UKRAINIAN MINISTRY OF PUBLIC HEALTH

Vinnytsya National Medical University n.a. M.I. Pyrogov

«APPROVED»
At the methodological meeting of the
internal medicine propedeutics
department
Chief of the department
____________ prof. Mostovoy Y.M.
«______»_______________ 200 ___ y.

Guidelines
for Third-year Students of the Medical Department

Subgect Propedeutics of the internal medicine

Modules 1,2
Enclosure module № 1-5
Course 3
Faculty Medical № 1

Methodical recommendations are made in accordance with educationally-qualifying

descriptions and educationally-professional programs of preparation of the specialists ratified
by Order MES of Ukraine from 16.05 2003 years № 239 and experimentally - curriculum, that is
developed on principles of the European credit-transfer system (ECTS) and Ukraine ratified by
the order of MPH of Ukraine from 31.01.2005 year № 52.

Vinnytsya- 2009
 TOPIC 1
Main complains of the patients with respiratory diseases. Management of
patients and writing anamnesis part of the case history
1. Importance of the topic
Inquiring patients is the basic, informative method of examination. It is the first
interaction between the patient and doctor. If it has been done correctly, it provides
valuable information that cannot be obtained in any other way. It allows recognizing
symptoms of disease and points, in the most cases, diagnostic search on the right way.
If patient suffers from the respiratory diseases he has a lot of specific and general
symptoms that must be reveal and rightly assess. It is very important part of the
diagnostic process.

2. Concrete aims:
─ asking about main respiratory symptoms
─ refinement respiratory symptoms
─ taking medical history
─ assessment of the obtained data

3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the airways and lungs, their blood supply and
innervation
Normal physiology Mechanics of breathing, gas exchange
Histology Ontogenesis of the respiratory tract, histological structure of
the respiratory tract and alveoli
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Definition
Wheezing Whistle and noise breathing with feeling breathlessness
Dyspnea Difficult breathing
Cough Reflective act for self-cleansing of the airway from physiologic or pathologic
contains
Hemoptysis Coughing up blood
Smoking Amount of cigarettes that patient smoke in a day multiply to number of
history smoking years and divide to 20 (pack/years)

4.2. Theoretical questions:

1. Rules of the interviewing respiratory patient.
2. Main respiratory symptoms
3. What is cough? Its refinement, features at the respiratory patients.
4. What is dyspnea? Its refinement, features at the respiratory patients.
5. What is wheezing? Which syndrome and diseases can it appear in?
6. What is hemoptysis? How is it differenced from lung bleeding?
7. Features of the chest pain in case of the respiratory diseases.
8. Peculiarities of taking history respiratory patients.
9. Assessment of the obtaining data during inquiring respiratory patient.
 4.3. Practical task that should be performed during practical training
1. Inquiring patient about respiratory symptoms
2. Refinement of the respiratory symptoms
3. Taking history of the respiratory patient
4. Assessment subjective data revealed at the respiratory patient
5. Write a part of the case history the respiratory patient.

Topic content
The main specific complaints of the respiratory patients are cough, sputum production,
dyspnea, wheezes, chest pain, and hemoptysis.
Cough (tussis) is a difficult reflex-protective act that arises up at the irritation of areas
cough:
 larynx,
 bifurcation of trachea and bronchi,
 gullet,
 pleurae sheets,
 external acoustic ducts.
There are many different factors (sputum, mucus, blood, dust, toxic gases, pieces of
meal and other) can provoke cough.
Cough occurs due to inflammatory, mechanical, chemical, thermal irritation of cough
receptors. In case of inflammation, exudative processes irritate the mucous membrane of the
respiratory tract (laryngitis, tracheitis, bronchitis, and bronchiolitis) as well as from the alveoli
(pneumonia, lung abscess). Mechanical irritants are small particles breathed in with the air
(dust) or disturbance of the respiratory tract patency due to compression or increased tone.
Thermal irritants are very cold or very hot air. Chemical irritants are gases with strong odor,
including cigarette smoke.
The clinical description of cough relies to its character, timing and sputum production.
According to the rhythm, three forms of cough can be distinguished: a cough is
permanent, periodic and fit-like. Permanent cough occurs in laryngitis, acute bronchitis,
bronchogenic tumor of the lungs and in certain forms of tuberculosis.
Periodic cough is characteristic of influenza, pneumonia, pulmonary tuberculosis, and
chronic bronchitis.
Certain aspects of the timing of coughing may give useful diagnostic clues. Morning
cough is characteristic chronic bronchitis and sometimes asthma. Nocturnal cough is
characteristic of tuberculosis, limphogranulomatosis, and tumor. Evening cough can happen at
the patients with pneumonia and acute bronchitis.
As to the character, the cough can be dry (without sputum, tussis sicca) and productive
or moist (with sputum, tussis humida). Dry cough is observed in bronchitis, pleura irritation,
miliary tuberculosis, in affection of the bronchopulmonary lymph nodes (pressure on the vagus
nerve), whooping cough, asthma; Productive cough is present in bronchitis, pneumonia, lung
tumor, purulent diseases of the lungs, bronchiectasis.
As to the timber, there are several patterns:
1) hacking cough, short and long, usually is accompanied by a painful mimic, is observed
in dry pleurisy, initial stages of pleuropneumonia;
2) stridor in trachea compression with a tumor, goiter, in hysteria, laryngeal diseases;
4) hoarse — in inflammation of the vocal cords;
5) soundless — in ulceration, edema of the vocal cords, general malaise.
According to perspective of the conditions causing cough or the phenomena
accompanying the cough, the following types can be distinguished:
1) cough caused by the changes in the position, observed when cavities in the lungs are
present (bronchiectasis, caverns, abscess, gangrene of the lungs);
2) cough associated with meals (especially when food particles are present in the
sputum), is seen when the esophagus is joined with the trachea or bronchus (esophageal
cancer perforated to the respiratory tract);
3) cough accompanied by abundant sputum discharge, characteristic for emptying
cavities, perforation of the abscess or empyema to the bronchus;
4) cough accompanied by vomiting, observed in whooping cough, pulmonary
tuberculosis, chronic pharyngitis.
The character of the sputum may be helpful in the differential diagnosis. Thus, a cough
producing frothy, pink-tinged sputum occurs in pulmonary edema; clear, white, mucoid sputum
suggests viral infection or longstanding bronchial irritation; thick, yellowish or pus-containing
(purulent) sputum suggests a bacterial infectious cause; rusty sputum suggests pneumococcal
pneumonia; blood-streaked sputum suggests tuberculosis, bronchiectasis, carcinoma of the
lung, or pulmonary infarction. Large amounts (copious) sputum is characterized bronchiectasis,
lung abscess.
Hemoptysis (haemoptoe). Hemoptysis is blood discharge at cough. If patient
expectorates more than 50 ml blood in a day this condition is named pulmonary bleeding. This
may be caused by the diseases of the lungs, airways (bronchi, trachea, larynx), cardiovascular
system.
The expectoration of blood or of sputum, either streaked or grossly contaminated with
blood, may be due to:
1) escape of red cells into the alveoli from congested vessels in the lungs (acute
pulmonary edema);
2) rupture of dilated endobronchial vessels that form collateral channels between the
pulmonary and bronchial venous systems (mitral stenosis);
3) necrosis and hemorrhage into the alveoli (pulmonary infarction);
4) ulceration of the bronchial mucosa or the slough of a caseous lesion (tuberculosis);
minor damage to the tracheobronchial mucosa, produced by excessive coughing of any cause,
can result in mild hemoptysis (viral infection);
5) vascular invasion (carcinoma of the lung);
6) necrosis of the mucosa with rupture of pulmonary-bronchial venous connections
(bronchiectasis).
Massive hemoptysis may also be due to rupture of a pulmonary arteriovenous fistula;
exsanguinating hemoptysis may occur with rupture of an aortic aneurysm into the
bronchopulmonary tree.
Hemoptysis associated with shortness of breath suggests mitral stenosis. Blood-tinged
sputum in patients with mitral stenosis may be due to transient pulmonary edema.
A history of hemoptysis associated with acute pleuritic chest pain suggests pulmonary
embolism with infarction.
Recurrent hemoptysis in a young, otherwise asymptomatic woman favors the diagnosis
of bronchial adenoma.
Hemoptysis associated with congenital heart disease and cyanosis suggests
Eisenmenger syndrome.
A history of recurrent hemoptysis with chronic excessive sputum production suggests
the diagnosis of bronchiectasis.
 Hemoptysis associated with the production of putrid sputum occurs in lung abscess,
whereas hemoptysis associated with weight loss and anorexia in a male smoker suggests
carcinoma of the lung.
When blunt trauma to the chest is followed by hemoptysis, lung contusion is the
probable cause.
A history of drug ingestion may be helpful in elucidating the etiology of hemoptysis; e.g.,
anticoagulants and immunosuppressive drugs can cause bleeding.
The blood may be bright red (in pulmonary tuberculosis, bronchogenic lung cancer,
actinomycosis, vasculitis, bronchiectasis) or rusty-colored (in pleuropneumonia, lung
infuriation) due to decomposition of the erythrocytes and hemosiderin formation.
Dyspnea (dyspnoea) is the subjective sensation of shotness of breath, often
exacerbated by exertion. May be due to
─ lung diseases: interstitial (pneumonia, tuberculosis, pulmonary emphysema,
peripheral lung cancer, idiopatic fibrous alveolitis, etc.), airways (COPD, Central
lung cancer, bronchial asthma, foreign body) and pleura affecting (pleura
obliteration, pleural effusion, pneumotorax, etc.),
─ cardiovascular diseases (mitral stenosis and other valve diseases, left ventricular
failure, pulmonary embolism),
─ anatomical – due to diseases of chest wall, muscles, nerves (kifosis, scoliosis,
myositis, neuritis, ribs fracture, obesity),
─ other – thyrotoxicosis, ketoacidosis, aspirin poisoning, anemia, psychogenic, ets.
Three types of dyspnoea can be distinguished as to the phase of respiration in which
the patient has difficulties: in difficult inspiration — inspiratory, in difficult expiration —
expiratory, in simultaneous difficulties in both breathing in and out — mixed dyspnoea.
 Inspiratory dyspnea (dyspnoea inspiratoria) occurs commonly at patients with
cardiovascular diseases (left ventricular failure) and sometimes appears in prolapse of the
tracheal or bronchial mucosa.
 Expiratory dyspnea (dyspnoea expiratoria) develops when opening of the small bronchi is
narrowed due to inflammatory swelling of the mucous membrane, bronchospasm (bronchial
asthma), hypersecretion which prevents reverse movement of the air from the alveoli.
 Mixed dyspnoea occurs in considerable reduction of the respiratory surface of the lungs
(thrombosis of the pulmonary artery, pneumonia, bronchiolitis, pleural effusion, pneumotorax
etc.).
Wheezes are whistle and noise breathing with feeling breathlessness caused by air passing
through narrowed airways and heard for a distance by patient. They are symptoms of bronchial
asthma, COPD.
During the attack of breathlessness patient occupies the forced position with fixing of
overhead humeral belt. The attack is accompanied by a fit-like dry cough. Exhalation is labored
with whistle and noise sounds. Its duration is from a few minutes till 24 hours. The attack is
stopped after the removal of allergen and using broncholitic medications. At the end of attack a
patient expectorates viscid glassy sputum.
In respiratory diseases, pleura involvement results in a chest pain (dolor in pectore),
because the pleura contains sensitive nerve endings, which are absent in the lung tissue.
The location of the pathological focus is responsible for the place of the pain. In dry
pleurisy the pain develops in the low lateral portions of the chest, "pain in the side". When the
diaphragmatic pleura are involved, the pain is felt in the abdomen and mimics such diseases as
appendicitis, acute cholecystitis, and pancreatitis. The pleural pain is piercing, becomes worse
on deep breathing, cough and when the patient is lying on the healthy side. In diaphragmatic
 pleurisy and spontaneous pneumothorax the pain is usually acute and intensive, accompanying
with dyspnea.
Features of history
During taking disease history patient should be asking about first symptoms, when they
started, what seemed to provoke them, how severe they are, what seems to make they better,
have they ever happened before, and the of any medications used to treat them. Subsequent
interviews should focus on any changes in the symptoms that may have occurred with
threatment or simply with the passing of time.
During taking life history risk factors of the respiratory diseases must be assessed:
 Humidity of apartment, overcooling
 Contact with patients who has respiratory inflectional diseases,
 Traveling, living in hotels, fast changing climate and other situations which require increasing
adaptation of patient,
 Professional to harmfulness (poultry houses, miners, chemical and cements productions
sewing factories and other)
 Smoking history more than 10 pack/year (amount cigarettes in a day*number years of
smoking/20)
 Family history of the respiratory disease (asthma, COPD, diopatic fibrosis alveolitis, ect)
 Allergy: main causes, allergic symptoms, investigations, specific treatment and its effectivness.

Conclusions of subjective examination of the respiratory patient

1. Highlight the main complaints indicated injured system.
2. Note the character of disease (chronic, acute, or subacute).
3. Indicate the most likely causes of the disease development.

Materials for self-control (added)

7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova. Propedeutics to internal medicine, Part 1. –

Vinnytsya: NOVA KNYHA, 2006. – p. 15-18, 70-76.
o Barkauskas VH, Baumann LL, Darling-Fisher CS. Health and physical assessment, ed 3, St
Louis, 2002, Mosby.
o Wilkins RL, Sheldon RL, Klider SJ. Clinical assessment in respiratory care, ed 4, St Louis, 2000,
Mosby.
 Test for self-control
1. What are the respiratory symptoms?
A. Chest pain, cough, dyspnea, wheezes, haemoptysis.
B. Pain in the heart region, palpitation, intermissions, oedema
C. Headache, dizziness, dysphagia, nausea, vomiting.
D. Pain in the right subcostal region, bitter taste, brown urine, skin itching, jaundice.
E. Back pain, dysuria, ishuria, eyes oedema, weakness.
2. What are the respiratory symptoms?
A. Abdominal pain, nausea, vomiting
B. Heartburning, faint (syncope), palpitation
C. Cough with rusty sputum, chest pain, dyspnea
D. Swelling abdomen, constipation, melena
E. Oedema, dysuria, haematuria
3. What feature does pleural pain have?
A. Be caused by physical extension
B. Radiate to the right hand
C. Appears and increases due to cough and deep breathing
D. Radiate to the left hand and scapula
E. Duration under 15 minutes.
4. What are the cough causes?
A. Irritation of the larynx receptors
B. Irritation of the trachea and bronchus receptors
C. Irritation of the pleural receptors
D. All mentioned above
E. Northing from above
5. If patient has laryngitis his cough is characterized with
A. harsh and hoarse sound
B. absent of sputum
C. it is permanent
D. it is loud
E. all mentioned above.
6. If patient has clear, thick sputum it is named
A. Mucoid
B. Purulent
C. Copious
D. Fetid
E. Hemoptysis
7. Chronic expectorating copious sputum is observed at patient with
A. Acute bronchitis
B. Asthma
C. Atelectasis
D. Emphysema
E. Bronchiectasis
8. What is an objective dyspnea?
A. Disorders of the respiratory rate
B. Disorders of the respiratory depth
C. Disorders of the respiratory rhythm
D. Disorders of the respiratory rate, depth, rhythm
E. Northing from above
9. Which type of dyspnea is observed at the patients with obstructive syndrome?
A. Expiratory
B. Inspiratory
C. Mixed
D. Changing
E. All mentioned above.
10. Which types of dyspnea do you know?
A. Mixed
B. Expiratory
C. Inspiratory
D. All mentioned above
E. Northing from above
11. Sputum production that contains pus is described by what term?
A. Purulent
B. Fetid
C. Copious
D. Colored
E. None of the above
12. Which of the following characteristics is not typical of pleuritic chest pain?
A. Increases with deep breathing
B. Increases with coughing
C. Radiates to the jaw
D. Is located laterally
E. Diminishes with splinting of the affected side
13. Which type of pulmonary problem usually causes a breathing pattern with a
prolonged expiratory time?
A. Chronic obstructive pulmonary disease
B. Atelectasis
C. Pulmonary edema
D. Pneumonia
E. Pleural effusion.
14. Inspiratory dyspnea is –
A. Difficult breathing during exhalation
B. Difficult breathing during inhalation
C. Difficult breathing during exhalation and inhalation
D. Difficult breathing during hyperventilation
E. Northing from above
15. Expiratory dyspnea is –
A. Difficult breathing during exhalation
B. Difficult breathing during inhalation
C. Difficult breathing during exhalation and inhalation
D. Difficult breathing during hyperventilation
E. Northing from above
16. Mixed dyspnea is –
A. Difficult breathing during exhalation
B. Difficult breathing during inhalation
C. Difficult breathing during exhalation and inhalation
D. Difficult breathing during hyperventilation
E. Northing from above
 17. Whistle and noise breathing with feeling breathlessness is named …
A. Dyspnea
B. Respiratory noise
C. Musical breathing
D Wheezing
E. All mentioned above
18. What quantity of the blood is characterized hemoptysis?
A. 20-50 ml
B. 60 – 70 ml
C. 140 - 250 ml
D. All mentioned above
E. Northing from above
19. Lung bleeding is a pathological condition when the blood expectorates from airways.
What quantity of the blood is characterized lung bleeding?
A. 15 - 20 ml
B. 30–40 ml
C. 240 - 250 ml
D. All mentioned above
E. Northing from above
20. Amount of cigarettes that patient smokes in a day multiply to number of smoking
years and divide to 20 (pack/years) use for calculating …
A. Smoking history
B. Smoking consumption
C. Smoking habit
D. Smoking abuse
E. All mentioned above.

Control questions
1. Main respiratory symptoms
2. What is cough? Its refinement, features at the respiratory patients.
3. What is dyspnea? Its refinement, features at the respiratory patients.
4. What is wheezing? Which syndrome and diseases can it appear in?
5. What is hemoptysis? How is it differenced from lung bleeding?
6. Features of the chest pain in case of the respiratory diseases.
7. Peculiarities of taking history respiratory patients.
8. Assessment of the obtaining data during inquiring respiratory patient.

Practical tasks
1. Asking patient about respiratory symptoms as main complaints
2. Refinement respiratory complains and their assessment
3. Taking disease history and its assessment
4. Taking life history patients with respiratory diseases and its assessment
5. Making conclusions after inquiring respiratory patient
6. Writing part of case history of the respiratory patient

Situation tasks
Task 1
25-year-old male patient suddenly felt breathlessness with audible whistle noise after
contact with dust. He noted similar respiratory disorders periodically during last 7 years.
1. Which respiratory symptom does patient have?
2. How should the symptom be specified?
3. What parts of life history are the most informative in this case?
Task 2
67-year-old female patient complains of dyspnea, cough and left side chest pain. The
symptoms appeared after hard work and overcooling 3 days before.
1. What additional questions should you ask for refinement the symptoms?
2. Is the disease acute or chronic? What should you ask for obtaining this data?
3. How may origin of the chest pain be established using interviewing?
Task 3
34-year-old female was admitted to pulmonology department with severe mixed dyspnea,
high fever (39°C), cough with rusty sputum, piercing chest pain.
1. What questions should be asked for refinement chest pain?
2. How should the anamnesis morbi be collected?
3. What parts of the anamnesis vitae must be take into account for prescribing treatment?
Task 4
70-year-old male patient notes increasing dyspnea, cough with purulent sputum production
during last week after overcooling. Mild dyspnea and periodical morning cough disturbed
patient long time (15 years). Patient is long time smoker (has been smoking 55 year, on
average 1 pack cigarettes in a day).
1. What type of dyspnea does patient have?
2. How is present condition of the patient named?
3. Calculate patients smoking history parameter.
 TOPIC 2
General visual inspection, visual inspection and palpation of the chest.
Diagnostic value
1. Importance of the topic
Visual inspection of patients is one of the basic, informative methods of examination.
Doctor performs it during the first contacts with the patient and inquiring him. Doctor
is assessing patient general condition, its severity and forming the first opinion about
patient. It allows recognizing visual signs of disease and points diagnostic search on
the right way. Respiratory patients sometimes have a lot of specific signs of diseases
that must be reveal and rightly assess. It is very important part of the diagnostic
process.

2. Concrete aims:
─ Master principles and methods of the general visual inspection
─ Revealing main signs of the respiratory diseases during general visual inspection
─ Performing and assessing static visual inspection of the chest
─ Performing and assessing dynamic visual inspection of the chest
─ Master method of palpation of the chest
─ assessment of the data obtained at palpation of the chest

3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the airways and lungs, their blood supply and
innervation
Normal physiology Mechanics of breathing, gas exchange in the lung and tissues of
system organs
Histology Ontogenesis of the respiratory tract, histological structure of
the respiratory tract and alveoli
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Definition
Active position the patient can change his position as he wants
Passive taken due to exclusively the law of gravity
position
Forced taken instinctively or consciously to elicit the suffering
position
Constitution Body-building
Cyanosis Bluish color of the skin
Hyperemia Reddish color of the skin due to increased blood circulation
Tachypnea Increased respiratory rate
Bradypnea Decreased respiratory rate
Barrel chest Increased rounded shape of the chest with horizontal position of the ribs,
equal front and side size
Paralytic chest Diminished and flat chest with vertical position of the ribs
Terminal types Breathing patient with severe injury of the respiratory center in the brain
of breathing (Cheyne-Stokes, Biot’s, Grocco’s, Kussmaul respiration)
 4.2. Theoretical questions:
10. Rules of general visual inspection of the respiratory patient.
11. Main sings of the respiratory disease that can be revealed at visual examination.
12. Static visual inspection of the chest
13. Types of the normal chest shape, their description.
14. Barrel chest, its description and diagnostic value.
15. Paralytic chest its description and diagnostic value.
16. Pigeon and funnel chests, their description and diagnostic value.
17. Scoliotic and kyphoscoliotic chest, its description and diagnostic value.
18. Dynamic visual inspection of the chest, rules and diagnostic value.
19. Pathologic types of breathing, their diagnostic value.
20. Rules of chest palpation, diagnostic value

4.3. Practical task that should be performed during practical training

6. Performing general visual inspection of the respiratory patient
7. Recognizing respiratory signs at visual examination.
8. Performing static visual inspection of the chest and assessing obtained data
9. Performing dynamic visual inspection of the chest and assessing obtained data
10. Palpation of the chest and assessing obtained data
Topic content
General inspection
The patient should be undressed; the examination room should be warm and well lit. An
anthropometric caliper and a measuring tape are used to do anthropometry.
The appearance of the patient is described: general condition, carriage, gait, position in
bed, consciousness, expression of the face, constitution, stature, chest circumference at calm
breathing, skin, visible mucosa, and conjunctiva, subcutaneous fat, edemas, muscles, bones,
joints.
General patient's condition may be good, satisfactory, moderate grave, grave, extremely
grave. The criteria's of patient's condition are the following clinical features: consciousness,
posture, gait, the facial expression, weight, and mental condition.
Good patient's condition is characterized by clear consciousness, active posture, free gait,
sensible facial expression, sufficient weight, and good mood. This condition occurs in patients
with remission of chronic disease favorable course of a disease, or during recovery.
Satisfactory patient's condition (status morboacili) is characterized by clear consciousness,
active or active with restriction posture, free or partial deranged (specific) gait, sensible facial
expression, and adequate mental reaction. This condition occurs in patients with remission of
prolong chronic disease, or during recovery from acute disease.
Moderate condition (status ingravescens) is characterized by deranged consciousness,
alteration of facial expression and posture (forced), uncertain gait, partial deranged mental
state and may be observed in patients with recurrence of chronic disease, acute diseases, or
due to the traumas and poisoning.
Grave condition (status morbogravi) is characterized by disorders of practically all clinical
features: deranged consciousness, changed facial expression (fear, suffer, hopelessness,
indifference). The patients have forced or passive posture, loss of weight, edema, and
inadequate mental state. Grave condition is observed in patients with infections and oncologic
diseases, heart failure, disorders of renal, liver functions, abnormalities of nervous and
endocrine systems, after operations, traumas.
Extremely grave condition (status gravissimus) is characterized by unconsciousness,
passive posture, and indifferent facial expression and observes in the patient with coma, shock,
and agony.
 The general condition of the patient is characterized by his/her position in bed and the
state of the consciousness.
Consciousness (sensorium) may be clear or deranged. The criteria's of consciousness
condition are the following features: orientation to the surroundings, adequate answers,
concentrated attention, reflexes, and pupil reaction on light.
Clear consciousness (sensorium lucidum) is characterized by adequate behavior, correct
orientation to the surroundings, timely answer to the question, and preservation of all reflexes.
The deranged consciousness develops due to the different causes: disorders of cerebral or
cardiac circulation; endogenic and exogenic intoxication; infectious affections; hormonal,
mineral, metabolic abnormalities; and traumas of the brain.
The deranged consciousness is divided into two groups - depressed (stupor, sopor, coma)
and excited consciousness (irritative disorder: hallucinations and delirium).
Attention should be paid to gait and carriage. In healthy persons the carriage is straight,
the gait is steady.
Position in bed. Three types of the patient's position are distinguished: active, passive,
forced.
An active position is that which the patient can change as he needs.
A passive position is taken due to exclusively the law of gravity; this is the sign of poor
condition of the patient.
A forced position is taken instinctively or consciously to elicit the suffering.
These positions can be specific and an experienced physician may determine the
character of the disease seeing the patient's position.
In dry pleurisy, lung abscess, bronchiectasis, the patient prefers to lie on the affected
side. In dry pleurisy, this position relieves the pain because it limits pleura movement; in
abscess, it relieves coughing because the content of the cavity does not get to the bronchial
tree.
During an attack of bronchial asthma the patient sits upright or resting the hands on the
edge of the table of chair, this position allows mobilizing accessory respiratory muscles.
Constitution (body-build)
Definition of patient’s constitution includes assessing the shape of the body, developing
muscles by measuring their size and subcutaneous layer by measuring the thickness of the skin
fold in the area of the left hypochondrium. If the thickness of the fold is >2 cm, development of
the subcutaneous fat is abundant, if <0,7 cm, this is insufficient.
Frequent causes of weight loss are chronic diseases of the respiratory system (COPD,
tuberculosis) or cancer.
The findings of the constitution investigation as well as measuring the stature and chest
circumference allow determining the constitution type. Constitution is the entity of the
congenital and acquired morphological and functional features of the person formed during the
lifetime under the environmental influence. According to M.V. Chernorutsky, normosthenic,
asthenic and hypersthenic types are distinguished.
In normosthenic constitution all parts of the body are proportional.
Asthenic constitution (habitus asthenicus) is characterized by the following features:
longitudinal dimensions of the body prevail, the chest is narrow and flat, the neck is thin and
long, the extremities are long and thin, the skull is long, the muscles are inactive, the shoulders
are narrow, the subcutaneous fat is poorly developed.
In hypersthenic constitution (habitus hypersthenicus) transverse dimensions prevail, the
patients are stocky, the chest is wide, the neck is short, the extremities are short and wide, the
skull is wide, the muscles and subcutaneous fat are well-developed, early holding is typical.
Examination of the skin.
 It is necessary to pay attention to the color, humidity, turgor, presence of hemorrhages,
rashes, scars, the state of the body hair and venous system.
Color of the skin. The normal skin is pale pink due to development of the vascular
network of the skin, the amount of the blood in the capillaries, morphological and chemical
composition of the blood, skin thickness.
The skin can be cyanotic, pale, hyperemic.
In a number of respiratory diseases, i.e. pneumonia, emphysema, pneumosclerosis,
pulmonary tuberculosis, supportive conditions of the lungs, as well as in patients with
pulmonary insufficiency, the skin and mucous membranes are cyanotic. Acute development of
cyanosis is seen in pulmonary embolism and spontaneous pneumothorax. The cause of
cyanosis is disturbances of gas exchange in the lungs resulting in accumulation of increased
amount of reduced hemoglobin.
A pronounced paleness is present in excessive pulmonary hemorrhage, decaying lung
tumor, cavities, bronchiectasis, vasculitis (Goodpasture's syndrome, Wegener's syndrome).
At the patients with pleuropneumonia, cyanotic face can be associated with hyperemia.
Increased humidity is observed in fever.
Turgor is skin elasticity. This is determined by touching the skin and depends on the
degree of subcutaneous fat development and the amount of fluid in the skin. Decreased turgor
is present in severely ill patients with dehydration.
When examining the skeletal muscles it is necessary to determine the degree of
development (good, moderate, weak), local hypertrophy, atrophy, tenderness, spasms.
Muscular tone is determined by palpations, this can be preserved, decreased, increased.
Muscular tone is decreased can be at the chronic infection diseases of lungs, cancer. Muscular
atrophy is developed at the COPD patient.
The digits are inspected for clubbing (abnormal enlargement of the distal phalanges).
Clubbing is a nonspecific finding often associated with chronic respiratory diseases (cystic
fibrosis, bronchiectasis, hypoplasia, fibrosing alveolitis, mesothelioma), lung cancer and some
chronic cardiac disorders (e.g., congenital cyanotic heart disease). The exact mechanism for it
remains unknown.
Visual examination of the chest.
Visual examination should be performed following the order: from the front, sides and
back.
Doing a static examination the physician should pay attention to the size of the both
halves without consideration of their participation in respiration.
Normosthenic chest (thorax normosthenicus). The transverse and anteroposterior sizes
are proportional with the ratio of transverse to anteroposterior diameters measured at the
same level 0,65-0,75. The angle between the both costal arches (epigastric angle) is about 90°.
The ribs are directed slightly obliquely downward. The intercostal spaces can be noticed but not
clearly marked. Supra- and subclavicular fossae are moderately developed, the collarbones do
not jut out. The shoulder blades moderately fit the back with the hands down.
Asthenic chest (thorax asthenicus). Anteroposterior to transverse chest size ratio is <
0,65 therefore the chest seems flat and narrow. The ribs are directed downward. The angle
between the ribs is acute, intercostal spaces are wider than at norm and are clearly seen.
Supra- and subclavicular fossae are distinct, the collarbones are well seen. The shoulders are let
down (at an obtuse angle to the shoulders). The shoulder blades are stuck out (winged scapula,
scapulae alatae). Sometimes the end of the tenth rib is free (costa decimafluctuans).
Hypersthenic chest (thorax hypersthenicus). Anteroposterior to transverse ratio is > 0,75,
therefore the transverse section of the chest is close to circle (in norm it is close to oval). The
chest is wide. The ribs are horizontal. The epigastric angle is obtuse. The intercostal spaces are
narrow and poorly marked, sometimes not seen. Supra- and subclavicular fossae are poorly
seen. The hypersthenic chest is associated not only with the skeleton features but also good
development of the chest muscles.
Pathological shape of the chest results from the changes in the skeleton (congenital
anomalies), changes of the vertebral column due to pathological processes in it or various
chronic diseases of the lungs and pleura.
An emphysemic or barrel chest (thorax emphysemicus) resembles hypersthenic but its
features are more pronounced. Unlike the latter it results from emphysematous enlargement of
the lungs. Due to reduction of the lung tissue elasticity in lung emphysema, the lungs collapse
insignificantly on expiration; therefore the chest is constantly in an inspiratory state and
resembles a hypersthenic chest. The ribs are horizontal, the intercostal spaces are narrow,
supra- and subclavicular fossae are not seen, the epigastric angle is obtuse. Initially shape of
chest likes trapezium (wide in the lower part and narrow in the upper), late it becames lake
cylinder (round and wide in the lower and the upper part). This shape of the chest is common
for COPD, severe asthmatic and emphysema patients.
A paralytic chest (thorax paralyticus) resembles an asthenic chest. This is caused by
severe chronic diseases of the lungs (tuberculosis, pneumosclerosis, cystic fibrosis,
bronchoectasis) resulting in shrinkage and reduction of the lung mass. Visual examination of
the patients with a paralytic chest also reveals muscular dystrophy, asymmetry of collarbones,
unequal supraclavicular fossae, different levels of scapulas moving synchronically during the act
of respiration.
Other thoracic deformities of note include pectus carinatum (pigeon breast),
characterized by the upper ribs bending inward and thrusting the sternum outwards like the
keel of a ship. This shape of the chest is a result of abnormal skeleton formation in childhood in
the patient with rachitis.
The "funnel breast" of pectus excavatum (the reverse of carinatum) is characterized by a
impression in the lower portion of the sternum near the xiphoid process. Severe deformation
can diminish vital capacity; however, it is usually a mild, asymptomatic, congenital defect of
cosmetic concern only.
Pathological shapes of the chest caused by various deformities of the spin as a result of
injuries, tuberculosis of the spine, rheumatoid arthritis, etc. There are four types of spine
deformities are distinguished:
Scoliosis - lateral curvature of the spine, is most common. It develops in schoolchildren
due to bad habitual posture.
Kyphosis -backward curvature of the spine, occurs less frequently.
Lordosis - forward curvature of the spine, generally in the lumber region, occurs in rare
cases.
Kyphoscoliosis - combination of the lateral and backward curvature of the spine.
The examiner should pay special attention to an exaggerated thoracic and lumbar spinal
curvature (kyphosis and scoliosis) because these findings may limit lung expansion, thus causing
a significant restrictive defect.
Enlargement of one half of the chest is noticed in accumulation of a considerable
amount of fluid in the pleural cavity (exudate, transudate, blood, pus), gas (pneumothorax).
This is characterized by smoothing and protrusion of intercostal spaces, asymmetric location of
the collarbones and shoulder blades, delay in the movement of this half during the act of
respiration.
Diminution of one hemithorax is observed in generalized processes of the lung tissue
shrinkage due to connective tissue growth (pneumosclerosis) as a result of pneumonia,
tuberculosis, syphilis of the lungs, lung abscess, bronchiectasis, lung infarct, actinomycosis,
pleural adhesions or complete imperforation of the pleural fissure after resorption of exudate,
after surgical removal of the lung or its portion, in atelectasis (collapse of the lung or its lobe)
resulting from occlusion of a large bronchus with a foreign body or obturating tumor in the
lumen. In these conditions the air does not enter the lung and absorption of the air from the
alveoli causes diminution of the lung and the respective hemithorax.
Due to the diminution of one half, the chest becomes asymmetrical: the shoulder on the
side of the affection goes down, the collarbone and shoulder blade are lower, their movement
at deep breathing in and out is slow and limited; supra – and subclavicular fossa sink down.
More pronounced sinking down on one side depends on diminution of the lung apex at fibrosis
development.
Dynamic visual inspection
The type of respiration can be thoracic, abdominal, mixed.
Thoracic respiration is accomplished mainly by contraction of the intercostal muscles.
The chest expands and goes up, during breathing out it diminishes and goes down. It is chiefly
observed in women.
Abdominal respiration is accomplished with the diaphragm participation. On breathing
in it contracts and goes down increasing negative pressure in the thoracic cavity, the air quickly
fills the lungs. The abdominal wall goes forward due to increased intra-abdominal pressure. On
breathing out the diaphragm relaxes and goes up, the abdominal wall goes to its place. This is
chiefly observed in men.
Mixed type of respiration is accomplished with simultaneous work of the intercostal
muscles and the diaphragm. This can be seen in elderly persons and in some diseases of the
respiratory and abdominal organs. In women with dry pleurisy, pleural adhesions, myositis,
thoracic radiculitis, respiratory movements are accomplished with an additional aid of the
diaphragm due to reduction in the contractile function of the intercostal muscles.
Respiratory rate is assessed counting the motions of the chest or abdominal wall. The
patient should not notice the calculation because, when his attention is attracted by the
procedure, he may change the rate. The physician holds the patient's hand as if counting the
pulse or puts his hand on the epigastric area. For accurate counting, respiratory rate should be
done for at least half a minute. At rest, an adult makes 16 —20 respiratory movements per
minute.
Respiratory rate may increase (tachypnea) or decrease (bradypnea).
Causes of tachypnea:
- physiological (at excitement, during and immediately after physical load, meals).
- The disease with reduction of the respiratory surface (pneumonia, tumors,
granulomas of the lungs, tuberculosis, vasculitis, bronchiolitis)
- Insufficient gas exchange and accumulation in the blood of carbon dioxide, which
stimulates the respiratory center.
- insufficient depth (surface respiration) in the result of difficult contraction of the
intercostal muscles or diaphragm in acute pains (dry pleurisy, acute myositis,
intercostal neuralgia, rib fracture or tumor metastases to the ribs)
- at acute increasing intra-abdominal pressure and high position of the diaphragm
(ascites, meteorism, pregnancy);
- at paralysis of the diaphragm; sometimes in hysteria
- loss of the lung elasticity (severe pulmonary emphysema),
- at the cardiovascular diseases,
- severe anemias causing hypoxemia.
Pathological reduction of the respiratory rate (bradypnea) occurs when the function of
the respiratory center is inhibited and its excitability is decreased. This can be due to several
causes:
- increased intracranial pressure due to brain tumors,
 - hemorrhage to the brain,
- brain edema,
- meningitis,
- action of toxic substances accumulating in the blood as a result of uremia,
- liver or diabetic coma,
- infectious diseases.
Depth of respiration is determined by the volume of the air inhaled and exhaled at rest.
In healthy adults the volume of air participating in respiration is about 500 ml. As to the depth,
respiration can be superficial or deep. Superficial respiration is observed in pathological
increase of the respiratory rate, when inspiration and expiration become shorter. In the
majority of cases, deep breathing is accompanied by pathological reduction of the respiratory
rate. Especially deep is so-called "Kussmaul's breathing".

a) normal respiration; b) accelerated superficial respiration;

c) atactic respiration (Biot's); d) Cheyne-Stokes respiration.

This can appear in patients with acidosis (diabetic, uremic, hepatic coma).
Rhythm of respiration. The respiration of healthy individuals is rhythmical, the depth
and duration of inspiration and expiration phases are constant. When the respiratory function
is disturbed, arrhythmic respiration can develop. Separate respiratory maneuvers are
performed with different frequency, the depth of separate respiratory maneuvers becomes
unequal. A respiratory center dysfunction can result in such dyspnea in which the respiratory
pause or a short delay (apnea) in respiration develop after a definite number of respiratory
maneuvers. This respiration is called periodic (e.g. Cheyne-Stokes and Biot's respiration).
Cheyne-Stokes respiration. After a prolonged (from several seconds to 1 minute) pause,
a noiseless superficial respiration increasing in depth and getting noisier develops and reaches
its maximum with the 5th—7th maneuver, then it decreases in the same manner and ends with a
short pause. The patients are poorly oriented during the pause or completely loose conscience,
this restores with restoration of the respiratory maneuvers. This rhythm disorder is observed in
the diseases causing acute orchronic brain hypoxia or in severe intoxications. It frequently
appears during sleep and can be noticed in elderly patients with marked atherosclerosis of the
brain arteries.
Biot's respiration is characterized by rhythmic deep respiratory maneuvers alternating
with long (from several second to one minute) pauses. It can be observed in meningitis, in
agonal states with profound disturbance of the brain circulation.
Grocca's wave-like respiration resembles Cheyne-Stokes respiration but instead of the
pause, weak superficial respiration followed by increase in the depth and later reduction in the
depth of respiratory maneuvers, is observed. This type of arrhythmic dyspnea can be
considered an early stage of the pathological processes causing Cheyne-Stokes respiration.
Doing a dynamic observation the examiner should pay abstention to the participation of
each half in the act of respiration.
 Examining the chest, it is necessary to pay attention to participation of the accessory
respiratory muscles in the act of respiration.
Participation of the accessory muscles is easily determined by the movement of the
wings of the nose, contraction of the intercostal ribs and m. sternocleidomastoideus. The latter
can hypertrophy and look like dense thick bands.
Participation of the accessory muscles in the act of respiration can be observed during
an attack of bronchial asthma, in pulmonary emphysema and some other diseases of the lungs
accompanied by disorders of the external respiration.
Examining the chest the physician should pay attention to the rate, depth, type, and
rhythm of respiration.
Chest palpation
Chest palpation reveals its elasticity, voice resonance, tenderness of the pleural points
and Potenger’s sign.
Chest palpation should be done with the both hands; the palmar surfaces are put on the
symmetrical areas of the left and right halves of the chest. This position of the hands allows
following the respiratory excursion, eliciting delay in one half, and determining the epigastric
angel. Palpation allows localizing the pain in the chest and determining the area. In rib fracture,
the pain is felt on a limited area, only in the site of the fracture, dislocation of the fragments
will give a crackling sound.
Tenderness of the pleural points is revealed by finger’s pressing along both sides of
vertebral column, middle axillary line and sternum where the subcostal nerves closer to skin.
These points are painfull if patient’s pleura infolved to inflammatory process (lobar pneumonia,
dry pleurisy, neuritis).
Resistance and elasticity of the chest are determined pressing the chest with the hands
in the posterior direction and at the sides with palpation of the intercostal spaces. In healthy
subjects this maneuver gives a feeling of elasticity and pliability. When fluid (transudate,
exudate) or tumor is present in the pleural cavity, the intercostal spaces over the affected areas
become rigid. Increased rigidity is generally observed due to ossification of the costal cartilages
and development of pulmonary emphysema. In this case, increased resistance is felt at
compression of the chest in the anteroposterior and lateral direction.
Voice resonance (fremitus pectoralis) is used to determine the force of the voice
radiation to the surface of the chest. Voice resonance is assessed with the both hands on
strictly symmetrical areas of the chest. The patient is asked to pronounce loudly the words
giving the strongest vibration of the voice. The vibration of the vocal cords is transmitted to the
underlying air in the bronchi, bronchioles and chest. If we use the same words for the test, we
can obtain a standard for comparison of the voice resonance. The pitch of voice should be low;
the lower the pitch, the better the vibrations radiate. The whole palmar surfaces of the
physician's hands should be pressed to the chests.
Voice resonance in physiological conditions. In men the voice resonance is stronger than
in women and children; in women with a high-pitched voice and in children the voice resonance
can be absent. Voice resonance is stronger in the upper portions of the chest and on the right
side, especially over the right apex, where the right shorter bronchus creates better conditions
for vibration radiation; on the left side of the chest and in the lower portions, the resonance is
weaker. This normal variability should always be born in mind. In pathological conditions of the
respiratory organs the resonance can increase, decrease or is not felt.
Increased voice resonance is observed in consolidation of the lung (lobular pneumonia,
infarction of the lung, tuberculosis, compression atelectasis).
 Decreased voice resonance is noted in patients with a weak voice (affection of the vocal
cords, severe illness), when a moderate amount of fluid or air in present in the pleural cavity, in
obturation atelectasis, in thickened chest wall (edema, fat).
Voice resonance may be completely absent when a large amount of fluid or air is
present in the pleural cavity.
Palpation sometimes allows to feel friction rub (in abundant accumulations of fibrin of
the pleura), dry buzzing rales due to bronchitis and crepitation due to subcutaneous
emphysema.
Potenzer’s sign is determined by symmetrical palpation of the trezius muscles. In a norm
or negative Potenzer’s sign palpation is painfulness and physician ’s sensation of tone and mass
of muscles is similar. Positive Potenzer’s sign is characterized with painful palpation and/or
changed tone, mass of muscle on affected side. The sign may be positive in case of lobar
pneumonia, tuberculosis, dry pleurisy and etc.

Materials for self-control (added)

7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –

Vinnytsya: NOVA KNYHA, 2006. – p. 19-20, 24-27, 30, 33-35, 39-44, 76-89.
 Test for self-control
1. If patient’s respiratory rate is 32 per minute he has…
a. Tachypnea
b. Bradypnea
c. Apnea
d. Polypnea
e. Dyspnea
2. What types of breathing does healthy man have in a rest?
a.Abdominal breathing
b.Thoracic breathing
c. Mixed breathing
d. All mentioned above
e. Northing from above
3. If patient doesn’t have respiratory moving his condition is named:
a. Tachypnea
b. Bradypnea
c. Apnea
d. Polypnea
e. Dyspnea
4. Kussmaul ‘s breathing is…
a. Disorder of breathing depth
b. Disorder of the respiratory rate
c. Disorder of the respiratory rhythm
d. Disorder of the respiratory types
e. Hyperventilation syndrome
5. Cheyne-Stokes breathing is …
a. Disorder of breathing depth
b. Disorder of the respiratory rate
c. Disorder of the respiratory rhythm
d. Disorder of the respiratory types
e. Hyperventilation syndrome
6.What is the normal respiratory rite in a rest?
a. 12-14 per 1 minute
b. 16-20 per 1 minute
c. 10-12 per 1 minute
d. 20-24 per 1 minute
e. 24-28 per 1 minute
7. What types of breathing does healthy woman have in a rest?
a. Abdominal breathing
b. Thoracic breathing
c. Mixed breathing
d. All mentioned above
e. Northing from above
8. If patient’s respiratory rate is 10 per minute he has…:
a. Tachypnea
b. Bradypnea
c. Apnea
d. Polypnea
e. Dyspnea
9. What types of breathing do you know?
a. Abdominal breathing
b. Thoracic breathing
c. Mixed breathing
d. All mentioned above
e. Northing from above
10. Which of the following conditions is associated with increased vocal fremitus?
a. Pneuomonia
b. Emphysema
c. Pneumothorax
d. Pleural effusion
e. Bronchial asthma
11. Which of the following condition is associated with asymmetrical diminished vocal
fremitus?
a. Pneumonia
b. Emphysema
c. Bronchial asthma
d. Chronic bronchitis
e. Pleural effusion
12. Which of the following condition is associated with painfulness of the pleural points?
a. Lobar pneumonia
b. Bronchial asthma
c. Pleural effusion
d. Emphysema
e. Chronic bronchitis
13. Which of the following condition is associated with increased chest resistance?
a. acute bronchitis
b. focal pneumonia
c. COPD
d. mild bronchial asthma
e. all mentioned above.
14. What does the general inspection start with?
a. Skin
b. Position in bed.
c. General condition
d. Edemas
e. Joints
15. What kind of posture is observed at the bronchial obstruction?
a. Upright
b. Sitting position fixing the shoulder girdle
c. Orthopnoea
d. Sitting posture bending forward
e. Knee-elbow posture
16. If patient skin has diffuse bluish tint, it is named:
a. Diffuse cyanosis
b. Diffuse erythema
c. Acrocyanosis
d. Pathological pallid skin
e. Northing mentioned above.
17. What mechanisms are caused by the cyanosis?
a Secondary pulmonary hypertension
b. Restricted pulmonary circulation
c. Artery-venous blood shunting
d. Primary pulmonary hypertension
e. Everything mentioned above
18. What kind of posture is observed at the left dry pleurisy?
a. Upright
b. Sitting position fixing the shoulder girdle
c. Orthopnoea
d. On the left side
e. Sitting posture bending forward
19. What kind of posture is observed at the right pleural effusion?
a. Orthopnea
b. On the right side
c. Sitting position fixing the shoulder girdle
d. On the left side
e. Sitting posture bending forward
20. What shape of the chest can be observed at the patient with chronic tuberculosis?
a. Normosthenic
b. Asthenic
c. Barrel
d. Paralytic
e. "Funnel breast"
21. What shape of the chest can be observed at the patient with emphysema?
a. Normosthenic
b. Asthenic
c. Barrel
d. Paralytic
e. "Funnel breast"
22. How is chest shape changed at the left side pneumothorax?
a. Enlarged left part of the chest
b. Reduced left part of the chest
c. Enlarged right part of the chest
d. Reduced right part of the chest
e. Not changed
Control questions
1. Main respiratory signs that can be revealed at the general visual inspection
2. What type of cyanosis can be observed at the respiratory patients? Describe mechanism
of its formation.
3. What types of the forced position do respiratory patients occupy? Describe and explain
their.
4. What normal shapes of the chest do you know? Describe their.
5. When can the barrel and paralytic chest be formed? Describe their.
6. What pathological shapes of the chest due to deformities of the spin do you know? How
they can influence to the respiratory function?
7. What normal and abnormal types of breathing do you know?
8. What data can you received performing chest palpation? Their diagnostic value.
 Practical tasks
1. Performing general visual inspection of the respiratory patient
2. Assess patient’s chest shape, revealing signs of the pathologic chest
3. Performing dynamic visual inspection of the chest
4. Assess data obtained at the dynamic visual inspection of the chest
5. Performing palpation of the chest and assessment of the obtained data.

Situation tasks
Task 1
29-year-old male patient noted repeated every day attacks of breathlessness during last 7
years. At the visual inspection patient skin is light cyanotic, the ribs are horizontal, the
intercostal spaces are narrow, supra- and subclavicular fossae are not seen, the epigastric
angle is obtuse. The upper portion of the chest is especially wide.
4. Why is the patient’s skin cyanotic?
5. What types of the chest does patient have?
6. What position in the bed does patient occupy during attack of breathlessness?
Task 2
57-year-old female patient complains of dyspnea, cough and left side chest pain. The
symptoms appeared after hard work and overcooling 3 days before. At the visual inspection
skin is pale and cyanotic, respiratory rate is 32 and left part of the chest is left behind from
right
4. How is increased respiratory rate named? Why does patient have this sign?
5. Why is one half of the chest left behind from other?
6. What position may patient occupy in the bed? Why?
Task 3
24-year-old female was admitted to pulmonology department with severe mixed dyspnea,
high fever (39°C), cough with rusty sputum, piercing chest pain. Her mother said the patient
was exited and had visual hallucinations. During examination patient is calm, her
respiratory rate is 36. Skin is red and hot.
4. What is general condition of the patient? Which department should patient be
admitted?
5. What disorder of consciousness does patient have? Why?
6. How should you palpate the patient chest? What signs of the respiratory disease may
you reveal?
Task 4
73-year-old male patient suffered from COPD during last 10 years, smoking, notes
increasing dyspnea, cough with purulent sputum production during last week after
overcooling. Patient condition is moderate severe. He sits fixing the shoulder girdle. His
exhalation is longer than inhalation. Skin is cyanotic.
1. What type of the chest shape may be at the patient? Why?
2. What change of his finger can you find? Why?
3. How is vocal fremitus changed at the patient? Why?
 TOPIC 3
Percussion as an objective method of patient examination.
Comparative and topographic percussion of the chest
1. Importance of the topic
Percussion of the chest is one of the basic, informative methods of examination of the
respiratory patients. It allows revealing diagnostic signs of the respiratory diseases without
modern additional investigations. Today, when doctor has a lot of additional diagnostic devices
importance of percussion is less then before. But if doctor uses percussion during patient
examination his diagnostic research becomes more efficient and fruitful. This method is very
useful when doctor could not perform modern investigation and in an emergency situation. It is
very important part of the diagnostic process.

2. Concrete aims:
─ Master principles, types and rules of percussion of the chest
─ Learn physical grounds of percussion
─ Perceive clear lung sound and it changes: dull and tympanic, their characteristics.
─ Performing and assessing comparative percussion of the chest
─ Know chest points and lines used for topographic percussion of the lung
─ Performing and assessing topographic percussion of the lung

3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the airways and lungs, their blood supply and innervation
Normal physiology Mechanics of breathing, gas exchange in the lung and tissues of
system organs
Histology Ontogenesis of the respiratory tract, histological structure of the
respiratory tract and alveoli
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Definition
Clear lung sound heard on percussion of the chest areas over an unchanged lung tissue
Dull sound heard over the solid tissue without air like dense parenchymatous organs
Tympanic sound heard over the tissue containing a lot of air
Passive excursion of lung Moving lower lung border when patient changes his position from stand to
lying
Active excursion of lung Moving lower lung border due to deep inhaler and exhaler

4.2. Theoretical questions:

1. What is percussion and which types of percussion do you know?
2. What are the rules of percussion? What methods of percussion do you know?
3. What are the physical grounds of percussion?
4. What percussion sounds do you know? Mechanism of their origin.
5. When may you hear dull sound over lung?
6. When may you hear tympanic sound over lung?
7. What are the main purposes of topographic percussion of the lung?
8. When may you find shifting up lower border of the lung?
9. When may you find shifting down lower border of the lung?
10. When may you find shifting down height of the lung apex?
11. When may you find shifting up height of the lung apex?
12. When may you find that active excursion of the lung is limited?

4.3. Practical task that should be performed during practical training

11.Performing comparative percussion of the chest
12.Recognizing percussion sounds.
13.Performing topographic percussion of the lung
14.Recognizing and assessing changes of percussion sound and position of the lung
Topic content
Percussion is a method of objective study consisting in tapping the patient's body to evaluate the
physical properties of the underlying organs according to the character of the artificially produced sounds.
 There are two types of percussion: immediate and mediate. Immediate (direct) percussion
consists in tapping the patient's body with one or several fingers. In indirect (mediate) percussion the
tapping is performed on some object applied to the studied area. A so-called plessimeter, a plate of a
dense material, is used. A finger of the doctor applied to the surface of the body may play a role of this
instrument. Striking the plessimeter is done using a percussion hammer or a finger. At direct percussion,
the sound is low and indistinct, as a large portion of the energy is used by compression of the soft tissues.
In indirect percussion, the plessimeter, compressing the soft tissue, limits the propagation of the energy
directing it to the depth. The sound is loud. This type of percussion is painless. The most frequent method
of indirect percussion is tapping with a finger on the finger.
Physical grounds of percussion
Percussion is based on obtaining a sound wave from the tissues as a result of their shacking on
striking. Vibrations of the sounding bodies are due to their elasticity (air, metallic plate) or are produced
under the influence of elasticity obtained with the body strain (string, membrane). Sound is produced by
striking a hard or liquid body.
From the physical perspective, the sounds can be classified as to the loudness, duration, pitch.
The former three properties depend largely on the mass, density and strain of the object as well as the
force of the strike. As the physician uses the taps of the same force and tissue mass is constant, the
properties of the sound depend mainly on the density and strain of the studied tissue.
Loudness of the percussion sound depends inversely on the density (strain) of the tissue. The
dense tissue produces quiet sound. The air in the cavities and tissues produces a loud sound.
The pitch of the sound directly depends on the tissue density. The greater is the density, the
higher is the frequency of vibrations, and the higher is the pitch. Low density, air contained tissue
produces rare vibrations that have lower pich.
Duration of the sound is in reverse dependence with the density of the tissue. Dense tissue
vibrates short time but air contained vibrates longer.
The liver, muscles, spleen, fluid accumulated in the pleural cavity as a solid tissue produce very
quiet, high pitch and short sound. Lung tissue, stomach, intestine, as air conteined tissue, produces loud,
low pitch and longer sound.
Three sounds clear (pulmonary), dull and tympanic can be heard on percussion.
The character of percussion sounds. Clear lung sound is heard on percussion of the chest areas
over an unchanged lung tissue. A clear sound is heard when the amount of air in the lungs, the tension of
the lung tissue, and the thickness of the covering structures are normal. A clear lung sound is loud, long,
low-pitched and not tympanic. It changes its properties depending on a number of conditions: the
properties of the chest, development of the muscles, and amount of subcutaneous fat.
Dull sound is heard in the areas neighboring with dense parenchymatous organs (heart, liver,
spleen). This sound is quiet, short, high-pitched, resembles the sound produced by tapping on the wood.
Tympanic resonance is produced in the areas neighboring with the air-filled cavities. Tympanic
resonance has a musical shade which occurs at beating a drum. In a healthy person, tympanic resonance
is heard only in one area of the chest, on the left lower anterior portion, so-called Traube's semilunar
space. The upper border of this space is limited by the lower edge of the liver, to the left - spleen, below -
costal arch. In this area, the thoracic wall adjoins the fundus of the stomach with an air sac, which is the
cause of the tympanic resonance in this area.
The rules of the percussion. To obtain clear percussion sound it is necessary to observe the
following rules:
1. The middle or the point finger of the left hand plays the role of the plessimeter.
2. The percussion taps are made with a soft portion of the end phalanx of the right-hand middle
finger on the middle phalanges of the plessimeter finger.
3. The hands of the physician should be warm not to produce unpleasant sensations.
4. The plessimeter finger is applied to the patient's body tightly but without excessive pressure.
When the pressure is strong, even a weak percussion tap gets the properties of a strong one, which is not
desired because its effect propagates to the depth and around the studied point. The point and the ring
fingers should be kept apart, sliding apart the skin of the patient.
5. The axis of the end phalanx of the tapping finger as well as the direction of the percussion
strike should be strictly perpendicular to the surface of the plessimeter finger. Only in this case the force
of the percussion strike will be used to penetrate deep inside, not around the studied place.
6. Percussion strike should be light and always of the same force. It is necessary to learn to bend
the hand only in the radioulnar joint, without moving the arm on tapping.
7. Percussion strike should be short and elastic.
8. Percussion of the lungs should be performed in an upright position, when the patient stands or
sits.
9. The examination room should be warm.
 Comparative and topographic percussion are distinguished. Topographic percussion is used to
determine the lower border of the lungs, their mobility, and the height of the lung apices and the width of
Kronig's fields.
Comparative percussion is used to evaluate the morphological state of the underlying tissue
considering the changes in the character of the sound.
Chest points and lines
To designate the location of the revealed normal or pathological findings it is convenient to use
vertical (ordinates) and horizontal (abscissas) lines. The ribs can play the role of abscissas, the vertical
lines drown through the definite points on the chest can serve as ordinates.
These lines are as follows:
1. Anterior median line (I. mediana) going vertically through the middle of the chest.
2. Right and left sternal lines (/. sternalis dextra at sinistra) going along the both edges of the
breastbone.
3. Right and left parasternal lines (I. parasternalis dextra et sinistra) going vertically between the
sternal and medioclavicular lines.
4. Right and left medioclavicular lines (I. medioclavuculare dextra at sinistra) going through the
middle of the both collarbones.
5. Right and left anterior axillary lines (I. axillare dextra et sinistra) going through the anterior
edges of the armpits.
6. Right and left middle axillary lines (I. axillare dextra et sinistra) going vertically through the
middle of the both armpits.
7. Right and left posterior axillary lines (I. axillare posterior dextra et sinistra) going vertically
through the posterior edges of the armpits.
8. Right and left scapular lines (7. scapulare dextra et sinistra) going vertically through the angles
of the shoulder blades.
9. Right and left paravertebral lines (7. paravertebral dextra et sinistra) going vertically between
the scapular lines and the line going through the processes of the vertebrae.
As these lines go through easily recognizable points they can be determined mentally. If a
change is noticed not in the place of crossing the rib and one of the lines, the distance to the nearest line
in centimeters is determined. The ribs are easily counted beginning from the second rib on the front, its
cartilage is attached to the breastbone at the level of the so-called angulus Ludovici (the angle between
the manubrium of sternum and its body). The rib of this angle is easily detected when drawing a line with
a finger downward along the breastbone. It is frequently seen like a roller in the upper portion of the
sternum. It is also easy to find the 7 rib as this is the last rib attached to the sternum with its cartilage.
Vertebral processes are used to orient on the back, the process of the 7 th cervical vertebra is felt as it is
prominent when the head is bend forward. If three vertebrae are prominent together, the middle one is the
7th cervical vertebra. Besides, the orienting points can be clavicles, the axis of the shoulder blade, is lower
angle, xiphoid process as well as fossae on the chest (supra-and subclavicular).
Percussion allows answering two important questions:
1. What changes has occurred in the studied organ?
2. What are the borders, size, and shape of the organ? The answer to the first question is
obtained at the so-called comparative percussion; topographic percussion answers the second question.
Comparative percussion of the lungs
Comparative percussion of the lungs allows determining the presence of pathological changes
judging by the changes in the character of the percussion sound. The obtained percussion sound is
compared with normal sounds.
Comparative percussion should be done thoroughly satisfying the following conditions:
1. The percussion should be done in symmetrical areas of the chest.
2. The percussion should be started from the healthy side if the physician can suggest the
location of the pathological process.
3. The position of the plessimeter finger and the force with which it is applied should be equal on
the symmetrical sides of the chest.
4. The loudness of the sound depends of the force of percussion strike. The taps should be made
with equal energy. It is necessary to remember that a moderate tap reaches the depth of 5 cm. It is
recommended to use alternatively both weak and strong percussion to avoid mistakes: weak percussion
may fail to reveal a deep affection, while strong percussion superficial.
5. Percussion should be done when the patient is maximally relaxed and breathe calmly.
Technique of comparative percussion Comparative percussion is performed in the following
order: 1) apices; 2) anterior surface of the lungs: along the intercostal spaces; 3) lateral surfaces: along
the axillary lines; 4) posterior surface: along the scapular lines over the shoulder and above the angle of
the scapula in the interscapular space. The following should be remembered:
1) percussion sound over the right apex is a little shorter due to its lower position when compared
with the left one and more pronounced development of the muscles of the right shoulder girdle;
 2) in the 2nd and 3rd intercostal spaces the percussion sound is shorter due to proximity of the
heart;
3) percussion sound in the right axillary area is shorter due to the liver; on the left it is loud with
tympanic shade due to proximity of a gas sac, i.e.the stomach (Traube's space).
A clear lung sound can become dull or tympanic.
Dullness of percussion sound is caused by reduction in the amount of air in the lung tissue, filling
the pleural cavity with fluid, thickening of the pleura: pneumosclerosis, fibrous focal pulmonary
tuberculosis, hepatization stage of lobular pneumonia, formation of a large cavity filled with inflammatory
fluid (lung abscess, echinococcus cyst), foreign air-free tissue (tumor), in lung infarction (filling the alveoli
with blood), complete atelectasis (collapse of the lung resulting from obstruction of the lumen or its
compression).
At presence of small infiltrated air-free foci located between large areas of an unchanged lung
tissue lying far from the surface, percussion sound can be clear. The larger are the air-free infiltrates, the
closer they are located to the surface, the larger is their number, the less is the number of the areas of
normal tissue between them, the more intensive is dullness. Percussion sound may become completely
dull if a large air-free infiltrated area adjoins the studied area.
Changes in the pleura is another cause of dullness, which impedes percussion conduction to the
air-containing tissue. Dullness can be observed in pleura thickening, tumors, presence of fluid in the
pleural cavity (hydrothorax, pyothorax, hemothorax, exudation pleuritis). If the layer of the fluid is thick
enough (>6 cm), the sound becomes dull. When effusion develops in the left pleural cavity and fills the left
pleural sinus, tympanic resonance over Traube's space disappears. First signs of dullness occur when
about 400 ml of fluid have accumulated in the lungs. But slight percussion sometimes allows determining
the presence of even smaller amounts.
The upper level of dullness at moderate accumulation of the inflammatory exudate in the pleural
cavity resembles a parabola, so-called Ellis-Damuaso line. The lowest point of this line is situated behind
the vertebral column; from this point the line goes in an arch-like manner to the level of the scapula angle,
further it goes down but at the level of the middle of the axillary area it goes up again and then down to
the lowest point near the sternum. The cause of this arch-like pattern of the dullness level is different
pliability of various areas of the lung to the accumulating fluid. The upper level of dullness will be higher in
the areas where pliability is greater. In exudative pleurisy both layers of the pleura adhere at the upper
level of the fluid due to sticky character of the exudate. That is why dullness outlines and Ellis-Damuaso
line do not change when the patient's position changes.
In exudation pleurisy a triangle space with dullness of the sound can be determined on the
healthy side of the chest behind and lower the spinal column. This right-angle triangle is called
Rauchfuss' triangle. Its hypotenuse is continuation of Ellis-Damuaso line on the healthy side of the chest,
one side is the vertebral column, the other lower border of the lung. The cause of dullness in this triangle
is displacement of the mediastinum organs to the healthy side.
Tympanic character of the sound is observed at increased amount of air or decreased elasticity of
the lung tissue. This may be observed at air accumulation in the pleural cavity (pneumothorax), at
presence of an air-filled cavity (lung abscess, tuberculosis), when the cavity is large enough (>3 —4 cm)
and located close to the chest wall. If he cavity is large (> 6 cm), located superficially, and has smooth
walls, low tympanic resonance resembling knocking at a metallic vessel is produced (bell tympanic
sound). Bell sound is also heard over pneumothorax.
If a large cavity in the lungs is close to the chest and joints with the bronchus by a narrow
opening, or in pneumothorax joined with the bronchus, a variety of tympanic resonance, high jingling
sound, is heard. It develops with exit of the air in several portions through one opening.
In pulmonary emphysema percussion sound is low tympanic due to increased filling with air and
decreased elastic tension of the lung tissue. This sound is termed vesiculotympanic (bandbox)
resonance.
Combination of decreased clearness of the sound (dullness) and indistinct tympanic timber, dull
tympanic sound, can sometimes be heard. It appears if at partially decreased filling with air the normal
elastic tension of the lung tissue decreases. This develops in:
1) onset and resolution of lobular pneumonia, when the pulmonary tissue relaxes with incomplete
infiltration;
2) in bronchopneumonia, if the foci of lung consolidation alternate with air-containing areas;
3) in effusive pleurisy, in the area located over the exudate where the lung tissue is poorly filled
with air and looses its tension due to compression with fluid (obturation atelectasis);
4) in incomplete obturation atelectasis, in incomplete obstruction of bronchioles with sputum, pus,
blood, tumor, when the pulmonary tissue tension decreases due to reduction of air amount in the alveoli;
5) in partial compression of the lung (compression atelectasis) with a tumor, highly located
diaphragm, pneumothorax, fluid in the pleural cavity;
6) when the alveoli are filled with air and fluid in lung edema, lung infarction.
 Besides, deadened tympanic sound can appear over large air-free areas of the lungs in acute
infiltration if a strong percussion tap reaches deeply located large bronchi or cavities (caverns,
abscesses) and causes vibration of the air in them.

Pathological changes of percussion sound

1 Incomplete or a) decreased air content in the Lung infiltration (pneumonia, tuberculosis),

complete (in some alveoli atelectasis, tumor; Effusive pleurisy,
cases) dullness b) fluid or solid formation in the adhesions of the pleural tumor
pleural cavity
2 Tympanic a) a large cavity in the lung Cavern, abscess; pneumothorax
resonance b) air in the pleural cavity
3 Vesicular tympanic Reduction of tissue elastic Pulmonary emphysema
resonance (bandbox tension at increased air content
sound)
4 Deadened tympanic a) reduction of elastic tissue Initial or final stage of pneumonia, partial
sound strain at decreased air content atelectasis, pulmonary edema; cavern, lung
b) air-free areas with deep abscess
cavities

Topographic percussion of the lungs

Determining the borders of the lungs is started from the lower border of the right lung
(pulmonohepatic border), percussion is done from the top (beginning with the subclavicular area)
downward along the parasternal, medioclavicular, axillary, scapular and paravertebral lines.
The position of the lower border of the lung is determined in the following way: the plessimeter
finger is applied to the second intercostal space parallel to the probable border. Weak taps are made
moving the plessimeter finger downward from one intercostal space to another until clear sound changes
into a dull one. The place of transition of a clear sound to a dull one is marked on the skin using a special
pencil. Having determined the location of the lower border of the lung on all lines (beginning from the
parasternal line) and marked this area, the points are joined by a line. This line is the projection of the
lower border of the lung on the chest wall. After having determined the lower edge of the lung on the
lateral surface of the chest wall (between the anterior and posterior axillary lines), the patient should be
asked to put the respective hand on the head. The lower border of the left lung is determined in the same
way, beginning the percussion from the anterior axillary line (cardiac dullness, the cardiac notch, is
located medially). Along the axillary and the other lines the lower border is determined in the same
manner as on the right side.

Place of percussion Right lung Left lung

Along the parasternal line 5th intercostal space —
Along the medioclavicular line 6th intercostal space —
along the anterior axillary line 7th intercostal space 7th intercostal space
along the median axillary line 8th intercostal space 8th intercostal space
along the posterior axillary line 9th intercostal space 9th intercostal space
along the scapular line 10th intercostal space 10th intercostal space
along the paravertebral line The process of the lit The thoracic vertebra

Determining the upper border of the lungs The upper border of the lung is determined using
percussion of the lung apices over the collarbone and the spine of scapula (spina scapulae). The
percussion is started from the middle of the supraclavicular fossa going upwards (silent percussion, the
plessimeter finger is parallel to the studied border). On the back, the percussion is done from the middle
of the fossa supraapinata to the process of the 7 th cervical rib. With this method, the apex is 3 —5 cm
above the collarbone, and at the level of the 7 th cervical vertebra on the back. Determining Kronig's fields
is also used. The Kronig's field is a 5-cm band of a clear percussion sound going through the shoulder
from the clavicle to the spine of scapula divided by the edge of the trapezius muscle into the anterior and
posterior portions. The percussion is started from the middle of the space going downwards and upwards
until dullness is heard, this is the way to find out external and internal borders of this field as well as its
width. In a healthy person the width of Kronig's fields is about 5 —6 cm (ranging from 3,5 to 8 cm).
Determining the lung border mobility Topographic percussion of the lungs is used to define the
degree of the lung border mobility. This can be active and passive. Active mobility is that to change the
position depending on the phase of respiration. Passive mobility is that of the borders to shift depending
on the changes in the position of the body.
 The volume of the lung border expiratory excursion is the distance between the positions of the
lung border at maximally deep breathing in and out. On the right side, it is determined along three lines:
medioclavicular, median axillary, scapular, on the left side along two lines: median axillary and scapular
and is due to elastic expanding and contracting of the lugs as well as the depth of the pleural sinus, to
which the border of the lung enters at respiratory expansion of the lung. The lower border of the lung has
the greatest respiratory mobility along the median axillary line. On deep breathing, the lower border of the
lung goes down 4 cm lower than on normal breathing. Thus, at the level of median axillary line the
respiratory excursion of the lower border of the lung is 8 cm. At the level of medioclavicular line it equals 4
cm.
Mobility of the lower border of the lungs is determined in the following way: first, the position of
the lower border of the lung on medium breathing is determined using percussion and marked with a
pencil. Then the patient is asked to take a deep breath and hold his breath. The position of the border is
determined once again and marked with the pencil. Then the patient breathes out maximally and holds
his breath. Percussion is done upwards until a clear lung sound appears and the third mark is made on
the borderline of the relative dullness. The distance between the second and third marks in centimeters is
the respiratory excursion of the lung border.
The position of the lower border of the lungs may change because of a number of causes:
pathology of the lungs, diaphragm, pleura, abdominal organs. The lower border of the lungs may shift
downward or upward the normal position, these changes can be both unilateral and bilateral. The lower
border can shift down in acute (an attack of bronchial asthma) or chronic (pulmonary emphysema)
expansion of the lungs as well as in pronounced weakening of the tone of the abdominal muscles
(splanchnoptosis).
Upward displacement of the lower border of the lungs is usually unilateral and accompanies
pneumosclerosis, obturation atelectasis, accumulation of fluid or air in the pleural cavity, significant
enlargement of the liver (cancer, echinococcus), enlargement of the spleen.
Bilateral displacement of the lower border is observed when intra-abdominal pressure is
increased, i.e. accumulation of fluid (ascites), air (due to acute perforated ulcer) in the abdominal cavity,
pronounced flatulence, obesity.
Reduced mobility of the lower border is present in pulmonary emphysema (reduction of the lung
elasticity), inflammatory infiltration of the lungs, presence of large amount of fluid in the pleural cavity, in
pleural obliteration.

Materials for self-control (added)

7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. – Vinnytsya: NOVA
KNYHA, 2006. – p. 62-68, 89-103.
 Test for self-control

1. What type of percussion sounds may you hear over health lung?
a. Tympanic
b. Clear lung
c. Dull
d. Stony dull
e. Resonant.
2. When may you hear dull percussion sound over lung?
a. Thickened pleura.
b. Collapse of lung.
c. Consolidation of lung.
d. Fluid in pleural cavity.
e. Everything mentioned above.
3. When may you hear hyper-resonant percussion sounds over the lung?
a. Emphysema,
b. Pneumothorax,
c. Above the level of pleural effusion
d. Large cavity
e. Everything mentioned above.
4. What pathological condition can produce dull percussion sound?
a. Pneumonia
b. Emphysema
c. Large cavity
d. Bronchitis
e. Pneumothorax.
5. What percussion sound is heard of the lobular pneumonia?
a. Tympanic
b. Impaired
c. Dull
d. Clear lung
e. Resonant.
6. What percussion sound is heard of emphysema?
a. Tympanic
b. Impaired
c. Dull
d. Clear lung
e. Resonant.
7. What percussion sound is heard of acute bronchial asthma?
a. Tympanitic
b. Impaired
c. Dull
d. Clear lung
e. Resonant.
8. What percussion sound is heard of pleural effusion?
a. Tympanic
b. Impaired
c. Dull
d. Clear lung
e. Resonant.

9. What percussion sound is heard of collapse of the lung lobe resulting from obstruction of the
bronchus lumen?
a. Tympanitic
b. Impaired
c. Dull
d. Stony dull
e. Resonant.
10. What percussion sound is heard of the focal pneumonia near root of lung?
a. Tympanitic
b. Impaired
c. Dull
d. Clear lung
 e. Resonant.
11. What is determined on topographic percussion of the lung?
a. Position of the height of the lung apex
b. Lung border mobility
c. Position of the lower border
d. Kronig's fields width
e. All mentioned above
12. What lines is topographic percussion done along?
a. Scapular
b. Paravertebral
c. Parasternal
d. Medioclavicular
e. Everything mentioned above.
13. What is the first line along which the lower border of the left lung is determined?
a. Scapular
b. Paravertebral
c. Parasternal
d. Medioclavicular
e. Axilar anterior
14. What is the first line along which the lower border of the right lung is determined?
a. Scapular
b. Paravertebral
c. Parasternal
d. Medioclavicular
e. Axilar anterior
15. What is position of the lower border of the right lung along medioclavicular line?
a. 6th interspace
b. 10th interspace
c. 7th interspace
d. 5th interspace
e. Not determine
16. What is position of the lower border of the left lung along medioclavicular line?
a. 6th interspace
b. 10th interspace
c. Not determine
d. 5th interspace
e. 8th interspace
17. What is the normal height of the lung apex?
a. 6-8 sm
b. 3-5 sm
c. 8-10 sm
d. 5-7 sm
e. 1-2 sm
18. What are the causes of increase height of the lung apex?
a. Pulmonary emphysema
b. Inflammatory infiltration of the lungs
c. Pleural effusion
d. Pleural obliteration
e. Everything mentioned above.
19. What are the causes of reduced mobility of the lower border?
a. pulmonary emphysema
b. inflammatory infiltration of the lungs
c. fluid in the pleural cavity
d. pleural obliteration
e. everything mentioned above.
20. What are the causes of upward displacement of the lower border?
a. pulmonary emphysema
b. pneumosclerosis
c. abscess
d. obturation atelectasis
e. everything mentioned above.
 Control questions
9. What is percussion?
10. What types of percussion do you know; their diagnostic importance?
11. What are purpose and rules of the comparative percussion?
12. What percussion sound may be obtained over health lung, mechanism of its origin?
13. What is dull percussion sound, its origin and diagnostic importance?
14. What is tympanic (resonance) percussion sound, its origin and diagnostic importance?
15. What distinguished lines and points on chest do you know?
16. What is normal position of the right lower border of the lung? How it can change in pathology?

Practical tasks
7. Performing comparative percussion of the chest of the respiratory patient
8. Assess findings of the comparative percussion
9. Determine position of the lower border of the left lung.
10. Determine position of the lower border of the right lung.
11. Determine height of the lung apex, assess obtained findings
12. Determine active excursion of the lower border of the lung, assess findings

Situation tasks
Task 1
30-year-old male patient noted repeated every day attacks of breathlessness during last 5 years. At
the comparative percussion you hear long, low and loud sound over all surface of the chest.
1. How is the sound named?
2. What is diagnostic value of the sign?
3. What may position of the lower border of lung be at patient and why?
Task 2
47-year-old female patient complains of dyspnea, cough and right side chest pain. The symptoms
appeared after hard work and overcooling 3 days before. At the comparative percussion you reveal
short, quiet and high pitch sound over lower right part of the chest.
1. How is the sound named?
2. What is diagnostic value of the sign?
3. What may position of the right lower border of lung be at patient and why?
Task 3
44-year-old male was admitted to pulmonology department with severe mixed dyspnea, high fever
(39°C), cough with copious purulent sputum, piercing chest pain in the upper left part. During the
comparative percussion you hear loud, long and low sound over limited region of the upper left part
of the chest.
1. How is the sound named?
2. What is diagnostic value of the sign?
3. What may position of the left upper border of lung be at patient and why?
Task 4
73-year-old male patient notes gradually increasing dyspnea, hemoptisis, weakness. Patient
condition is moderate severe. Skin is cyanotic. During the comparative percussion you hear shorter,
quieter and higher than clear pulmonary sound over the anterior lower right part of the chest.
1. How is the sound named?
2. What is diagnostic value of the sign?
3. How may the mobility of the lower edge of the right lung be changed at the patient? Why?
 TOPIC 4
Auscultation of the lungs as an objective method of patient examination.
Procedure of the lung auscultation. Main respiratory sounds
1. Importance of the topic
Auscultation of the chest is one of the basic, informative methods of examination of
the respiratory patients. It allows hearing normal and pathological changed sounds
produced during act of breathing. Most of the respiratory diseases are accompanied
with certain auscultation phenomena their determining is one of clues at the
diagnostic process of the respiratory patients.

2. Concrete aims:
─ Master principles, types and rules of auscultation of the chest
─ Learn physical grounds of auscultation, mechanisms of production of normal and
abnormal respiratory sounds
─ Characteristics of the bronchial and vesicular respiratory sound, their distinguishing
─ Qualitative and quantative changes of the vesicular respiratory sound, their
diagnostic importance.
─ Pathological bronchial respiratory sound, mechanism of its production
─ The mechanisms for bronchophony, whispered pectoriloquy

3. Basic training level

Previous subject Obtained skill

Biological physics Principles of sound formation and spreading
Normal anatomy Anatomy of the airways and lungs, their blood supply and
innervation
Normal physiology Mechanics of breathing, gas exchange in the lung and tissues of
system organs
Histology Ontogenesis of the respiratory tract, histological structure of
the respiratory tract and alveoli
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Definition
Bronchial breath sound Heard over trachea and major bronchus, formed in vocal fissure due
to moving airflow through it
Vesicular breath sound heard over all areas of the chest distal to the central airways, formed
in alveoli due to their walls vibration at the pitch of inspiration
Bronchophony Louder and clearer voice sounds over the affected lung area
Stridor Indicates narrowing of the upper airway, loud sound can be heard at
a distance from the patient
Whispered Clarity transmitting whispering to the chest wall at the patient with
pectoriloquy consolidation of the lung tissue

4.2. Theoretical questions:

1. What is auscultation and which types of auscultation do you know?
2. What are the rules of auscultation?
3. What are the physical grounds of auscultation?
 4. How is a bronchial breath sound formed, where is it heard in a norm, its
characteristics?
5. How is a vesicular breath sound formed, where is it heard in a norm, its
characteristics?
6. What is a stridor, its formation, diagnostic importance?
7. What changes of the vesicular breath sound do you know? Their diagnostic
importance.
8. What is a pathological bronchial breath sound, how is it formed? Its diagnostic
importance.

4.3. Practical task that should be performed during practical training

1. Auscultation of the lungs
2. Assessment normal lung sounds.
3. Assessment changes of the lung sounds
4. Recognizing and assessing bronchophony and whispered pectorophony
Topic content
Auscultation of the lungs
Auscultation is an objective method of study based on listening and evaluation of
acoustic phenomena, which naturally occur in the functioning organisms.
The difference between auscultation and percussion is that on percussion we produce
vibrations of the tissues artificially, on auscultation we listen to the sounds produced in the
organ due to the changes of the tissue tension on their functioning. As a result, the sounds
obtained on percussion are loud enough to be heard at a distance. Auscultation sounds are
weaker and can be heard when applying the physician's ear to the patient's body, or with the
help of sound-conducting tubes (stethoscopes).
As to the way of listening two types of auscultation are distinguished:
1) direct auscultation performed applying the ear to the patient's body;
2) indirect auscultation performed with the help of a special tube, a stethoscope (from
Greek sthetos - chest, scopeo - look).
Thus, indirect auscultation uses an instrument. It has a number of advantages: the
funnel of the stethoscope is smaller than the auricle of the ear; this allows listening to the
acoustic phenomena at a smaller area. It is more convenient prom hygienic perspective. It
allows listening to the areas inaccessible for the ear (supraclavicular, axillary).
Auscultation rules
1. The chest of the patient should be bare as the shuffling of the clothes may mix with
the sound.
2. The examination room should be warm and silent.
3. The stethoscope should be applied to the body tightly, with the whole edge of the
funnel (not with its portion as, firstly, it can cause pain, secondly, the air between the body and
the funnel increases the sound by resonance and changes it). Sliding of an untightly applied
stethoscope may also produce accessory sounds.
4. It is not necessary to use excessive force to apply the stethoscope. It can cause pain
and hinder vibrations of the chest wall in the studied area, in this way weakening conduction of
the vibrations from the underlying tissues to the air and the ear.
5. It is not necessary to hold the tube of the stethoscope with the hand as the minute
motions of the holding fingers can add sounds.
6. It is necessary to use one and the same stethoscope. Various stethoscopes and
phonendoscopes are available for indirect auscultation. This method allows avoiding some
disadvantages of direct auscultation mentioned above, besides the instrument aids conduction
of the sound to the physician's ear and limits the studied area.
Stethoscopes, which can enhance acoustic phenomena, have been made recently. They
are termed phonendoscopes. Their shape can be various, but all of them can enhance the
sound. The terminal portion of a phonendoscope is a metal cavity covered with a membrane.
This portion is applied to the studied area. The acoustic phenomena in one or another organ
(heart, lungs) are conducted to the membrane, which starts vibrating. The cavity covered with
the membrane enhances the sound. The enhanced sound is conducted through the tubes.
Physical grounds of auscultation. Sound is defined as propagation of energy by a
mechanical wave through matter. Sound is produced when a mechanical disturbance occurs
and a compressional wave of energy spreads out from the source to the site of detection. In
case of auscultation it is physician’s ears.
Two important measures of sound are frequency (the number of vibrations per second)
and amplitude (the power/velocity of the sound wave). Subjective indicators of these
measurements are pitch and loudness, respectively.
The most important factor that determines the speed of sound conductance is the
density of the medium. Structures with greater density conduct sound at higher speed and with
greater efficiency. Structures with a low density do not conduct sound waves effectively.
Attenuation is the decrease in sound as it travels through time and space. The three
primary factors that determine attenuation in the body are inverse square loss, absorption, and
reflection. Obstacles to sound conduction cause the sound waves to be absorbed or reflected
back toward the sound source. In either case, sound detection distal to the obstacle is impeded.
Reflection of sound waves also occurs when they attempt to pass across tissues of
significantly different acoustical impedance characteristics (e.g., air to bone or vice versa).
Lung sounds can be divided into two major categories: breath sounds and adventitious
lung sounds. Breath sounds are normal noises that can be heard on the chest wall with
breathing. Adventitious lung sounds are abnormal sounds superimposed on the breath sounds
and usually indicate some types of respiratory disorder.
Main breath sounds may be divided into two types: vesicular and bronchial breath
sounds.
In a norm the bronchial breath sound is heard over the larynx (lower portion of the
neck), trachea and large bronchi (upper portion of the chest). The sound is harsh, loud, and high
pitched, like pronouncing "h" sound. It is heard during inspiration and expiration that is louder
and longer than inspiration. This sound is produced in the larynx when the air passes trough the
fissure of the glottis due to air circulation above the vocal cords at breathing in and under the
vocal cords at breathing out.
The vesicular breath sound is heard over all areas of the chest distal to the central
airways. It is soft, low pitch, blowing like "f' sound, heard during inspiration and one-third
expiration. The sound is produced in the lung parenchyma when the air enters the alveoli and
their walls get strained. Vibrations, producing the sound, occur as a result. A great number of
alveoli vibrate at the same time and all alveoli expand consequently. As a result of summing the
sounds, a pulmonary sound of vesicular respiration is heard. During expiration due to alveoli
collapse the tension in the walls rapidly decreases, their ability to vibrate decreases, that is why
the respiratory sound is heard only at the beginning of breathing out.
Changes of vesicular breath sound can be quantitative and qualitative. Quantitative
changes of vesicular breath sound manifest by weakening or strengthening of the respiration.
Physiological weakening of vesicular respiration is observed in thickening of the chest wall due
to abundant development of its muscles or increased fat amount. Main causes of weakened
vesicular respiration are difficult air passage to the lungs; insufficient expansion of the lungs at
breathing in; an obstacle for the sound conduction to the ear of the physician.
Weakening of vesicular respiration may be caused by decreased expansion, alveolar
wall tension with lower vibration amplitude. When the larynx and trachea are narrowed,
vesicular respiration is evenly weak in the both halves of the chest. The difficulties in the air
passage to the lungs may be due to narrowing of airways with a foreign body, tumor or
compression of the larynx, trachea, and bronchi by an external lymph node, tumor, and scar. In
bronchus narrowing, weakened vesicular respiration is heard over the portion of the lung
supplied through the narrowed bronchus.
In complete obstruction to the bronchus with a foreign body or a tumor respiration is
not heard in the respective portion of the chest.
Weakened vesicular respiration due to insufficient expansion of the alveoli on
inspiration is observed at some lung diseases, i.e. emphysema due to decreased respiratory
excursion of the lungs and reduction of their elasticity; at focal pneumonia in the area of
inflammation due to exclusion of the alveoli from the act of respiration; at the initial stages or
resolution of lobular pneumonia when the alveoli are not filled with dense infiltration, but the
tension of the walls, saturated with exudates, is decreased.
Weakened vesicular respiration is observed at reflex reduction of respiratory mobility of
one half of the chest with pain appearing on breathing (in dry pleurisy, rib fracture, intercostal
neuralgia). The alveoli of the respective lung expand less than normal hence the vesicular
respiration on this half is weaker.
A frequent cause of weakened vesicular respiration is obstacles for conduction of the
respiratory sound to the ear of the physician. They are accumulation of air or fluid in the pleural
cavity; displacement of the lung from the chest wall with a thickened pleura or tumor;
considerable thickening of the chest (edema, subcutaneous emphysema).
Increased vesicular respiration is observed in cases when alveoli expansion on
breathing in is more forceful.
Strengthening of vesicular respiration develops on physical exercise, increase of body
temperature, at a thin chest. Strengthening of respiration over one lung is observed when
respiration in the other lung is absent (compressed with pleural effusion or pathological process
in it). This increased breathing is termed compensatory.
Qualitative changes in vesicular respiration . Rough breath sounds appear when the
lumen of the bronchus is unevenly narrowed, as a result, the sound of the air passing through
the narrowed bronchi with a changed wall is mixed to vesicular respiration. They appear in case
of bronchitis.
Vesicular respiration with prolonged expiration: not only inspiration and the initial
stage of expiration but also the whole phase of expiration are heard. The breath sound with
prolonged expiration is a sign of bronchial obstruction and usually is heard at patients with
bronchial asthma, COPD, acute obstructive bronchitis.
Interrupted respiration is vesicular respiration which is not continuous as usually, but
consists of separate short inspirations interrupted by short pauses. This may be due to
contraction of the respiratory muscles (fatigue, muscular trembling) and in this case is heard
over the whole surface of the lung. In the both cases interrupted respiration appears because
the air enters the alveoli in several movements. It developed in case neurous disorders.
Pathological bronchial respiration. If bronchial respiration is heard over one area of the
chest besides the areas where it is heard in healthy individuals, this is called pathological and
suggests the changes in the physical properties of the lung.
Pathological bronchial respiration appears when vesicular respiration is absent and
bronchial respiration is conducted to this particular area from the place of its origin. Main
condition for this is consolidation of the lung tissue due to filling the alveoli with inflammatory
exudate (hepatization stage of lobular pneumonia), blood (lung infarction), and compression
atelectasis. In all these conditions vibrations of the alveolar walls are absent and the dense lung
tissue becomes a good conductor for the sound waves of the laryngotracheal respiration to the
chest surface. Consolidation of the lung can result from replacement of the lung tissue with a
connective tissue (pneumosclerosis, cornification of the lobe).
Pathological bronchial respiration may be of various intensity and timber which depend
on the degree of consolidation and location in the lung. A loud bronchial respiration is heard
when there is a large area of dense pulmonary tissue. In this case the timber of the bronchial
respiration is higher (this can be heard in the 2 nd stage of lobular pneumonia). More silent
bronchial respiration with low timber is heard when only a segment of the lung or its deep
portion is dense (focal pneumonia). Especially silent low-timber bronchial respiration is present
in compression atelectasis.
Pathological bronchial respiration can be hard when a free cavity or abscess joined with
the bronchus is present in the lung. Consolidation of the lung tissue around the cavity facilitates
better conduction of the sound waves to the surface of the chest. In this case the character of
bronchial respiration can be distinctive (either amphoric or bell breath sounds). These types of
bronchial respiration are observed when the following are present: a considerable size of the
cavity (>5—-6 cm), smooth inner surface of the cavity, moderate degree of filling with pus.
Amphoric breath sounds (from Greek amphora - a vessel with a narrow neck) is a low
empty sound resembling that which is produced by forceful blowing over the neck of an empty
bottle. It appears when the walls of the cavity are smooth and it communicates with a large
bronchus. The resonance facilitates appearance of accessory high overtones in addition to the
main low sound of laryngotracheal respiration. The change the timber of the main sound.
Bell bronchial sound is loud, high-pitched, ringing like metal. This is characteristic for
open pneumothorax (pneumothorax in which the pleural cavity communicates with the outer
air and the air pressure in it is high).
It is necessary to remember that the conditions of good resonance responsible for
amphoric and bell sounds can appear due to proximity of large smooth-walled air-containing
cavities, therefore mistakes are possible.

Materials for self-control (added)

7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –

Vinnytsya: NOVA KNYHA, 2006. – p. 103-111.
 Test for self-control

1. Where is bronchial breath sound formed?

a. in larynx
b. in trachea
c. in bronchus
d. in alveoli
e. in pleural cavity
2. Where is vesicular breath sound formed?
a. in the larynx
b. in the trachea
c. in the bronchus
d. in the alveoli
e. in the pleural cavity
3. Which of the following properties is not appropriate to bronchial breath sound?
a. Heard over trachea and major bronchi
b. Loud and rough
c. Heard only during inspiration
d. Sound like “h” heard during inspiration and expiration
e. Formed in the larynx
4. Which of the following properties is not appropriate to vesicular breath sound?
a. Heard over trachea and major bronchi
b. Soft sound
c. Heard during inspiration and one third of expiration
d. Sound like “f” heard during inspiration and expiration
e. Formed in the alveoli
5. When can the weakened vesicular breath sound be heard?
a. 2nd stage of lobar pneumonia
b. Acute bronchitis
c. Large cavity in the lung
d. Emphysema
e. Complete atelectasis
6. When can not the weakened vesicular breath sound be heard?
a. Emphysema
b. Focal pneumonia
c. Dry pleurisy
d. Large cavity in the lung
e. Pneumosclerosis
7. When can the amphoric breath sound be heard?
a. Emphysema
b. lobar pneumonia
c. Dry pleurisy
d. Large cavity in the lung
e. Pneumosclerosis
8. What auscultation phenomenon is heard of the large pleural effusion?
a. Absent of the breath sound
b. Vesicular breath sound with prorogated exhalation
c. Rough vesicular breath sound
d. Bronchial breath sound
 e. Weakened vesicular breath sound
9. What auscultation phenomenon is heard of the bronchial asthma?
a. Absent of the breath sound
b. Vesicular breath sound with prorogated exhalation
c. Rough vesicular breath sound
d. Bronchial breath sound
e. Weakened vesicular breath sound
10. What breath sound is heard of the focal pneumonia near root of lung?
a. Normal vesicular breath sound
b. Vesicular breath sound with prorogated exhalation
c. Rough vesicular breath sound
d. Bronchial breath sound
e. Weakened vesicular breath sound
11. How vesicular breath sound is changed in case of pneumotorax?
a. Not change
b. Became weakened
c. Became pathological bronchial
d. Became amphoric
e. Became rough
12. How vesicular breath sound changed is in case of acute bronchitis?
a. Not change
b. Became weakened
c. Became pathological bronchial
d. Became amphoric
e. Became rough
13. How vesicular breath sound is changed in case of the 2nd stage of the lobar pneumonia?
a. Not change
b. Became weakened
c. Became pathological bronchial
d. Became amphoric
e. Became rough
14. How vesicular breath sound is changed in case of emphysema?
a. Not change
b. Became weakened
c. Became pathological bronchial
d. Became amphoric
e. Became rough
15 When can the stridor be heard?
a. Emphysema
b. Atelectasis
c. Pleural effusion
d. Obstruction of the trachea and major bronchi
e. Pneumosclerosis
16. How vesicular breath sound is changed in case of COPD exacerbation?
a. Not change
b. Became weakened
c. Became pathological bronchial
d. Became amphoric
e. Became rough with prorogated exhalation
17. How vesicular breath sound is changed in case of the 1nd and 3rd stage of the lobar
pneumonia?
a. Not change
b. Became weakened
c. Became pathological bronchial
d. Became amphoric
e. Became rough
18. How vesicular breath sound is changed in case of the dry pleurisy?
a. Not change
b. Became weakened
c. Became pathological bronchial
d. Became amphoric
e. Became rough
19. When can bronchophony be heard?
a. pulmonary emphysema
b. lobar infiltration of the lungs
c. fluid in the pleural cavity
d. pleural obliteration
e. Everything mentioned above.
20. What auscultation phenomenon is heard of the complete atelectasis of the lower right
lung lobe?
a. Absent of the breath sound
b. Vesicular breath sound with prorogated exhalation
c. Rough vesicular breath sound
d. Bronchial breath sound
e. Weakened vesicular breath sound

Control questions
1. What is auscultation? What types of auscultation do you know?
2. What types of the normal breath sounds do you know? Their properties and differences.
3. How the vesicular breath sound is changed in pathology? Diagnostic importance of the
quantitative changes.
4. What are qualitative changes of vesicular breath sound, their diagnostic importance?
5. What is pathological bronchial breath sound, its diagnostic importance?
6. What is a stridor, its formation, diagnostic importance?

Practical tasks
1. Auscultation of the lungs
2. Assessment normal lung sounds.
3. Assessment changes of the lung sounds
4. Recognizing and assessing bronchophony and whispered pectoriloquy

Situation tasks
Task 1
21-year-old male patient complains on attacks of breathlessness. He occupied the forced
position with fixed shoulder girdle, his skin is cyanotic. At auscultation you hear louder than
normal vesicular breathe sound during inhalation and long exhalation. You suppose acute
asthma attack.
1. How the vesicular breath sound change is named?
2. Why do the changes happen?
3. How the percussion sound is changed at the patient?
Task 2
59-year-old female patient complains of dyspnea, cough and left side chest pain. The
symptoms appeared after hard work and overcooling 3 days before. At the visual inspection
skin is pale and cyanotic, respiratory rate is 32 and left part of the chest is left behind from
right. At percussion you find dull sound over lower lobe of the left lung. At auscultation you
hear loud and rough breath sound during inhalation and exhalation, like sound “H ” over the
lower lobe of the left lung. X-ray examination has revealed lobar infiltration.
1. How the breath sound is named?
2. What is mechanism of their origin?
3. What position may patient occupy in the bed? Why?
Task 3
34-year-old female was admitted to pulmonology department with high fever (39°C), cough
with mucus sputum. During examination patient’s general condition is moderate severe, at
auscultation - vesicular breath sound calmer over right upper lobe than left.
1. How the vesicular breath sound change is named?
2. Why do the changes happen?
3. How the percussion sound is changed at the patient?
Task 4
67-year-old male patient notes increasing dyspnea, cough with purulent sputum production
during last week after overcooling. Patient condition is moderate severe. He sits fixing the
shoulder girdle. His exhalation is longer than inhalation. Skin is cyanotic. At auscultation
vesicular sound is louder than normal with light metallic tone.
1. How the vesicular breath sound change is named?
2. Why do the changes happen?
3. How the percussion sound is changed at the patient?
 Topic 5
Auscultation of the lungs as an objective method of patient examination.
Adventitious lung sounds.
1.Importance of the topic
Auscultation of the chest is one of the basic, informative methods of examination of the
respiratory patients. Commonly adventitious lung sounds appear when pathological process
changes normal properties of the airways, alveoli or pleural sheets. It means that adventitious
lung sounds are the most important signs of the respiratory diseases. Most of the respiratory
diseases are accompanied with certain auscultation phenomena: changes of main sounds and
appearance of the adventitious lung sounds, their determining is one of clues at the diagnostic
process of the respiratory patients.

2. Concrete aims:
─ Study classification of the adventitious lung sounds (rales, crepitation and pleural friction
rub)
─ Learn causes and mechanisms of the producing dry and wet rales and their types
─ Understand diagnostic importance of the consonating (sonorous) and non-consonating
(non-sonorous) rales
─ Study conditions of arising crepitation and pleural friction rub.
─ Differential signs of the adventitious sounds

3. Basic training level

Previous subject Obtained skill

Biological physics Principles of sound formation and spreading
Normal anatomy Anatomy of the airways and lungs, their blood supply and
innervation
Normal physiology Mechanics of breathing, gas exchange in the lung and tissues of
system organs
Histology Ontogenesis of the respiratory tract, histological structure of the
respiratory tract and alveoli
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Definition
Rales Adventitious lung sounds that are generated in bronchi and bronchioles
Dry rales Continuous musical sounds, persist throughout the respiratory cycle and
vary greatly in their character, pitch, and intensity, formed due to narrowing
airways
Moist or wet rales Are generated in bronchi and cavities in the lungs in presence of liquid
secretions
Crepitation Is generated in alveoli when they contain small amount of liquid secretion
due to separating alveolar walls at the end of inspiration with slight cracking
sound
Pleural friction rub Appears when pleural layers lost their smoothness and produced non-
musical creaking sound during breathing movements of the lungs

4.2. Theoretical questions:

21. What is adventitious lung sounds, their classification?
22. Mechanism of producing dry rales, their classification and diagnostic importance.
23. Mechanism of producing moist (wet) rales, their classification and diagnostic importance
24. Mechanism of producing crepitation, their diagnostic importance
 25. Mechanism of producing pleural friction rub, their diagnostic importance
26. What are differential signs between the moist rales and crepitation?
27. What are differential signs between the moist rales, crepitation and pleural friction rub?

4.3. Practical task that should be performed during practical training

15. Auscultation of the lungs
16. Recognizing and assessment main and adventitious lung sounds.
17. Differentiation rales, crepitation and pleural friction rub
Topic content
Adventitious lung sounds
Adventitious lung sounds (ALS) are produced in the trachea, bronchi, alveoli, between the
pleural sheets, pathological cavity in the lungs due to the foreign bodies or material in them (exudates,
pus, blood, mucus, fluid, sputum). These masses can be moved by the air passing through the trachea
and bronchi and produce vibrations responsible for accessory sounds.
Three types of the ALS can be heard at the respiratory diseases: rales, crepitation, pleural
friction rub.
Rales are ALS occurring in the trachea, bronchi, and lung cavities. They can be moist and dry.
Dry rales occur only in the bronchi at narrowing of the lumina. This narrowing can be caused by:
1. Swelling of the bronchial mucosa due to inflammation.
2. Spasm of the smooth muscles of small bronchi.
3. Accumulation of viscous sputum, which can adhere to the bronchial walls and narrow the
lumen.
4. Formation of fibrous tissue in the walls of separate bronchi.
5. Vibration of the viscous sputum at moving along the large and medium-sized bronchi during
expiration and inspiration.
Depending on the acoustic sensations dry rales are divided into wheezes and buzzing rales. They
are heard in the phase of inspiration and expiration. Dry rales differ in timber, pitch, loudness. As to the
pitch and timber they are divided into high pitched sibilant (wheeze) and sonorous or buzzing rales.
Wheeze develops as a result of narrowing of the lumina of the small bronchi. Buzzing rales occur in
narrowing of larger bronchi or when viscous sputum accumulates in them.
The intensity of dry rales depends on the intensity of respiration, the degree of involvement,
depth of the involved bronchi.
The amount of dry rales can be different: from solitary to numerous, disseminated all over the
lungs (bronchial asthma, generalized bronchitis).
Dry rales always are sign of bronchitis.
Moist rales are formed as a result of accumulation of fluid secretion (sputum, blood, pus) in the
bronchi or in the pathological cavity when the air is passing through this secretion, air bubbles of various
sizes are formed, burst and produce noise. Such sounds can be heard when air bubbles are burst if air is
blown in water through a narrow tube. These sounds are called moist rales. Moist rales are heard both
at the phase of inspiration and the phase of expiration, but at inspiration they are louder.
Moist rales may be fine bubbling, medium bubbling, and coarse bubbling according to the size of
the bronchi or cavity where they develop. Fine bubbling rales are formed in small bronchi, coarse
bubbling in large bronchi, large bronchiectases, cavities which communicate with large bronchi and are
filled with secretion. The mechanism of the rales formation in the large cavities is the same as in the
bronchi, because they always contain fluid. Fine rales are usually more numerous then coarse. They are
softer, briefer and more high-pitched than coarse ones. The sound of coarse rales is louder, longer, and
low-pitched. The rales can be heard in symmetrical areas of the lungs (diffuse bronchitis, marked
congestion in the lungs) or on a limited area of the chest (cavity in the lung, bronchiectasis, focal
pneumonia).
Moist rales are divided into two groups: sonorous and non-sonorous. Sonorous character of the
rales results from the presence of consolidated tissue around the bronchi with fluid secretion or
smooth-walled cavities of the lungs which are good conductors of the sound. The resonator is the cavity
itself. Coarse sonorous rales are also called cavitary.
 Dry rales either result from mucosa swelling or presence of viscous sputum in the bronchi. They
are heard in the initial stages of bronchitis or when exudation is stopped. Moist rales develop when the
content of the bronchi is liquid. They are heard at the height of bronchitis when exudation is liquid or in
edema of the lungs when fluid accumulated in the bronchi or in hemorrhage to the lungs when the
bronchi are overfilled with blood or in lung abscess or cavity. It means that moist rales have higher
prognostic significance than dry rales. From moist rales the most significant are fine rales because they
indicate location of the inflammatory process in the small bronchi, which, on the one hand, can be a sign
of ascending bronchitis, on the other is a danger of transition of the inflammatory process from the
small bronchi to the alveoli that is bronchitis can be complicated with pneumonia. This is especially
important in the cases when fine rales are heard over a limited area.
But there are cases when coarse rales are important. It is when they are heard in the areas of
the lungs where there are no large bronchi (lung apices or lower lobes). These coarse rales develop in
pathological cavities in the lung tissue. These may be abscesses, caverns, bronchiectases.
Crepitation is an auscultation phenomenon that develops in the alveoli. It is close to the moist
rales. It looks like a fine soft crack appearing when a small bundle of hairs is smoothed out above the
ear. Crepitation appears when alveolar walls are imbued with exudates or transudes. In the phase of
expiration the walls adhere, in the phase of inspiration they depart at the height of the maneuver.
Therefore crepitation is heard at the height of inspiration.
Crepitation suggests the presence of the changes in the alveoli and involvement of the lung
tissue itself. Crepitation is heard at inflammation of the lung tissue (initial and final stages of lobular
pneumonia), lung atelectasis, congestion, lung infarction.
At the lobular pneumonia, when the exudate only begins to saturate the walls of the alveoli
induction crepitation develops, at the period of resolution, when the exudate starts resolve, it is called
reduction crepitation.
Crepitation may be physiological. Transient crepitation may develop in elderly persons with
physiological atelectasis (when for a long time the lungs do not participate in respiration and are
collapsed).
At the pulmonary edema profound crepitation is heard at the beginning when the fluid starts
filling the alveoli, later moist rales develop. At the collapse of lung tissue crepitation appears when air
enters into the collapsed portions of the lungs.
Crepitation sounds resemble fine moist rales, but as their significance is different, because
crepitation are formed in the alveoli, but rales - in the bronchi. It is necessary to differentiate them. The
distinctive features are:
1. Crepitation is heard only at the height of inspiration; fine rales both during inspiration and
expiration.
2. Crepitation develops in the alveoli of similar size, the sounds are similar in character; fine
rales develop in bronchi of different size, the sounds are various.
3. Crepitation is more profound that fine rales because each acoustic sphere involves greater
amount of alveoli than bronchi.
4. Crepitation develops simultaneously like a burst; fine rales develop over a time.
5. Crepitation does not change after coughing, while fine rales change (increase in number,
disappear, change their character).
Pleura friction rub develops due to friction of the layers of the pleura, which has become rough,
uneven and dry as a result of a pathological process. In healthy individuals the visceral and parietal
layers of the pleura are smooth; their movement in the process of respiration is noiseless. Various
pathological processes can result in disturbances of the physical properties of the pleura, which is
responsible for more intensive friction of the layers and appearance of adventitious respiratory sound
named a pleura friction rub. These changes are mainly due to inflammation (pleurisy), which is
characterized by fibrin sedimentation on the pleura followed by formation of thick and uneven areas on
its surface. Other factors may also be responsible for pleura friction rub: tumor of the pleura, toxic
involvement (uremia), and dehydration of the organism (pleura dryness). Pleura friction rub is heard
both on inspiration and expiration.
The character of the sound is various: it may resemble tender friction, scratching, rustling of
paper, crunch of snow, and squeak of new leather. The character of the pleura friction rub can be
reproduced when two fingers are rubbed near the ear. Considerably pronounced pleura friction rub can
felt with a hand. Pleura friction rub is characterized by the following: 1) this is heard both on inspiration
and expiration; 2) the sound does not propagate considerably (when compared with rales) though it
sometimes involves larger areas, 3) the sound is intermittent, it develops in several maneuvers; 4) the
sound is superficial, it is heard near the ear, 5) the sound changes, it appears and disappears. At the
chronic diseases of pleura friction rub may be unchanged for years, 6) pain in the chest is frequent.
Pleura friction rub is usually heard along the median axillary line in the inferolateral portions of
the chest, where the respiratory excursion of the lungs is the greatest.
Not infrequently, it is difficult to differentiate pleura friction rub from moist rales. In this case
the following should be done:
1) Pressing the stethoscope increases pleura friction rub, rales do not change.
2) Cough and deep breathing in do not change pleura friction rub while rales change and even
disappear after coughing.
3) After breathing out the patient is asked to close the mouth and nose and to pull in and out
the abdomen like as abdominal respiration. The movement of the diaphragm causes sliding of the layers
of pleura, if the unclear phenomena are pleura friction rub, they would reappear; if they are moist rales,
they would stop because the air does not move through the airways and there are no conditions for
respiratory sound.
Pleura friction can be heard after pleurisy and is due to shrinkage or uneven thickening of the
layers of pleura.
Accessory respiratory sounds may appear in hydrothorax. They are splashing sound, dripping
sound.
Splashing sound (succussio Hippocratis) can be heard at shaking any cavity containing air and
fluid. This is present in hydropneumothorax. The sound is heard when the physician puts both hands on
the shoulders of the patient and quickly shakes the upper part of the patient's body. Splashing sound is
heard with the ear over the chest of the patient.
Dripping sound also appears in hydro- or pneumothorax, sometimes in a large cavern. It appears
when the drops of fluid drop from the upper cupola of the cavity on the surface of the fluid. It appears if
the patient sits up. Similar bell sound may appear due to a good resonance at formation of moist rales in
a large cavity with smooth walls.
Bronchophony (bronchophonia) is voice conduction felt as voice resonance. Bronchophony
results from conduction of the voice from the larynx through the air column in the bronchi to the
surface of the chest. This is determined by auscultation. This is heard on symmetrical sides of the chest.
The patient is asked to pronounce the words with low-pitch sounds.
In healthy subjects, the voice conducted to the surface of the chest is poorly heard and similar
on the both sides in symmetrical points. Speech in healthy individuals is felt like as unclear noise only in
the places where normal bronchial respiration is heard.
Bronchophony is heard when voice resonance increases and bronchial respiration appears, that
can be at the case of consolidation, infiltration or cavity formation. Sometimes bronchophony may be
amphoric or bell, separate words can be distinguished. This increased bronchophony (when the voice
appears in the place of auscultation) is called pectoriloquy.
Sometimes marked nasal squeaky tinkling sound resembling a goat's bleating may appear. This
is called egophony. The causes are unclear. It is frequently observed in pleural effusions over the upper
border and disappears when the exudate becomes large and reaches the top. Listening not only to
speech but also to whisper is of diagnostic significance. Whisper is heard only in the areas of the chest
(sternum, the area between the shoulder) where only bronchial respiration is normally heard.
In pathological conditions (a dense lung) conduction of whisper may propagate all over the lung.
Over the dense lungs, the whispered words become clear.
Listening to whispering has some advantages over bronchophony. This is a more sensitive
method of examination than listening to speech and demonstrates smaller dense foci than
bronchophony does. Owing to this sensitivity listening to whisper may be used to determine the borders
of large dense areas. At last, listening to whisper is a sparing method which can be used in severely ill
patients.
 The areas of the chest which require special attention at auscultation and percussion of the
lungs
1. Axillary area. Initial phenomena of pneumonia are frequently noted there; besides changes in
tuberculous infiltration located in the subclavicular area are heard high in the armpit.
2. Subscapular area corresponds to the base of the lungs and auxiliary pleural space; the signs of
compression and pleural effusion are first revealed in this area.
3. On the back and in axillary area corresponding tot he projection of the main interlobar cleft,
the changes in pneumonia can be revealed with auscultation and percussion.
4. The area between the scapulas corresponds to posterior mediastinum, upper portion to the
lung root, lower to the bronchi. The signs of enlargement of tracheobronchial lymph nodes, bronchial
compression, mediastinitis are determined in this area.
General information about the acoustic changes in the lung and pleura on percussion and
auscultation are shown in the following table.

Materials for self-control (added)

7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. – Vinnytsya: NOVA
KNYHA, 2006. – p. 112-119.
 Test for self-control
1. Which adventitious lung sound is formed in alveoli?
a. wheeze
b. moist rales
c. pleural frictional rub
d. crepitation
e. nothing mentioned above
2. Where is wheeze formed?
a. in the larynx
b. in the trachea
c. in the small bronchus
d. in the alveoli
e. in the pleural cavity
3. Where are buzzing dry rales formed?
a. in the larynx
b. in the trachea and big bronchi
c. in the small bronchi
d. in the alveoli
e. in the pleural cavity
4. Which phenomena are the adventitious lung sounds?
a. Rales
b. Crepitation
c. Pleural friction rub
d. All mentioned above
e. Northing mentioned above
5. Where is pleural friction rub formed?
a. in the larynx
b. in the trachea and big bronchi
c. in the small bronchi
d. in the alveoli
e. in the pleural cavity
6. Where are moist rales formed?
a. In the pleural cavity
b. In the alveoli
c. In the bronchi and lung cavities
d. In the bronchi
e. In the lung cavities
7. What is the main mechanism of the dry rales forming?
a. Swelling mucous membrane of the bronchus
b. Storing viscous secretion in the bronchus
c. Storing viscous secretion over the pleural sheets
d. Infiltration of the alveolar walls and their saturating with exudate that result in their adhering
e. Storing liquid secretion in the bronchi
8. What is the main mechanism of the moist rales forming?
a. Swelling mucous membrane of the bronchus
b. Storing viscous secretion in the bronchus
c. Storing viscous secretion over the pleural sheets
d. Infiltration of the alveolar walls and their saturating with exudate that result in their adhering
e. Storing liquid secretion in the bronchi
9. What is the main mechanism of the pleural friction rub forming?
a. Swelling mucous membrane of the bronchus
b. Storing viscous secretion in the bronchus
c. Storing viscous secretion over the pleural sheets
d. Infiltration of the alveolar walls and their saturating with exudate that result in their adhering
 e. Storing liquid secretion in the bronchi or lung cavities
10. What is the main mechanism of the crepitation forming?
a. Swelling mucous membrane of the bronchus
b. Storing viscous secretion in the bronchus
c. Storing viscous secretion over the pleural sheets
d. Infiltration of the alveolar walls and their saturating with exudate that result in their adhering
e. Storing liquid secretion in the bronchi or lung cavities
11. What adventitious lung sounds can be heard at the bronchial asthma?
f. Crepitation
g. Pleural friction rub
h. Wheezes
i. Moist rales
j. Nothing from adventitious lung sounds
12. What adventitious lung sound can be heard at the 1st stage of lobar pneumonia?
a. Crepitation
b. Pleural friction rub
c. Wheezes
d. Non-sonorous moist rales
e. Nothing from adventitious lung sounds
13. What adventitious lung sound can be heard at the dry pleurisy?
a. Crepitation
b. Pleural friction rub
c. Wheezes
d. Non-sonorous moist rales
e. Nothing from adventitious lung sounds
14. What adventitious lung sound can be heard at the pulmonary edema?
a. Crepitation
b. Pleural friction rub
c. Wheezes
d. Non-sonorous moist rales
e. Nothing from adventitious lung sounds
15 The sonorous moist rales are signs of…
f. Emphysema
g. Bronchitis
h. Pleural effusion
i. Pneumonia
j. Bronchial asthma
16. The buzzing dry rales are sign of…
a. Emphysema
b. Bronchitis
c. Pleural effusion
d. Pneumonia
e. Bronchial asthma
17. The non-sonorous moist rales are sign of …
a. Bronchial asthma
b. Fibrinous pleurisy
c. Lobar pneumonia
d. Exudative pleurisy
e. All answers are wrong
18. Appearance of the pleural friction rub at the patient with exudative pleurisy is sing of …
a. Increasing exudate
b. Obturative atelectasis in the lung collapse region
c. Decreasing exudate
d. Pneumothorax
 e. All answers are right depending on clinical situation
19. The sonorous coarse bubbling rales can be heard at the patient with…
a. Emphysema
b. Chronic abscess
c. Pleural effusion
d. Lobar pneumonia
e. Compressive atelectasis
20. The sonorous medium bubbling rales can be heard at the patient with …?
a. Emphysema
b. bronchiectasis
c. Acute bronchitis
d. Pleural effusion
e. Obturative atelectasis

Control questions
1. What is adventitious lung sounds, their classification?
2. Mechanism of producing dry rales, their classification and diagnostic importance.
3. Mechanism of producing moist (wet) rales, their classification and diagnostic importance
4. Mechanism of producing crepitation, their diagnostic importance
5. Mechanism of producing pleural friction rub, their diagnostic importance
6. What are differential signs between the moist rales and crepitation?
7. What are differential signs between the moist rales, crepitation and pleural friction rub?
Practical tasks
5. Auscultation of the lungs
6. Assessment main and adventitious lung sounds.
7. Distinguishing different adventitious lung sounds
8. Describing auscultation finding

Situation tasks
Task 1
28-year-old male patient complains on attacks of breathlessness. He occupied the forced position
with fixed shoulder girdle, his skin is cyanotic. At auscultation you hear rough vesicular breathe with
prolonged expiration and a lot of whistle sounds. You suppose acute asthma attack.
4. How the adventitious breath sounds is named?
5. Why do they appear?
6. How the percussion sound is changed at the patient?
Task 2
39-year-old female patient complains of dyspnea, cough and left side chest pain. The symptoms
appeared after hard work and overcooling 3 days before. At the visual inspection skin is pale and
cyanotic, respiratory rate is 32 and left part of the chest is left behind from right. At auscultation
you hear weakened vesicular breath sound and a fine soft crack in a pitch of the inspiration.
7. How the adventitious breath sound is named?
8. What is mechanism of their origin?
9. When this phenomenon can appear else?
Task 3
74-year-old female was admitted to pulmonology department with high fever (39°C), cough with
mucus sputum. During examination patient’s general condition is moderate severe, at auscultation
– weakened vesicular breath sound and sonorous fine bubbling sounds over lower right lobe.
7. How the auscultation phenomenon is named?
8. Why does it appear?
9. How the percussion sound is changed at the patient?
Task 4
47-year-old male patient notes dry cough and left side chest pain increasing at the deep breathing
and cough. Patient condition is moderate severe, left part of the chest is left behind from right. At
auscultation – weakened vesicular sound and rough like rustling of paper sound over lower left
lobe.
1. How the auscultation phenomenon is named?
2. Which disease is this phenomenon heard at?
3. Which position at the bed does patient occupy?
 TOPIC 6
Instrumental and laboratory methods of examination of the respiratory system
1.Importance of the topic
Instrumental and laboratory diagnostic procedures are used for establishing suspected
diagnosis or obtaining data that can help to reveal unclear or unexplained changes at the
patient’s condition. Modern additional methods of examination are very various and
informative. They are very important and indispensable for accurate and timely diagnostics of
the respiratory diseases.

2. Concrete aims:
─ Study main indications and methods of performing lung function tests (spirometry, peak
expiratory flow )
─ Learn main lung function parameters in a norm and their change at the obstructive and
restrictive defects
─ Study pulse oximetry and its diagnostic importance
─ Understand diagnostic importance of the bronchoscopy
─ Study method of performing pleural aspiration, its diagnostic importance
─ Study the laboratory examination of pleural fluid and sputum
─ Study X-ray and computer tomography investigations of the chest, main indications and
diagnostic importance

3. Basic training level

Previous subject Obtained skill

Biological physics Principles of radiology and optics
Normal anatomy Anatomy of the airways and lungs, their blood supply and
innervation
Normal physiology Mechanics of breathing, gas exchange in the lung and tissues of
system organs
Histology Ontogenesis of the respiratory tract, histological structure of the
respiratory tract and alveoli
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Definition
Peak expiratory flow The highest speed of flow in the beginning of forced expiration
Pulse oximetry Non-invasive assessment of peripheral O2 saturation
Obstructive defect Reduced speed parameters more than volume ones
Restrictive defect Reduced volume parameters more than speed ones
Fibreoptic bronchoscopy Assessment of the large airways using fibreoptic tube inserted into their
Pleural puncture Inserted special needle into pleural cavity for diagnostic or therapeutic
aspiration pleural fluid at the patient with pleural effusion

4.2. Theoretical questions:

28. What are the main indications for lung function test?
29. What parameter can be assessed using spirometry?
30. What pathologic changes of lung function are known?
31. What is diagnostic importance and indications to pulse oximetry?
32. What is diagnostic importance and indications to fibreoptic bronchoscopy?
33. What is diagnostic importance and indications to pleural aspiration?
34. Which parameters are investigated at the pleural fluid?
35. How is sputum investigated?
36. What are indications and diagnostic importance of the X-ray examination of the chest?
 37. What are indications and diagnostic importance of the computer tomography of the chest?
4.3. Practical task that should be performed during practical training
18. Assessment of the lung function reports
19. Assessment of the pulse oximetry report
20. Assessment of the X-ray films
21. Assessment of the sputum analysis
22. Assessment of the pleural fluid analysis
Topic content
Lung function tests
Spirometry is a measure of airflow and lung volumes during a forced expiratory maneuver from
full inspiration. It is the simplest of all respiratory functional tests. Indication for Lung function tests:
1. To evaluate for presence of lung disease
2. To assess severity and progression of known lung disease
3. To diagnose/differentiate obstructive vs restrictive lung disease
4. To assess the effectiveness of therapy
5. To evaluate the amount of disability
6. To assess postoperative complications.
Correct interpretation of spirometry requires that it be performed correctly. To obtain an
accurate recording the subject should be told to:
 stand or sit up straight
 inhale maximally ('breathe in all the way')
 get a good seal around the mouthpiece of the spirometer
 blow out as hard and as fast as possible ('blast out')
 continue to exhale until he or she can blow no more. In practice this is when less
than 50 mL has been exhaled over 2 seconds. Expiration should continue for at least
6 seconds and up to 15 seconds if necessary (some patients will find this exhausting
and prolonged manoeuvres should be used with caution)
 repeat until three technically acceptable maneuvers (no coughs, air leaks, false-
starts) are completed
Two FEV1s and FVCs within 200 mL and within 5% of each other should be obtained.
Using spirometry tidal volume (VT), vital capacity (VC), inspiratory reserve volume (IRV),
expiratory reserve volume (ERV), forced vital capacity (FVC), forced expiratory volume in 1s (FEV1),
forced expiratory flow between 25% and 75% of FVC (FEF25-75%), peak expiratory flow (PEF), maximum
voluntary ventilation (MVV) can be measured.
All spirometry parameters depend on patient age, sex, height and weight. They are calculated by
computer programs of spirometer and named predictor value. For patient normal values of lung
function are 80% and more from predictor.
The FEV1/FVC ratio gives a good estimate of severity of airflow obstruction; normal ratio is 75-
80%.
In case of obstructive defects (for example COPD or asthma) FEV1 is reduced more than the FVC
and FEV1/FVC ratio is< 70%.
In case of restrictive defects (for example lung fibrosis, sarcoidosis, pneumoconiosis, interstitial
pneumonias, connective tissue diseases, pleural effusion, obesity, kyphoscoliosis, neuromuscular
problems) FVC is reduced and the FEV1/FVC ratio is normal or raised.
Peak expiratory flow (PEF) is measured by a maximal forced expiration through a peak flow
meter. It correlates well with the forced expiratory volume in 1 second (FEV1) and is used as an
estimate of airway caliber. Peak flow rates should be measured regularly in asthmatics to
monitor response to therapy and disease control.
Pulse oximetry allows non-invasive assessment of peripheral O 2 saturation. It provides a useful
tool for monitoring those who are acutely ill or at risk of deterioration. On most pulse
oximeters, the alarm is set at 90%. An oxygen saturation of <80% is clearly abnormal and action
is required (unless this is normal for the patient, eg in COPD. Here, check arterial blood gases
(ABG) as PaCO2 may be rising despite a normal P aO2). Erroneous readings may be caused by:
poor perfusion, motion, excess light, skin pigmentation, nail varnish, dyshaemoglobinaemias,
and carbon monoxide poisoning.
Fibreoptic bronchoscopy is an essential tool in the investigation of many forms of
respiratory diseases. Under local anaesthesia, the flexible bronchoscope is passed through the
nose, pharynx and larynx, down the trachea, and the bronchial tree is then inspected.
Diagnostic indications:
 suspected lung cancer,
 slowly resolving pneumonia,
 pneumonia in the immunosuppressed,
 interstitial lung disease.
Bronchial lavage fluid may be sent to the lab for microscopy, culture, and cytology.
Mucosal abnormalities may be brushed (cytology) and biopsied (histopathology). Flexible
biopsy forceps are passed down a channel inside the bronchoscope, and are used to obtain
tissue samples for histological examination. In diffuse interstitial lung disease, such as
sarcoidosis or pulmonary fibrosis, the technique of transbronchial biopsy can be used to obtain
small specimens of lung parenchyma for histological examination and confirmation of the
diagnosis.
Therapeutic indications:
 aspiration of mucus plugs causing lobar collapse,
 removal of foreign bodies,
 stopping lung bleeding.
Complications: respiratory depression, bleeding, pneumothorax
Roentgenography or X-ray examination is commonly and widely used for diagnostics of
the different respiratory diseases. It is obviously for confirming pneumonia, tuberculosis,
pleural effusion, pneumotorax and revealing some form of lung cancer and other. For
diagnostics of the respiratory diseases it should be performed in two positions:
posterioranterior and lateral. If patient is bedridden anteriorposterior position is used but films
of this position are inferior to posterioranterior view. Assessing X-ray film of the chest includes
position, shadow of soft tissue (breast at women or subcutaneous layer at obesity patients,
muscle and other), bones, diaphragm position, clear, opacity, different types of nodular
shadows, mediastinum, heart and roots (hilum).
Computed tomography is cross-sectional scanning of the chest. This technique is more
sensitive than plain radiography in detecting respiratory abnormalities. Computed tomography
makes possible to distinguish more accurate tumors, small indurations, cavities and caverns in
the lungs. This method is far better than radiographic studies at characterizing tissue density,
distinguishing subtle differences in density between adjacent structures, and providing
accurate size assessment of lesions. Indications for computed tomography:
 Evaluation of suspected interstitial lung diseases, pulmonary nodules and
subpleural lesions when X-ray is normal or nonspecific
 Characterization of interstitial lung diseases or solitary pulmonary nodules
 Diagnosis of bronchiectasis (it replaced bronchography)
 Detecting or confirming presence of mediastinal mass and its size
 Differentiating pleural from parenchymal masses/ abnormalities
Magnetic resonance imaging provides a less detailed view of the pulmonary parenchyma
as well as poor spatial resolution. However, magnetic resonance imaging offers several
advantages over computed tomography in certain clinical settings: for imaging abnormalities
near the lung apex, the spine, and the thoracoabdominal junction. Vascular structures can be
distinguished from nonvascular without the need of contrast.
Bronchography is an integral part of the diagnosis evaluation of diseases of bronchi. The
standard technique requires the injection of contrast medium, usually iodolipol, into the
bronchi lumen. This may be done through a catheter passed via the nose or mouth through the
anaesthetized larynx. Then radiographs are taken, that give a distinct patterns of the bronchial
tree. This procedure is of particular importance to the evaluation of bronchiectasis, abscesses,
caverns in the lungs, and compression of the bronchi by tumor.
Sputum examination Collect a good sample; if necessary ask a physiotherapist to help. Note
the appearance: clear and colourless (chronic bronchitis), yellow/green (pulmonary infection),
red (haemoptysis), black (smoke, coal), or frothy white/pink (pulmonary oedema). Send the
sample to the laboratory for microscopy (Gram stain and auramine/ZN stain, if indicated),
culture, and cytology.
Thoracentesis is performed to aspirate pleural fluid for diagnostic purposes and in case of a
large effusion to remove fluid from pleural cavity.
Laboratory assessment of pleural fluid:
1. Common – visual assessment, comparative density, Rivalt test
2. Biochemistry for measurement of protein, LDH, glucose, cholesterol, triglycerides, amylase,
depending on the clinical circumstances.
3. Cytology for examination for malignant cells and differential cell count
4. Microbiology for Gram stain and microscopy, culture, MBT examination
Is the pleural effusion a transudates or exudates?
Sign transudates exudates
comparative density < 1,015-1,018 >1,018
Rivalt test negative positive
protein <30 g/l >30 g/l
Pleural fluid protein/serum protein ratio <0,5 >0,5
LDH <1,6 mMol/l >1,6 mMol/l
Pleural fluid LDG/serum LDG ratio <0,6 >0,6
erythrocytes <10*109/l >100*109/l
leucocytes <1*109/l >1*109/l
pH >7,3 <7,3
glucose 3,3-5,5 mMol/l <3,3 mMol/l

Materials for self-control (added)

7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. – Vinnytsya: NOVA
KNYHA, 2006. – p. 119-137.
 Test for self-control
1. What is a spirometry?
a. Measuring airflow and lung volumes during a forced expiratory maneuver from full inspiration
b. Measuring inspiratory volume
c. Measuring tidal volume
d. Measuring airflow
e. All mentioned above
2. Which parameters can be measured with open spirometry?
a. FEV1, FVC
b. TLC, RAV
c. O2 saturation
d. O2 consumption
e. all mentioned above
3. Which types of the ventilation disorders do you know?
a. obstruction
b. restriction
c. mixed
d. all mentioned above
e. northing mentioned above
4. If patient’s FEV1 is low and FVC is normal, he has…
f. Normal lung function
g. Restriction
h. Obstruction
i. mixed disorder
j. Northing mentioned above
5. If patient’s FVC is low and FEV1 is normal, he has…
a. Normal lung function
b. Restriction
c. Obstruction
d. mixed disorder
e. Northing mentioned above
6. What is the lower limit of the normal parameters of lung function?
f. 100% from predicted
g. 90% from predicted
h. 85% from predicted
i. 80% from predicted
j. 70% from predicted
7. Ratio FEV1/FVC is used for diagnostics of
f. Severity of lung function disorders
g. Types of lung function disorders
h. This ratio is obsolete and now is useless
i. Patient’s constitution
j. Northing mentioned above
8. What is a peak flowmetry?
f. Measuring speed of the airflow
g. Measuring expiratory volume
h. Measuring inspiratory volume
i. Measuring vital capacity
j. Measuring minute volume
9. What is pulse oximetry?
f. Non-invasive method of estimation O2 saturation
g. Measuring blood gas (CO2 and O2) pressure
h. Measuring blood O2 concentration
i. Method of measuring pulse and respiratory rate
 j. Method of measuring pulse and pulmonary blood pressure
10. What is normal level of the O2 saturation?
f. 75-80%
g. 80-85%
h. > 70%
i. > 90%
j. 85-90%
11. What is diagnostic indication for bronchoscopy?
k. Suspected lung cancer
l. Slowly resolving pneumonia
m. Interstitial lung disease
n. Pneumonia in the immunosuppressed patients
o. All mentioned above
12. What is therapeutic indication for bronchoscopy?
f. aspiration of mucus plugs causing lobar collapse
g. removal of foreign bodies
h. stopping lung bleeding
i. aspiration purulent copious sputum at the debilitated patient
j. All mentioned above
13. Which radiologic method of lung examination is routinely used?
f. Computed tomography
g. Magnetic resonance imaging
h. Bronchography
i. X-ray
j. Nothing from above
14. Which radiologic method of lung examination has the highest level of resolution for distinguishing
the smallest lung structures?
a. Computed tomography
b. Magnetic resonance imaging
c. Bronchography
d. X-ray
e. Nothing from above
15 Which method of sputum examination is used for establishing the pathogen of pneumonia?
k. General macro- and microscopic
l. Cytological
m. histological
n. Cultural
o. Northing from above
16. Which method of sputum examination is used for establishing revealing tuberculosis
mycobacterium?
a. Microscopic with Gram staining
b. Microscopic with Ziehl-Nielsen staining
c. Microscopic with Romanovskiy-Himza staining
d. Microscopic without staining
e. Macroscopic
17. Which method of sputum examination may help to establish lung cancer?
a. General macroscopic
b. Cytological
c. General microscopic
d. Cultural
e. Northing from above
18. How long should be sputum transported to laboratory for bacteriological investigation?
 a. Urgent delivery
b. Under 1 hour
c. Under 2 hours
d. Under 24 hours
e. Under 24-72 hours
19. Which property could not transudes have?
a. Light yellow color
b. Protein 60 g/l
c. Negative Rivalt test
d. 1-5 leucocytes
e. 2-3 epitheliocytes
20. Which property could not exudates have?
a. Light yellow color
b. Protein 60 g/l
c. Negative Rivalt test
d. 15-20 leucocytes
e. 5-7 epitheliocytes

Control questions
38. What are the main indications for lung function test?
39. What parameter can be assessed using spirometry?
40. What pathologic changes of lung function are known?
41. What is diagnostic importance and indications to pulse oximetry?
42. What is diagnostic importance and indications to fibreoptic bronchoscopy?
43. What is diagnostic importance and indications to pleural aspiration?
44. Which parameters are investigated at the pleural fluid?
45. How is sputum investigated?
46. What are indications and diagnostic importance of the X-ray examination of the chest?
47. What are indications and diagnostic importance of the computer tomography of the chest?
4.3. Practical task that should be performed during practical training
23. Assessment of the lung function reports
24. Assessment of the pulse oximetry report
25. Assessment of the X-ray films
26. Assessment of the sputum analysis
27. Assessment of the pleural fluid analysis

Situation tasks
Task 1
20-year-old male patient, height 170 sm, never smoked, complaints of episodic wheeze and chest
tightness, particularly in the early morning and during exercise. At auscultation you hear rough
vesicular breathe.
7. Which functional method of examination should be performed for establishing diagnosis?
8. Which functional method of examination should be administered for control of the patient
condition?
9. Which test must be performed for confirming reversibility of obstruction?
Task 2
39-year-old female patient complains of dyspnea, cough with purulent sputum and left side chest
pain. The symptoms appeared after hard work and overcooling 3 days before. At the visual
inspection skin is pale and cyanotic, respiratory rate is 32 and left part of the chest is left behind
from right. At auscultation you hear weakened vesicular breath sound and a fine soft crack in a pitch
of the inspiration.
10. Which investigation must be performed for establishing diagnosis?
11. How must sputum be examined?
12. What method allows assessing respiratory failure?
Task 3
74-year-old male was admitted to pulmonology department with hemoptysis. During examination
patient’s general condition is moderate severe, at auscultation – weakened vesicular breath sound
over lower right lobe. You suppose a lung cancer.
1. Does the sputum examination useful in this case? Why?
2. How should patient be investigated?
3. Which method can help you to confirm diagnosis?
Task 4
47-year-old female patient notes dry cough and left side chest pain increasing at the deep breathing
and cough. Patient condition is moderate severe, diffuse cyanosis; left part of the chest is left
behind from right. At auscultation – absent of vesicular breathing over lower left lobe. You suppose
a pleural effusion.
4. Which change can be at the patient’s X-ray film?
5. What procedure is mandatory in this case?
6. What investigations of the pleural fluid must be performed for establishing diagnosis?
 TOPIC 7
Syndromes of lobar and focal consolidations of lung tissue, pleural
effusion, pneumothorax, atelectasis
2. Importance of the topic
Syndromic diagnostics is one of the important components at the diagnostic process.
Revealing pathogenic relation between different symptoms and signs forms integral estimate
about patient’s condition. It is indispensable to correct diagnosis and treatment.

2. Concrete aims:
─ Study main symptoms and signs of the syndromes of focal and lobar consolidation of the
lung tissue
─ Learn main instrumental methods that can help to establish consolidation of the lung tissue
─ Study main symptoms and signs of the syndrome of pleural effusion
─ Learn basic investigations that should be performed for confirming pleural effusion and
laboratory examinations of the pleural fluid
─ Study main symptoms, signs of pneumothorax, its instrumental diagnostics
─ Master causes, symptoms and signs of the different types of atelectasis, their instrumental
diagnostics

3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the airways and lungs, their blood supply and
innervation
Normal physiology Mechanics of breathing, gas exchange in the lung and tissues of
system organs
Histology Ontogenesis of the respiratory tract, histological structure of the
respiratory tract and alveoli
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine respiratory patients
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Definition
Consolidation of the lung Pathologic process when alveoli are felt with inflammatory exudates,
tissue transudates, blood tumor cells or others
Pleural effusion Accumulation of fluid in the pleural cavity
Transudates Non-inflammatory fluid that can accumulate in pleural cavity, alveoli,
bronchus and others
Exudates Inflammatory fluid that can accumulate in pleural cavity, alveoli, bronchus
and others
Pneumothorax Accumulation of air in the pleural cavity
Atelectasis Collapse of lung tissue

4.2. Theoretical questions:

1. What is definition and causes of syndromes of lobar and focal consolidation of lung tissue?
2. What are symptoms and signs of the lobar and focal consolidation of the lung tissue?
3. How can consolidation of the lung tissue be confirmed by instrumental examination?
4. What is definition and causes of the pleural effusion?
5. What are symptoms and signs of the pleural effusion?
6. How pleural effusion can be confirmed by instrumental examination?
 7. How pleural fluid should be investigated with laboratory methods
8. What is definition and causes of the pneumothorax?
9. What are symptoms and signs of the pneumothorax?
10. What is definition and causes of the atelectasis?
11. Which types of atelectasis do you know; their distinguishing symptoms and signs?
4.3. Practical task that should be performed during practical training
28. Revealing and assessment of symptoms and signs of focal and lobar consolidation of the lung tissue
29. Revealing and assessment of symptoms and signs of pleural effusion
30. Revealing and assessment of symptoms and signs of pneumothorax
31. Revealing and assessment of symptoms and signs of atelectasis
32. Assessment of the pleural fluid analysis
Topic content
Lobar and focal consolidation of lung tissue is the complex of symptoms that appears after effect on the
lung different pathogenic mechanisms resulting to pulmonary infiltrate or proliferation. The lobar
consolidation involves some segments or whole lobe of lung. The focal consolidation involves small site
of lung tissue.
Causes of the lobar consolidation of lung tissue:
1. Community-acquired and nosocomial pneumonia – infiltration of lung by inflammatory cells due
to non specific inflammation
2. Lobar tuberculosis - infiltration of lung by inflammatory cells due to specific inflammation
3. Lobar pneumofibrosis – proliferation at lung by connective tissue
4. Lung cancer and tumor - proliferation at lung by tumorous tissue
5. Infarction-pneumonia at patients with sub-massive pulmonary embolism - infiltration of lung by
blood and inflammatory cells
Causes of the focal consolidation of lung tissue
1. Community-acquired, nosocomial, aspiration pneumonia
2. Focal tuberculosis
3. Focal pneumofibrosis
4. Lung tumor
Symptoms of the focal consolidation of lung tissue: Sometimes there is breathlessness because small
part of lung is involved, lung function and gas exchange is not limited.
Cough can be dry or with purulent sputum. It is depended from stage of disease.
Signs of the focal consolidation of lung tissue:
Visual examination of the chest
Sometimes there is limitation of the chest moving at the affected side.
Palpation of the chest
May be, there is a tenderness of the pleural points, positive Potendzher symptom, amplifying of voice
resonance if the site of consolidation is near surface of chest.
Percussion of the chest
Comparative percussion: If site of consolidation is near of the chest surface it can be dullness of
percussion sound. Because account of solid components of lung tissue increase due to infiltration but air
presents in alveoli which haven’t been involved to pathological process and they get to percussion
sphere. If site of consolidation is deeply in lung percussion sound is clear without change.
Topographic percussion: Some change can be if site of consolidation is near of chest surface. There is
dimension of lower lung border excursion.
Auscultation of the lung
There is diminished vesicular breathing because less alveoli involve to act of breathing. There are
sonorous bubbling (moist) rales. They are formed in bronchus which around by consolidated lung tissue.
Such tissue conduct sounds from bronchus better then healthy and we can hear them as sonorous.
Sometimes if site of consolidation is near chest surface crepitations can be heard.
X-ray signs of the focal pulmonary consolidation: There is peribronchial and perivascular and/or focal
infiltration of lung tissue.
Symptoms of the lobar consolidation of lung tissue:
 o Breathlessness occurs due to large injury of lung that result to diminution of it function and
changing of gas content of blood.
o Chest pain happens due to involving of pleura in inflammatory process.
o Cough can be dry or with purulent bloody sputum. It is depended from stage or form of disease.
Signs of the lobar consolidation of lung tissue
Visual examination: It is severe condition of the patient. He has redness in cheek at the affected side,
herpes on his lips, sometimes prefers to lie on the affected side. There is tachypnea, cyanosis.
Visual examination of the chest: There is limitation of the chest moving at the affected side. Auxiliary
muscles take part in breathing.
Palpation of the chest
There is a tenderness of the pleural points, positive Potendzher symptom, because large part of lung
with pleura is involved to inflammatory process and surrounded tissues react to this. It is obtained
amplifying of voice resonance according to the affected lobe or segments, because consolidated lung
tissue conducts acoustic waves better than normal one.
Percussion of the chest
Comparative percussion: Over the consolidated lobe the percussion sound is dull because only solid
components of infiltrated lung tissue get to percussion sphere.
Topographic percussion: The lower border of the affected lung lifts up if pathological process localizes in
lower lobe. The height of lung apex pulls down. But size of the lung doesn ’t change. It is obtaining due to
increasing of solidity of lung tissue. There is dimension of lower lung border excursion.
Auscultation of the lung
There is pathological bronchial breathing because all alveoli are filled up with inflammatory exudates,
whispering pectoriloquy. There is pleural rub due to inflamed pleura rubbing against each other. You can
hear depressed vesicular or bronchial breathing and crepitations in the beginning or end of pathological
process.
X-ray signs of lobar pulmonary consolidation: There is intensive and homogeneous infiltration of lobe
or segments.
A pleural effusion results from the accumulation of abnormal volumes (>10-20 ml) of fluid in the pleural
space. According to causes of pleural effusion and content of pleural fluid there are two types –
exudates and transudates.
Causes of the pleural effusion:
1. Cardiac failure
2. Pneumonia
3. Tuberculosis
4. Malignancy
5. Pulmonary embolism
6. Chest injury
7. Liver cirrhosis, pancreatitis and other
Symptoms of the pleural effusion:
It may be asymptomatic if little quantity of fluid accumulates in pleural space.
It is associated with breathlessness, dry cough, chest pain (suggesting pleural inflammation), chest
“heaviness”, palpitation, if quantity of fluid is large (more than 400-500 ml).
Signs of the pleural effusion:
Visual examination
It is a severe condition of the patient. There is tachypnea, cyanosis and limitation of the chest moving at
the affected side. Patient prefers to lie on the affected side because it facilitates his breathing.
Palpation of the chest
It is obtained reduced or absent tactile vocal fremitus, because fluid damps acoustic waves, and
increased chest resistance. Sometimes, may be positive Potendzher symptom.
Percussion of the chest
Comparative percussion: It is dullness over fluid.
Topographic percussion: Lower lung border has shape named Ellis-Damuazo line which begins near
column and rises to scapular then descends to axillary region and continues horizontally. This shape of
line makes conditional upon different property of lung tissue to be squeezed.
Auscultation of the lung
There are no any sounds over the fluid. But sometimes may be diminished vesicular breathing if it is
little quantity of fluid. You can hear diminished bronchial breathing if quantity of fluid much and
squeezed lung has similar density as fluid. Above the fluid it is diminished vesicular breathing and,
sometimes, pleural rub.
X-ray signs of the pleural effusion: It is usually detected effusion volumes of 200 ml or more by
posterior-anterior position. Lateral chest X-ray is more sensitive and may detect as little as 50 ml pleural
fluid. Classical chest X-ray appearance is of basal opacity obscuring hemidiaphragm, with concave upper
border. Massive effusion may result in a ‘white-out ’ of the hemithorax, with mediastinal displacement
away from the effusion. Lack of the mediastinal shift in such cases raises the possibility of associated
volume loss due to bronchial obstruction from a primary lung cancer.
Ultrasound is extremely sensitive at detecting fluid volumes of 100 ml or more, and is useful for
distinguishing pleural fluid from pleural masses or thickening, and for demonstrating loculation.
Laboratory assessment of pleural fluid:
1. Common – visual assessment, comparative density, Rivalt test
2. Biochemistry for measurement of protein, LDH, glucose, cholesterol, triglycerides, amylase,
depending on the clinical circumstances.
3. Cytology for examination for malignant cells and differential cell count
4. Microbiology for Gram stain and microscopy, culture, MBT examination
Is the pleural effusion a transudates or exudates?
Sign transudates exudates
comparative density < 1,015-1,018 >1,018
Rivalt test negative positive
protein <30 g/l >30 g/l
Pleural fluid protein/serum protein ratio <0,5 >0,5
LDH <1,6 mMol/l >1,6 mMol/l
Pleural fluid LDG/serum LDG ratio <0,6 >0,6
erythrocytes <10*109/l >100*109/l
leucocytes <1*109/l >1*109/l
pH >7,3 <7,3
glucose 3,3-5,5 mMol/l <3,3 mMol/l
A pneumothorax is an air in the pleural space; may occur with apparently normal lungs (primary
pneumothorax) or in the presence of underlying lung disease (secondary pneumothorax); may occur
spontaneously or following trauma.
Causes of pneumothorax:
1. It occurs following an air leak from apical bullae.
2. Underlying diseases: COPD, asthma, interstitial lung disease, necrotizing pneumonia,
tuberculosis, Pneumocystis carinii pneumonia, cystic fibrosis, Langerhans’cell histiocytosis,
lymphangioleiomyomatosis, Marfan’s syndrome, oesophageal rupture, lung cancer, catamenial
pneumothorax, pulmonary infarction.
Spontaneous – due to rupture of blebs, usually in thin tall young males with history of smoking
Traumatic – iatragenic (i.e. subclavian central line insertion, excessive PPV, thoracic surgery,
transbronchial lung biopsy) or penetrating chest trauma (knife, bullet).
Tension – most serious: air enters on inspiration but cannot escape on expiration = pneumothorax
size increases with each breath. Lung eventually collapses under increasing pressures.
Symptoms of pneumothorax:
o Acute pleuritic chest pain due to rupture of pleura
o Acute breathlessness. It is often minimal in young patients and is more severe in secondary
pneumothorax and if it is tension pneumothorax/
o Sometimes can be dry cough.
Signs of pneumothorax
Visual examination: It is severe condition of the patient. He has tachypnea, cyanosis, tachycardia. May
be feel “bubbles” and “crackles” under the skin of the torso and neck if there is subcutaneous
emphysema.
Visual examination of the chest: Chest is asymmetric – affected side is increased. There is diminished
chest excursion on the affected side. Auxiliary muscles take part in breathing.
Palpation of the chest
It is obtained absent tactile vocal fremitus, because air in pleural space damps acoustic waves. Chest
resistance is increased. Sometimes there is a tenderness of the pleural points, positive Potendzher
symptom; because pleura is involved to pathology process and surrounded tissues react to this.
Percussion of the chest
Comparative percussion: Over affected lung the percussion sound is hyper-resonant.
Topographic percussion: Erroneously the lower border of the affected lung descends down and apex of
lung lifts up when you make percussion but in reality lung collapses. Lower lung border excursion is
absent.
Auscultation of the lung
There is quiet or absent breath sounds on the pneumothorax side.
X-ray signs of pneumothorax: no lung markings on affected side peripheral to edge of collapsed lung
and depressed diaphragm, tracheal/mediastinal shift to unaffected side.
Atelectasis is complex of symptoms and signs when part of lung or whole lung doesn ’t content air or
content less air than normal and it collapses.
Classification:
Obstructive – due to occlusion of the airways
Compressive – due to pressure of lung by fluid or air in pleural space.
Causes of obstructive atelectasis:
1. Central lung cancer
2. Characinoid of bronchus
3. Foreign body of bronchus
4. Tumor of mediastinum
5. Enlarged lymphonodules of mediastinum or tracheal-bronchial, bronchial-pulmonary ones due
to tuberculosis or metastasis.
Causes of compressive atelectasis:
1. Pleural effusion
2. Pneumothorax
3. Tumor of pleura
4. Deformation of chest.
Sign and symptoms of obstructive atelectasis
Breathlessness
Visual examination
If atelectasis large, there is severe condition o patient, tachypnea, cyanosis. Chest is asymmetric –
affected side and chest excursion is diminished.
Palpation of the chest
It is obtained diminished or absent tactile vocal fremitus, because collapsed lung tissue damps acoustic
waves. Chest resistance is increased.
Comparative percussion: It is dullness over atelectasis.
Topographic percussion: Lower lung border is lifted up by collapsed segments.
Auscultation of the lung
There are no any sounds over the atelectasis because air doesn ’t come into alveoli.
Sign and symptoms of compressive atelectasis
Breathlessness
Visual examination
If atelectasis large, there is severe condition o patient, tachypnea, cyanosis. Chest is asymmetric –
affected side is bigger than normal and chest excursion is diminished.
Palpation of the chest
It is obtained diminished or absent tactile vocal fremitus, because collapsed lung tissue damps acoustic
waves. Chest resistance is increased.
Comparative percussion: It is dullness over atelectasis.
Topographic percussion: Lower lung border is lifted up by collapsed segments.
Auscultation of the lung
There is diminished bronchial sound over the atelectasis because collapsed lung tissue conducts acoustic
waves from bronchus.
X-ray signs of atelectasis and addicted methods of diagnostics of atelectasis.
Diminished volume and elevated hemidiaphragm on affected side; mediastinal shift to affected side;
increased opacity; scattered densities.
Materials for self-control (added)

7. Reference source

o Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000 – P.85-86, 658-659, 668-669.

 Test for self-control
1. Syndrome of the focal consolidation of the lung tissue can be if patient has:
a. focal pneumonia;
b. focal pneumofibrosis;
c. focal tuberculosis;
d. lung cancer;
e. all mentioned above.
2. Syndrome of the lobar consolidation of the lung does not reveal at patient with…
a. Lobar pneumonia
b. Infiltrative tuberculosis
c. Pulmonary embolism with infarction-pneumonia
d. COPD
e. Lung cancer
3.At the patient with lobar consolidation at palpation of the chest can be obtained
a. Amplifying vocal fremitus on the affected side
b. Weakened vocal fremitus on the affected side
c. Vocal fremitus does not change
d. Vocal fremitus is absent
e. Amplifying vocal fremitus on the health side
4.At the patient with focal consolidation near the root of lung at palpation of the chest can be
obtained
a. Amplifying vocal fremitus on the affected side
b. Weakened vocal fremitus on the affected side
c. Vocal fremitus does not change
d. Vocal fremitus is absent
e. Amplifying vocal fremitus on the health side
5.Pathological bronchial breathing is heard at patients with:
a. focal consolidation
b. lobar consolidation
c. pleural effusion
d. emphysema
e. acute bronchitis
6.Percussion sound of the lobar consolidation of lung tissue is:
a. tympanic
b. clear
c. resonance
d. dull
e. small dull
7.Auscultation signs of the focal consolidation is:
a. Vesicular breathing with prorogated exhalation and wheeze
b. Absent of the any breath sound
c. Diminished vesicular breathing and sonorous bubbling (moist) rales
d. Unchanged vesicular breathing
e. Pathological bronchial breathing
8.Auscultation signs of the lobar consolidation is:
f. Vesicular breathing with prorogated exhalation and wheeze
g. Absent of the any breath sound
h. Diminished vesicular breathing and sonorous bubbling (moist) rales
i. Unchanged vesicular breathing
j. Pathological bronchial breathing
9. Obstructive atelectasis can be if patient has:
a. Lung cancer;
b. Metastasis into pulmonary lymphonodes;
c. Foreign body of bronchus;
 d. Tuberculosis of the pulmonary lymphonodes;
e. all mentioned above.
10. Compressive atelectasis can be if patient has:
a. Pleural tumor (mesotelioma);
b. Massive pleural effesion;
c. Pneumothorax;
d. Deformation of the chest;
e. all mentioned above.
11. Percussion sound over massive pleural effusion:
a. tympanic
b. clear
c. resonance
d. dull
e. small dull
12. Percussion sound over pneumothorax:
a. tympanic
b. clear
c. resonance
d. dull
e. small dull
13. Auscultation signs of pneumothorax:
a. Diminished vesicular breathing and wheeze
b. Diminished vesicular breathing and crackles
c. absent of breath sounds
d. unchanged breath sound
e. Pathological bronchial breathing
14. Auscultation signs of massive pleural effusion:
a. Diminished vesicular breathing and wheeze
b. Diminished vesicular breathing and crackles
c. absent of breath sounds
d. unchanged breath sound
e. Pathological bronchial breathing
15. If patient has massive pleural effusion vocal fremitus is:
a. Absent on the affected side
b. Increased on the affected side
c. Diminished on the affected side
d. Normal
e. Increased on the health side
16. Percussion sound over small pleural effusion:
a. tympanic
b. clear
c. resonance
d. dull
e. small dull
17.If patient has small pleural effusion vocal fremitus is:
a. Absent on the affected side
b. Increased on the affected side
c. Diminished on the affected side
d. Normal
e. Increased on the health side
18. Which properties does transudate have?
f. Light yellow color
g. Protein < 30 g/l
h. Negative Rivalt test
 i. 1-5 leucocytes and 2-6 mezoteliocytes
j. All mentioned above
19. Which properties does not exudate have?
a. Comparative density < 1,018
b. Protein > 30 g/l
c. Positive Rivalt test
d. 10-25 leucocytes and 2-6 mezoteliocytes
e. Yellow color
20. Percussion sound of the focal consolidation of lung tissue is:
a. tympanic
b. clear
c. resonance
d. dull
e. small dull

Control questions
1. What is definition and causes of syndromes of lobar and focal consolidation of lung tissue?
2. What are symptoms and signs of the lobar and focal consolidation of the lung tissue?
3. How can consolidation of the lung tissue be confirmed by instrumental examination?
4. What is definition and causes of the pleural effusion?
5. What are symptoms and signs of the pleural effusion?
6. How pleural effusion can be confirmed by instrumental examination?
7. How pleural fluid should be investigated with laboratory methods
8. What is definition and causes of the pneumothorax?
9. What are symptoms and signs of the pneumothorax?
10. What is definition and causes of the atelectasis?
11. Which types of atelectasis do you know; their distinguishing symptoms and signs?
4.3. Practical task that should be performed during practical training
1. Revealing and assessment of symptoms and signs of focal and lobar consolidation of the lung
tissue
2. Revealing and assessment of symptoms and signs of pleural effusion
3. Revealing and assessment of symptoms and signs of pneumothorax
4. Revealing and assessment of symptoms and signs of atelectasis
5. Assessment of the pleural fluid analysis

Situation tasks
Task 1
40-year-old male patient, height 180 sm, long time smoked, suddenly feels knife-like pain in the
chest and breathlessness after physical extension. At visual examination left part of the chest
enlarged and is left behind from right in breathing, at percussion – resonant sound, at auscultation –
breathing is absent.
10. What syndrome has developed at the patient?
11. Which investigation should be performed to confirm it?
12. How is respiratory rate changed at the patient?
Task 2
19-year-old female patient complains of dyspnea, cough with purulent sputum and left side chest
pain. The symptoms appeared after hard work and overcooling 3 days before. At the visual
inspection skin is pale and cyanotic, respiratory rate is 32 and left part of the chest is left behind
from right. At auscultation you hear pathological bronchial breathing.
13. What syndrome has developed at the patient?
14. What signs of the syndrome can be obtained by percussion?
15. What investigation should be used for confirming syndrome?
Task 3
79-year-old male was admitted to pulmonology department with hemoptysis and breathlessness.
During examination patient’s general condition is moderate severe, skin is pale and cyanotic; at
auscultation – weakened vesicular breath sound over lower right lobe. You suppose a central lung
cancer.
4. What syndrome has developed at the patient?
5. What signs of the syndrome can be obtained by percussion?
6. Which method can help you to confirm diagnosis?
Task 4
55-year-old female patient notes dry cough, breathlessness and palpitation. Patient condition is
severe, diffuse cyanosis; right part of the chest is left behind from left. At percussion – dull sound
over lower right lobe.
7. What syndrome has developed at the patient?
8. What signs of the syndrome can be obtained by auscultation?
9. What investigations are mandatory for establishing diagnosis?
 TOPIC 8
Clinical presentation of community-acquired pneumonia, pleurisies, lung cancer
and pneumosclerosis
3. Importance of the topic
Pneumonias, pleurisies and lung cancer are common respiratory diseases. Sometimes
they have similar clinical presentation. It is very important to know distinguishing
these pathologic conditions because patient’s life, its quality and ability depend on
right, timely diagnostics of the diseases.

2. Concrete aims:
─ Study main symptoms and signs of the pneumonias, their classification
─ Study main symptoms and signs of the dry and exudative pleurisies
─ Learn types, main symptoms and signs of the lung cancer
─ Master causes, symptoms and signs of pneumosclerosis

3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the airways and lungs, their blood supply and
innervation
Normal physiology Mechanics of breathing, gas exchange in the lung and tissues of
system organs
Histology Ontogenesis of the respiratory tract, histological structure of
the respiratory tract and alveoli
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine respiratory patients
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Community-acquired pneumonia Nosocomial or hospital-acquired pneumonia
Peripheral lung cancer Atypical pneumonia
Dry pleurisy Aspiration pneumonia
Exudative pleurisy Pneumonia at the immunocompromised patients
Pneumosclerosis Central lung cancer

4.2. Theoretical questions:

12. What is classification of pneumonias?
13. What is definition and etiology of community-acquired pneumonia?
14. What are symptoms and signs of lobar and focal community-acquired pneumonia?
15. Which features does atypical pneumonia have?
16. What is classification and causes of pleurisies?
17. What are symptoms and signs of the dry pleurisy?
18. What are symptoms and signs of the exudative pleurisy?
19. How pleural fluid should be investigated with laboratory methods?
20. What types of lung cancer do you know?
21. What are symptoms and signs of lung cancer?
22. What is definition and causes of the pneumosclerosis?
 4.3. Practical task that should be performed during practical training
33. Revealing and assessment of symptoms and signs of focal and lobar pneumonias
34. Revealing and assessment of symptoms and signs of pleurisies
35. Revealing and assessment of symptoms and signs of lung cancer
36. Revealing and assessment of symptoms and signs of pneumosclerosis
37. Assessment of the pleural fluid analysis
Topic content
Pneumonia is an infection of lung parenchyma, which leads to inflammation and exudates
filling air spaces with fluid (consolidation). This leads to reduced lung compliance and
ventilation-perfusion mismatch or shunt, which results in decreased oxygenation.
Classification:
Community-acquired pneumonia (CAP) acquired outside the hospital; common in nonimmuno-
compromised individuals, may be primary or secondary to underlying disease.
Hospital-acquired pneumonia develops after 48-72 hours after hospital admission and is not
apparent at admission.
Aspiration pneumonia follows the aspiration of exogenous material or endogenous secretions
into the lower respiratory tract. Can be in patients with stroke, myasthenia, bulbar palsies,
diminished consciousness (post-ictal, drunk), oesophageal disease (achalasia, reflux), or with
poor dental hygiene, risk aspirating oropharyngeal anaerobes.
Pneumonia at immunocompromised patients (AIDS, prolonged systemic corticosteroids and
other immunosuppressive therapy)
Causes of CAP:
S. pneumoniae, M. pneumoniae, C. pneumoniae, H. influenzae, S. aureus, Legionella spp., M.
catarrhalis, Gram-negative bacilli and Viruses.
Clinical features of lobar CAP
o Breathlessness occurs due to large injury of lung that results to diminution of it function
and changing of gas content of blood.
o Chest pain happens due to involving of pleura in inflammatory process.
o Cough can be dry or with purulent bloody sputum. It is depended from stage or form of
disease.
o Fever, rigors, malaise, anorexia
Signs of lobar CAP
Visual examination: It is severe condition of the patient; confusion (may be the only sign in the
elderly). He has redness in cheek at the affected side, herpes on his lips, sometimes prefers to
lie on the affected side. There is tachypnea, cyanosis, tachycardia, hypotension.
Visual examination of the chest: There is limitation of the chest moving at the affected side.
Auxiliary muscles take part in breathing.
Palpation of the chest
There is a tenderness of the pleural points, positive Potendzher symptom, because large part of
lung with pleura is involved to inflammatory process and surrounded tissues react to this. It is
obtained amplifying of voice resonance according to the affected lobe or segments, because
consolidated lung tissue conducts acoustic waves better than normal one.
Percussion of the chest
Comparative percussion: Over the consolidated lobe the percussion sound is dull because only
solid components of infiltrated lung tissue get to percussion sphere.
Topographic percussion: The lower border of the affected lung lifts up if pathological process
localizes in lower lobe. The height of lung apex pulls down if infiltration of the upper lobe is
presented. But size of the lung doesn’t change. It is obtaining due to increasing of solidity of
lung tissue. There is dimension of lower lung border excursion.
Auscultation of the lung
There is pathological bronchial breathing because all alveoli are filled up with inflammatory
exudates, whispering pectoriloquy. There is pleural rub due to inflamed pleura rubbing against
each other. You can hear depressed vesicular or bronchial breathing and crepitations in the
beginning or end of pathological process.
Lobar CAP has three stages: rising tide, high point and resolution.
During rising tide inflammation process is begun and alveolus walls are impregnated with
exudation fluid became adhesive. When air get to them alveoli fill out with sound due to
sticking off. This added sound is named crepitations (crackles). The main sound is diminished
vesicular during this stage. By percussion you can obtain dullness with tympanic inflection.
During high point alveoli full up with exudates and air cannot gets to them. Vesicular breathing
isn’t formed, crackles disappear, but consolidation lung conducts bronchial breathing and
whispering speech from vocal cords. By percussion you can obtain dullness.
During resolution exudates gradually disappears from alveoli and changes of their walls same
as the first stage. By percussion and auscultation you can receive similar data.
X-ray signs of lobar CAP: There is intensive and homogeneous infiltration of lobe or segments.
Symptoms of the focal CAP: Sometimes there is breathlessness because small part of lung is
involved, lung function and gas exchange is not limited.
Cough can be dry or with purulent sputum. It is depended from stage of disease. Sometimes
can be subfebrile fever, not significant rigors, malaise.
Signs of the focal CAP:
Visual examination
It is satisfactory or moderate serious. Sometimes there is limitation of the chest moving at the
affected side.
Palpation of the chest
May be, there is a tenderness of the pleural points, positive Potendzher symptom, amplifying of
voice resonance if the site of consolidation is near surface of chest.
Percussion of the chest
Comparative percussion: If site of consolidation is near of the chest surface it can be dullness of
percussion sound. Because account of solid components of lung tissue increase due to
infiltration but air presents in alveoli which haven’t been involved to pathological process and
they get to percussion sphere. If site of consolidation is deeply in lung percussion sound is clear
without change.
Topographic percussion: Some change can be if site of consolidation is near of chest surface.
There is dimension of lower lung border excursion.
Auscultation of the lung
There is diminished vesicular breathing because less alveoli involve to act of breathing. There
are sonorous bubbling (moist) rales. They are formed in bronchus which around by
consolidated lung tissue. Such tissue conduct sounds from bronchus better then healthy and we
can hear them as sonorous. Sometimes if site of consolidation is near chest surface crepitations
can be heard.
X-ray signs of the focal CAP: There is peribronchial and perivascular and/or focal infiltration of
lung tissue.
Data of additional methods of examination of CAP:
Assess oxygenation: oxygen saturation (if SaO2 <92% analysis of blood gas)
Blood test:
Full blood count: leukocytosis, left shift of blood formula – increasing young forms of
neutrophiles.
Urine and enzymes (ALT, AST, LDH), C-reactive protein are increased if CAP severe.
Blood culture and/or sputum culture are positive if patient has bacteriemia and purulent
sputum.
If patient has large CAP restrictive pattern of ventilatory disorders is developed.
Pleurisy is inflammation of parietal and visceral pleura. It is secondary condition.
Pleurisy can be dry if small quantity of fluid is in pleura cavity (less than 50 ml). Exudative
pleurisy is if more than 50 ml of fluid in pleura cavity.
Symptoms and signs of dry pleurisy:
It is dry cough due to irritation of cough receptors of pleura. It is pleuric chest pain due to
irritation of painful receptors of pleura. There is fever, malaise and other symptoms of primary
disease.
At the visual examination condition of patient depends from primary disease. There is limitation
of the chest moving at the affected side, a tenderness of the pleural points, positive Potendzher
symptom and diminished vocal fremitus. You obtain light dullness and dimension of lower lung
border excursion by percussion. Vesicular breathing is diminished and rough pleural rub is
heard.
X-ray examination can obtain thickening of pleura and its adhesion.
Exudative pleurisy has all symptoms and signs of pleural effusion.
Symptoms of the pleural effusion:
It may be asymptomatic if little quantity of fluid accumulates in pleural space.
It is associated with breathlessness, dry cough, chest pain (suggesting pleural inflammation),
chest “heaviness”, palpitation, if quantity of fluid is large (more than 400-500 ml).
Signs of the pleural effusion:
Visual examination
It is a severe condition of the patient. There is tachypnea, cyanosis and limitation of the chest
moving at the affected side. Patient prefers to lie on the affected side because it facilitates his
breathing.
Palpation of the chest
It is obtained reduced or absent tactile vocal fremitus, because fluid damps acoustic waves, and
increased chest resistance. Sometimes, may be positive Potendzher symptom.
Percussion of the chest
Comparative percussion: It is dullness over fluid.
Topographic percussion: Lower lung border has shape named Ellis-Damuazo line which begins
near column and rises to scapular then descends to axillary region and continues horizontally.
This shape of line makes conditional upon different property of lung tissue to be squeezed.
Auscultation of the lung
There are no any sounds over the fluid. But sometimes may be diminished vesicular breathing if
it is little quantity of fluid. You can hear diminished bronchial breathing if quantity of fluid much
and squeezed lung has similar density as fluid. Above the fluid it is diminished vesicular
breathing and, sometimes, pleural rub.
X-ray signs of the pleural effusion: It is usually detected effusion volumes of 200 ml or more by
posterior-anterior position. Lateral chest X-ray is more sensitive and may detect as little as 50
ml pleural fluid. Classical chest X-ray appearance is of basal opacity obscuring hemidiaphragm,
with concave upper border. Massive effusion may result in a ‘white-out’ of the hemithorax, with
mediastinal displacement away from the effusion. Lack of the mediastinal shift in such cases
raises the possibility of associated volume loss due to bronchial obstruction from a primary lung
cancer.
Ultrasound is extremely sensitive at detecting fluid volumes of 100 ml or more, and is useful for
distinguishing pleural fluid from pleural masses or thickening, and for demonstrating
localization.
Laboratory assessment of pleural fluid:
1. Common – visual assessment, comparative density, Rivalt test
2. Biochemistry for measurement of protein, LDH, glucose, cholesterol, triglycerides, amylase,
depending on the clinical circumstances.
3. Cytology for examination for malignant cells and differential cell count
4. Microbiology for Gram stain and microscopy, culture, MBT examination
Laboratory signs of transudates and exudates
Sign transudates exudates
comparative density < 1,015-1,018 >1,018
Rivalt test negative positive
protein <30 g/l >30 g/l
Pleural fluid protein/serum protein ratio <0,5 >0,5
LDH <1,6 mMol/l >1,6 mMol/l
Pleural fluid LDG/serum LDG ratio <0,6 >0,6
9
erythrocytes <10*10 /l >100*109/l
9
leucocytes <1*10 /l >1*109/l
pH >7,3 <7,3
glucose 3,3-5,5 mMol/l <3,3 mMol/l
Lung cancer usually develops within the wall or epithelium of the bronchial tree. If it develops
in the proximal big bronchi it is named central. If it is developed in the distal small bronchi or in
the bronchioles it is named peripheral.
Long-time smoking, inhalation of carcinogenic pollutants, work with asbestos can result in lung
cancer.
Early-stage lung cancer does not produce symptoms. The following late-stage symptoms are:
chronic cough with bloody sputum, hoarseness, wheezing, dyspnea and chest pain, weakness,
weight loss, anorexia and shoulder pain.
In case of the central lung cancer symptoms and signs of obstructive atelectasis are
developed: Breathlessness, tachypnea, cyanosis. Chest is asymmetric – affected side and chest
excursion is diminished; tactile vocal fremitus is diminished or absent, because collapsed lung tissue
damps acoustic waves. Chest resistance is increased. Percussion sound is dull over atelectasis. Lower
lung border is lifted up by collapsed segments. There are no any sounds over the atelectasis by
auscultation because air doesn’t come into alveoli.
In case of the peripheral lung cancer symptoms and signs of consolidation are developed.
This type of cancer becomes apparent like lobar pneumonia. But it has not been resolved after
antimicrobial treatment.
Diagnostic investigations:
Chest X-ray usually shows an advanced lesion, but it can detect a lesion up to 2 years before
symptoms appear.
Sputum cytology, which is 75% reliable, requires a specimen coughed up from the lungs and
tracheobronchial tree, not postnasal secretions or saliva.
Computered tomography scan of the chest may help to delineate the tumor ’s size and its
relationship to surrounding structures.
Bronchoscopy can locate the tumor site and take material for cytologic and histologic
examination by a needle biopsy.
Tissue biopsy of accessible metastatic sites includes supreclavicular and mediastinal nodes and
pleural biopsies.
Thoracentesis allows chemical and cytologic examination of pleural fluid.
Pneumosclerosis – last stage of any inflammatory of degenerative process in the lung tissue. It
can develop after pneumonia, tuberculosis, chronic bronchitis, interstitial lung diseases and
other. Clinical presentation depends on spreading of the process and usually manifests by
progressive mixed dyspnea and respiratory failure.

7. Reference source

o Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000 – P.508-510, 660, 663-666.

 TOPIC 9
Syndromes of bronchial obstruction, emphysema and respiratory failure
1.Importance of the topic
Syndromic diagnostics is one of the important components at the diagnostic process.
Revealing pathogenic relation between different symptoms and signs forms integral estimate
about patient’s condition. It is indispensable to correct diagnosis and treatment.

2. Concrete aims:
─ Study main symptoms and signs of the syndrome of bronchial obstruction
─ Learn main instrumental methods that can help to establish bronchial obstruction
─ Study main symptoms and signs of the syndrome of emphysema
─ Learn basic investigations that should be performed for confirming emphysema
─ Study main symptoms, signs and investigations of respiratory failure

3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the airways and lungs, their blood supply and
innervation
Normal physiology Mechanics of breathing, gas exchange in the lung and tissues of
system organs
Histology Ontogenesis of the respiratory tract, histological structure of the
respiratory tract and alveoli
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine respiratory patients
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Bronchial obstruction Hyperinflation
Reversibility of obstruction Respiratory failure
Emphysema Asthma attack

4.2. Theoretical questions:

1. Definition of syndromes of bronchial obstruction
2. Causes of bronchial obstruction
3. Symptoms of bronchial obstruction
4. Signs of bronchial obstruction
5. Instrumental and laboratory methods of examination of patients with bronchial obstruction,
its diagnostic importance
6. Definition of emphysema
7. Symptoms and signs of emphysema
8. Data of additional methods of examination of patients with emphysema.
9. . Definition of respiratory failure, its causes.
10. Clinical presentation of respiratory failure
4.3. Practical task that should be performed during practical training
38. Revealing and assessment of symptoms and signs of bronchial obstruction
39. Revealing and assessment of symptoms and signs of emphysema
40. Revealing and assessment of symptoms and signs of respiratory failure
Topic content
Bronchial obstruction is the complex of symptoms that develops due to limitation of air passing through
narrowed airway or increasing of resistance against air flow during ventilation.
Causes of bronchial obstruction:
 6. Organic – bronchial obstruction isn’t reversible – endobronchial or exobronchial tumor,
enlarged lymphonodes, metastasis, foreign body of branchus, deformation of bronchus, rumen
of bronchus.
7. Functional - bronchial obstruction is reversible bronchus smooth muscles contraction, hyper-
and dyscrinia, oedema of bronchial mucous.
Bronchial obstruction can be at patients with bronchial asthma, COPD, pneumonia with obstructive
syndrome, bronchiectasis, and cystic fibrosis.
Symptoms of bronchial obstruction:
Cough is mostly dry, episodic, morning or nocturnal.
Shortness of breath – difficulty during expiration from light dyspnoe to severe asthma attack.
Wheeze
Chest tightness
Signs of bronchial obstruction:
Visual examination:
The patient sits upright and leans on the edge of the table or chair with hands. This position mobilizes
accessory respiratory muscles, does exhalation active and facilitates breathing. There is cyanosis,
tachypnea and lengthened exhalation. Auxiliary muscles take part in breathing. If patient is sick during 5
or more year his chest has barrel shape.
Palpation of the chest
Vocal fremitus is diminished. Potenzher symptom is negative and pleural points are painless. Chest has
increased resistance.
Percussion of the chest
Comparative percussion: There is resonant percussion sound over chest. Because account of air in lung
increases due to dysfunction of breathing.
Topographic percussion: The lower borders of the lungs descend down and apexes of lungs lift up. There
is dimension of lower lung border excursion.
Auscultation of the lung
There is diminished rough vesicular breathing with prolonged exhalation, polyphonic wheezes due to
narrowing of airways of differing caliber.
Instrumental and laboratory methods of examination of patients with bronchial obstruction, its
diagnostic importance:
1. Spirometry with reversibility and provocative test.
2. Sputum examination
3. Pulse oximetry and arterial blood gas analysis.
4. X-ray examination
5. Fibreoptic bronchoscopy.
Spirometry: FEV1, FEV1/FCV, PEF, FEF 25-75% is reduced less than 80% for FEV1, PEF, 70% for
FEV1/FCV, and 60% for FEF 25-75% from predicted value.
Reversibility test is performed for patient with obstruction and allow to establish level of its
reversibility. Obstruction is reversible if diminished index of spirograme (FEV1, PEF) increase to 12%
from initial value.
Provocative tests are performed for establishing hypersensitivity of bronchus when obstructive
syndrome occurs episodically. Patient does some physical exercises (exercise test) or inhale
histamine or methacholine aerosol (non-specific tests) or allergen aerosol (specific test) and after
that he performs spirometry. If index decrease less than 15% test is considered positive.
Sputum examination: mucoid, white, clear with eosinophiles in microscopy.
Pulse oximetry - O 2 saturation diminishes less than 90% if patient with obstruction has respiratory
failure.
X-ray examination – hyperinflation or evidence of localized abnormality simulating wheeze, e.g.
adenoma.
Fibreoptic bronchoscopy – Its main use to exclude an obstructive airway tumor (e.g. carcinoid).
Emphysema is a pathological condition due to alveolar wall destruction causing irreversible enlargement
of air spaces distal to the terminal bronchiole (the acinus), with subsequent loss of elastic recoil and
hyperinflated lungs. There is primary (due to congenital α1-antitrypsin deficiency and other pathology of
connective tissue) and secondary (due to COPD, occupation (musician, glassblower), senility).
Symptoms: The most common is dyspnoe (shortness of breath). It has mixed character: during
inhalation and exhalation. Patient notes decreased exercise tolerance and rare dry cough.
Signs of emphysema:
Visual examination: There is barrel shape of the chest, cyanosis, tachypnea. Auxiliary muscles take part
in breathing.
Palpation of the chest
Vocal fremitus is diminished. Potenzher symptom is negative and pleural points are painless. Chest has
increased resistance.
Percussion of the chest
Comparative percussion: There is resonant percussion sound over chest because volume of air in the
lungs increase due to dysfunction of breathing.
Topographic percussion: The lower borders of the lungs descend down and apexes of lungs lift up. There
is dimension of lower lung border excursion.
Auscultation of the lung
There is diminished rough vesicular breathing with prolonged exhalation
Data of additional methods of examination of patients with emphysema:
In blood analysis compensatory erhytrocytosis and hyperhemoglobinemia are obtained due to
decreasing gas exchange I lung.
X-ray examination – hyperinflated lung fields with attenuation of peripheral vasculature – “black lung
sign”, flattened diaphragms, more horizontal ribs, may see bullae, especially in the lung apices, which if
large can be mistaken for a pneumothorax due to the loss of lung markings.
Spirometry – mixed pattern of disorder: reduced VC, FVC and FEV1, PEF. Total lung capacity and residual
volume are increased.
Respiratory failure occurs when gas exchange is inadequate, resulting in hypoxia. There are 2 types of
respiratory failure.
Type I is defined as hypoxia (PaO2<50mmHg) with a normal or low P aCO2. It is caused primarily by
ventilation/perfusion mismatch. Causes include:
- pneumonia
- pulmonary oedema
- pulmonary embolism
- asthma
- Emphysema
- Fibrosing alveolitis
- ARDS
Type II is defined as hypoxia (PaO2<50mmHg) with hypercapnia (PaCO2>45 mmHg). This is caused by
alveolar hypoventilation, with or without ventilation/perfusion mismatch. Causes include:
- Pulmonary diseases: asthma, COPD, Pneumonia, pulmonary fibrosis, obstructive sleep
apnoea;
- Reduced respiratory drive: sedative drugs, central nervous system tumor, or trauma;
- Neuromuscular diseases: cervical cord lesion, diaphragmatic paralysis, poliomyelitis,
myasthenia gravis.
- Thoracic wall diseases: flail chest, kyphoscoliosis.
Clinical features are those of the underlying cause together with symptoms and signs of hypoxia, with or
without hypercapnia.
Hypoxia includes dyspnoea; restlessness; agitation; confusion; central cyanosis. If londitudinal hypoxia:
polycythaemia; pulmonary hypertension and development cor pulmonale.
Hypercapnia includes headache; peripheral vasodilatation; tachycardia; bounding pulse; tremor/flap;
confusion; drowsiness; coma.
Visual examination: diffuse cyanosis, tachypnea. Auxiliary muscles take part in breathing.
Investigation includes arterial blood gas analysis. Heparinized blood is taken from the radial, brachial or
femoral artery and pH, PaO2, PaCO2 are measured using an automated analyzer. Normal range of P aO2 is
70-100 mm Hg, PaCO2 – 35-45 mm Hg, pH 7,35-7,45.
Pulse oximetry is a quick noninvasive estimation of O 2 saturation (SpO2) of Hb in arterial blood. Normal
range SpO2 95-99%. If SpO2 is reduced less than 90% patient needs oxygen therapy.
Classification of respiratory failure:
- Acute is developed during some hours.
- Chronic is developed during some months or years.
According to severity:
I (mild): dyspnoea during physical exercises that was not before.
II (moderate): dyspnoea during small physical effort.
III (severe): dyspnoea in rest
 TOPIC 10
Clinical presentation of chronic obstructive pulmonary diseases, bronchial
asthma
4. Importance of the topic
Bronchial asthma and chronic obstructive pulmonary disease (COPD) are widely
spread internal diseases. They produce serious problems with health. Prevalence of
COPD a-is increasing from year to year and now it is one from frequent cause of death
in the world. Ability to recognizing COPD and bronchial asthma is very important for
every doctor or student, because sometimes these diseases appear with emergency
life-threatened condition that should be resolved immediately.

2. Concrete aims:
─ Study main symptoms and signs of the bronchial asthma
─ Learn main instrumental methods that can help to establish bronchial asthma
─ Learn classification of bronchial asthma
─ Study main symptoms and signs of COPD
─ Learn instrumental and functional exanimation patients with COPD
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the airways and lungs, their blood supply and
innervation
Normal physiology Mechanics of breathing, gas exchange in the lung and tissues of
system organs
Histology Ontogenesis of the respiratory tract, histological structure of
the respiratory tract and alveoli
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine respiratory patients
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Bronchial obstruction Hyperinflation
Reversibility of obstruction Respiratory failure
Emphysema Asthma attack

4.2. Theoretical questions:

11. Definition of bronchial asthma
12. Causes of bronchial asthma and its classification
13. Symptoms of bronchial asthma
14. Signs of bronchial asthma
15. Instrumental and laboratory methods of examination of patients with bronchial
asthma
16. Definition of COPD
17. Symptoms and signs of COPD
18. Data of additional methods of examination of patients with COPD.
19. . Classification of COPD.
4.3. Practical task that should be performed during practical training
41. Revealing and assessment of symptoms and signs of bronchial asthma
42. Revealing and assessment of symptoms and signs of COPD
43. Revealing and assessment of functional data at patients with bronchial asthma and COPD
Topic content
Bronchial asthma is a chronic inflammatory disease of the airways resulting in airflow
obstruction secondary to airway edema, increased mucus production, bronchospasm and
infiltration of the airway with leukocytes (eosinophils, lymphocytes and neutrophiles). It is
usually reversible either spontaneously or with treatment. May be allergic and non-allergic and
genetic burden.
Clinical presentation:
Episodic dyspnea
Wheezing
Cough dry and nocturnal or morning or episodic as asthma attack equivalent
Episodic chest tightness
Signs of reversible bronchial obstructive syndrome
Visual examination:
The patient sits upright and leans on the edge of the table or chair with hands. This position
mobilizes accessory respiratory muscles, does exhalation active and facilitates breathing. There
is cyanosis, tachypnea and lengthened exhalation. Auxiliary muscles take part in breathing. If
patient is sick during 5 or more year his chest has barrel shape.
Palpation of the chest
Vocal fremitus is diminished. Potenzher symptom is negative and pleural points are painless.
Chest has increased resistance.
Percussion of the chest
Comparative percussion: There is resonant percussion sound over chest. Because account of air
in lung increases due to dysfunction of breathing.
Topographic percussion: The lower borders of the lungs descend down and apexes of lungs lift
up. There is dimension of lower lung border excursion.
Auscultation of the lung
There is diminished rough vesicular breathing with prolonged exhalation, polyphonic wheezes
due to narrowing of airways of differing caliber.
Investigations:
Lung function tests: pre- and post-bronchodilator test – FEV1 is increased by> 12% and > 200
ml.
Peak expiratory flow rate: difference of > 20% between morning and afternoon PEF may
suggest asthma
Bronchoprovocation test: test for airway hyperreactivity. Test positive if FEV1 drop to 20%.
Classification of bronchial asthma:
I step – Intermittent symptoms rare than 1 a week and night symptoms less than 1 a 2 week
(PEF, FEV1> 80%)
II step – mild persistent - symptoms rare than 1 a day and night symptoms less than 1 a 2 week
(PEF, FEV1> 80%)
III step – moderate persistent – daily symptoms and night symptoms one a week (PEF, FEV1
80-60%)
IV step – severe persistent – continua day symptoms and frequent night symptoms
(PEF, FEV1<60%)
Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow
limitation that is not fully reversible. The airflow limitation is usually both progressive and
associated with an abnormal inflammatory response of the lungs to noxious particles or gases.
Risk factors: smoking, occupational dust and chemicals, air pollution and chronic recurrent
respiratory infections, hereditary α-1 antitrypsin deficiency.
Symptoms of COPD:
Cough is productive, slowly progressive dyspnoe with difficulty during expiration, wheeze,
decreased exercise tolerance.
Significant airflow obstruction may be present before the patient is aware of it.
Signs of bronchial obstruction:
Visual examination:
The patient sits upright and leans on the edge of the table or chair with hands. This position
mobilizes accessory respiratory muscles, does exhalation active and facilitates breathing. There
is cyanosis, tachypnea and lengthened exhalation. Auxiliary muscles take part in breathing. The
chest has barrel shape.
Palpation of the chest
Vocal fremitus is diminished. Potenzher symptom is negative and pleural points are painless.
Chest has increased resistance.
Percussion of the chest
Comparative percussion: There is resonant percussion sound over chest. Topographic
percussion: The lower borders of the lungs descend down and apexes of lungs lift up. There is
dimension of lower lung border excursion.
Auscultation of the lung
There is quiet breath sounds with prolonged exhalation, wheezes, quiet heart sounds (due to
overlying hyperinflated lung)
Signs of Cor pulmonale and CO2 retention (ankle oedema, raised jugular vein pulse, warm
peripheries, plethoric conjunctivae, bounding pulse, polycythaemia. Flapping tremor if CO 2
acutely raised).
Investigations:
6. Lung function tests: obstructive spirometry and flow-volume loops, reduced FEV1
to<80% predicted, FEV1/FVC< 70%, reversibility less than 12%, raised total lung volume,
FRC and residual volume because of emphysema, air trapping and loss of elastic recoil.
7. Chest X-ray shows data of emphysema.
8. Sputum examination is significant if patient has exacerbation (microscopy and culture)
9. Pulse oximetry and arterial blood gas analysis - Pa O2 decreased, Sa O2 <95%.
Classification of COPD by severity (GOLD):
Stage 0, at risk: Lung function still normal; chronic symptoms (chronic cough and sputum
production).
Stage I, Mild COPD: Mild airways limitation (FEV1/FVC<70%, but FEV1≥80% predicted) and
usually, but not always, chronic cough and sputum production.
Stage II, Moderate COPD: Worsening airways limitation (FEV1/FVC<70%, 50%≤FEV1<80%
predicted) and usually progression of symptoms, with shortness of breath typically developing
on exertion.
Stage III, Severe COPD: Further worsening of airflow limitation (FEV1/FVC<70%, 30%≤FEV1<50%
predicted) progression of symptoms with shortness of breath and exacerbations which have
impact on patient’s quality of life.
Stage IV, Very severe COPD: severe airflow limitation (FEV1/FVC<70%, FEV1<30% predicted) or
FEV1<50% plus chronic respiratory failure. Quality of life is very appreciably impaired and
exacerbations may be life-threatening.
7. Reference source

o Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000 – P.79-82, 206-210.

Professor assistant Demchuk H.V.
 Test for self-control
1. Bronchial asthma is a…
f. Acute inflammatory disease;
g. Acute infective disease;
h. Chonic infective disease;
i. Chonic iinflammatory disease;
j. northing from above.
2. Chronic obstructive pulmonary disease is a…
f. chronic inflammatory of trachea and large bronchus
g. chronic inflammatory of large and medium bronchus
h. chronic inflammatory of medium, small bronchus with involving lung parenchyma and
vessels
i. All from above
j. Northing from above
3. Which symptoms characterize bronchial asthma?
f. Mixed dyspnea, cough with purulent sputum
g. Episodic dry cough, tightness of the chest, wheezing
h. Chest pain with radiation to jaw, inspiratory dyspnea
i. Permanent expiratory dyspnea, cough
j. Episodic hemoptysis and dyspnea due to physical effort
4. Which symptoms characterize COPD?
a. Mixed dyspnea, dry cough, chest pain
b. Episodic dry cough, tightness of the chest, wheezing
c. Chest pain with radiation to jaw, inspiratory dyspnea
d. Permanent expiratory dyspnea, cough, sputum production
e. Episodic hemoptysis and dyspnea due to physical effort
5. What symptom doesn’t characterize bronchial asthma?
f. Wheezing
g. cough
h. tightness in the chest
i. dyspnea
j. purulent sputum
6. What symptom doesn’t characterize COPD?
a. Wheezing
b. cough
c. chest pain
d. dyspnea
e. purulent sputum
7. What change of vocal fremitus can be at the patient with COPD?
a. Amplifying
b. Decreasing
c. Absence
d. Not changed
e. Change depends on clinical situation
8. What change of vocal fremitus can be at the patient with bronchial asthma?
a. Amplifying
b. Decreasing
c. Absence
d. Not changed
e. Change depends on clinical situation
9. If patient has asthma symptoms 1-2 times in a week, 1 night awaking in a mouth, he has…
f. Intermitend asthma;
g. Mild persistent asthma;
h. Moderate persistent asthma;
i. Severe persistent asthma;
j. depends on clinical situation
10. If patient has asthma symptoms 1-2 times in a day, 1 night awaking in a week, he has…
a. Intermitend asthma;
b. Mild persistent asthma;
c. Moderate persistent asthma;
d. Severe persistent asthma;
e. depends on clinical situation
11. If patient has asthma symptoms 1-2 times in a year, night awaking is absent, he has…
a. Intermitend asthma;
b. Mild persistent asthma;
c. Moderate persistent asthma;
d. Severe persistent asthma;
e. depends on clinical situation
12. If patient has asthma symptoms 8-10 times in a day, every night awaking, he has…
a. Intermitend asthma;
b. Mild persistent asthma;
c. Moderate persistent asthma;
d. Severe persistent asthma;
e. depends on clinical situation
13. How percussion sound is changed at the patient with COPD?
a. unchanged
b. dull
c. small box sound
d. tympanic
e. depend on clinical situation
14. How mobility of the lung border is changed at the patient with COPD?
a. unchanged
b. limited
c. increased
d. became immovable
e. depend on clinical situation
15. How percussion sound is changed at the patient with mild asthma?
a. unchanged
b. dull
c. small box sound
d. tympanic
e. depend on clinical situation
16. What are auscultation findings at the patient with asthma attack?
f. Vesicular rough breathing with prorogated expiration, wheezing
g. Diminished vesicular breathing,
h. Diminished vesicular breathing and moist rales
i. Diminished vesicular breathing and crepitation
j. Vesicular breathing and pleural friction rub
17. What are auscultation findings at the patient with COPD?
a. Vesicular rough breathing
b. Diminished vesicular breathing with prolongated expiration, wheezing
c. Diminished vesicular breathing and moist rales
d. Diminished vesicular breathing and crepitation
e. Vesicular breathing and pleural friction rub
18. How is FEV1 increased after bronchial spasmolytic if patient has reversible obstruction?
k. >12% from initial
l. >20% from initial
m. >25% from initial
n. > 30% from initial
o. > 10% from initial
19. If patient has permanent expiratory dyspnea during physical effort, FEV1 is 52% from
predicted and FEV1/FVC 55% he has…
a. Mild COPD
b. Moderate COPD
c. Severe COPD
d. Very severe COPD
e. Depend on clinical situation
20. If patient has permanent expiratory dyspnea in a rest, FEV1 is 22% from predicted and
FEV1/FVC 45% he has…
a. Mild COPD
b. Moderate COPD
c. Severe COPD
d. Very severe COPD
e. Depend on clinical situation

Control questions:
1. What is a bronchial asthma?
2. What are causes of bronchial asthma?
3. What stage of bronchial asthma do you know?
4. What are the main symptoms of bronchial asthma?
5. What are signs of bronchial asthma?
6. Which instrumental and laboratory investigations are used for establishing bronchial
asthma?
7. What is COPD?
8. What are risk factors of COPD?
9. What are the main symptoms and signs of COPD?
10. What are findings of instrumental investigations of patients with COPD?
11. What stage of COPD do you know?
4.3. Practical task that should be performed during practical training
1. Revealing and assessment of symptoms and signs of bronchial asthma
2. Revealing and assessment of symptoms and signs of COPD
3. Revealing and assessment of functional data at patients with bronchial asthma and
COPD
 TOPIC 11
Taking history and general visual inspection patients with cardiovascular
diseases. Management of the patients and writing part of the case history
1.Importance of the topic
Cardiovascular diseases are the most spread in the world. They are the leading cause of death.
Distinguishing heart pathology is very important and every doctor must know main cardiac
symptoms and can recognize patient’s appearance and complexity.

2. Concrete aims:
1. Study principles of taking history at the patient with cardiovascular diseases
2. Learn general examination features of patient with cardiovascular diseases
3. Assessment of obtaining data
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart and vessels
Normal physiology Mechanics of heart working and blood circulation
Histology Ontogenesis of the cardiovascular system, histological structure of
the heart and vessels
Boimedical physics Principles of liquid flow in a tube
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
palpitation Syncope
Angina pectoris Cardiac edema
dizziness acrocyanosis

4.2. Theoretical questions:

1. Principal complaints and there refinement at patients with cardiovascular diseases.
2. Features of disease history (anamnesis morbi) and life history (anamnesis vitae) of
patients suffering from cardiovascular diseases.
3. Peculiarities of general inspection of patients with cardiovascular diseases.
4.3. Practical task that should be performed during practical training
44. Revealing and assessment of symptoms of cardiovascular disease
45. Performing general visual inspection of the patients with cardiovascular diseases
46. Assessment of obtaining finding
Topic content
The symptoms are caused by heart disease result most commonly from myocardial ischemia,
from disturbance of the contraction and/or relaxation of the myocardium, from obstruction to blood
flow, or from an abnormal cardiac rhythm or rate.

Complaints in the cardiovascular diseases

Specific Nonspecific
Pain in the heart region; Fever; Sweatiness; Weight loss;
Intermissions; Palpitation; Fatigue; Headache; Dizziness;
Dyspnea; Asphyxia; Cough; Sleeplessness; Deranged vision and
Hemoptysis; Syncope, hearing; Voice changes; Dysphagia;
heaviness at the right subcostal Dyspepsia; Thirst; Pain in the
region, oedema abdomen; Pain in the joints

Specific complaints
 Pain in the heart region. Pain in the region is one of the most frequent complaints of the
patients in the internal diseases clinic.
Diagnostic approach to the patients with pain in the heart region
1. Location: retrosternal, in the apex region, to the left of the sternum...
2. Intensity: severe, rather intense, moderate, mild...
3. Character:
a) superficial or profound ("deep");
b) type of the pain: squeezing, pressing, stabbing, piersing, burning, boring, gnawing, feeling of
tightness, shooting;
4. Frequency: seldom, every day, every week, several times a day (to indicate how many times);
5. Duration: transitory, constant, intermittent, attacks of pain (to indicate in seconds, minutes,
hours);
6. Radiation: to the left shoulder, left arm, left shoulder-blade, left supraclavicular and
subclavicular region, to the back, interscapular region, to the left of the neck, lower jaw, to the
epigastric region, to the right half of the chest;
7. Associated features: morbid fear of death, palpitation, intermissions, dyspnoea, weakness,
trembling in the body, cramps, feeling of air deficit, dizziness, excessive urination;
8. Provocation: during insignificant physical exertion - during walk: quick, ordinary, slow;
ascending the stairs or hill; frosty day; in going out of doors in 10-20 minutes; emotional factors;
excessive meal; after alcohol use, smoking; in considerable physical loading; without visible cause.
9. Relieving conditions: is abated by nitroglycerin (how many tablets a day, pain relieve at once,
in few seconds, in few minutes); at rest; changing position; physical or emotional exertion; talking; is
abated by analgetics.
A number of key characteristic help to distinguish cardiac pain from other causes
Tab.2.2. Differential diagnosis of pain in the heart region from history

Pain features Disease

Retrosternal, constricting, feeling of heaviness, from few seconds to 15 Favours angina pectoris
min, radiate to the left arm, scapula, jaws, the neck, associated with (ischemic pain)
morbid fear of death, comes on with exertion, is relieved by rest, is relieved
by nitrates.
Pain as above but prolonged, continuous pain > 20-30 min, more severe, Favours myocardial
tight or burning, resist at rest, and does not respond to nitrates. infarction
Retrosternal, extremely severe, sharp and tearing, piercing, radiate to the Consider aortic dissection
spinal column, moves gradually along coarse of the aorta, associated with
collapse, syncope, cyanosis, with very sudden onset.
Middle of the sternum or heart apex or entire heart region, stabbing, Consider pericarditis
shooting, feeling of heaviness, persist several days or may arise in attack
during inspiration, coughing, radiate to the left scapular, the neck,
epigastric region, left arm, varies in intensity with movements, the phase
of respiration, and under the pressure of stetoscope.
Behind manubrium sterni, permanent, does not respond to exertion Consider aortitis
Very variable in site and intensity, may vary with posture or movement, Consider musculosceletal
very commonly accompanied by local tenderness over the rib or costal cause
cartilage.
Intermission is solitary beats at various intervals, sometimes one, two, three, and more beats,
accompanied by feeling of sinking heart, arrest, lack of air are characteristic for preliminary heart
contractions, i.e. extrasystolic arrhythmia, which is often is not a consequence of anorganic heart
disease but occurs in regulation disorders. It is said that the more unpleasant is the feeling of
extrasystole, the more probable is their functional origin.
Extrasystoles are frequently found in healthy subjects (emotional exertion, in heavy smokers, in
coffee, strong tee, and alcohol abuse), and their prevalence increases with age. Extrasystoles can occur
in hyperthyroidism, menopause, digitalis and adrenaline toxicity as well as by reflex in the diseases of
the abdominal organs. Premature beats are common in patients with coronary heart disease (especially
in acute myocardial infarction), hypertension, rheumatic heart valvular disease, myocarditis, and heart
failure. Patients with premature cardiac contraction feel their heart missing a beat (escape beat) with
subsequent strong stroke.
Palpitation is subjective feeling of accelerated and intensified heart contractions onto the chest
wall. This is a symptom experienced by most people at some time in their lives. Heart palpitation is
clinical sign of tachycardia. Accurate assessment of palpitation requires an exact description of the
sensation and it is often helpful to ask patients to explain their symptoms by taping out the heart beat
on their chest or a table top.
Palpitation is a symptom, mainly, of organic affection of the cardiovascular system. In this case,
it has lingering character, more expressive without any external causes, and moreover, accompanied by
the pain in the heart region, disorders of the heart rate, feeling of compression in the chest, feeling of
fear, stoppage of breathing, headache, noise in the ears, and "net" before eyes.
The evaluation of palpitation: important questions
(Davidson's principles and practice of medicine, 1999).
 Is the palpitation continuous or intermittent?
 Is the heart beat regular or irregular?
 What is the approximate heart rate?
 Do the symptoms occur in discrete attacks?
 Is the onset abrupt?
 How do attacks terminate?
 Are there any associated symptoms? e.g. chest pain
 Lightheadedness
 Polyuria (a feature of supraventricular tachycardia)
 Are there any precipitating factors? e.g. exercise, alcohol
 Is there clinical evidence of structural heart disease? e.g. Coronary
heart disease, Valvular heart disease
Palpitation periodic, of not long duration, appeared regular after moderate physical activity, is a
symptom of the heart failure. In increased pressure in the lesser circulation, elevated pressure in the
orifice of the vena cava by reflex through the sympathetic nerve accelerates cardiac rate (Bainbrigde
reflex) to unload lesser circulation.
Palpitation often develops as a reflex in diseases of some internal organs: in disease of the
central nervous system, neurosis, endocrine pathology (thyrotoxicosis), in fever, anemia, hypotension,
and in many infectious diseases.
Palpitation causes
Pathological
Physiological
Cardiac diseases Noncardiac causes
Physical exertion Coronary heart disease Diseases of the central
Rheumocarditis nervous system,
Emotional exertion Pericarditis neurosis
Strong tea, coffee, alcohol Heart valvular disease Endocrine pathology
Cardiac tumor Digestive diseases
Drugs (adrenaline, Myocardiopathy
caffeine, atropine sulfate) Mitral valve prolapse Fever
Ventricular preexcitation syndromes (Wolf-
Parkinson-White Syndrome, Clerk-Levi-Critesko
Synrome)

Dyspnoea (breathlessness). The term "dyspnoea" is derived from the Greek roots dys (difficult,
painful) and pnoia (breathing). Breathlessness or dyspnoea is disorder of the respiratory ventilation of
the lungs, manifested by unreasonably accelerated and intensified breathing. Patients describe
dyspnoea as 'the sensation of difficult, laboured, uncomfortable breathing', as 'distressing feeling of air
deficit', and as 'the consciousness of the necessity for increased respiratory effort'. Often dyspnea
accompanied by the feeling of the fear and alarm, and by others unpleasant feelings.
Dyspnoea is a cardinal symptom of left heart failure and occurs in many others cardiovascular
conditions.
Some common causes of dyspnoea
Types of
Cardiovascular causes Other causes
dyspnoea
Exertional Left heart failure left ventricular failure acute and Lung disease
dyspnoea chronic, mitral valve disease, Atrial myxoma Upper airways
Congenital heart disease obstruction
Pulmonary vascular disease pulmonary embolism, Fluid overload
acute and chronic other causes of pulmonary Anaemia
hypertension Obesity
Angina equivalent Psychogenic
Orthopnoea Left heart failure Lung disease
Diaphragmatic weakness
Paroxysmal Left heart failure Nocturnal asthma
nocturnal Gastro-oesophageal
dyspnoea reflux with aspiration
Acute dyspnoea Acute myocardial infarction Supraventricular or Asthma
at rest ventricular tachycardia Acute dissection of the aortic root Pneumothorax
Mitral chordal or papillary muscle rupture Large Aspiration/inn aled
pulmonary embolism Mitral obstruction by left atrial ball foreign body
thrombus or left atrial myxoma Obstruction or Metabolic acidosis
dehiscence of an artificial valve Infundibular spasm of Massive haemorrhage
Fallot's tetralogy

Different types of dyspnoea can be distinguished in clinical practice, although they often coexist.
1. Exertional dyspnoea: this may be graded according to the revised New York Heart Association
scale. The severity of cardiac disease may be underestimated if the patient's physical activities are
restricted for any other reason - sedentary habit, intermittent claudication, or arthritis.
2. Orthopnoea: dyspnoea worse when lying flat than when sitting up or standing is common.
3. Paroxysmal nocturnal dyspnoea: acute dyspnoea waking the patient from sleep.
Characteristically the patient sits or stands up, and may throw open the windows for air. Paroxysmal
nocturnal dyspnoea can be crudely graded by the number of pillows that patient uses to prop himself up
to allow uninterrupted sleep.
4. Acute dyspnoea: this is uncommon. It may complicate myocardial infarction, severe
arrhythmias, or number of other catastrophic events.
Other respiratory symptoms may occur with dyspnoea in cardiovascular disease:
1. Acute pulmonary oedema: acute severe dyspnoea accompanied by cough producing copious
white or pale pink frothy sputum. There is usually cyanosis, sweating, tachycardia, and raised systemic
blood pressure. Dyspnoea with copious pale pink frothy sputum also occurs in the rare condition of
alveolar cell carcinoma of the lung.
2. Dry cough: a persistent dry cough may occur in chronic left heart failure, particularly after
exercise and whenlying flat in bed at night. A dry cough may persist for about half an hour after an
episode of paroxysmal nocturnal dyspnoea. Treatment with angiotensin-converting enzyme inhibitors
sometimes causes troublesome cough.
3. Haemoptysis: coughing large amounts of blood is a dramatic symptom and has many causes.
Small haemoptysis occur in severe mitral stenosis and occasionally in severe left ventricular failure.
Massive or exsanguinating haemoptysis may occur with rupture of a thoracic aortic aneurysm,
pulmonary artery aneurysm, or arteriovenous malformation.
 4. Irregular respiration: Cheyne-Stokes periodic respiration is well known to occur in advanced
cardiac failure, but is uncommon. Cyclical variation in ventilation without frank apnoeic phases is
relatively common during sleep in moderate and severe heart failure.
Cardiac dyspnoea is caused by upset gas exchange and accumulation of underoxidized
metabolites in the blood, which stimulate the respiratory center to accelerate and deepen respiration.
Especially pronounced disorders in gas exchange arise in blood congestion in the lesser circulation, when
the respiratory surface and respiratory excursion of the lungs decrease.
Asphyxia is attack of grave dyspnoea that occur due to acute congestion in the lungs and upset
of gas exchange in acute left ventricular failure, and observes in the patients with myocardial infarction,
aortic stenosis and regurgitation, and in essential hypertension. Attacks of asphyxia, which are known as
cardiac asthma, arise suddenly at rest or soon after physical or emotional stress, and usually during night
sleep. This can be explained by an increased vagus tonus during sleep, which causes narrowing of the
coronary arteries and thus impairs nutrition of the myocardium.
During an attack of cardiac asthma in patients appears feeling of intense pressure in the chest,
acute lack of air; the patient suffocates, catches the air by the mouth, marked weakness develops, and
appears cold sweat. The skin becomes pallid and cyanotic. The face of the patient, not infrequently,
expresses the fear and suffering. Respiration becomes superficial and accelerated, inspiratory dyspnoea
develops. The patient become coughing and expectorated tenacious sputum. During an attack of cardiac
asthma the patient has to assume forced position - orthopnoea, or stands up. If congestion in the lesser
circulation progresses, edema of the lungs develops. The feeling of suffocation and cough intensify still
more, respiration becomes stertorous, ample foaming sputum with traces of blood (pink or red) is
expectorated. Edema of the lungs requires prompt and energetic measure to be taken to prevent
possible death of the patient.
Cough in the patients with cardiovascular diseases is due to congestion in the lesser circulation.
Cough, as a rule, at first dry, arises during exertion, and particularly in the lying posture of the patient. In
prolonged congestion cough is with sputum.
Symptomatic features in the differential diagnosis of cardiac cough
Cough features Causes of cough Disease
Periodic, dry, persistent, sonorous, comes on with Congestion in the lesser Chronic heart failure
exertion, at rest, in the lying position, at night circulation, increases of
bronchial secretion
Periodic with insignificant bloody sputum, comes on Significant hypertension in Mitral stenosis
with exertion, in lying position the lesser circulation
In attacks, dry, mainly at night, comes on directly Aggravation of the septic Long-standing septic
before the beginning of the night sleep or in 1-2 process and spreading of endocarditis
hours of staying in the bed. In the morning the cough infection to the upper
resumes, but slightly of lesser intensity, after respiratory tract
expectorating of the mucus sputum the condition of
the patient relieves
Dry, transitory, sharp rending, accompanied by Irritation of the pleural Pericarditis
sensation of pain in the heart coughing zone
Strong, sonorous, dry, barking, and dull. Pressure of enlarged great Aortic or pulmonary
vessels on bronchi and aneurysm
trachea
Haemoptysis. Coughing up blood is an alarming symptom and nearly always brings the patient
to the doctor. Haemoptysis in cardiac pathology is mostly due to congestion in the lesser circulation and
rupture of fine bronchial vessels during coughing.
Tab. 2.10. Symptomatic features in the differential diagnosis of haemoptysis in cardiovascular
pathology
Haemoptysis Causes of haemoptysis Disease
features
In a form of streaks Congestion in the lesser circulation, rupture of fine Mitral stenosis
of the blood in the bronchial vessels during coughing
sputum
In a form of ample Sudden significant pressure elevation in the lesser Acute left ventricular
foaming sputum circulation, erythrocytes diapedesis through the vessels failure (pulmonary
with traces of blood walls into respiratory tract edema)
(pink or red)
Traces of blood in a Pulmonary hypertension, erythrocytes diapedesis Pulmonary
form of streaks or through the vessels walls into respiratory tract thromboembolism
clots Pulmonary infarction
Traces of blood or Break of the aortic aneurysm to the bronchi, trachea, Aortic aneurysm
bleeding lungs dissection
In a form of streaks Disorders of vessels penetrability, erythrocytes In elderly patients with
of blood in diapedesis atherosclerosis of
insignificant rnucus pulmonary and bronchial
sputum arteries

Syncope - is sudden loss of consciousness. Cardiac syncope is caused by a sudden drop in cardiac
output and recoverable loss of adequate blood supply to the brain (cerebral ischemia) due to an
arrhythmic or a mechanical problem (Tab.2.11)
A faint is often preceded by a brief feeling of "lightheadness"; vision then darkens and there
may be ringing in the ears.
Vasovagal syncope may be provoked by some emotionally charged event (e.g. venepuncture)
and almost always occurs from the standing position.
Cardiac syncope may be provoked by exertion (e.g. with severe aortic stenosis) or occur
completely "out of the blue" (as in heart block). The loss of consciousness is brief, and the patient
recovers quickly as long as he or she has assumed the horizontal position.
Common causes of cardiac syncope
Arrhythmia Bradycardia (especially sick sinus syndrome, complete atrio-ventricular block)
Tachycardia (especially ventricular tachycardia)
Ventricular preexitation syndromes (WPW, CLC)
Atrial fibrillation and flutter)
Mechanical Ischemic left ventricular dysfunction
Aortic stenosis
Mitral valve prolapse Hypertrophic obstructive cardiomyopathy

In vasovagal syncope the loss of consciousness is gradual and rarely associated with injury.
There is no amnesia for events that occur after regaining awareness. During a syncopal attack
incontinence of urine can occur and there may be some stiffening of the limbs and even some brief
twitching of the limbs, but tongue-biting never occurs.
Whenever possible, an accurate description of syncope should be obtained from the patient and
a witness. A careful history will often reveal the cause of syncope without recourse to complex and
expensive investigations.
Typical features of cardiac and neurogenic syncope
Features Cardiac syncope Neurogenic syncope
Premonitory Lightheadness Palpitation Chest pain Headache
symptoms Breathlessness Confusion
Hyperexcitability
Olfactory hallucinations
"Aura"
Unconscious Extreme "death-like" pallor Prolonged (> 1 min) unconsciousness
period Motor seizure activity*
Tongue-biting Urinary incontinence
Recovery Rapid recovery (<1min) Prolonged confusion (> 5 min) Headache
Flushing Focal neurological signs
*NB. Cardiac syncope can also cause convulsions by inducing cerebral anoxia.

General condition depends on severity of the disease. Condition is satisfactory in the patients
with cardiovascular pathology in compensation stage. Condition becomes worse in progression of
pathological process and associated with complications.
Posture of the cardiac patients may be active, passive or forced. Active posture is in patients
with heart valvular diseases, arterial hypertension, and coronary heart disease without sighs of the heart
failure. Passive posture - horizontal with low head of the bed is observed in the patients with acute
vascular failure. In some cardiac diseases patients assume forced posture.
Forced posture of the patients in cardiovascular diseases
Posture Pathological condition Pathophysiological mechanisms
Upright Attack of angina Tissue oxygen demand reduce at rest, decreased myocardial
pectoris ischemia
On the right side Chronic heart failure of Re-distribution of blood into the iow extremities, reducing of
with high head II degree circulating blood volume, decreasing
of the bed
Orthopnoea Acute left ventricular blood volume, decreasing of venous pressure in the lesser
failure, chronic heart circulation, improvement of gas exchange in the "alveoli-
failure of II-III degree pulmonary capillaries" system, displacement of ascitis fluid

Sitting posture Dry pericarditis Pericardial layers presses to one another, reduce their
bending forward movement that decrease irritation of pain receptors in
pericardium
Knee-elbow Effusive pericarditis Improvement of diastolic cardiac function
posture

Consciousness of the patients with various cardiovascular diseases is clear. Significant hypoxia,
as a result of acute and chronic heart failure, is accompanied by consciousness disorders in a form of
stupor or sopor.
Skin and visible mucosa colour changes is of important diagnostic significance.
Changes of skin and visible mucosa colour in cardiovascular pathology.

Color Pathological conditions Mechanisms of color changes

Cyanosis Mitral valvular diseases Secondary pulmonary hypertension
Acute and chronic left Restricted pulmonary circulation
ventricularfailure Artery-venous blood shunting
Thromboembolism of the Primary pulmonary hypertension
pulmonary artery
Congenital heart diseases
Aerz's syndrom

Constant pallor Aortic stenosis Low stoke volume

Aortic regurgitation Low diastolic pressure
Transitory pallor Acute vascular failure Low storke volume, peripheral vascular spasms,
redistribution of blood

Growing pallor Aortic aneurysm dissection Bleeding, shock

Pallor with yellowish Infectious endocarditis Anaemia increase hemolysis of erythrocytes
tint (coffee with milk)

Jaundice Chronic right ventricular failure Cardiac liver cirrhosis, infectious-toxic hepatitis
Infectious endocarditis
Jaundice with Total heart failure Cardiac liver cirrhosis, slow peripheral
acrocyanosis circulation
Inspection of the face and the neck.
'Fades mitrale' is characterized by cyanotic blush on the cheeks, cyanotic lips, tip of the nose,
ears, young-looking, observes in the patients with mitral stenosis.
Face of the patient with aortic regurgitation is pale, rhythmic movements of the head,
synchronous with carotid arteries pulsation - Musset's symptom is observed.
'Corvisart 'sface' observes in patients with severe heart failure. The face is edematous, pale
yellowish with cyanotic tint, the eyes are dull and eyelids are sticky, always open mouth, cyanotic lips.
Excitement, fear of death, suffering expression of the face are typical to the patients with acute
left ventricular failure.
In myocardial infarction complicated by cardiogenic shock the face of the patient is pale with
cyanotic hue, covered by cold sweat.
'Stokes' collar' — marked dilation of neck veins, oedema of the neck, head, shoulders. These
signs arise as a result of compression of superior vena cava by aortic aneurysm, tumor of mediastinum,
and enlarged mediastinal lymph nodes.
Cardiac oedema. Right heart failure produces a high jugular venous pressure, with hepatic
congestion and dependent peripheral oedema. Oedema is caused by penetration of fluid through the
capillary walls and its accumulation in tissues. Cardiac oedema can first be latent. Retention of fluid in
the body does not immediately cause visible oedema but provokes a rapid gain in the patient's weight
and his decreased urination. Oedema becomes visible in the first instance in the malleolus region, on
the dorsal side of the foot, shins (if the patient sits or stands), and in sacral region (if the patient keeps
bed). Oedema first develops only in the evening annd resolves during the night sleep. If the heart failure
progresses, oedema increases, and transudate may accumulate in the body's cavities: in the abdominal
cavity (ascitis), pleural cavity (hydrothorax), and in the pericardium (hydropericardium). General
distribution of oedema throughout the entire body is called anasarca.
There are following methods of oedema revelation: inspection, palpation, patient weighing, and
diuresis control.
Methods of oedema revelation
Method Features
Inspection Swollen glossy skin. The specific relief features of the oedema-affected parts
of the body disappear due to the leveling of all irregularities on the body
surface. Stretched and tense skin appears transparent, and is especially
transparent on loose subcutaneous tissues (the eyelids, the scrotum, etc.)

Palpation When the pressed by the finger, the oedematous skin overlying bones
(external surface of the leg, malleolus, loin, etc) remains depressed for 1-2
minutes after the pressure is released
Weighing of the patient Gain of the body mass
Diuresis control The amount of intake fluid exceeds the amount of urine

For revelation of cavities oedema percussion, auscultation, X-ray and ultrasound examination
methods are also used.
It should be remembered that general oedema can be caused not only by cardiac pathology, but
also by renal diseases (Tab. 2.17), hypofunction of the thyroid gland, and by long-standing starvation.
Considerable oedema of low limbs, accompanied by cyanosis of the low part of the body, dilated venous
network in the navel region, ascitis that are caused by obstruction to blood flow in vena cava inferior
trunk are classified as vena cava inferior syndrome.
Symptomatic features in the differential diagnosis of cardiac and renal oedema

Features Cardiac oedema Renal oedema

Location, character Ascending character, starts from low Descending character, starts from the
extremities and spread upward face and spread downward
Time of arising More pronounced in the evening More pronounced in the morning
Colour of the skin Cyanotic Pallor
Temperature of Cold Warm
the skin
Skeletal and muscular system. Marfan's syndrome is characterized by affection of the aorta in a
form of aneurysm, coarctation, regurgitation and others congenital heart valvular diseases. Phenotype
of the patients - tall, long narrow limbs, arachnodactyly, kyphoscoliosis, deformation of the sternum,
and hypermobility of the joints.
Drum-stick (Hippocratic) fingers - clubbing of the terminal phalanges of the fingers and toes,
nails in a form of 'hour glass' -are characteristic of congenital heart valvular diseases, subacute septic
endocarditis, and chronic cor pulmonale.
In aortic coarctation disproportion of the muscular system of upper and low limbs are observed:
muscles of upper limbs are hypertrophied, and on the other hand, muscles of low limbs are relatively
hypotrophied.
7. Reference source

1. Zh. D. Semidotskaya, O.S. Bilchenko, I.A. Cherniacova, K.P. Zharko Introduction to the course of
internal disease. Book 1. Diagnosis // Kharkiv, 2005. – P. 112-123.
2. Barbara Bates, Lynn S. Bickley, Robert A. Hoekelman Physical Examination and History Taking //
J.P. Lippincott Company, Philadelphia. – P. 241-250.
 Test for self-control
1. What are the cardiovascular symptoms?
A. Chest pain, cough, dyspnea, wheezes, haemoptysis.
B. Pain in the heart region, palpitation, intermissions, oedema
C. Headache, dizziness, dysphagia, nausea, vomiting.
D. Pain in the right subcostal region, bitter taste, brown urine, skin itching, jaundice.
E. Back pain, dysuria, ishuria, eyes oedema, weakness.
2. What are the cardiovascular symptoms?
A. Abdominal pain, nausea, vomiting
B. Dyspnea, faint (syncope), palpitation, dry cough
C. Cough with rusty sputum, chest pain, dyspnea
D. Swelling abdomen, constipation, melena
E. Oedema, dysuria, haematuria
3. What feature does the pain at angina pectoris have?
A. Be caused by physical extension
B. Duration under 15 minutes
C. Constricting, feeling of heaviness
D. Radiate to the left hand and scapula
E..All mentioned above
4. What feature does not the pain at myocardial infarction have?
A. Prolonged, continuous > 20-30 min.
B. Severe, tight or burning.
C Relief at rest.
D. Does not respond to nitrates.
E. Radiate to both hands, jaws, neck.
5. If patient has heart failure his cough is characterized with
A. appearing at lying position
B. a lot of rusty sputum
C. it is permanent
D. it is loud
E. all mentioned above.
6. If patient has feeling of solitary beats at various intervals it is named
A. exrtasistole
B. palpitation
C. syncope
D. dizziness
E. heart dyspnea
7. If patient has feeling of accelerated and intensified heart contractions onto the chest wall it is
named
A. exrtasistole
B. palpitation
C. syncope
D. heart dyspnea
E. heart pain
8. If patient has a lot of foamy pink liquid sputum it means he has
A. Pulmonary edema
B. Pulmonary embolism
C. Aortic aneurysm dissection
D. all from above
E. Northing from above
9. Which type of dyspnea is observed at the patients with cardiovascular diseases?
A. Expiratory
B. Inspiratory
C. Mixed
 D. Changing
E. All mentioned above.
10. What is feature of dyspnea at patient with cardiac asthma attack?
A. Appear at night
B. Accompanying with dry cough
C. Inspiratory
D. Ortopnea position in the bed
E. all mentioned above
11. Which of the following disorders is not likely to be associated with hemoptysis?
A. Mitral stenosis
B. Pulmonary embolism
C. Pulmonary edema
D. Pericarditis
E. None of the above
12. What characteristics of edema at patient with heart failure?
A. Asymmetrical on the part of body which patient lies on.
B. Firstly on the face than gradually spreads to body down.
C Firstly on the legs than gradually spreads to body up
D. Hear the heart region
E. Only on abdomen and hands
13. What position does a patient with cardiovascular insufficiency occupy?
A. . A forced sitting position with the legs let down.
B. The patient prefers to lie on the affected side.
C. The patient sits upright or resting the hands on the edge of the table of chair.
D. A lying position on the side (lateral recumbent position) with the head thrown back and the
bent legs pulled up to the abdomen.
E. A forced knee-elbow position.
14. What mechanisms are caused by the orthopnoea posture?
A. Tissue oxygen demand reduce at rest, decreased myocardial ischemia
B. Re-distribution of blood into the iow extremities, reducing of circulating blood volume,
C. Decreasing blood volume, decreasing of venous pressure in the lesser circulation,
improvement of gas exchange in the "alveoli-pulmonary capillaries" system, displacement of
ascitis fluid
D. Pericardial layers presses to one another, reduce their movement that decrease irritation of
pain receptors in pericardium
E. Improvement of diastolic cardiac function
15. What kind of posture is observed at angina pectopis?
A. Upright
B. On the right side with high head of the bed
C. Orthopnoea
D. Sitting posture bending forward
E. Knee-elbow posture
16. What kind of posture is observed at acute left ventricular failure?
A. Upright
B. On the right side with high head of the bed
C. Orthopnoea
D. Sitting posture bending forward
E. Knee-elbow posture
17. What cardiovascular disease is characterized with constant pale skin color?
A. Angina pectoris
B. Mitral stenosis
C. aortic valve diseases
D Essential hypertension
E. All mentioned above
18. Which of the following conditions is least to produce jugular venous distention?
A. right heart failure
B. Chronic left heart failure
C. Chronic hypoxemia
D. Liver failure
E. circulation insufficiency
19. What kind of cyanosis is usually observed at patient with cardiovascular diseases?
A. Central, warm
B. peripheral, cold
C. peripheral warm
D. Local (near heart region), cold
E. Diffuse warm
20. Which method can we use for establishing edema
A. Visual inspection
B. Palpation
C. weighing patient
D. measuring leg circumstance
E. All mentioned above.

Control questions:
12. What are features of chest pain at angina pectoris?
13. What are features of chest pain at myocardial infarction?
14. What is a palpitation and which diseases it accompanies?
15. What are intermissions and which diseases they accompany?
16. What is syncope and which diseases it accompanies?
17. What are features of dyspnoea at cardiovascular patients?
18. What are features of cough at cardiovascular patients?
19. What are features of hemoptysis at cardiovascular patients?
20. What postures in the bed can patient with cardiovascular disease occupy?
21. What are features of cyanosis at cardiovascular patients?
22. What are features of oedema at cardiovascular patients?
4.3. Practical task that should be performed during practical training
4. Asking patient about cardiovascular symptoms
5. Taking history of cardiovascular patient
6. Doing general visual inspection of cardiovascular patient
7. Assessing obtaining data
 TOPIC 12
Pulse investigations and measuring blood pressure. Local visual
inspection and palpation of near heart area. Obtaining borders of
absolute and relative cardiac dullness
Importance of the topic
Pulse and blood pressure are the vitals signs as temperature and respiratory rate. Their
assessment is very important for establishing patient condition especially if he has
cardiovascular disorders. Local visual inspection of the heart region and palpation of the apex
beat helps to reveal chronic pathology of heart and point diagnostic research to right way.
Percussion of the relative and absolute dullness of heart borders allows finding roughly
enlargement of heart or change its shape that also help to direct diagnostic process at right
way.
2. Concrete aims:
─ Master taking pulse and assessing its properties
─ Master measuring blood pressure and assessing its level
─ Performing and assessing local visual inspection of the heart region
─ Master of palpation and assessment properties of the apex beat
─ Master determining and assessing borders of the relative and absolute heart dullness
─ Master determining and assessing wideness of vascular bundle
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart and vessels
Normal physiology Mechanics of heart working and blood circulation
Histology Ontogenesis of the cardiovascular system, histological structure of
the heart and vessels
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Humpback Hypertension
Apex beat Hypotension
“cat’s purr” symptom Pulse different
Relative heart dullness Irregular pulse
Absolute heart dullness Bradycardia
Wideness of vascular bundle Tachycardia
Pulse deficit Pulse tension
Pulse volume Pulse size

4.2. Theoretical questions:

48. Rules of taking pulse.
49. Basic properties of pulse and their assessment.
50. Rules of blood pressure measurement and normal value of the blood pressure.
51. Main signs obtaining by visual inspection of the heart region.
52. Rules of the apex beat palpation.
53. Main properties of the apex beat, their assessment and diagnostic importance.
54. Rules of the determination of borders of the relative heart dullness.
55. Changes of borders of the relative heart dullness at pathology
56. Rules of the determination of borders of the absolute heart dullness and their changes in
pathology, diagnostic importance.
57. Rules of the determination of the vascular bundle wideness, their diagnostic value.
4.3. Practical task that should be performed during practical training
47. taking pulse and assessing its properties
48. measuring and assessing blood pressure
49. Performing visual inspection of the heart region.
50. Palpation and assessment of the apex beat
51. Percussion and assessment of the borders of the relative and absolute heart dullness
52. Percussion and assessment of the vascular bundle wideness

Topic content
Investigation of the pulse and arterial pressure
Periodic, simultaneous with the work of the heart vibrations of the arterial walls are called
arterial pulse. The most frequent place to study the pulse is the radial artery as it is located superficially
under the skin between the styloid process and the tendon of the inner radial muscle. The topography
of the radial artery allows to press the vessel to the bone, which facilitates the study of the pulse. The
hand of the patient is held with the physician's right hand in the area of the radioulnar joint, the thumb
of the physician should be on the elbow side, the fingers on the radial side. After the artery is felt it is
pressed with the point and middle fingers. When the wave passes the artery, the physician feels dilation
of the artery, that is the pulse. First, it is necessary to study the properties of the radial artery. The
fingers of the physician should glide along the artery in transverse and longitudinal direction. The
normal sensation is that of a thin, soft, even, elastic, pulsating tube.
Then it is necessary to determine whether the pulses are equal on the both hands. Normally
they are equal. If the pulses are unequal, this is called pulsus differens.
After comparison of the pulse on the both hands, it is necessary to study the properties the
pulse on one hand. If the pulse is different on the both hands, it is studied on the hand where it is more
intensive.
The following properties are to be determined.
Pulse rate , the number of pulse beats per minute. In healthy individuals pulse rate is 60-80
beats per minute.
Rhythm of the pulse, the beats follow with equal intervals and are equal, i.e. regular pulse
(pulsus regularis). In disturbances of the heart function, this regularity changes, it becomes arrhythmical,
irregular, an irregular pulse (pulsus irregularis).
If the pulse is arrhythmical, it is necessary to determine if the number of the pulse waves
corresponds to the number of the heart contractions. The difference between the number of the heart
contractions and pulse waves per one minute is termed pulse deficiency, the pulse is called a deficiency
pulse (pulsus deficiens).
Pulse tension is the pressure of the blood exercised on the wall of the artery. It is determined by
the force, which should be exercised to compress the artery completely in order to arrest the blood flow
in it. This property of the pulse gives the information about the state of the vascular system and the
arterial pressure. In healthy persons the pulse tension is satisfactory.
Pulse filling is the amount of blood in the vessel. This property is most difficult to determine,
namely according to the maximum and minimum volume of the vessel (how the diameter of the vessel
changes in the period of dilation and collapse). To do this, proximal fingers on the radial artery should
press the vessel gradually, the distal finger determines its maximum filling. In healthy persons the pulse
is satisfactory.
Pulse value is a collective concept, uniting such properties as filling and tension. It depends of
the degree of the artery widening during systole and its collapse during diastole. In healthy persons the
pulse is sufficient.
The shape or rate of the pulse is the rate of dilation and the following contraction of the artery.
This property depends of the rate of the pressure changes in the arterial system during systole and
diastole. In aortic valve incompetence, an abrupt pulse (pulsus celer) or a bouncing pulse (pulsus silens)
as well as pulsus altus: the stroke blood volume and systolic blood pressure are increased, during
diastole the pressure drops quickly as the blood returns from the aorta to the left ventricle can be
present.
 Slow pulse (pulsus tardus) is opposite to an abrupt pulse. This is associated with slow increase of
the blood pressure in thearterial system and its small fluctuations during a cardiac cycle. This is observed
of aortic stenosis.
Dicrotic pulse (pulsus dicroticus) is a second additional wave after reduction of a normal pulse
wave. In healthy subjects it is not pulpated but registered on sphygmogram. A dicrotic pulse is present in
reduced tone of the peripheral arteries (fever, infections, severe pneumonia, fig. 47a).
An alternating pulse (pulsus alterans) is alterations of large and small pulse waves when the
pulse is rhythmical (severe affection of the myocardium, i.e. myocarditis, cardiomyopathy, fig. 47b).
A paradoxical pulse (pulsus paradoxus) is reduction of the pulse waves during breathing in (in
adhesion of the pericardium layers due to compression of the large veins and reduction of the heart
filling during expiration (Fig. 47c).
Arterial blood pressure and methods to measure it
Arterial pressure is the stress exerted by the blood on the walls of the vessels (lateral pressure)
and the column of the blood from the site of the pressure to periphery (end pressure).
During left ventricle systole, blood pressure in the arteries is the highest, this is systolic or
maximal blood pressure. During diastole it is the lowest, minimum or diastolic pressure. The difference
between maximum and minimum pressure is termed pulse pressure.
Investigation technique The most practical is an auscultation method proposed by N. S.
Korotkoff in 1905. The pressure is usually measured on the brachial artery. The cuff is wrapped and
fastened around the bare upper arm of the patient. The cuff should be tightened to allow only one
finger between it and the patient's skin. The edge of the cuff with the rubber tube should face
downward. The zero level of the apparatus, the artery and the patient's heart should be at the same
level. The patient's arm should rest comfortably with the palm upright and the muscles relaxed. Than
the valve of the apparatus is turned off and the cuff is inflated with air until the pressure in it exceeds
the 30 mm the level when pulsation of the brachial and radial artery is not felt. After that the valve is
turned on and the air is allowed to escape slowly from the cuff. When the pressure in the cuff is a little
lower than systolic pressure, sounds simultaneous with the heartbeat are heard with a phonendoscope
over the brachial artery. When the sound appears, the values noticed correspond to systolic pressure.
When the pressure in the cuff equals diastolic pressure, the obstacle to the blood flow disappears, the
vibrations decrease sharply. This moment is characterized by evident weakening and disappearing
sounds and corresponds to diastolic pressure.
Arterial pressure is measured in millimeters mercury. Normal systolic pressure ranges within
100—140 mm Hg (13—18 kPa), diastolic pressure 60 —90 mm Hg (8 —11 kPa).
Inspection of the heart region
Examination plan:
1. Presence of deformation of the chest in the heart region:
a) cardiac "humpback",
b) effusive pericarditis;
2. Presence of the apex beat;
3. Presence of the pathological pulsation in the heart region;
4. Presence of the remoted pathological pulsation.
Inspection of the heat region.
Symptoms description Arising conditions States
1 2 3
Cardiac "humpback" -constant, Enlargement of the heart chambers 1. Congenital heart valvular
diffuse bulging of the area over the in childhood, when the chest is diseases.
heart liable to changes 2. Heart valvular diseases acquired
in childhood
Temporary, diffuse and general Effusion in the pericardium cavity Effusive pericarditis
protrusion of the cardiac region and
leveling of the costal interspaces

Apex beat - limited rhythmic The thrust of the heart apex against Observed in healthy persons with
pulsation in the site of projection of chest wall moderately developed
the heart apex, synchronous to the subcutaneous fat and wide
left ventricle contraction intercostals spaces
Negative apex beat -precordial Adhesion of the parietal and visceral Adhesive pericarditis,
depression during systole. layers of the pericardium. mediastinopericarditis
Cardiac beat - spread pulsation in Dilation and hypertrophy of the Mitral valvular diseases, tricuspid
the III-IV interspaces along left edge right ventricle regurgitation, chronic cor pulmonale
of the sternum with synchronous i
pulsation in the epigastric region

Systolic depression and diastolic Decreased volume of the right Tricuspid regurgitation
bulging of the chest in the IH-IV ventricle during systole and
interspaces along left edge of the considerable enlargement of it
sternum during diastole
Weak restricted pulsation in the IH- Presence of the bulging in the Aneurysm of the left ventricular
IV interspaces somewhat laterally ventricular wall after myocardial anterior wall
from the left sternal edge infarction
Pulsated bulging in the jugular Dilation of the aortic arch Aneurysm of the aortic arch
fossae
Pulsation in the II interspace to the Dilation of the ascending part of the Aneurysm of the ascending part of
right of the sternum edge aorta the aorta, aortic regurgitation,
syphilitic mesoartritis
Pulsation in the II interspace to the Pulmonary hypertension, Mitral stenosis
left of the sternum edge poststenotic dilation of the
pulmonary artery
Epigastric pulsation, which Hypertrophy and dilation of the Mitral valvular diseases, tricuspid
increased in deep inspiration right ventricle regurgitation, chronic cor pulmonale
Epigastric pulsation, which Pulsation of the abdominal aorta In healthy persons with
decreased in deep inspiration underdeveloped subcutaneous fat,
enteroptosis, aneurysm of the
abdominal aorta
Palpation of the heart
Examination plan:
1. Estimation of location and properties of the apex beat;
2. Determination of the "cat's purr" symptom presence;
3. Palpation of pulsated liver.
Palpation of the apex beat
Technique. Place the palm of your right hand on the chest about at the level of and parallel to
the 3r - 6th ribs. Flex the terminal phalanges of three fingers and slide them medially along the
interspaces until the moderately pressing fingers feel the movement of the heart apex. If the apex beat
is diffuse, extreme left and lower point is considered to be the point of me apex beat. The apex beat can
be better detected if patient slightly leans forward, or during deep expiration: in this position the heart
is pressed closer to the chest wall.
Location. A normal apex beat is found in the 5 intercostal space 1-1,5 centimeters toward to the
sternum from the left midclavicular line (Fig. 2.3a). If the patient slightly leans forward or during deep
inspiration you can better detect apex beat, because in these positions the heart presses closer to the
chest wall. When the patient lies on his left side, the beat is displaced 3-4 cm to the left, and on right
side - 1-1,5 cm to the right. In about one third of cases the apex beat is impalpable: covered by rib.
Displacement of the apex beat may depend on noncardiac and cardiac causes
Causes of the apex beat displacement.
Physiological Pathological
 Noncardiac Cardiac
Respiration phases Position on Changes of pressure in the chest and Changes of the heart
the left, right side, lying, diaphragm level Changes of pressure in the chambers size
standing position pleural cavities Tumor of the lungs and
Constitutional types mediastinum

In changes of the heart chambers size there may be different variants of the apex beat
displacement. In left ventricular hypertrophy apex beat is displaced outward, in dilation of left
ventricular cavity apex beat is displaced downward, in combination of hypertrophy and dilation apex
beat is displaced outward and downward.
Diagnostic significance of the apex beat displacement
Apex beat is displaced outward Hypertrophy of the left ventricle: mitral regurgitation, aortic stenosis,
essential hypertension, atherosclerotic cardiosclerosis,
hypertrophic cardiomyopathy. Hypertrophy and dilation of the right
ventricle: mitral stenosis, tricuspid
regurgitation, cor pulmonale. Extracardiac causes: right-sided effusive
pleurisy, hydrothorax, left- sided obstructive atelectasis
Apex beat is displaced outward Considerable hypertrophy and dilation of the left ventricle: aortic
and downward regurgitation, considerable dilation of the left ventricle - dilative
myocardiopathy
Apex beat is displaced outward Elevated pressure in abdominal cavity, high diaphragm level: ascitis,
and upward meteorism, pregnancy, hepatomegaly
Apex beat is displaced inward Right-sided obstructive atelectasis

Apex beat is displaced inward Low diaphragm level: asthenic constitution, visceroptosis
and downward.

Apex beat properties: area, height, strength (or resistance).

Area of normal apex beat is near 2 cm 2. Different physiological or pathological conditions can
cause diffuse or restricted apex beat.
Causes of the diffuse apex beat
Causes
Physiological Deep inspiration, pregnancy, in subjects with thin chest wall, wide intercostal
spaces (asthenic chest)
Pathological Tumor of mediastinum, high diaphragm level (ascitis, meteorism), sclerotic affection
of the lower border of the left lung, hypertrophy and dilation of the left ventricle
(aortic regurgitation, aortic stenosis, arterial hypertension in myogenic dilation
stage)

Causes of restricted apex beat

Causes
Physiological Deep expiration
Low diaphragm level
Pathological Pulmonary emphysema
Left-sided effusive pleurisy*
Left-sided pneumothorax*
Effusive pericarditis (in considerable accumulation of fluid or air apex beat is
impalpable)
Height of the apex beat is the amplitude of vibration of the chest wall (Fig. 2.4).
Usually, the height varies with the area. High and low apex beats are differentiated.
Physiological causes of the apex beat height changes
Properties
 High Low
Physical exertion Emotional exertion Obesity Overdeveloped muscles

Pathological causes of the apex beat height changes

Causes Properties
High Low
Noncardiac Tumor of posterior mediastinum Pulmonary emphysema
Diffuse toxic goiter (Basedow's disease) Effusive pleurisy
Fever Pneumothorax
Cardiac Left ventricular hypertrophy Effusive pericarditis
Strength of the apex beat is determined by resistance of the heart apex to palpated fingers
during systole. Strong or resistant apex beat - sign of the left ventricular hypertrophy in aortic valvular
diseases, arterial hypertension, and mitral regurgitation.
Weak apex beat is determined in pulmonary emphysema, obesity, left-sided effusive pleurisy,
effusive pericarditis (in small amount of fluid).
Dome-like apex beat in VI - VII intercostals spaces on left anterior or midaxillary line, diffuse,
high, strong is determined in aortic regurgitation.
Cat's purr symptom is thrill of the chest wall in the heart region, low vibrating murmur, which
resembles purring of the cat. This sign is of great diagnostic significance. The cat's purr symptom is
palpatory equivalent of cardiac murmur in organic heart valvular diseases.
Depend on cardiac cycle phases systolic and diastolic thrill are differentiated.
Cat's purr symptom

Palpation of the pulsated liver. True and transmitted pulsations are distinguished. True pulsation
is observed in tricuspid regurgitation due to regurgitation of blood from the right ventricle to the right
atrium during the systole, overfilling of the vena cava superior and liver veins. Therefore liver is enlarged
during systole and positive venous pulse is determined. Transmitted pulsation is characterized by
movement of the liver in the one direction, and is caused by transmission of heart contractions.
Percussion of the heart
Examination plan:
1. Borders of the relative cardiac dullness;
2. Transverse length of the heart;
3. Borders of the vascular bundle;
4. Configuration of the heart;
 5. Borders of the absolute cardiac dullness. Determination of the size, position, and shape of
the heart is based on the distinction between percussion sounds. Being the airless organ, the heart gives
dull percussion sound. But since it is partly covered by the lungs on its sides, the sound here is
intermediate. The heart is surrounded by the lungs, which give clear pulmonary sound in percussion.
The right contour of the heart is formed by the right atrium at the bottom and by the superior
vena cava to the upper edge of the 3 r rib. The left contour is formed by the arch of the aorta, pulmonary
trunk, auricle of the left atrium, and downward by the narrow strip of the left ventricle. Relative cardiac
dullness - is the projection of its anterior surface onto the chest. The relative cardiac dullness
corresponds to the true borders of the heart.
Technique. Percussion can be done with the patient in both erect and lying position. It should,
however, be remembered that the area of cardiac dullness in the vertical position is smaller than in
horizontal. This is due to mobility of the heart and the displacement of the diaphragm as the patient
change posture. The percussion stroke should be of medium strength.
In order to determine the borders of the relative cardiac dullness the remotest points of cardiac
contour are first found on the right, then at the top, and finally on the left.
The right border. As known the position of the heart depends on the diaphragm level, which is
indicated by the lower border of the lung. The lower border of the right lung by loud percussion is,
therefore, first determined in the midclavicular line (normally at the level of the 5 th interspace). Then
move your pleximeter-finger one interspace above, place it parallel to the sternum and change the
percussion technique - medium strength percussion stroke. Continue percussion by moving the
pleximeter-finger along the interspace toward the heart until the sound change. The right border of the
relative cardiac dullness is marked by the edge of the finger directed to the more clear sound. The
normal right border of the relative cardiac dullness is in the 4 th intercostal space 1 cm outward from the
right edge of the sternum.
The upper border. In order to determine the upper border of the relative cardiac dullness place
pleximeter-finger in the 1st intercostal space in the left parasternal line and move it downward until the
percussion sound change. The normal upper border of the relative cardiac dullness is in the 3 rd
intercostal space in the left parasternal line.
The left border is determined in the interspace, where the apex beat is palpated. Place your
pleximeter-finger laterally in this intercostal space parallel to the sought border and move it toward the
sternum. In the apex beat is impalpable you should start percussion in the 5 th intercostal space from the
left anterior axillary line. The left border of the relative cardiac dullness is in the 5 th intercostal space 1,5
cm medially of the left midclavicular line.
Borders of the relative cardiac dullness.
Borders Location Formed by
th
Right 4 intercostal space 1 cm laterally of the right Right atrium
edge of the sternum
Upper 3rd intercostal space in the left parasternal line Cone of the pulmonary artery, the auricle of
the left atrium
Left 5th intercostal space 1,5 cm medially of the left Left ventricle
midclavicular line

The borders of the relative cardiac dullness can be modified by physiological and pathological
factors.
Displacement of the relative cardiac dullness borders. Phvsioloaical and pathological causes.
Extracardiac Cardiac
Physiological Pathological
Position of the body Pulmonary pathology Changes of the heart chambers
Constitutional types Fluid, air in the pleural cavity size and volume
Diaphragm level Diaphragm level (ascitis)
(pregnancy)
There are different clinical variants either isolated and combined displacement of the relative
cardiac dullness borders.
Clinical variants of the relative cardiac dullness borders displacement
Heart borders Changes of the heart chambers size and volume
Extracardiac causes
displacement Conditions Clinical variants
To the right Left-sided pneumothorax, Dilation of the right Pulmonary artery stenosis
effusive pleurisy, hydrothorax. ventricle Dilation of the Tricuspid stenosis, chronic
Right-sided obstructive right atrium and pulmonary diseases (cor pulmonale)
atelectasis ventricle
To the right Dilation of the right Mitral stenosis
and upward ventricle and left atrium
Upward and to Dilation of the left Mitral regurgitation
the left atrium and ventricle,
protrusion of the
pulmonary artery cone
To the left Right-sided pneumothorax, Dilation of the right Mitral stenosis Aortic stenosis,
effusive pleurisy, hydrothorax. ventricle Hypertrophy arterial hypertension, atherosclerotic
Left-sided obstructive and dilation of the left cardiosclerosis
atelectasis ventricle
To the left and Dilation of the left Aortic regurgitation
downward ventricle

Transverse length of the heart is the sum of distance from the right border of the relative
cardiac dullness to the anterior median line (3-4 cm) and from the left border of the relative cardiac
dullness to the median line (8-9 cm). The transverse length is measured by a measuring tape, and
normally is 11-13 cm.
Enlargement of the cardiac transverse length is observed in hypertrophy and dilation of the
heart chambers.
The borders of the vascular bundle are determined by light percussion in the 2 nd intercostal
space from midclavicular line to the right and left toward the sternum. The borders of the vascular
bundle are normally found along the edges of the sternum. The normal width of the vascular bundle is
4-6 cm.
The width of the vascular bundle is increased in:
• Dilation of the pulmonary artery in elevated pressure in it;
• Aortic aneurysm;
• Syphilitic mesoaortitis.
The angle formed by the bundle of the great vessels and left ventricle is called waist of the
heart. In normal configuration of the heart this angle is dull.
Absolute cardiac dullness is the projection of the anterior surface of the heart, which is not
covered by the lungs onto the chest. Absolute cardiac dullness is formed by the right ventricle.
Technique. The right border of the absolute cardiac dullness is first elicited. Place your
pleximeter-finger on the right border of the relative cardiac dullness parallel to the sternum, and using
light percussion stroke move it medially to dullness.
To determine the upper border place pleximeter-finger on the upper border of the relative
cardiac dullness and move downward to dullness.
To outline the left border place pleximeter-finger slightly outside the left border of the relative
cardiac dullness and move medially.
Normal borders of the absolute cardiac dullness:
The right - along the left edge of the sternum from 4 th to 6th rib;
The upper - lower edge of the 4th rib in the site of its connection with the left sternal edge;
The left - 5th intercostal space 0.5 cm medially of the left border of the relative cardiac dullness.
Changes of absolute cardiac dullness area
Decreasing Increasing
Low diaphragm level Pregnancy
Pulmonary emphysema High diaphragm level (ascitis, meteorism)
Left-sided pneumothorax Tumor of mediastinum
Dilation, hypertrophy of the right ventricle

Materials for self-control (added)

7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. – Vinnytsya: NOVA
KNYHA, 2006. – p. 166-184, 208-216, 220-222.

Professor assistant Demchuk H.V., Kushiruk N.V.

 Test for self-control
1. The normal pulse rate is:
A.70 – 80 in a min.
B.50 – 70 in a min.
C. 60 – 80 in a min.
D. 80 – 100 in a min.
E. 50-90 in a min
2. Arising condition to cardiac '' humpback'':
A. enlargement of the heart chambers in childhood
B. effusion in the pericardium cavity
C. the thrust of the heart apex against chest wall
D. dilation and hypertrophy of the right ventricle
E. adhesion of the parietal and visceral layers of the pericardium
3. Arising condition of pulsated bulging in the jugular fossae:
A. dilation of the ascending part of the aorta
B. hypertrophy and dilation of the right ventricle
C. pulmonary hypertension
D. dilation of the aortic arch
E. left atrium dilatation
4. Arising conditions of pulsation in the II interspace to the right of the sternum edge:
A. dilation of the ascending part of the aorta
B. hypertrophy and dilation of the right ventricle
C. pulmonary hypertension
D. dilation of the aortic arch
E. left atrium dilatation
5. Arising conditions of epigastric pulsation that increases in deep inspiration:
A. dilation of the ascending part of the aorta
B. pulsation of the abdominal aorta
C. pulmonary hypertension
D. dilation of the aortic arch
E. Left ventricle hypertrophy
6. A normal apex beat is found:
A. in the 5th intercostal space in 1-1,5 cm medially from the left midclavicular line
B. in the 6th intercostal space 0-1 cm medially from the left midclavicular line
C. in the 4th intercostal space on the left midclavicular line
D. in the 5th intercostal space in 1-1,5 cm laterally from the left midclavicular line
E. in the 6th intercostal space on the left left midclavicular line
7. If patient has left ventricle hypertrophy his apex beat sift…
A. leftward
B. downward
C. upward
D. rightward
E. unchenged
8. Apex beat properties is:
A. localization, area, height, strenght (or resistence)
B. area, height
C. height, strenght
D. area, exertion, strength
E. localization, height
9. Area of normal apex beat is:
A. near 2 cm2
B. near 3 cm2
C. near 1 cm2
D. near 1,5 cm2
E. near 4,5 cm
10. The normal right border of the relative cardiac dullness is:
A. 4th interspace 1 cm laterally of the right edge of the sternum
B. 4th interspace 1,5 cm laterally of the right edge of the sternum
C. 4th interspace 2 cm laterally of the right edge of the sternum
D. 4th interspace 2,5 cm laterally of the right edge of the sternum
E. 4th interspace near the right edge of the sternum
11. The normal upper border of the relative cardiac dullness is:
A. 3th interspace at the left parasternal line
B.3th interspace at the right parasternal line
C.2th interspace at the left parasternal line
D.2th interspace at the right parasternal line
E. 4th interspace at the left parasternal line
12. The normal left border of the relative cardiac dullness is:
A. 5th interspace 2,5 cm medially of the left midclavicular line
B. 5th interspace 1,5 cm medially of the left midclavicular line
C.5th interspace 2 cm medially of the left midclavicular line
D.5th interspace 3 cm medially of the left midclavicular line
E. 5th interspace on the left midclavicular line
13. Right border of the relative heart dullness is displaced to the right in case of:
A. Dilation and hyper trophy of the left ventricle
B. Dilation of the left atrium
C. Atelectasis of the left lung
D. Dilation and hypertrophy of the right ventricle and/or right atrium
E. Pneumothorax of the right lung
14. Left border of the relative heart dullness is displaced to the left in case of:
A. dilation and hypertrophy of the right ventricle
B. dilation of the right atrium
C. hypertrophy and dilation of the left ventricle
D. dilation of the right ventricle and right atrium
E. dilation of the left atrium
15. The normal right borders of the absolute cardiac dullness:
A. along the left edge of the sternum in 5 th interspace
B. along the left edge of the sternum from 4 th to 6th rib
C. along the right edge of the sternum from 5 th to 6th rib
D. along the right edge of the sternum from 3 th interspace
E. along the middle of the sternum between 5 th rib
16. The normal upper borders of the absolute cardiac dullness:
A. lower edge of the 3 th rib along left parasternal line
B. lower edge of the 4th rib along left parasternal line
C. lower edge of the 5th rib along left parasternal line
D. lower edge of the 4th rib along right parasternal line
E. lower edge of the 5 th rib along right parasternal line
17. The upper border of the relative heart dullness shift upward in a case of:
A. mitral stenosis
B. aortic stenosis
C. tricuspid regurgitation
D. pulmonary stenosis
E. pulmonary regurgitation
18. Transverse length of the heart in a norm is:
A. 8 – 10 cm
B. 11 – 13 cm
C. 12 – 14 cm
D. 6 – 7 cm
E.15-17 cm
19. The normal width of the vascular bundle is:
A. 4 – 6 cm
B. 5 – 7 cm
C. 6 – 8 cm
D. 2–3 cm
E. 1,5-2,5 cm
20. The normal range of blood pressure is:
А. 120 – 149/70-99 mm. Hg
В. 90 – 159/60 – 109 mm. Hg
С. 80 – 129/50 – 99mm.Hg
D. 100 – 139/60 – 89 mm. Hg
E. 110-149/40-79 mm Hg

Control questions
17. Main respiratory signs that can be revealed at the general visual inspection
18. What type of cyanosis can be observed at the respiratory patients? Describe mechanism of its
formation.
19. What types of the forced position do respiratory patients occupy? Describe and explain their.
20. What normal shapes of the chest do you know? Describe their.
21. When can the barrel and paralytic chest be formed? Describe their.
22. What pathological shapes of the chest due to deformities of the spin do you know? How they can
influence to the respiratory function?
23. What normal and abnormal types of breathing do you know?
24. What data can you received performing chest palpation? Their diagnostic value.

Practical tasks
13. Performing general visual inspection of the respiratory patient
14. Assess patient’s chest shape, revealing signs of the pathologic chest
15. Performing dynamic visual inspection of the chest
16. Assess data obtained at the dynamic visual inspection of the chest
17. Performing palpation of the chest and assessment of the obtained data.

Situation tasks
Task 1
29-year-old male patient noted repeated every day attacks of breathlessness during last 7 years. At
the visual inspection patient skin is light cyanotic, the ribs are horizontal, the intercostal spaces are
narrow, supra- and subclavicular fossae are not seen, the epigastric angle is obtuse. The upper
portion of the chest is especially wide.
7. Why is patient skin cyanotic?
8. What types of the chest does patient have?
9. What position in the bed does patient occupy during attack of breathlessness?
Task 2
57-year-old female patient complains of dyspnea, cough and left side chest pain. The symptoms
appeared after hard work and overcooling 3 days before. At the visual inspection skin is pale and
cyanotic, respiratory rate is 32 and left part of the chest is left behind from right
16. How is increased respiratory rate named? Why does patient have this sign?
17. Why is one half of the chest left behind from other?
18. What position may patient occupy in the bed? Why?
Task 3
24-year-old female was admitted to pulmonology department with severe mixed dyspnea, high
fever (39°C), cough with rusty sputum, piercing chest pain. Her mother said the patient was exited
and had visual hallucinations. During examination patient is calm, her respiratory rate is 36. Skin is
red and hot.
10. What is general condition of the patient? Which department should patient be admitted?
11. What disorder of consciousness does patient have? Why?
12. How should you palpate the patient chest? What signs of the respiratory disease may you
reveal?
Task 4
73-year-old male patient notes increasing dyspnea, cough with purulent sputum production during
last week after overcooling. Patient condition is moderate severe. He sits fixing the shoulder girdle.
His exhalation is longer than inhalation. Skin is cyanotic.
2. What type of the chest shape may be at the patient? Why?
3. What change of his finger can you find? Why?
4. How is vocal fremitus changed at the patient? Why?
 Topic 13
Auscultation of the heart in a norm
1.Importance of the topic
Auscultation is one of the important physical methods of heart examination. It allows
revealing different changes of the heart sounds and help to establish valve diseases,
find signs of myocarditis, pericarditis, essential hypertension and others. Auscultation
of the heart has a great diagnostic importance.
2. Concrete aims:
─ Study rules of the heart auscultation
─ Study components of the first and second heart sound
─ Study properties of the first and second heart sound
─ Master distinguishing normal first and second heart sounds
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart and vessels
Normal physiology Mechanics of heart working and blood circulation
Histology Ontogenesis of the cardiovascular system, histological
structure of the heart and vessels
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training
Term Term
First heart sound Components of the heart sound
Second heart sound

4.2. Theoretical questions:

58. Rules of heart auscultation.
59. Formation of the first heart sound, its components.
60. Formation of the second heart sound, its components.
61. Features of the normal first heart sound.
62. Features of the normal second heart sound.
63. How can the first and second heart sound be distinguished?
4.3. Practical task that should be performed during practical training
53. Auscultation normal heart sounds
54. Assessment of the normal heart sounds

Topic content
Auscultation of the heart is an objective method based on listening a noise within the
heart during cardiac cycle. Examination plan:
1. Heart rhythm;
2. Heart rate;
3. Heart sounds (loudness, timbre);
4. Presence of the splitting and additional sounds;
5. Presence of the heart murmurs.
Technique. To obtain the most information from cardiac auscultation and to assess
correctly the findings, it is necessary to know the sites of valves projection on the chest wall and
listening points of the heart.
Since the sites of the valves projection on the chest are very close to each another, it is
difficult to assess which valve is affected if listen them in the points of their actual projection.
Therefore the heart sounds are auscultated in the certain listening points where sounds of each
valve can be better heard.
Auscultation should be performed in the order of decreasing frequency of valves
affection: 1 - mitral valve, 2 - aortic valve, pulmonary valve, 4 - tricuspid valve. The fifth listening
point to the left of the sternum at the 3 rd and 4th costosternal articulation- so-called Botkin-
Erb's point, was proposed to assess aortic valve sound.
Projection of the heart valves on the chest wall and standard listenine points of the
heart.
Valve Mitral Aortic Pulmonary Tricuspid
nd
Site of To the left of the In the middle of the In the 2 intercostalOn the sternum
projection sternum at the level sternum at the level space 1-1,5 cm to midway between 3 rd
of the 3rd of the 3rd the left of the left and 5th right
costosternal costosternal sternum costosternal
articulation articulation articulation
Listening Heart apex 2nd intercostal space nd
2 intercostal space Base of the xiphoid
point to the right of the to the left of the process
sternum sternum

Cardiac auscultation is performed using a stethoscope in a quiet room to avoid the

distracting noises of normal activity. Heart sounds are better heard if the patient keeps breath
for short period so that the respiratory sounds should not interfere with auscultation of the
heart. The mitral valve sound in its pathology is better heard when the patient lies on the left
side; aortic valve sound - in the upright posture of the patient or when he lies on the right side.
Normal heart sounds. The noise produced by a working heart is called heart sounds. In
auscultation two sounds can well heard in healthy subjects: the first sound (S1, which is
produced during systole, and the second sound (S2), which occur during diastole.
S1 consists of four pair components: atrial component: 1 -tension and contraction of the
right atrium, 2 - tension and contraction of the left atrium; valvular component: 3 - closure and
vibration of mitral valve cusps, 4 - closure and vibration of tricuspid valve cusps; muscular
component: 5 - isometric tension and contraction of the right ventricle, 6 - isometric tension
and contraction of the left ventricle; vascular component: 7 -vibration of the initial portion of
the aorta, 8 - vibration of the initial portion of the pulmonary trunk. S2 consists of two pair
components: valvular component: 1 - closure and vibration of the aortic valve cusps, 2 - closure
and vibration of the pulmonary valve cusps; vascular component: 3 -vibration of the aortic
walls, 4 - vibration of pulmonary trunk walls.
The first heart sound, a dull, prolonged 'lub' marks the onset of the ventricular systole.
The second heart sound, a short, sharp 'dup' occurs at the beginning of ventricular diastole.
Diastole is subdivided in protodiastole, mesodiastole, and presystole. Both heart sounds can be
heard over precordium, but their intensity changes depend on nearness of valves that take part
in formation of S1 or S2.
In rhythmic heart activity S1 and S2 can be differentiate according following signs.

Differential siens of S1 and S2.

Main sign First sound Second sound
Listening point Heart apex Heart base
Relation to cardiac pause Follows the long pause Follows the short pause
Duration 0,09-0,12 s 0,05-0,07 s
Relation to apex beat Synchronous Follows the apex beat
 Relation to carotidpulse Synchronous Asynchronous

A weak, low-pitched, dull third sound (S3) is sometimes heard and is thought to be
caused by vibration of the walls of the ventricles when they are suddenly distended by blood
from atria (passive rapid filling), occurs 0,12-0,15 s after the onset of S2- The third sound is
heard most clearly at the apex of the heart with the bell of a stethoscope; it may be normal in
children, adolescents, or very thin adults, or in patients with high cardiac output.
The fourth heart sound (S4) is a low-pitched, presystolic sound produced in the ventricle
during ventricular filling; it is associated with an effective atrial contraction and is best heard
with the bell piece of the stethoscope.
Cardiac rhythm. In healthy subjects S1 and S2, S2 and S1 follow each another at regular
intervals: the heart activity is said to be rhythmic or regular. When the cardiac activity is
arrhythmic, the heart sounds follow at irregular intervals.
Heart rate (HR) in normal conditions is 60-80 beats per minute. Acceleration of the heart
rate to more than 90 beats per minute is called tachycardia. A heart rate less than 60 beat per
minute is called bradycardia.
In heart sounds analysis their loudness and timbre should be assessed. Loudness of the
heart sounds depends on several factors.

Loudness of the heart sounds depends on the point of auscultation.

In the first and fourth listening points first heart sound is louder than second one S 1 >
S2, in the second and third - second heart sound is louder than the first S 1 < S2, the second
sound over aorta and pulmonary artery is of the same loudness A 2 = P2.

Materials for self-control (added)

7. Reference source
o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –
Vinnytsya: NOVA KNYHA, 2006. – p. 185-190.
 Test for self-control
1. Where is the mitral valve on the front chest wall projected?
a. 2nd intercostal space to the left of the sternum
b. On the sternum midway between 3rd left and 5th right costosternal articulation
c. To the left of the sternum at the level of the 3rd costosternal articulation
d. To the left of the sternum at the level of the 4th costosternal articulation
e. On the sternum midway between 3rd left and 3th right costosternal articulation
2. Where is the tricuspid valve on the front chest wall projected?
a. 2nd intercostal space to the left of the sternum
b. On the sternum midway between 3rd left and 5th right costosternal articulation
c. To the left of the sternum at the level of the 3rd costosternal articulation
d. To the left of the sternum at the level of the 4th costosternal articulation
e. On the sternum midway between 3rd left and 3th right costosternal articulation
3. Where is the pulmonary artery valve on the front chest wall projected?
a. 2nd intercostal space to the left of the sternum
b. On the sternum midway between 3rd left and 5th right costosternal articulation
c. To the left of the sternum at the level of the 3rd costosternal articulation
d. To the left of the sternum at the level of the 4th costosternal articulation
e. On the sternum midway between 3rd left and 3th right costosternal articulation
4. Where is the aortic valve on the front chest wall projected?
a. 2nd intercostal space to the left of the sternum
b. On the sternum midway between 3rd left and 5th right costosternal articulation
c. To the left of the sternum at the level of the 3rd costosternal articulation
d. To the left of the sternum at the level of the 4th costosternal articulation
e. On the sternum midway between 3rd left and 3th right costosternal articulation
5. Where is listening point for tricuspid valve?
a. heart apex
b. 2nd intercostals space right from the sternum
c. 2nd intercostals space left from the sternum
d. Base of the xiphoid process
e. 3rd intercostals space left from the sternum
6. Where is listening point for mitral valve?
a. heart apex
b. 2nd intercostals space right from the sternum
c. 2nd intercostals space left from the sternum
d. Base of the xiphoid process
e. 3rd intercostals space left from the sternum
7. Where is listening point for aortic valve?
a. heart apex
b. 2nd intercostals space right from the sternum
c. 2nd intercostals space left from the sternum
d. Base of the xiphoid process
e. 3rd intercostals space left from the sternum
8. Where is listening point for pulmonary artery valve?
a. heart apex
b. 2nd intercostals space right from the sternum
c. 2nd intercostals space left from the sternum
d. Base of the xiphoid process
e. 3rd intercostals space left from the sternum
9. Which auscultation point coincides with heart valve projection on the chest wall?
a. 1st auscultation point
b. 2nd auscultation point
c. 3rd auscultation point
d. 4th auscultation point
e. 5th auscultation point
10. Where is placed Botkin-Erb’s listening point?
a. 2nd intercostal space to the right of the sternum
b. 2nd – 3rd intercostal space to the left of the sternum
c. 3rd – 4th intercostal space to the left of the sternum
d. 4th – 5th intercostal space to the left of the sternum
e. 3rd – 4th intercostal space to the right of the sternum
11. Which components does the second heart sound consist of?
a. Muscular, valvular and vascular
b. Muscular and valvular
c. Valvular and vascular
d. Valvular, vascular and atrial
e. None of variants
12. From which components consists the first heart sound?
a. Muscular, valvular and vascular
b. Valvular, vascular and atrial
c. Valvular and vascular
d. Muscular, valvular, vascular and atrial
e. None of variants
13. What produces the third heart sound?
a. The ventricular systole
b. The closure of the aortic and pulmonary valves
c. The vibration of the ventricular diastole
d. The closure of the bicuspid and tricuspid valves
e. The vibration of the ventricular during passive rapid filling
14. When can the forth heart sound be listened?
a. At the beginning of the ventricular systole
b. At the end of the ventricular systole
c. At the beginning of the ventricular diastole
d. At the end of the ventricular diastole
e. At the beginning of the precordial systole
15 Which auscultation points are used for the first sound assessment?
a. 1st and 2nd auscultation points
b. 2nd and 3rd auscultation points
c. 3rd and 4th auscultation points
d. 1st and 3rd auscultation points
e. 1st and 4th auscultation point
16. Which auscultation points are used for the second sound assessment?
a. 1st and 2nd auscultation points
b. 2nd and 3rd auscultation points
c. 3rd and 4th auscultation points
d. 1st and 3rd auscultation points
e. 1st and 4th auscultation point
17. Which sound follows the short pause?
 a. The 1st heart sound
b. The 2st heart sound
c. The 3st heart sound
d. The 4st heart sound
e. Depends on clinical situation
18. Which sound follows the long pause?
f. The 1st heart sound
g. The 2st heart sound
h. The 3st heart sound
i. The 4st heart sound
j. Depends on clinical situation
19. What can be assessed by heart auscultation?
p. Heart rhythm
q. Heart rate
r. Heart sounds
s. Heart murmurs
t. All mentioned above
20. What cannot be assessed by heart auscultation?
u. Heart rhythm
v. Cardiac index
w. Heart rate
x. Heart sounds
y. Heart murmurs

Control questions
1. Rules of heart auscultation.
2. Formation of the first heart sound, its components.
3. Formation of the second heart sound, its components.
4. Features of the normal first heart sound.
5. Features of the normal second heart sound.
6. How can the first and second heart sound be distinguished?

Practical tasks
55. Auscultation normal heart sounds
56. Assessment of the normal heart sounds

Situation task 1
Auscultation of the heart is carried out in a defined sequence.
Questions:
1) Why is the auscultation of the heart carried out by such sequence?
2) Where is the 5th auscultation point situated?
3) Which purpose is the auscultation in the 5th point used with?

Situation task 2
During the auscultation of the heart defines rapid heart rate and weakness of the first heart
sound on the heart apex.

Question: How to define, which heart sound is the first?

 Situation task 3
The patient has pulmonary emphysema. It’s impossible to define, during the auscultation,
which heart sound is the first.

Question: How to define, which heart sound is the first and why?

Situation task 4
The doctor, listening to the patient, defines which heart sound is the first. He uses the method
of accordance with the pulse on a. radialis and also defines one of the pulse characteristics.

Question:
1) Can he define the accordance of the first heart sound? In which cases?
2) Which characteristics of the pulse does the doctor define?
 TOPIC 14
Auscultation of the heart: changes in pathology
1.Importance of the topic
Auscultation of a heart is the most valuable method of its analyses. With the help of auscultation
one can diagnose pathologic rates of a heart ’s activity and give a diagnostic assessment of a clinical
pattern of a disease.

2.Concrete aims:
- Changes in heart sounds strength and timbre
-Sounds reduplication and splitting
-Triple rates
-Pendulous rate and embryocardia

3.Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart and vessels
Normal physiology Mechanics of heart working and blood circulation
Histology Ontogenesis of the cardiovascular system, histological structure of the heart
and vessels
Boimedical physics Principles of liquid flow in a tube

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

myocarditis mitral stenosis hypertension Gallop rhythm

myocardiosclerosis aortic snenosis reduplication of the heart Triple rhythm
sound
myocardiopathy extrasystolic arrhythmia splitting of the heart Systolic clicks
sound
myocardial infarction tachycardia „рistol-shot” sound Embryocardial or
pendulum rhythm

4.2.Theoretical questions:
1. Changes of the 2nd heart sound, diagnostic importance.
2. Changes of the 1st heart sound, diagnostic importance.
3. Reduplication and splitting of the heart sounds, diagnostic importance.
4. "Gallop" rhythms of diagnostic importance.
5. "Quails" rhythm, diagnostic importance.

4.3. Practical task that should be performed during practical training

1. Auscultation of the heart
2. Auscultation of the heart in a norm.
3. Auscultation of the heart in a patholigy.
Topic content
Auscultation of the heart is an objective method based on listening a noise within the heart
during cardiac cycle. Examination plan:
1. Heart rhythm;
2. Heart rate;
3. Heart sounds (loudness, timbre);
4. Presence of the splitting and additional sounds;
 5. Presence of the heart murmurs.
Technique. To obtain the most information from cardiac auscultation and to assess correctly the
findings, it is necessary to know the sites of valves projection on the chest wall and listening points of
the heart.
Since the sites of the valves projection on the chest are very close to each another, it is difficult
to assess which valve is affected if listen them in the points of their actual projection. Therefore the
heart sounds are auscultated in the certain listening points where sounds of each valve can be better
heard.
Auscultation should be performed in the order of decreasing frequency of valves affection: 1 -
mitral valve, 2 - aortic valve, pulmonary valve, 4 - tricuspid valve. The fifth listening point to the left of
the sternum at the 3 rd and 4th costosternal articulation- so-called Botkin-Erb's point, was proposed to
assess aortic valve sound.
In heart sounds analysis their loudness and timbre should be assessed. Loudness of the heart
sounds depends on several factors.
Loudness of the heart sounds influenced factors
Sounds
Factors
S1 s2 S1+s2
1 .Listening point + +
2.Condition of atrioventricular valves +
3.Ventricular contractility + + +
4. Volume of ventricular filling by blood +
5.Speed of ventricular contraction +
6.Condition of semilunar valves of the aorta and +
pulmonary artery
7.Condition of initial portion of the aorta +
8.Pressure in the lesser and greater circulation +
9.Properties of the sound wave transmission +
10. Properties of the nearest to the heart organs +
Loudness of the heart sounds depends on the point of auscultation.
In the first and fourth listening points first heart sound is louder than second one S 1 > S2, in the
second and third - second heart sound is louder than the first S 1 < S2, the second sound over aorta and
pulmonary artery is of the same loudness A2 = P2.
The loudness of the heart sounds can be changed in several physiological and pathological
conditions. Loudness of one or both heart sounds may increase or decrease.
Both heart sounds increasing (in all listening points)
CAUSES
Physiological Pathological
Thin chest wall Thyrotoxicosis
Nervous excitement Wrinkled pulmonary edges
Hard physical exertion Inflammatory consolidation of pulmonary edges
Fever
Both heart sounds decreasing (in all listening points)
CAUSES
Extracardiac Cardiac
Physiological Pathological Primary Secondary
Excessive muscles Obesity Swelling of the chest wall Myocarditis Anemia
development Pulmonary emphysema Myocardiosclerosis Collapse
Effusive pericarditis Myocardial infarction Shock
Effusive left-sided pleurisy Myocardiopathy
Changes in only one heart sound are very important diagnostically.
Increased loudness of the first heart sound at the heart apex
Causes Mechanism
 Mitral stenosis Tachycardia Not adequate filling of the left ventricular
Left ventricular extrasystole Complete cavity during diastole, quick and intense
atrioventricular block in synchronous contraction of contraction of the myocardium
atria and ventricles - 'pistol-shot' sound according
Strazhesko
Decreased loudness of the first heart sound at the heart apex
Causes Mechanism
Mitral regurgitation Anatomic abnormalities of the valve
Aortic regurgitation Absence of closed valve period
Aortic stenosis Overfilling of the left ventricular cavity
Different loudness of the first heart sound at the heart apex

Causes Mechanism
Complete heat block Different ventricular filling in each cardiac cycle
Atrial fibrillation
Extrasystolic arrhythmia
Ventricular flutter
Accentuated second heart sound over aorta
Causes
Physiological Pathological Mechanism
Emotional exertion Essential hypertension Pressure elevation in the greater circulation,
Physical exertion Symptomatic decreased elasticity of the aorta
hypertension
Aortic atherosclerosis
Syphilitic mesoaortitis

Decreased second sound over aorta

Causes Mechanism
Aortic regurgitation (A) Anatomic changes of valve (A)
Aortic stenosis (B) Low pressure if the aorta at the beginning of the diastole (B)

Accentuated second heart sound over pulmonary artery

Causes
Mechanism
Physiological Pathological
In children Mitral valvular diseases Pressure elevation in
Thin chest wall Diseases of the broncho-pulmonary system the pulmonary
Adhesion of the pleural layers circulation
Kyphoskoliotic chest

Decreased second sound over pulmonary artery

Decreased loudness of the first heart sound at the base of the sternum

Causes Mechanism
Tricuspid regurgitation Anatomic changes of the valve
Absence of closed valves period
Overfilling of the right ventricular cavity

Reduplication and splitting of the heart sounds may be revealed in auscultation, which are
caused by asynchronous work of right and left chambers of the heart.
 Reduplication - two short sounds follow one another are heard instead S1 or S2.
Splitting - two short sounds follow one another at a short interval, and therefore they are not
perceived as two separate sounds.
Splitting of the two high-pitched components of S1 by 10-30 ms is a normal phenomenon, which
is recorded by phonocardiography. The third component of S1, is attributed to mitral valve closure, and
the fourth to tricuspid valve closure. Widening of the interval between these two components is heard
as S1 splitting or reduplication at the heart apex or at the base of the xiphoid process.
Physiological splitting of S1, is heard in the upright position of the patient during very deep
expiration, when the blood delivers to the left atrium with a greater force to prevent the closure of
theThree-sound rhythms, caused by appearance of additional sounds
Triple rhythm is three-sound rhythm, which is heard at the heart anex in the patient with mitral
stenosis.
Triple rhythm quail’s rhythm consists of loud (snapping) S1, normal S2 and additional sound,
which is heard 0.07-0.13 s following S2, and termed OS (opening snap). The cusps of the normal mitral
valve open noiseless; they are freely forced back by the blood flow ejected from the atria to the
ventricle. In mitral stenosis blood thrusts against the sclerosed valve, cusps of which cannot freely move,
to produce OS. The opening snap is a brief, high-pitched, early diastolic sound. This phenomenon is of
considerable diagnostic value because it is heard only in the mitral stenosis.
Gallop rhythm.
Three-sound rhythm of a peculiar acoustic character, termed gallop rhythm (bruit de galop or
rythme de galop according to Laubry and Pezzi), is also of considerable diagnostic value. The sounds of
gallop rhythm are usually soft and low, resemble the galloping of a horse, and are best heard in direct
auscultation. Gallop rhythm is heard as three separate audibly distinct sounds in approximately equal
intervals.
Gallop rhythm is classified as presystolic (at the end of diastole), protodiastolic (at the beginning
of diastole), and mesodiastolic (at the middle of the diastole) depend on the time of appearance of the
extra sound in diastole.
Presystolic gallop rhythm occurs due to delayed atrioventricular conduction, when atrial systole
is separated from the ventricular systole by a longer than normal period, and is heard as separate sound.
Three-sound rhythm at the heart apex, in which S1 is decreased, S2 is normal, and the first
sound is weakest - is presystolic gallop rhythm.
Presystolic gallop rhythm is heard in the patients with:
• Rheumocarditis;
• Cardiosclerosis;
• Essential hypertension;
• Chronic nephritis with arterial hypertension syndrome;
• Mitral stenosis;
• Toxic and infectious affection of the myocardium.
Protodiastolic gallop rhythm is caused by appearance of pathological additional sound 0.12 -
0.02 s after S2 as a result of considerably decreased tone of the ventricular myocardium. Ventricles
distended quickly during their filling with blood at the beginning of the diastole and the vibrations thus
generated are audible as an extra sound.
Three-sound rhythm at the heart apex, in which S1and S2 are decreased, and the third sound is
increased - is protodiastolic gallop rhythm.
This auscultation phenomenon is observed in the patients with:
• Acute and chronic myocarditis;
• Myocardiosclerosis;
• Heart failure;
• Toxicosis;
• Thyrotoxicosis;
• Anaemias.
Mesodiastolic (summation) gallop rhythm arises in severe dystrophic affection of the
myocardium in the patients with myocardial infarction, essential hypertension, heart valvular diseases,
myocarditis and chronic nephritis. Mesodiastolic gallop rhythm is characterized by appearance of the
additional sound in the middle of diastole caused by increase intensity of the S3 and S4, which are heard
as one gallop sound.
Systolic clicks - auscultation phenomenon, which denote prolapse of one or both cusps of the
mitral valve. They also may be caused by tricuspid valve prolapse. Auscultation symptomatic may be
very different: systolic clicks may be single or multiple, they may occur at any time in systole with or
without a late systolic murmur. Typical peculiarity - changes of the auscultation data depend on position
of the patient and exercise test. If the patient squat click and murmur slightly delayed; in the upright
posture click and murmur are closer to S1.
Pericardial knock - high-pitched sound occurs 0.01 -0.06s after S2 in the patients with
constrictive pericarditis due to vibration of the adherent pericardium in abrupt dilation of the ventricle
at the beginning of diastole. Pericardial knock is better heard at the heart apex or medially toward to
ziphoid.
Embryocardial or pendulum rhythm occurs in severe heart failure, attacks of paroxysmal tachycardia,
high fever, etc. Tachycardia makes diastolic pause almost as short as the systolic one. A peculiar
auscultative picture, in which heart sounds are similar in intensity, resembles foetal rhythm is termed
embryocardia.

Reference source
o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. – Vinnytsya: NOVA
KNYHA, 2006. – p. 189-200.
 Materials for self-control (added)

1.Loud first sound in the cardiac apex is auscultated in case of:

A. Myocardiac infarction
B. Myocarditis
C. Myocardiac sclerosis
D. Synchronic systole of atriums and ventricles in case of full atrioventricular blockade

2.Weakening of the first sound in the cardiac apex is auscultated with:

A. Stenosis of mitral orifice
B. Insufficiency of mitral valve
C. Synchronic systole of auricles and ventricles in case of full atrioventricular heart block
D. Extrasystole

3.Weakening of both heart sounds is auscultated in case of:

A. Myocardiac infarction
B. Myocarditis
C. Emphysema of lungs
D. All mentioned cases

4.Loud second sound in aorta is auscultated in case of:

A. Insufficiency of aortic valve
B. Aortic stenosis
C. Essential hypertension
D. Mitral stenosis

5.Loud second sound in pulmonary artery is auscultated in case of:

A. Aortic ostium stenosis
B. Mitral stenosis
C. Essential hypertension
D. Aortic insufficiency

6.Loud both sounds in heart apex in case of:

A. Lungs limbus shrinkage
B. Posterior mediastinum tumors
C. Forward inclination of body
D. All mentioned reasons

7.Loud first sound in the cardiac apex is auscultated in case of:

A. Mitral stenosis
B. Ciliary arrhythmia
C. Full atrioventricular blockade
D. All mentioned cases
E.No right answer

8.Loud second sound in pulmonary artery is auscultated in case of:

A. Emphysema of lungs
B. Chronic obstructive lung disease
C. Pneumosclerosis
D. All mentioned reasons
E.No right answer

9.‘Quail’ rate is:

A. Loud ‘flapping’ first sound
B. Loud ‘flapping’ first sound, second sound, opening snap of mitral valve
C. Opening snap of mitral valve
D. No right answer

10. Loud ‘flapping’ first sound in heart apex is auscultated in case of:
A. Mitral stenosis
B. Mitral insufficiency
C. Aortic ostium stenosis
D. aortic insufficiency

11. In the basis of second tone accent appearance in pulmonary artery there is:
A. High pressure in greater circulation
B. High pressure in lesser circulation
C. All above mentioned
D. No right answer

12. In the basis of second tone accent appearance above aorta there is:
A. High pressure in greater circulation
B. High pressure in lesser circulation
C. All above mentioned
D. No right answer

13. ‘Gallop’ rhythm is auscultated in case of:

A. Diffuse myocarditis
B. Cardiac infarction
C. Dilatational cardiomyopathy
D. Cardiac insufficiency
E.All mentioned variants
F.No right answer

14. First sound when ausculating ‘gallop’ rhythm:

A. Intensified
B. Bifurcated
C. Weakened
D. All variants are right
E.No right answer

15. Reduplication of first sound appears in case of:

A. Asynchronous right and left ventricle contraction
B. Block of bundle of His
C. Bisystolia (systole in 2 portions)
D. All mentioned variants
E.No right answer

16. Reduplication of second tone appears more often in:

A. Aorta
B. Pulmonary artery
C. Apex
D. All mentioned variants

17. Reduplication of second sound in pulmonary artery is connected with:

A. High pressure in lesser circulation
B. Asynchronous aortic and pulmonary artery valve closing
C. Breathing
 D. All mentioned is true
E.No right answer

18. Presystolic ‘gallop’ rhythm is auscultated in case of:

A. Cardiosclerosis
B. Rheumatic carditis
C. Chronic nephritis with hypertensive syndrome
D. All above mentioned cases
E.No right variant

19. Protodiastolic ‘gallop’ rhythm is auscultated in case of:

A. Mitral stenosis
B. Tricuspid insufficiency
C. Pneumonia
D. All above mentioned cases
E.No right variant

20. Embryocardia or pendulous rate appears in case of:

A. High fever
B. Paroxysmal tachycardia
C. Cardiac insufficiency
D. No right answer
E.All mentioned variants
Control questions:
6. Changes of the 2nd heart sound, diagnostic importance.
7. Changes of the 1st heart sound, diagnostic importance.
8. Reduplication and splitting of the heart sounds, diagnostic importance.
9. "Gallop" rhythms of diagnostic importance.
10. "Quails" rhythm, diagnostic importance.

Practical task
1. Auscultation of the heart
2. Auscultation of the heart in a norm.
3. Auscultation of the heart in a patholigy

Tasks
1.Left limit shift of relative heart dullness ectad from left middle clavicle line is observed in a
patient with essential hypertension.
A. How will the loudness of second sound be changing?
B. What term designates this change of second sound?
C. Why does the shift of left heart limit appear?

2.Weakening of first sound in heart apex is auscultated in a patient with mitral insufficiency.
A. Explain the mechanism of weakening of first sound.
B. How will the loudness of second sound be changing?
C. How will the heart limits be changing?

3.When ausculating a patient’s heart in the 1 st point a triple rate is auscultated: ‘flapping ’ first
sound, second sound and additional third sound which appears at once after the second sound.
A. How is the mentioned rate called?
B. In what pathological state is it auscultated?
C. What is the mechanism of additional sound appearance?
 4.When auscultating the heart in the apex a triple rate is auscultated: weakened first sound,
second sound, third sound.
A. How is the mentioned rate called?
B. In what pathological state is it auscultated?
C. What is the mechanism of additional sound appearance?
 TOPIC 15
Auscultation of the heart: heart murmurs
1.Importance of the topic
Auscultation of a heart is the most valuable method of its analyses. With the help of
auscultation one can diagnose pathologic rates of a heart ’s activity and give a diagnostic
assessment of a clinical pattern of a disease. Murmurs usually appear at the different
pathologic conditions that can be related with heart and blood circulation. Revealing murmurs
and distinguishing their reasons have a great diagnostic importance.

2.Concrete aims:
- Study of classification of the cardiac murmurs
Study characteristics of the systolic murmurs in different clinic situation
-Study characteristics of the diastolic murmurs in different clinic situation
-study feature and causes of functional cardiac murmurs
- study feature and causes of pleuropericardial and pericardial friction rubs
3.Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart and vessels
Normal physiology Mechanics of heart working and blood circulation
Histology Ontogenesis of the cardiovascular system, histological structure of the
heart and vessels
Boimedical physics Principles of liquid flow in a tube

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

Diastolic murmur mitral stenosis

Systolic murmur aortic snenosis
Functional murmur Mitral regurgitation
Pericardial friction rub Aortic regurgitation

4.2.Theoretical questions:
11. Definition and physical base of murmur appearance.
12. Classification of cardiac murmurs.
13. Systolic cardiac murmurs, their characteristics at the different clinical situation.
14. Diastolic cardiac murmurs, their characteristics at the different clinical situation.
15. Functional cardiac murmurs, their characteristics at the different clinical situation.
16. How functional cardiac murmurs can be distinguished from organic?
17. Pericardial friction rub, its characteristics and causes.
18. Pleuropericardial friction rub, its characteristics and causes.

4.3. Practical task that should be performed during practical training

1. Auscultation of the heart
2. Auscultation of the heart in a norm and pathology.
3. Auscultation of the cardiac murmur.
4. Assessment of the heart auscultation
Topic content
Cardiac murmurs
In addition to the normal heart sounds, abnormal sounds known as murmurs may be
heard in auscultation. Cardiac murmurs may both endocardiac and exocardiac. Endocardiac
murmurs occur in dysfunction of the intact valves - functional murmurs or in anatomical
changes in the structure of the heart valves - organic murmurs.
Organic cardiac murmurs.
When a valve is stenotic or damaged, the abnormal turbulent flow of blood produces a
murmur, which can be heard during the normally quiet times of systole or diastole.
The mechanisms of cardiac murmurs can be explained by the physics laws concerning
the flow of liquids in tubes.
Such condition as liquid flowing through a partially narrowed portion of the tube can
cause turbulent flow. The intensity of noise depends on the extent of narrowing: the narrower
lumen of the tube, the more intense noise. In significant narrowing of the tube, noise may
weaken or even disappears. Liquid flowing from a smaller portion of the tube to a larger one
can also cause vortex movement. Murmur can be caused by blood flow in the vascular lumen
partially obstructed by atherosclerotic plaque or thrombus.
Following characteristics used to describe cardiac murmurs are timing, intensity, pitch,
quality, configuration, duration, location and radiation.
Murmurs are defined in terms of their timing within the cardiac cycle. Systolic murmur
terminates between S1 and S2 or begins instead of significantly decreased S1. Diastolic murmur
begins with or after S2 and terminates at or before the subsequent S1.
The intensity of the murmurs is graded according to the Levine scale:
• Grade I - Lowest intensity, difficult to hear even by expert listeners
• Grade II - Low intensity, but usually audible by all listeners
• Grade III - Medium intensity, easy to hear even be inexperienced listeners, but
without a palpable thrill
• Grade IV - Medium intensity with a palpable thrill
• Grade V - Loud intensity with a palpable thrill. Audible even with the stethoscope
placed on the chest with the edge of the diaphragm
• Grade VI - Loudest intensity with a palpable thrill. Audible even with stethoscope
raised above the chest.
A cardiac murmur's pitch varies from high to low.
Common descriptive terms of a murmur's quality include rumbling, blowing, machinery,
scratchy, harsh, rough, squeaky, or musical.
The configuration of murmur is defined by changes in their intensity during systole and
diastole as recorded on a phonocardiogram.
A decrescendo murmur gradually decreases in intensity, a crescendo murmur gradually
increases in intensity, a crescendo-decrescendo murmur (a diamond-shaped) first increases in
intensity, and then decreases in intensity, and a plateau murmur is equal in intensity
throughout the murmur.
A murmur's duration can be of different length.
Location. Cardiac murmurs may not be not audible over all areas of the chest, and it is
important to note where it is heard best and where it radiate to. The location on the chest wall
where the murmur is best heard and the areas to which it radiates can be helpful in identifying
the cardiac structure from which the murmur originates.
Best auscultatory areas of a cardiac murmurs. Topographic classification of murmurs
Auscultatory areas Murmur Heart valvular disease
Heart apex Systolic Mitral regurgitation
 Diastolic Mitral stenosis
Second intercostal space Systolic Aortic stenosis
at the right sternal edge Diastolic Aortic regurgitation

Second intercostal space Systolic Pulmonary stenosis

at the left sternal edge Diastolic Pulmonary regurgitation

Base of the ziphoid Systolic Tricuspid regurgitation

Diastolic Tricuspid stenosis
Radiation. Some cardiac murmurs may be heard not only in standard auscultatory areas
but also transmitted in the direction of blood flow. This phenomenon is known as radiation.
Murmurs radiate in either a forward (ejection murmurs) or backward direction
(regurgitation murmurs).

Auscultatory areas and radiation of murmurs in heart valvular diseases.

Heart valvular
Murmur Auscultatory areas Radiation areas
disease
Mitral Systolic Heart apex Axillary region
regurgitation
Mitral stenosis Diastolic Heart apex No radiation
Aortic Diastolic Second Botkin-Erb's point,
regurgitation intercostals space sometimes heart
at the right sternal apex
edge
Aortic stenosis Systolic Second intercostal Subclavian,
space at the right carotid arteries,
sternal edge interscapular
region
SYSTOLIC MURMURS
Aortic stenosis.
One of the most frequent pathologic systolic murmurs is due to aortic stenosis. The
murmur of aortic stenosis heard best over "aortic area", second intercostal space along right
sternalborder, with radiation into the neck, along carotid arteries, into the interscapular region
(ejection murmur). The intensity of murmur varies directly with the cardiac output. It has a
harsh quality, are usually crescendo-decrescendo in configuration (as the velocity of ejection
increases, the murmur gets stronger, and as ejection declines, its diminished), is typically
midsystolic murmur (starts shortly after S 1, when the left ventricular pressure becomes enough
to open aortic valve; ends before left ventricular pressure falls enough to permit closure of the
aortic leaflets).
Pulmonary stenosis.
The murmur of pulmonary stenosis is heard best in the "pulmonic area", second
intercostal space along the left sternal border. The murmur can be heard radiating into the neck
or the back (ejection murmur), has a harsh quality, a crescendo-decrescendo shape, and
midsystolic duration.
Mitral regurgitation.
Systolic murmur in mitral regurgitation is best heard at the heart apex, with radiation
into the axilla (regurgitant murmur). The quality of murmur is usually described as blowing,
frequency - as high-pitched, the configuration of murmur may vary considerably, and its
duration is holosystolic.
 Tricuspid regurgitation.
The holosystolic murmur of tricuspid regurgitation is best heard at the base of the
sternum, generally softer than that of mitral regurgitation, and frequently increases during
inspiration.
DIASTOLIC MURMURS
Aortic regurgitation.
The murmur of aortic regurgitation best heard in the second intercostal space along left
sternal edge, it widely radiates along the left sternal border (Botkin-Erb's point) and to be well
transmitted to the heart apex (regurgitant murmur). This murmur is usually characterized as
blowing, generally high-pitched, decrescendo (since there is progressive decline in the volume
of regurgitationduring diastole), and early diastolic murmur. In severe regurgitation, it may be
holodiastolic. The soft, rumbling, low-pitched, mid- to late diastolic murmur at the heart apex
(Austin Flint murmur) may be detected in severe aortic regurgitation. It is thought to be due to
a functional mitral stenosis, as the backflow blood from the aorta presses on the mitral valve,
slightly occluding the flow from the left atrium.
Pulmonary regurgitation.
The murmur of pulmonary regurgitation is best heard in the second intercostal space to
the left of the sternum, with radiation along left sternal edge (regurgitant murmur), high-
pitched, decrescendo, early diastolic murmur. The diastolic murmur of pulmonary regurgitation
without pulmonary hypertension is softer, and low- to medium-pitched.
In mitral stenosis functional early diastolic, high-pitched, with a decrescendo quality
murmur is heard over the pulmonic area. This murmur, known as Graham Steel murmur, begins
with accentuated S2, and is caused by dilation of the pulmonary artery due to significant
pulmonary hypertension.
Mitral stenosis.
The murmur of mitral stenosis is best heard at the heart apex with a little radiation. It is
usually described as low-pitched, rumbling, characteristically follows OS, and can be heard best
with the patient in the left lateral decubitus position. The murmur is nearly holodiastolic with
presystolic accentuation, or presystolic crescendo, or early diastolic (protodiastolic)
decrescendo.
Tricuspid stenosis.
The diastolic murmur associated with tricuspid stenosis is localized to a relatively limited
area over the ziphoid, low-pitched, rumbling, and like most right-sided events, may be stronger
during inspiration.
Extracardiac murmurs: pleuropericardial friction rub and pericardial friction rub
Pericardial friction rub may be heard when the pericardial sac becomes inflamed. The
surface of pericardium becomes shaggy due to fibrin over its.
Pericardial friction rub is heard:
1. Dry pericarditis
2. At the beginning or at the end of exudative pericarditis
3. Uremia
4. Myocardial infarction (Dressler syndrome)
5. Polyserositis (autoimmunity diseases)
Signs of pericardial friction rub
1. Is heard during systole and diastole
2. Character – may be soft or rough, like snow crunches
3. The best place for listening – area of absolute dullness of heart
4. Not radiation
 5. Increases if patient band front or if the funeral of the stethoscope is pressed to
the chest
Pleuropericardial friction rub may be heard when the pleura near the heart is inflamed.
Signs of the pleuropericardial friction rub:
1. Associated with breathing
2. Increases during deep inspiration
3. The best place for listening is the left edge of the relative cardiac dullness

Reference source
o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –
Vinnytsya: NOVA KNYHA, 2006. – p. 200-208.
 Materials for self-control (added)
1. What heart diseases listed below can you find organic systolic cardiac murmurs at?
A. mitral stenosis
B. Aortic stenosis
C. Aortic regurgitation
D. Pulmonary regurgitation
E. Tricuspid stenosis
2. What heart diseases listed below can you find organic diastolic cardiac murmurs at?
A. Stenosis of mitral foramen
B. Stenosis of orifice of aorta
C. Mitral valve deficiency
D. Stenosis of lung arteries orifice
E. Threecaspidalis valve deficiency
3. The best point for hearing the systolic murmurs at aortic stenosis is
A. The heart apex
B. The Botkin – Erb point
C. The second intercostal space, to the right from the breastbone
D. The second intercostal space, to the left from the breastbone
E. On the middle of the breastbone on the level of third rib
4. The best point for hearing the diastolic murmurs at aortic regurgitation is
A. The heart apex
B. The Botkin – Erb point
C. The second intercostal space, to the right from the breastbone
D. The second intercostal space, to the left from the breastbone
E. On the middle of the breastbone on the level of third rib
5. Anaemic functional murmur is more often:
A. Systolic
B. Diastolic
C. Protodiastolic
D. Presystolic
E. Systola-diastolic
6. Anaemic murmur is heard better
A. Above the lung artery
B. At Bodkin’s point
C. Above all valve orifices
D. On the apex of the heart
E. Above the aorta
7. Haemodinamical functional murmurs can be auscultated at
A. Thyrotoxicosis
B. Mitral stenosis
C. Myocarditis
D. Cardiosclerosis
E. Hypertension disease
8. How is functional systolic murmur differed from organic one?
A. It is not ruled by periods of breathing
B. Loud, harsh, prolonged
C. Do not change during exercises
D. Do not have irradiative zones
 E. Often supported by feeling of systolic “cat purr”
9. The pericardial friction pub is better heard
A. On the heart apex
B. on the Botkin-Erb point
C. Above the absolute heart’s dullness zone
D. On heart’s base
E. Near the xiphoid process
10. The pericardial friction rub usually appears at
A. Uremia
B. Hydropericardium
C. Cardiomegaly
D. Angina pectoris
E. Adhesion of pericardium and pleura
11. The pericardial friction rub differs from organic murmurs in that it is
A. More delicate
B. Heard like far away
C. Heard near the ear
D. Always coincide with systole
E. Well radiate to other auscultatic zones
12. The pericardial friction rub differs from organic in that it is
A. Become stronger during pressing the chest
B. Becomes weaker if patient bends forward
C. Heard above zones, projections and places of the best auscultation of heart ’s vavles
D. Do not coincidance with cardiac periods
E. Never gives tactile sings
13. The pericardial friction rub differs from organic in that it is
A. Never gives any tactile fillings
B. Becomes stronger if patient bends forward
C. Coincidance with systola and diastola
D. Well irradiate to other auscultatic zones
E. Loud
14. Which organic murmur gives the filling of “cat purr” on the heart apex?
A. Systolic murmur of mitral regurgitation
B. Diastolic murmur of mitral stenosis
C. Systolic murmur of aortic stenosis
D. Diastolic murmur of aortic regurgitation
E. Systolic murmur of tricuspid regurgitation
15 Which organic murmur gives the filling of “cat purr” in the second intercostal space right
from the breastbone?
A. Systolic murmur of mitral regurgitation
B. Diastolic murmur of mitral stenosis
C. Systolic murmur of aortic stenosis
D. Diastolic murmur of aortic regurgitation
E. Systolic murmur of tricuspid regurgitation
16. Which cardiac murmur gives tactile filling above absolute cardiac dullness that becomes
stronger while bending the body forward?
A. Systolic murmur of mitral regurgitation
B. Diastolic murmur of mitral stenosis
C. Systolic murmur of aortic stenosis
 D. Diastolic murmur of aortic regurgitation
E. Systole-diastolic pericardial friction rub.
17. Which functional murmur can be heard at aortic regurgitation?
A. Systolic hydremic
B. Systolic hemodynamic
C. Flint’s murmur
D. Coombs’ murmur
E. Graham-Steel murmur
18. Systolic murmur of aortic stenosis irradiates
A. To the heart apex and to Botkin’s point
B. To the left axillary region
C. To the second left intercostal space
D. To the area of xiphoid process
E. To the carotid and subclavical arteries
19. What are the reasons for Flint’s murmur in aorta valve deficiency
A. Relative mitral regurgitation
B. Relative mitral stenosis
C. Relative aortic stenosis
D. Relative tricuspid regurgitation
E. Relative pulmonary stenosis
20. Which functional murmur can be heard at mitral stenosis?
A. Systolic hydremic
B. Systolic hemodynamic
C. Systolic muscular
D. Kumbs’ murmur
E. Graham-Steel murmur
Control questions:
19. Definition and physical base of murmur appearance.
20. Classification of cardiac murmurs.
21. Systolic cardiac murmurs, their characteristics at the different clinical situation.
22. Diastolic cardiac murmurs, their characteristics at the different clinical situation.
23. Functional cardiac murmurs, their characteristics at the different clinical situation.
24. How functional cardiac murmurs can be distinguished from organic?
25. Pericardial friction rub, its characteristics and causes.
26. Pleuropericardial friction rub, its characteristics and causes.

Practical task
1. Auscultation of the heart
2. Auscultation of the heart in a norm and pathology.
3. Auscultation of the cardiac murmur.
4. Assessment of the heart auscultation

Situation task 1
The boy, 16 years old, has short systolic murmur above the lung artery, which don ’t irradiate.
Heart’s tones don’t change
A. Are such processes typical for organic or functional murmur?
B. What process helps to find the difference in organic and functional murmurs?
C. What conditions promote the formation of functional murmur
 Situation task 2
During the auscultation of the patient it was found that, the first tone is weaken and the sharp
systolic murmur which irradiates to the arteries of neck is heard in the second intercostal space
to the right from breast-bone
A. During what heart disease such systolic murmur is heard?
B. What is the mechanism of its origin?
C. What symptoms during palpation do this patient have?

Situation task 3
During the patient’s auscultation the louder firs tone and presystolic murmur is heard above the
top of the heart
A. For which pathology this murmur is typical?
B. How to explain its origin?
C. Does this murmur irradiate?
Situation task 4
During the auscultation of the heart the murmur which takes systole and diastole is heard in
the fourth intercostal space to the right from the breast-bone
A. How is it named
B. For which pathology this murmur is typical?
C. What are the typical features of this murmur?
 TOPIC 16
Method of the ECG recording and evaluation. ECG signs of atrial and ventricular hypertrophy
1. Importance of the topic
Electrocardiography (ECG) is a simple, useful, and practical diagnostic test. The ECG should be
interpreted with knowledge of the entire clinical picture and must never be the sole basis for judging a
patient’s cardiac status. Abnormalities of cardiac function and structure can occur without changes of
the ECG. Similarly, ECG change may occur without structural and functional abnormality of the heart.

2. Concrete aims:
- Study principles of the ECG records
- Learn rules of ECG interpretation
- Study characteristics of the waves and intervals at the normal ECG record
- learn topical features of the ECG assessing
- Study ECG-signs of the left and right atrium hypertrophy
- Study ECG-signs of the left and right ventricle hypertrophy
Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart, its conduction systems
Normal physiology Principles of the heart automaticity, conductivity
Histology histological structure of the heart
Boimedical physics Principles of electricity activity of the heart and its records with ECG device

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

automaticity refractoriness pacemaker

conductivity ECG leads electrical axis of the heart
depolarization ECG waves Electrical systole
repolarization ECG intervales Electrical diastole

4.2. Theoretical questions:

27. Main principles of the ECG records.
28. Rules for the ECG assessment.
29. Characteristics of the normal ECG waves and ECG intervals.
30. Topical diagnostics of ECG changes.
31. ECG signs of the right ventricle hypertrophy.
32. ECG signs of the right atrial hypertrophy
33. ECG signs of the left ventricle hypertrophy.
34. ECG signs of the left atrial hypertrophy.

4.3. Practical task that should be performed during practical training

1. Recognizing normal and pathological ECG waves and intervals
2. Recognizing cardiac pacemaker
3. Assessing cardiac rhythm and rate by ECG record.
4. Recognizing hypertrophy of the heart chambers

Topic content
ECG is a record of electrical activity of cardiac muscle on paper, recorded by attaching
electrodes to the body and using ECG machine.
Under resting state (polarized state), the cardiac muscle has negative charge inside and positive
charge outside. When cardiac muscle is stimulated by electric current, its charge becomes reverse, i.e.
the interior of muscle becomes positively charged while the exterior negatively charged. This change is
called "depolarization". When wave of excitation is over, again, there is reversal to original state, i.e.
there is negative charge inside and positive charge outside the cardiac muscle. This process of reversal
to resting state is called "repolarization".

CONDUCTION OF CARDIAC IMPULSE

Pacemaker of the heart (S.A. node) is located at the junction of superior vena cava and right
atrial appendage. It is buried in the endocardial surface of the posterior wall.
It initiates the electrical impulse in the form of a depolarization wave which spreads to whole of
the myocardium. From S.A. node, the wave of depolarization spreads to the atria.
After the stimulation of atria, the wave of depolarization reaches the A.V. node from A.V. node
to A.V. bundle and then to left and right bundle branches.
Eventually, the wave travels through the Purkinje system of fibers and initiates the
depolarization of ventricles. After depolarization, repolarization starts. The part depolarized in the last is
first to be repolarized. Apex of the heart is depolarized in the last, so it is first to be repolarised. In this
way the wave of the repolarization spreads from the apex to the base of the heart.

CARDIAC AXIS
The flow of current from one point to another is represented by an arrow. This arrow is called
"Vector".
A vector indicates two things:-
1) The direction of flow of current, i.e. the arrow point is always towards the positive direction.
2) The length of the arrow represents the voltage uenerated by the current i.e. greater the
voltage of current, longer is the length of arrow.
Normal cardiac axis is downwards towards the left in the direction of + 59°. The range of cardiac
axis (for adults more then 40 years) is 0° to +90. Beyond this limit, it is said to be "deviated".

LEADS
A standard ECG is composed of six limb and six chest leads,
Limb leads.
These are recorded by placing electrodes on-the right and left arms and left leg respectively.
Lead I:
This is recorded by placing + ve electrode on the left arm, while - ve electrode is on the right
arm.
Lead II:
This is recorded by placing - ve electrode on right arm, while + ve electrode is on the left leg.
Lead III:
This is recorded by placing + ve electrode on the left leg, while the - ve electrode is on the left
arm.
Augmental leads:
aVR. This reflects right cavity potential. In this, we use right arm as + ve and all other limb
electrodes as common negative.
aVL. This reflects left cavity potential. In this, we use left arm as + ve and all other limb
electrodes as common negative.
aVF. This reflects left ventricular epicardial potential. In this, we use left leg as +ve, while all
other limb electrodes as common negative.
For this, a+ve electrode is placed at six different positions around the chest.
VI. The electrode is placed in the 4th i.c.s. at right sternal edge.
V2. The electrode is placed in the 4th i.c.s on the left sternal edge.
V3. The electrode is placed between V 2 and V4.
V4. The electrode is placed in the 5th i.c.s. on midclavicular line.
V5 The electrode is placed at the point where the left anterior axillary line and a horizontal line
from V4 meet each other.
 V6. The electrode is placed at the point where the horizontal line from V4 meets the left mid
axillary line.

NORMAL ECG
The normal electrocardiogram is composed of waves produced by depolarization and
repolarization of the atria and ventricles. The waves of ECG are labelled as P,Q,R,S,T.
P wave:
This is produced by atrial depolarization. This has duration 0.1 seconds and height to 2.5 mm.
Usually it is positive, but it may be inverted in leads aVR and V 1 in a norm.
QRS complex:
This is from the beginning of the Q wave to the end of S wave and its normal duration is 0,06-
0.11 seconds. Its height is biggest in the II lead, and usually we begin to assess wave and intervals from
this lead.
Q wave is always negative, it reflects beginning of the ventricle depolarization. Its duration is not
more than 0,03 seconds and depth is not more than 1/3 of relative R wave.
R wave is always positive. The height of R is biggest in II lead and AVL. At the chest leads it
gradually increased from V1 to V4 and then becomes lower at V5, V6.
S wave is always negative. Its depth is the lowest at II lead from standard ones and AVF. At the
chest leads it is the deepest in V 1, gradually its depth is decreased to V 4 and at the V5,6 S wave
disappears. At the V3 S wave depth and R wave height becomes equal – it is transitional zone.
T wave:
It is, usually, more than 2 mm. high and up in all leads except in lead aVR. It may also be inverted
in leads III, aVF, V1 and V2 at normal individuals.

NORMAL INTERVALS
P-R Interval.
This is from the beginning of P wave to the beginning of Q wave. Normal duration is 0.2 seconds
when the heart rate is 70/min.
VAT (Ventricular activation time). It is time required for ventricular depolarization. This is from
the onset of QRS complex to the peak of R wave. Normally/it is 0.03 to 0.05 seconds for left ventricle.
Q-T interval. This extends from the beginning of QRS complex to the end of T wave. It is
electrical systole of the heart. Normally, it is less than 0.42 -0.45 seconds.
ST interval should be on the isoelectric line in a norm.

SYSTEMATIC APPROACH TO ECG INTERPRETATION

The ECG is interpretated according to the following scheme:
1. Determination of the Cardiac Rhythm Pacemaker Site.
2. Determination of the Cardiac Rhythm Regularity.
3. Calculation of the Heart Rate.
4. Determination of the Electrical Axis of the Heart.
5. Estimation of the Conductivity.
6. Measurement of the duration and amplitude of the ECG waves and intervals.
7. ECG conclusion. In the ECG conclusion it is necessary to note following:
a) The cardiac rhythm pacemaker (sinus or not sinus rhythm);
b) Regularity of the cardiac rhythm (regular or irregular);
c) The heart rate;
d) Position of the electrical axis of the heart;
e) Presence of the four ECG syndromes: arrhythmias, abnormalities of conductivity, atrial and
ventricular hypertrophy, myocardial damage (ischemia, injury, necrosis, scar).
Rhythm: can be sinus or non-sinus. We assess this looking at P-wave. If it is normal and has
relative link with QRS rhythm is sinus. In the other case rhythm is non-sinus.
Regularity: This is checked by the intervals between two "R" peaks or two "S" waves. If the
number of large or small squares between two "R" or "S" waves is equal in all leads, the rhythm is said
to be regular and if it is not, the rhythm is said to be irregular.- If rhythm is irregular note whether it is
regularly irregular or irregularly irregular. If the irregularity is after regular intervals, the rhythm is
regularly irregular, otherwise irregularly irregular.
Irregular rhythm is called Arrhythmia.
Rate: Before discussing how to calculate heart rate, one should have knowledge about ECG
paper.
ECG Paper
This is long roll of paper with a coated surface and is composed of number of small squares
which are 1 mm. wide and 1 mm. high. On the ECG paper, there are thick lines. Between two thick lines,
there are 5 small squares. When ECG machine works, the speed at which the roll of paper moves is 25
mm or 50 mm. per second (however the speed can be varied accordingly). So, we can say, horizontally,
the small squares represent time. The time interval of each small square can be calculated as follows:
25 mm represent = 1 second, or 50 mm represent = 1 second
1 mm. will represent = 1 = 0.04 seconds or 0.02 seconds. So each small square represents the
time interval of 0.04 or 0.02 seconds and each large square (which has width of 5 mm.) represents time
interval of 0.2 or 0.1 seconds.
Vertically, the small square represents the amount of electrical potential. The ECG machine is
standardized in such a manner, that an impulse of 1 millivolt will cause a deflection of 10 small squares
i.e. 10 mm.
How to calculate heart rate:
There are two methods:
1. When rhythm is regular.
2. When rhythm is irregular.
When rhythm is regular:
To calculate the heart-rate/min, count the number of small squares in between two "R" peaks of
same lead. Now divide 60 sec by number of squares and multiply on 0,04 if speed of paper is 25 mm/sec
or 0,02 if speed is 50 mm/sec . This will give us the heart rate/min.
A quick method to count the heart rate is as follows:
If there is one big square between two R peaks, the heart rate will be 300/min.
If there are two big squares, the heart rate will be 150/min.
If there are 3 big squares, the heart rate will be 100/min.
If there are 4 big squares, the heart rate will be 75/min.
If there are 5 big squares, the heart rate will be 60/min
If there are 6 big squares, the heart rate will be 50/min.
When rhythm is irregular.
In this connection, the QRS complex will be at variable distances. So, we calculate the heart rate
as follows:
Count the QRS complexes falling in 15 large squares and - multiply it with 20. This will give the
heart rate/mm.
AXIS DEVIATION
There are two types:
Rt. axis deviation.
Lt. axis deviation. 215
Right axis deviation.
As already has been mentioned, mean cardiac axis lying between 0° to + 90° is normal. Axis
more than 90° is called as "right axis deviation".
1. There will be deep S waves in lead aVL and lead I.
2. There will be tall R waves in lead aVF and lead III.
N.B. If lead I is put above and lead aVF below, their major QRS deflections will converge towards
each other in case of right axis deviation.
Left Axis deviation.
Mean cardiac axis less than 0° is called as "left axis deviation".
1. There will be tall R waves in lead I and lead aVL.
2. There will be deep S waves in lead III and lead aVF.
 N.B. If lead I is put above and lead aVF is put below, their major QRS deflections will diverge
away from each another in case of Left axis deviation.

VENTRICULAR HYPERTROPHY
Following are the important electro-physiological point regarding the ECG of ventricular
hypertrophy.
There is direct relationship between the voltage of R wave and thickness of muscle. Thicker the
muscle, greater is the voltage (height) of R wave. So there will be prominent R waves in the respective
ventricular leads.
ST segment and T wave changes: Due to relative endocardia ischaemia, there will be depression
of ST segment and inversion of T wave in respective ventricular leads.
When only ST segment and T wave changes are present without other changes, this is called as
"Strain Pattern".
RIGHT VENTRICULAR HYPERTROPHY:
This results mostly from mitral stenosis, cor pulmonale and Tetralogy of Fallot, pulmonary
embolism.
ECG will show the following pattern:
1. R wave at the III greater in height than R wave in II, I
2. S deeper at the I than the II, III.
3. R wave greater in height V1 than in a norm.
4. Transitional zone shifts to V4 or V5
5. S wave persisting in V5 and V6.
6. ST segment depression and T wave inversion in III, V 1,2

LEFT VENTRICULAR HYPERTROPHY

This results mostly from hypertension, aortic valvular lesion, mitral incompetence and various
congenital heart diseases i.e. P.D.A., VSD, Coarctation of aorta.
Lett ventricular Hypertrophy There will be:
1. R wave at the I greater in height than R wave at II, III
2. S deeper at the III than the II, I.
3. R wave greater in height V5,6 than in a norm.
4. Transitional zone shifts to V1 or V2
5. ST segment depression and T wave inversion in I, II, AVL, V 5,6
.

P wave
P wave: P wave is formed by the contractions (due to the stimulation of cardiac impulse) or both
right arid left atria. First half of P wave is due to the contraction of right atrium and second half is due to
the contraction of left atrium.
Abnormal P wave. It includes the following:
P pulmonale,
P mitrale.
P-Pulmonale (cor pulmonale due to lung diseases): This is tall and peaked wave with normal
duration but greater than in a norm height. It is produced due to right atrial hypertrophy. It is best seen
in lead II. Ill and aVF
P-Mitrale (mitral valve diseases): This is produced due to left atrial hypertrophy and is seen in
cases of mitral stenosis. This is large, wide and bifid. First peak is due to right atrial activity and second
peak is due to left atrial activity. It is best seen in leads I, II, AVL and V5.

Reference source
o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. – Vinnytsya: NOVA
KNYHA, 2006. – p. 227-255.
 Materials for self-control (added, ECG)
Control questions:
35. Main principles of the ECG records.
36. Rules for the ECG assessment.
37. Characteristics of the normal ECG waves and ECG intervals.
38. Topical diagnostics of ECG changes.
39. ECG signs of the right ventricle hypertrophy.
40. ECG signs of the right atrial hypertrophy
41. ECG signs of the left ventricle hypertrophy.
42. ECG signs of the left atrial hypertrophy.

Practical task
1. Recognizing normal and pathological ECG waves and intervals
2. Recognizing cardiac pacemaker
3. Assessing cardiac rhythm and rate by ECG record.
4. Recognizing hypertrophy of the heart chambers
 TOPIC 17
ECG signs of heart automatism and excitability dysfunctions
3. Importance of the topic
Electrocardiography (ECG) is a simple, useful, and practical diagnostic test. The ECG should be
interpreted with knowledge of the entire clinical picture and must never be the sole basis for judging a
patient’s cardiac status. Abnormalities of cardiac function and structure can occur without changes of
the ECG. Similarly, ECG change may occur without structural and functional abnormality of the heart.

4. Concrete aims:
- Study abnormalities of the impulse formation due to altered automaticity of the sinoatrial node:
Sinus tachycardia
Sinus bradycardia
Sinus arrhythmia
- Study abnormalities of the impulse formation due to increased automaticity of an ectopic
pacemaker: nodal (av) rhythm
- Study abnormalities of the impulse formation due to increased excitability of the myocardium:
premature heart beat (supraventricular, ventricular)
paroxysmal tachycardia (supraventricular, ventricular)
atrial and ventricular flutter and fibrillation

Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart, its conduction systems
Normal physiology Principles of the heart automaticity, conductivity
Histology histological structure of the heart
Boimedical physics Principles of electricity activity of the heart and its records with ECG device

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

automaticity Paroxysmal tachicardia pacemaker

conductivity Atrial flutter Ventricular extrasystole
Nodal rhythm Atrial fibrillation Ventricular paroxysmal
tachicardia
Supraventricular Ventricular flutter Ventricular fibrillation
extrasistole

4.2. Theoretical questions:

1.ECG signs of the altered automaticity of the sinoatrial node (sinus tachycardia, sinus
bradycardia, sinus arrhythmia).
2.ECG signs of nodal (av) rhythms.
3.ECG signs of premature heart beat (supraventricular, ventricular).
4.ECG signs of paroxysmal tachycardia (supraventricular, ventricular).
5. ECG signs of atrial and ventricular flutter and fibrillation.

4.3. Practical task that should be performed during practical training

1. Recognizing normal and pathological ECG waves and intervals
2. Recognizing cardiac pacemaker
3. Assessing cardiac rhythm and rate by ECG record.
4. Recognizing arrhysmias
Topic content
Diagnostic ECG signs of sinus tachycardia
1 . Decreased duration of the R-R intervals, increased heart rate to 90-150
per minute.
2. Regular sinus rhythm: the P waves are easily seen, upright in the leads I,
II, aVF, V4, V5, Vfi. The conduction to the ventricles is 1:1, the P-P and
R-R intervals are constant.
3. The P-Q interval is 0.12 second or more.
4. The ORS complexes are normal.
Diagnostic ECG signs of sinus bradycardia
The impulse is initiated in the sinus node and spreads in normal sequence through the conducting
system of the ventricles.
1. Increased duration of the R-R intervals, slow heart rate less than 60 beats
per minute.
2. Regular sinus rhythm: the P waves are easily seen, upright in the leads I,
II, aVF, V4, V5, V6. The conduction to the ventricles is 1:1, the P-P and
R-R intervals are constant.
3. The P-Q interval is between 0.12 and 0.20 second, although at very slow
rates it may be slightly longer.
4. The QRS complexes are normal.
Diagnostic ECG signs of sinus arrhythmia
1. The P-P and R-R intervals vary significantly and rhythmically in such manner that the R-R
intervals gradually shorten and lengthen with the respiratory cycles. The R-R intervals length
may vary by 0.16 second or more.
2. Regular sinus rhythm: the P waves are upright in the leads I, II, aVF, V 4, V5, V6. The conduction to
the ventricles is 1:1.
3. The P-Q intervals are constant.
4. The QRS complexes are normal.
Diagnostic ECG signs of nodal rhythm
1. Heart rate is 40-60 beats per minute.
2. An inverted P wave in leads II, III, and aVF may be seen just preceding
or following the QRS complexes; sometimes no P wave is seen.
3. The P-Q interval duration is more than 0.2 second.
4. The QRS complex is usually normal.
ECG signs of atrial premature contractions
1. Premature appearance of the P wave following by the QRS complex.
2. Changes of the P wave polarity depend on the site of the ectopic focus.
3. Normal configuration of the QRST complex.
4. Presence of the incomplete compensatory pause after the atrial premature
contraction.
ECG signs of the nodal premature contractions.
1. Premature appearance of the normal QRS complex.
2. Inverted P wave before, after, or within the QRS complex.
3. Presence of incomplete compensatory pause.
ECG signs of Premature ventricular contractions (PVCs).
1. Premature appearance of significantly wide and distorted QRS complex.
2. The S-T segment and T wave of PVC opposite in direction to the main deflection of the QRS complex.
3. The QRS complexes of PVCs are not preceded by a P wave.
4. Presence of the complete compensatory pause after PVCs.
PVCs from the same site have the same configuration in the same lead, and is called – unifocalPVCs.
PVCs that originate from the different site have different configuration when recorded in the same lead,
and is called – multifocalPVCs. Ventricular bigeminy occurs when PVCs alternate with normal con-
tractions. Trigeminy is a term applied to a grouping of the PVCs in runs of three, such as two normal
beats followed by a PVC.
 ECG signs of paroxysmal supraventricular tachycardia.
1. Sudden acceleration of heart rate 150 to 220 beats per minute.
2. The QRS complexes configuration is normal.
3. Inverted P wave before, after, or simultaneously with QRS complex.
ECG signs of paroxysmal ventricular tachycardia.
1. Abrupt starts and stops of the heart rate acceleration 150 to 200 beats per
minute in regular rhythm.
2. Deformation and broadening of the QRS complex with opposite to the
main QRS deflection S-T segment and T wave.
3. AV dissociation (independent atrial and ventricular rhythms). P wave is absent.
Ventricular Flutter and Fibrillation.
Ventricular flutter is characterized by fairy regular, oscillating waves of large amplitude with no
isoelectric interval, and a rate between 200-300 cycles per minute. In ventricular fibrillation, electrical
and mechanical activity of the heart is totally disorganized. There is no cardiac output; clinical cardiac
arrest is present. The ECG is bizarre, with complete absence of the characteristic P, QRS, and T waves; it
shows irregular waves of varying amplitude and shape occurring 250 to 500 times per minute. Both
rhythms usually result in death unless they are quickly converted by drugs or electrical defibrillation.
Atrial Flutter
Atrial flutter may result from a rapid series of impulses arising from a single ectopic focus, a series
of impulses from multiple ectopic atrial foci, or a circus movement. The atrial rate is usually between
240 and 350 beats per minute.
The ECG in atrial flutter is usually characterized by a uniformly appearing series of flutter waves (F
waves), often described as resembling a picket fence, or as having a saw-toothed appearance. These
waves are usually best seen in leads II, III, aVF, and V 1. There is a sharp upstroke with a more gradual
down-stroke, and no isoelectric interval exists between the waves.
At rest, the AV node will not allow more than 150-180 impulses per minute to pass. Therefore,
when atrial flutter is present in its untreated state, the conduction to the ventricles is blocked (2:1, 3:1,
4:1 ets).
ECG signs of atrial flutter.
1. Presence of rapid (150-180 per minute) regular, uniform atrial F waves,
which are best seen in leads II, III, aVF, V1.
2. Regular ventricular rhythm with equal R-R intervals.
3. The QRS complex is usually normal in configuration.
4. The conduction to the ventricles is 2:1 or 3:1, or 4:1 ets.
Atrial Fibrillation
In atrial fibrillation the atria are beating very rapidly and irregularly. The rate is between 350 and
700 beats per minute. Most of these impulses are blocked in the AV node, so the ventricular rate is
much slower, but totally irregular. Many impulses reach the nodal tissue while it is still refractory from
preceding impulses. Actually, some impulses may not reach the nodal tissue at all, and the impulses that
do arrive and conduct to the ventricle do so quite irregularity, giving rise to rapid and very irregular
ventricular response. Usually the ventricular rate is between 110 and 160. There are no definite P
waves; there are, instead, continuous irregular undulations of the baseline of varying amplitude,
spacing, and contour. These are known as fibrillation waves (f waves). The QRS complexes have
relatively normal configuration.
ECG signs of atrial fibrillation.
1. Instead P wave irregular undulations of varying shape and amplitude (f
waves), which are best seen in leads II, III, aVF, V 1.
2. Irregular ventricular rhythm with different R-R intervals.
3. The QRS complexes have relatively normal configuration.

Reference source
o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. – Vinnytsya: NOVA
KNYHA, 2006. – p. 260-279.
Professor assistant Demchuk A.V.
 Materials for self-control (added) - ECGs
Control questions:
1.ECG signs of the altered automaticity of the sinoatrial node (sinus tachycardia, sinus
bradycardia, sinus arrhythmia).
2.ECG signs of nodal (av) rhythms.
3.ECG signs of premature heart beat (supraventricular, ventricular).
4.ECG signs of paroxysmal tachycardia (supraventricular, ventricular).
5. ECG signs of atrial and ventricular flutter and fibrillation.

Practical task
1. Recognizing normal and pathological ECG waves and intervals
2. Recognizing cardiac pacemaker
3. Assessing cardiac rhythm and rate by ECG record.
4. Recognizing arrhysmias
 TOPIC 18
ECG signs of conductivity disorders. Basis of the electropulsed therapy
1.Importance of the topic
Electrocardiography (ECG) is a simple, useful, and practical diagnostic test. The ECG should
be interpreted with knowledge of the entire clinical picture and must never be the sole basis for
judging a patient’s cardiac status. Abnormalities of cardiac function and structure can occur
without changes of the ECG. Similarly, ECG change may occur without structural and functional
abnormality of the heart.

2.Concrete aims:
- to study abnormalities of the conductivity:
Sinoatrial node block
Intraatrial block
Incomplete atrioventricular block (the first-degree, second-degree)
Complete atrioventricular block
Intraventricular block

3.Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart, its conduction systems
Normal physiology Principles of the heart automaticity, conductivity
Histology histological structure of the heart
Boimedical physics Principles of electricity activity of the heart and its records with ECG
device

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

automaticity Incomplete Right bundle brunch

atrioventricular block block
conductivity Complete Mobitz type I second-
atrioventricular block degree block
Sinoatrial block Left bundle brunch block Mobitz type II second-
degree block

4.2. Theoretical questions:

6. ECG signs of the sinoatrial block.
7. ECG signs of the intaatrial block.
8. ECG signs of the incomplete atrioventrical blocks.
9. ECG signs of the complete atrioventrical block.
10. ECG signs of the intraventrical block.

4.3. Practical task that should be performed during practical training

1. Recognizing normal and pathological ECG waves and intervals
2. Recognizing cardiac pacemaker
3. Assessing cardiac rhythm and rate by ECG record.
4. Recognizing blocks
Topic content
Abnormalities of Conduction. Heart Blocks
Heart block is an electrocardiographic diagnosis arising from situations that delay or
interrupt the passage of an electrical impulse into any part of conduction system of the heart.
Incomplete block indicates defect, functional or organic, in the conduction system that slows,
but does not interrupt, the transmission of the impulses. Complete heart block indicates defect
in the conduction system that interrupt the transmission of the electrical impulses.
Depending on the site of conduction abnormalities the following heart blocks are
distinguished:
1. Sinoatrial Block.
2. Atrioventricular Block.
3. Intraventricular Block.
Sinoatrial Block
Sinoatrial (SA) block indicates failure of the sinus node to form impulses or impaired
conduction of the impulse from sinus node to the atrial myocardium. Since the sinus impulse
itself produces no ECG deflection, a sinus block is indirectly diagnosed by the absence of one or
more expected P wave with the associated QRS complex.

Sinoatrial block. The normal impulse is formed within the SA node, but is not conducted to the
atrium. The regular sinus rhythm is present, after which there is a pause during which no P-
QRS-T complex occurs. The pause is double the R-R interval of the beats displaying sinus
rhythm.

Sinus block occur most frequently in patients with increased vagal tone and often during
acute diaphragmatic myocardial infarction. Ischemia, hemorrahage, rheumatic fever, diphtheria,
other acute infections, and drug toxicity (digitalis, quinidine, atropine, salicylates) may also cause
SA block.
ECG signs of the sinoatrlal block.
1. Periodic missing of the separate cardiac cycle (P wave and QRST complex) in the regular
sinus rhythm.
2. The pause is double the P-P or R-R interval of the beats displaying sinus rhythm.
Abnormalities of the Atrial Conduction are developed due to dilatation and
hypertrophy of the cambers and appears as
P-Pulmonale (cor pulmonale due to lung diseases): This is tall and peaked wave with
normal duration but greater than in a norm height. It is produced due to right atrial
hypertrophy. It is best seen in lead II. Ill and aVF
P-Mitrale (mitral valve diseases): This is produced due to left atrial hypertrophy and is
seen in cases of mitral stenosis. This is large, wide and bifid. First peak is due to right atrial
activity and second peak is due to left atrial activity. It is best seen in leads I, II, AVL and V5..
Atrioventricular Block
Atrioventricular block (AV block) is an important and frequent cause of slow rhythms. The
greatest delay in normal transmission of an impulse from the atria to the ventricles occurs in the AV
junctional tissues. AV blocks observe in the patients with atherosclerosis, coronary heart disease with
acute myocardial infarction, rheumocarditis, and in drug toxicity.
By tradition, AV block has been divided into three degrees of block, depending on changes in
the P-Q interval and relationship between the P wave and QRS complex.
 The First-Degree AV Block
In the first-degree AV block the P-Q interval is prolonged over 0.21 second, but all sinus
impulses are conducted to the ventricles: every sinus beat (P wave) is followed by a ventricular
complex QRS. Since the ventricles are activated in the usual manner, the QRS complex is normal
in configuration. Ordinarily, the P-Q interval is constant at a given heart rate. In the normal
heart, the P-Q interval tends to shorten as the rate increases. When some forms of conduction
disturbances are present, the P-Q interval lengthens as the heart rate increases.
ECG signs of the first-degree AV block.
1. Prolonged P-Q interval to more than 0.21 second.
2. The QRS complexes normal in configuration.
Second-Degree AV Block
In second-degree AV block, some impulses are blocked and fail to reach the ventricles
(some P wave are not followed by a QRS complex). The more atrial impulses blocked from
reaching the ventricles, the slower the ventricular rate. Thus, second-degree AV block often
causes bradycardia.
Three types of second-degree AV block have been described: Mobitz type I, Mobitz type II,
and type III.
Mobitz (Wenchenbach) type I
In type I second-degree heart block involving AV node, the P-Q interval progressively
lengthens until the atrial impulse fails to conduct to the ventricles (P wave not followed by
QRS complex), and then the cycle repeats. The ECG sequence starting with the first conducted
beat following by the ventricular pause, and ending with the next blocked atrial beat,
constitutes a Samoilov-Wenchenbach period. The basic principle of the Wenchebach
phenomenon is that conduction time progressively lengthens until it is blocked for a one beat,
producing a pause. Following the pause the conduction time shortens and then progressively
lengthens again. Since the ventricles are activated in the usual manner, the QRS complex is
normal in configuration.

ECG signs of Mobitz type I second-degree AV block.

1. The P-Q interval is progressively prolonged until P wave is completely blocked.
2. The R-R interval is progressively shortened until the block occurs.
3. The P-Q interval after the blocked impulse is shorter than P-Q interval before the blocked
impulse.
4. The R-R interval following block impulse is longer than the R-R interval preceding the blocked
impulse.
5. The long interval due to the blocked impulse is less than twice the preceding R-R interval.
6. The QRS complex is normal in configuration.
Mobitz type II
In this type of block, an impulse from the atria suddenly fails to conduct to the ventricles without
antecedent progressive lengthening of the P-Q interval. The P-Q intervals are constant before and
after the pause
ECG signs of Mobitz type II second-degree AV block.
1. The P-Q interval is constant.
2. Irregular missing of the ventricular QRST complex.
Type III second-degree AV block or incomplete AV block
Type III shows a specific ratio of blocked beat. The ratio of P waves to QRS complexes varies: 2:1,
3:1, 4:1, etc.
ECG signs of type III second-degree AV block.
1. Every second (2:1) ventricular complex is blocked, or two and more in succession (3:1,4:1,
etc).
2. The R-R intervals are regular.
Complete AV block
Complete AV block indicates a complete interruption of AV conduction. In this arrhythmia,
no atrial impulses (P waves) activate the ventricles. The QRS originates from a junctional or
ventricular pacemaker site. Therefore, the P waves and QRS complexes occur independently.
Both the P waves and QRS complexes occur regularly, but there is no relationship between
them. The atria are controlled by SA node at a rate of 70-80 per minute; the ventricular rate is
60-30 beats per minute. The lower ventricular pacemaker, the slower ventricular rate, the more
bizarre the QRS complex.
ECG signs of complete AV block.
1. The P waves bear no relation to the QRS complexes.
2. The P wave may be before, after, or superimposed on the QRS complex or on the T wave to
cause their deformation.
3. The R-R and P-P intervals are constant, but R-R intervals are longer than P-P intervals.
4. If the site of the block is high in the AV junction, the QRS complexes will be normal in
configuration. The ventricular rate is not less than 45-60 beats per minute.
5. If the site of the block is below the bifurcation of the common His bundle, the QRS complex is
wide and deformed because the ectopic ventricular pacemaker causes the ventricles aberrantly
to be activated. The ventricular rate is not more than 40-45 beats per minute.
Abnormalities of the Ventricular Conduction.
Bundle-Branch Block.

Bundle-branch block is an obstruction in the right or left ventricular conduction pathway.

When this occurs, the impulse travels first through the unobstructed branch and is then
transmitted by nonspecialized myocardial tissue to the opposite ventricle. This aberrant pathway
requires a longer time for activation of the ventricles, and the resulting QRS is greater than 0.12
second and of abnormal configuration. Origin of this beat is from the SA node. Therefore, a P
wave will precede the wide QRS complex.

Right Bundle-Branch Block

When the right bundle-branch is blocked, the impulse travels first through the left
ventricle. Therefore, the initial electrical activation on the left side of the heart is normal, but
the right ventricle is the last portion of the heart to be activated.
ECG signs of right bundle-branch block (Fig. 4.106).
1. The M-shaped QRS complex in leads V1, V2 (rarer in leads III, aVF), where R'>r. R' - is
produced by delayed onset of ventricular activation in a rightward direction, r - activation of
the left ventricle.
2. A decidedly slurred, broad S wave, produced by the late right ventricular and septal
activation, in leads V5, V6, 1, aVL.
3. QRS widened to more than 0.12 second. The prolongation of the QRS interval is
due to the delayed onset of right ventricular activation and the slow conduction in the right
ventricle due to muscle cell-to-cell conduction through the septum and the right ventricular
wall.
4. S-T segment and T wave changes in the leads over the right ventricle. The right
precordial leads Vp V2 (rarer lead III) show depressed S-T segment and an inverted T wave. The
course of activation is altered, with a resultant change in the course of repolarization. In
general, the T wave is opposite in direction from the terminal part of the QRS complex.
Left Bundle-Branch Block.
If the entire left bundle-branch is blocked, the impulse first depolarizes the right side of the
heart and then through aberrant pathways - the left ventricle.
ECG signs of left bundle-branch block .
1. Increased amplitude of ventricular complex QRS with notched or slurring peak of the R
wave in leads V5, V6, I, II, aVL. Because left ventricular stimulation is delayed,
unopposed by right ventricular activation, the resultant potential is of greater
than normal magnitude. I.
2. A wide and deep ventricular complex by QS type with a slurred, broad S wave in
leads V1, V2, III, aVF.
3. QRS widened to more than 0.12 second. The late arrival of the depolarization wave at the left
ventricle produces this change.
4. S-T segment and T wave changes in the leads over the left ventricle. The left precordial
leads V5, V6, and leads I, aVL have depressed S-T segment and an inverted T wave, because
abnormal depolarization results in abnormal repolarization. In general, the S-T segment and T
wave are discordant (opposite) in direction from the terminal part of the QRS complex.

Reference source
o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. – Vinnytsya: NOVA KNYHA,
2006. – p. 280-287.
 Materials for self-control (added) - ECGs
Control questions:
1. ECG signs of the sinoatrial block.
2. ECG signs of the intaatrial block.
3. ECG signs of the incomplete atrioventrical blocks.
4. ECG signs of the complete atrioventrical block.
5. ECG signs of the intraventrical block.

Practical tasks
1. Recognizing normal and pathological ECG waves and intervals
2. Recognizing cardiac pacemaker
3. Assessing cardiac rhythm and rate by ECG record.
4. Recognizing blocks
 TOPIC 19
Instrumental investigation of the cardiovascular system

1.Importance of the topic

Modern instrumental investigations of the cardiovascular system play very important role in
diagnostic process today. These methods allow revealing and establishing different severe and difficult
in diagnostics heart and vascular diseases. They help to assess severity of diseases, property of their
treatment and correct therapy in time. Thanks to using instrumental investigations, medical care
cardiovascular patients have become more qualified.
2.Concrete aims:
-Study main principles and methods of echocardiography
-Learn the most important echocardiographic parameters of the heart
-Study main principles of Doppler echocardiography of the heart and vessels
- Study main principles of Holter daily ECG monitoring and blood pressure monitoring
- Study main principles of coronarography, its diagnostic importance
- Learn main principles of exercise testing cardiovascular patients

3.Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart, its conduction systems
Normal physiology Principles of the heart automaticity, conductivity
Histology histological structure of the heart
Boimedical physics Principles of ultrasound scanning, Doppler wave spreading

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

echocardiography End diastolic diameter Daily ECG monitoring

Doppler principles End systolic diameter Daily BP monitoring
End diastolic volume Stroke volume Coronorography
End systolic volume Ejection fraction Treadmill

4.2. Theoretical questions:

11. What is echocardiography, its main principles?
12. The normal value of the main Echocardiographic heart parameters? Their diagnostic
value.
13. What are main principles of Doppler echocardiography of the heart and vessels?
14. What purpose do we use daily ECG monitoring with? Its diagnostic importance.
15. What purpose do we use daily blood pressure monitoring with? Its diagnostic
importance.
16. What are main principles of coronarography? Its diagnostic importance.
17. What purpose do we use exercise testing cardiovascular patients with?
4.3. Practical task that should be performed during practical training
1. Assessing echocardiographic conclusion
2. Assessing daily ECG monitoring records
3. Assessing daily blood pressure monitoring records

Topic content
Echocardiography
This non-invasive technique uses the differing ability of various structures within the heart to reflect
ultrasound waves. It not only demonstrates anatomy but provides a continuous display of the
functioning heart throughout its cycle. There are various types of scan:
M-mode (motion mode). Scans are displayed on light-sensitive paper moving at constant
speed to produce a permanent single dimension (time) image.
2-dimentional (real time): A 2-dimentional, fan-shaped image of a segment of the heart is
produced on the screen, which may be 'frozen' and hard-copied. Several views are possible and the 4
commonest are: long axis, short axis, 4-chamber, and subcostal. 2-D echocardiography is good for
visualizing conditions such as: congenital heart disease, left ventricular aneurysm, mural thrombus, left
atrial myxoma, septal defects.
Doppler and color-flow echocardiography: Different colored jets illustrate flow and gradients across
valves and septal defects. Trans-oesophageal echocardiography (TOE) is more sensitive than
transthoracic echocardiography (TTE) because the transducer is nearer to the heart. Indications:
diagnosis aortic dissections; assessing prosthetic valves; finding cardiac source of emboli, and
endocarditis. Don't do if oesphageal disease or cervical spine instability.
Stress echocardiography: Used to evaluate ventricular function, ejection fraction, myocardial thickening,
and regional wall motion pre- and post-exercise. Dobutamine or dipyridamole may be used if the patient
cannot exercise. It is inexpensive and as sensitive/specific as a thallium scan.
Uses of echocardiography
Quantification of global left ventricle function: Heart failure may be due to systolic or diastolic
ventricular impairment (or both). Echo helps by measuring end-diastolic volume. If this is large, systolic
dysfunction is the likely cause. If it is small, it ’s diastolic. Pure forms of diastolic dysfunction are rare.
Differentiation is important, as vasodilators are less useful in diastolic dysfunction as a high ventricular
filling pressure is required.
Echo is also useful for detecting focal and global hypokinesia, left ventricular aneurysm. mural
thrombus, and left ventricular hypertrophy (echo is 5-10 times more sensitive than the ECG in detecting
this).
Estimating right heart haemodynamics: Doppler studies of pulmonary artery flow allow evaluation of
right ventricale function and pressures. Valve disease: Measurement of pressure gradients and valve
orifice areas in stenotic lesions. Detecting valvular regurgitation and estimating its significance is less
accurate. Evaluating function of prosthetic valves is another role. Congenital heart disease: Establishing
the presence of lesions and determining their functional significance.
Endocarditis: Vegetations may not be seen if <2mm in size. TTE with colour doppler is best for aortic
regurgitation (AR). TOE is useful for visualizing mitral valve vegetations, leaflet perforation, or looking
for an aortic root abscess.
Pericardial effusion is best diagnosed by echo. Fluid may first accumulate between the posterior
pericardium and the left ventricle, then anterior to both ventricles and anterior and lateral to the right
atrium. There may be paradoxical septal motion.
Hypertrophic obstructive cardiomyopathy: Echo features include asymmetrical septal hypertrophy, small
left ventricle cavity, dilated left atrium, and systolic anterior motion of the mitral valve.
Normal value of the echo-CG parameters (sm):
Right ventricle – < 3,8
End diastolic diameter – 4,9-5,5
End systolic diameter – 3,3-3,8
Thickness of the left ventricle posterior wall – 1,0+ 0,2
Thickness of the intraventricular wall (diastolic/systolic) – 0,7-0,9
Left atrium – 3,0-3,6
Amplitude of the aortic valve opening > 1,4
Amplitude of the mitral valve opening >2,5
End diastolic volume – 122+6 ml (female 59, male 157 )
End systolic volume – 45+3 ml ( female 18-65, male 33-68 )
Ejection fraction 60-66%
Exercise ECG testing
The patient undergoes a graduated, treadmill exercise test, with continuous 12-lead ECG and blood
pressure monitoring. There are numerous treadmill protocols; the 'Bruce protocol' is the most widely
used.
Indications:
• To help confirm a suspected diagnosis of IHD.
• Assessment of cardiac function and exercise tolerance.
• Prognosis following myocardial infarction. Often done pre-discharge (if positive, possibility of
worse outcome increases)
• Evaluation of response to treatment (drugs, angioplasty, coronary artery bypass grafting).
•Assessment of exercise-induced arrhythmias.
Contraindications:
•Unstable angina
• Recent Q wave myocardial infarction (<5day)
• Severe aortic stenosis
• Uncontrolled arrhythmia, hypertension, or heart failure.
Be cautious about arranging tests that will be hard to perform or interpret
• Complete heart block, left bundle branch block
• Pacemaker patients
• Osteoarthritis, COPD, stroke, or other limitations to exercise.
Stop the test if:
• Chest pain or dyspnoea occurs.
•The patient feels faint, exhausted, or is in danger of falling.
• ST segment elevation/depression >2mm (with or without chest pain).
• Atrial or ventricular arrhythmia (not just ectopics).
• Fall in blood pressure, failure of heart rate or blood pressure to rise with effort, or excessive rise
in blood pressure (systolic >230mmHg).
• Development of AV block or left bundle branch block.
• Maximal or 90% maximal heart rate for age is achieved.
Interpreting the test A positive test only allows one to assess the probability that the patient has IHD.
75% with significant coronary artery disease have positive test, but so do 5% of people with normal
arteries (the false positive rate is even higher in middle-aged women, eg 20%). The more positive the
result, the higher the predictive accuracy. Down-sloping ST depression is much more significant than up-
sloping, eg 1mm j-point depression with down-sloping ST segment is 99% predictive of 2-3 vessel
disease. Morbidity: 24 in 100,000. Mortality: 10 in 100,000.

Daily ECG monitoring (Holter) are used for assessment ECG change during 24 hour when patient
gives his routine life. This method allows finding changes of ECG (disorders of rhythm, conductivity,
variability of rhythm and QT interval, change of T-wave, ST position) that could not be revealed by one
moment ECG records.
Indications for dairy ECG monitoring
 Symptoms could be related with rhythm disorders (palpitation, interruption, faintness,
dizziness).
 Diseases with high risk of fatal arrhythmias and sudden death: prolonged QT, dilatational and
hypertrophic cardiomyopathy, idiopathic ventricular tachycardia, sinus sick syndrome, primary
pulmonary hypertension, resent myocardial infarction with heart failure or arrhythmias.
 Estimating efficacy of the antiarrhythmic therapy
 Assessing circadian variability of the sinus rhythm at patient with myocardial infarction, heart
failure, obstructive sleep apnea syndrome
 Revealing of ischemic disorders (ischemic heart disease)
Inexpediency of performing dairy ECG monitoring:
 At patients with stable angina pectoris if they don ’t have heart failure of rhythm disorders,
  At patients with occupational arrhythmias with faint (very low probability of rhythm disorder
recording),
 At patient with atrial fibrillation (excepting diagnostics of ischemic episodes and therapy
control).
Rhythm disorders that may be found at healthy person during dairy monitoring ECG:
Night bradycardia > 40 beats per min, sinus arrhythmia, ventricular premature beats (10-50
during day), AV block I or II stage at older person, episodes of RR duration < 2-3 seconds.
Dairy blood pressure monitoring allows revealing BP circadian dairy pattern, estimating efficacy
of the antihypertensive treatment and establishing changes of blood pressure at healthy and sick
people.
Indications for dairy BP monitoring:
Diagnostics of the ‘white coat’ hypertension, border hypertension, symptomatic hypertension,
neurocirculatory dystonia, hypotension due to myocardial infarction, heart failure, suprarenal failure,
vegetative disorders, obstructive sleep apnea syndrome, disorders of fat and carbohydrates metabolism,
during treatment of hypertensive crisis, resistant hypertension, control of antihypertensive therapy.
Estimated parameters:
Average dairy blood pressure (systolic, diastolic, during day and night),
Time index (% of measurements when BP over than normal),
Value of tension area under the increased BP curve,
Dairy index characterizes level of the night depression of blood pressure,
Variability of the blood pressure.
Classification of the patients according to dairy rhythm of BP:
Normal night depression of BP – dipper
Insufficient night depression of the BP – non-dipper
Increased night BP – hyper-non-dipper
Constant increased BP during night – night peacker

Reference source
o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. – Vinnytsya: NOVA
KNYHA, 2006. – p. 288-302.
 Materials for self-control (added)
1. Which pathological conditions can be confirmed by 2-dimenshional echocardiography?
a. congenital heart disease,
b. left ventricular aneurysm
c. mural thrombus
d. Valve heart diseases
e. All mentioned above
2. Doppler echocardiography used for revealing …
a. flow and gradients across valves and septal defects
b. left ventricular hypertrophy
c. ejection fraction
d. stroke volume
e. northing from above
3. Normal value of ejection fraction is …
a. 60-66%
b. 45-50%
c. 50-55%
d. 66-75%
e. 40-45%
4. Normal value of posterior wall thickness in diastole is …
a. 0,8-1,1 sm
b. 0,6-0,7 sm
c. 1,3-1,4 sm
d. 0,4-0,5 sm
e. 1,5-1,6 sm
5. If patient has diastolic dysfunction which echocardiographic parameter can confirm it?
a. End systolic volume
b. End diastolic volume
c. Stroke volume
d. Ejection fraction
e. Minute volume
6. If patient has left ventricular hypertrophy which parameters are changed?
a. Posterior wall thickness
b. Ejection fraction
c. End diastolic volume
d. Diameter of the interventricular septum
e. a and d.
7. Indications for exercise ECG testing are:
a. confirming a suspected diagnosis of IHD
b. Assessment of cardiac function and exercise tolerance
c. Prognosis following myocardial infarction
d. Evaluation of response to treatment
e. All mentioned above
8. Contraindication for exercise ECG testing:
a. Unstable angina
b. Recent Q wave myocardial infarction (<5day)
c. Severe aortic stenosis
d. Uncontrolled arrhythmia, hypertension, or heart failure
e. All mentioned above
9. Indication for dairy ECG monitoring
a. Symptoms could be related with rhythm disorders
b. Diseases with high risk of fatal arrhythmias and sudden
death
 c. Assessing circadian variability of the sinus rhythm at patient with myocardial infarction,
heart failure, obstructive sleep apnea syndrome
d. Revealing of ischemic disorders (ischemic heart disease)
e. All mentioned above
10. Indication for dairy blood pressure monitoring:
a. Diagnostics of the ‘white coat’ hypertension,
b. Diagnostics of the border hypertension,
c. Diagnostics of the symptomatic hypertension
d. Control of antihypertensive therapy.
e. All mentioned above
Control questions:
1.What is echocardiography, its main principles?
2.The normal value of the main Echocardiographic heart parameters? Their diagnostic value.
3.What are main principles of Doppler echocardiography of the heart and vessels?
4. What purpose do we use daily ECG monitoring with? Its diagnostic importance.
5. What purpose do we use daily blood pressure monitoring with? Its diagnostic
importance.
6. What are main principles of coronarography? Its diagnostic importance.
7. What purpose do we use exercise testing cardiovascular patients with?
Practical task
1. Assessing echocardiographic conclusion
2. Assessing daily ECG monitoring records
3. Assessing daily blood pressure monitoring records
 TOPIC 20
Clinical, laboratory and instrumental examinations of patients with mitral valve
disease
1.Importance of the topic
Valve mitral diseases are important structural pathology of the heart. They can be formed
due to different pathological process and usually could not be resolved without surgery.
Knowledge about causes, hemodynamics, symptoms and signs of the mitral valve diseases has a
great role in the study of the cardiovascular diseases.
2.Concrete aims:
To learn and understand hemodynamics, symptoms, signs, laboratory and instrumental
data at patients with the mitral valve disease.
3.Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart, its conduction systems
Normal physiology Principles of the heart automaticity, conductivity
Histology histological structure of the heart
Propedeutics to Symptoms of the cardiovascular diseases, data of general and local visual
internal diseases inspection, palpation, percussion, auscultation of the heart, main ECG-
signs, Echo-CG signs of the mitral valve diseases

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

“Cat purring” Kitaev reflex cardiac asthma

Active pulmonary Systolic murmur facies mitralis
hypertension
Passive pulmonary Diastolic murmur “symptom of yoke”
hypertension
Pulmonary edema Quail rhythm Graham Steel murmur

4.2. Theoretical questions:

1. Causes and hemodynamics of mitral stenosis.
2. Symptoms and signs of mitral stenosis.
3. Data of additional methods of investigation at patients with mitral stenosis.
4. Causes and hemodynamics of mitral regurgitation.
5. Symptoms and signs of mitral regurgitation.
6. Data of additional methods of investigation at patients with mitral regurgitation.
4.3. Practical task that should be performed during practical training
1. Collecting symptoms at patient with mitral valve diseases
2. Revealing signs of the mitral valve diseases
3. Assessing data of ECG, Echocardiography and X-ray examination of the mitral valve diseases
patient

Topic content
Causes of mitral stenosis:
Rheumatic fever,
congenital disease,
 septic endocarditis,
mucopolysaccharidoses,
endocardial fibroelastosis,
malignant carcinoid,
prosthetic valve.
Hemodynamics of the mitral stenosis is impaired if the mitral opening is decreased
from normal 4-6 sm2 until 1,5 sm2 and less. During diastole blood doesn’t have time to flow
from the left atrium to the left ventricular. Some account of blood rests in the atrium. This
content is added with new portion of blood from the pulmonary veins. It leads to overfilling of
the atrium and increasing pressure in one which is compensated with straitened contraction of
the atrium and its hypertrophy. But muscles of the left atrium is very weak to compensates the
narrow mitral opening long time, so the contractile ability of the muscle decreases, the atrium
is extended, pressure in it increases even higher. It causes increasing pressure in the pulmonary
veins, reflective spasm of the pulmonary arterioles (Kitaev reflex) and rise of pressure in the
pulmonary artery. It requires greater work of the right ventricular. After a time, the right
ventricular becomes hypertrophic. The left ventricular receives less blood than normal it leads
to diminished ones sizes. It is developed diastolic dysfunction of the left ventricular.
Symptoms and signs of mitral stenosis: Symptoms appear if mitral stenosis has
decompensated. There is dyspnoea, fatigue, palpitation, chest pain, and heamoptysis.
Dyspnoea appears at blood congestion in the pulmonary veins resulting in reduction of
the pulmonary tissue elasticity. At first, dyspnoea appears only on physical effort, later at rest
when the patient is lying (orthopnea) and, at last it does not disappear even in an upright
position. Dyspnoea is frequently mixed with difficulty in inspiration and expiration as well as
involvement of the auxiliary respiratory muscles in the act of respiration.
Exercise dyspnoea is always a sign of blood congestion in the lungs. It is accompanied by
accelerated superficial breathing (superficial polypnea).
Later dyspnoea appears when the patient takes a lying position (orthopnea), increases
when the patient is lying on the left side (trepopnea). To relieve the dyspnoea the patients have
to put several pillows and even sleep in a sitting position.
Dyspnoea sometimes appears suddenly at night as attack of cardiac asthma with dry
cough or heamoptysis. The most severe complication of this disease is pulmonary oedema.
At the visual examination a cheek flush, cyanotic lips and nose back (facies mitralis) is
observed. If mitral stenosis was developed at childhood physical developmental lagging and
cardiac hump due to hypertrophy of right ventricular could be formed.
Pulse is low-volume, different. Commonly patient has atrium fibrillation with pulse
deficit.
You can obtain diastolic trembling of chest at the apex region named “cat purring ”. It is
palpation sensation of murmur which appears during going flow blood through narrowing
mitral opening.
The upper border of relative heart dullness shifts up due to enlarged left atrium and
right ones shifts right due to hypertrophy right ventricular.
On auscultation loud flapping first heart sound, accent of the second heart sound on
pulmonary artery (due to pulmonary hypertension) and opening snap are heard. This
phenomenon is named “quail’s rhythm”. Also rumbling mid-diastolic murmur is heard best in
expiration, as the patient lies on his left side. It is accentuated presystolically if heart is still in
sinus rhythm.
Later early diastolic murmur (Graham Steel murmur) could be heard on pulmonary
artery due to pulmonary hypertension and pulmonary regurgitation.
 If the stenosis becomes more severe the diastolic murmur is longer and closer the
opening snap is to second heart sound.
Chest X-ray examination: Mitral configuration of the heart at the front position: flat waist
of heart; left atrium and pulmonary artery enlargement. At the left side position enlargement of
right ventricle and left atrium is observed. Sometimes may pulmonary oedema and mitral valve
calcification.
ECG: If patient has sinus rhythm there is p-mitrale, right ventricle hypertrophy, and
progressive right axis deviation. Commonly it is atrium fibrillation.
Echocardiography: Collateral and like “n” moving of mitral valve flaps, fibrosis and
calcification of valve, reduction of mitral opening square (normal – 4-6 cm 2), enlargement of left
atrium and right ventricular cavities, diminution of left ventricular cavity, pulmonary
hypertension signs are revealed.
Causes of mitral insufficiency or mitral regurgitation:
Functional (left ventricular deviation): arterial hypertension, coarctation of aorta, aortic
valve diseases, severe myocarditis, dilatation myocardiopathy, left ventricular aneurism;
Annular calcification (elderly);
Rheumatic fever, infective endocarditis;
Mitral valve prolapse, ruptured chordae tendinae;
Papillary muscle dysfunction/rupture;
Connective tissue disorders (Ehlers-Danlos, Marfan’s)
Congenital (may be associated with other defects, such as atrial septal defect).
Hemodynamics of the mitral regurgitation: At the incomplete closing of the mitral
valve flaps during the systole of the left ventricle part of blood goes back into a left
atrium. Filling of atrium is multiplied, because to the ordinary volume of blood, acting
from pulmonary veins, part of blood, returning from a left ventricle, is added.
Pressure in a left atrium rises, it is enlarged and hypertrophied.
During a diastole from the overfull left atrium greater than in a norm quantity of blood,
goes to left ventricle that results in its overfilling and stretching. The left ventricle must work
with the increased loading, what its hypertrophy is developed. The increased work of left
ventricle compensates mitral insufficiency protractedly. When contractile ability of left
ventricle decreases diastole pressure rises in it and the left atrium.
The increase of pressure in a left atrium results in the increase of pressure in
pulmonary veins, and the last due to irritation of baro-receptor causes the reflex narrowing
of pulmonary arterioles (the Kitaev reflex). The spasm of arterioles considerably increases
pressure in a pulmonary artery. It augments loading of right ventricle and causes its
hypertrophy.
Symptoms and signs of the mitral regurgitation: Symptoms appear if mitral regurgitation
has decompensated and congestive changes in pulmonary circulation are developed. Patients
feel dyspnoea, palpitations, fatigue, cardiac asthma attacks, heart pain, heaviness in the right
under rib, leg oedema.
At the visual examination peripheral cyanosis, facies mitralis and peripheral edemas are
obtained. Sometimes can be cardiac fibrillation.
At the palpation of apex it is displaced downwards to the left to the anterior axillary line
and the 6th intercostal space, enlarged, high and hyperdinamic.
The left border of relative heart dullness shifts left to the anterior axillary line due to
enlarged left ventricle. The upper border shifts up due to enlarged left atrium and right ones
shifts right due to hypertrophy right ventricular.
On auscultation the weakened first heart sound (due to the mitral valve leaflets fail to
close property, hypertrophy and overfilling of the left ventricle), split or accent of the second
heart sound on pulmonary artery (due to non-synchronous closing of pulmonary artery and
aortic valves, pulmonary hypertension) are heard.
There is pansystolic moderate loudness, blowing, noisy, whistling, rough and musical
murmur at the apex radiating to axillary zone. It increases in left decubitus and in a lying
position.
Graham Steel murmur could be heard on pulmonary artery due to pulmonary
hypertension and relative pulmonary regurgitation.
Chest X-ray examination: Mitral configuration of the heart at the front position: flat waist
of heart; left ventricle, atrium and pulmonary artery enlargement. There is balloting moving of
left atrium during systole of ventricle which appears pulsing of contrasted oesophagus, named
“symptom of yoke”.
Pulmonary congestive changes and mitral valve calcification may observe.
ECG: If patient has sinus rhythm there is p-mitrale, left ventricle hypertrophy. Commonly
it is atrium fibrillation.
Echocardiography: Fibrosis and calcification of valve, enlargement of left atrium and
ventricular cavities, pulmonary hypertension signs are revealed. Doppler echo allow assessing
size and site of regurgitation. Cardiac catheterization confirms diagnosis (size of left ventricular
cavity, contractility of left ventricle and level of regurgitation), excludes other valve disease,
assesses coronary artery disease.

Reference source
o Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000 – P.892-893
 Materials for self-control (added)
1. How is the first sound changed at the patient with mitral stenosis?
A. Amplified;
B. Diminished;
С. Split;
D. not changed;
E. Depend on clinical situation.
2. How is the second sound changed at the patient with mitral stenosis?
A. increased above the aorta
B. increased above the pulmonary artery;
C. diminished above the aorta;
D. diminished above the pulmonary artery;
E. not changed.
3. What murmur can be heard at the patient with mitral stenosis?
A. pansystolic
B. presystolic;
C. systolic and diastolic;
D. murmur is absent;
E. short systolic
4. What are ECG changes at the patients with mitral stenosis?
A. hypertrophy left atrium
B. hypertrophy of right atrium;
C. hypertrophy of right ventricle;
D. hypertrophy of left ventricle;
E. all mentioned above.
5. What border of the relative heart dullness is shift at the patient with mitral stenosis?
A. right is shift right
B. left is shift left and downward;
C. upper is shift upward;
D. upper is shift upward and right is shift right;
E. borders of the relative heart dullness are not changed.

6. How is the first sound changed at the patient with mitral regurgitation?
A. Amplified;
B. Diminished;
С. Split;
D. not changed;
E. Depend on clinical situation.
7. What border of the relative heart dullness is shift at the patient with mitral
regurgitation?
A. right is shift right
B. left is shift left and downward;
C. upper is shift upward;
D. right answers A, B, and C;
E. borders of the relative heart dullness are not changed.
8. What murmur at the heart apex can be heard at the patient with mitral regurgitation?
A. systolic
B. diastolic;
C. systolic and diastolic;
 D. murmur is absent;
E. depend on clinical situation
9. Which area does the systolic murmur at the patient with mitral regurgitation conduct
to?
A. neck vessels
B. axillary region
C. interscapular region
D. Botkin-Erb point
E. does not conduct.
10. What are the symptoms of decompensated mitral stenosis?
A. Dyspnea and fatigue,
B. palpitation,
C. chest pain,
D. heamoptysis
E. All mentioned above
11. What are the main reasons for development of mitral valve disease?
A. Rheumatic fever
B. Atherosclerosis of the valves
C. Septical endocarditic
D. Disease of consolidative tissue
E. All mentioned above
12. What are the main reasons for development of mitral stenosis?
A. Mixoma of the heart
B. Pericarditis
C. Myocarditis
D. Trauma of the chest
E. All answers are wrong
13. What is the main additional method of the verification of the mitral valves defects?
А. ECG
B. echocardiography
C. daily ECG - monitoring
D. exercise ECG testing
E. All mentioned above
14. How is the apex beat changed at the patients with mitral regurgitation?
A. It doesn’t palpate
B. It shifts to the left
C. It shifts to the right
D. It shifts upward
E. All answers are wrong
15. How are the borders of the relative heart dullness changed at the mitral stenosis?
A. shift to the left
B. shift to upward and to the righ
C. shift to downward and to the left
D. don’t change
E. shift to the all sides
16. How are the borders of the relative heart dullness changed at the mitral regurgitation?
A. shift to the left
B. shift to upward and to the right
C. shift to the left, upward and to the right
 D. don’t change
E. shift to the downward
17. How is the first sound changed at the patient with mitral regurgitation?
A. Amplified;
B. Diminished;
С. Split;
D. not changed;
E. Depend on clinical situation.

18. How is the second sound changed at the patient with mitral regurgitation?
A. increased above the aorta
B. increased above the pulmonary artery;
C. diminished above the aorta;
D. diminished above the pulmonary artery;
E. not changed.
19. What murmur can be heard at the patient with mitral regurgitation?
A. pansystolic
B. presystolic;
C. systolic and diastolic;
D. murmur is absent;
E. short systolic
20. What area does the dyastolic murmur at the patient with mitral stenosis conduct to?
A. neck vessels
B. axillary region
C. interscapular region
D. Botkin-Erb point
E. does not conduct.
Control questions:
1. Causes and hemodynamics of mitral stenosis.
2. Symptoms and signs of mitral stenosis.
3. Data of additional methods of investigation at patients with mitral stenosis.
4. Causes and hemodynamics of mitral regurgitation.
5. Symptoms and signs of mitral regurgitation.
6. Data of additional methods of investigation at patients with mitral regurgitation.
Practical task
1. Collecting symptoms at patient with mitral valve diseases
2. Revealing signs of the mitral valve diseases
3. Assessing data of ECG, Echocardiography and X-ray examination of the mitral valve
diseases patient
 TOPIC 21
Clinical, laboratory and instrumental examinations of patients with aortic
valve disease
5. Importance of the topic
Valve aortic diseases are important structural pathology of the heart. They can be formed due to
different pathological process and usually could not be resolved without surgery. Knowledge about
causes, hemodynamics, symptoms and signs of the aortic valve diseases has a great role in the study of
the cardiovascular diseases.
6. Concrete aims:
To learn and understand hemodynamics, symptoms, signs, laboratory and instrumental data at
patients with the aortic valve diseases.
Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart, its conduction systems
Normal physiology Principles of the heart automaticity, conductivity
Histology histological structure of the heart
Propedeutics to Symptoms of the cardiovascular diseases, data of general and local visual
internal diseases inspection, palpation, percussion, auscultation of the heart, main ECG-signs,
Echo-CG signs of the aortic valve diseases

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

“Cat purring” Capillary pulse cardiac asthma

Systolic murmur syncope ‘parvus and tardus’ pulse
Diastolic murmur carotid pulsation (‘pulsus celer, altus,
magnus’
Pulmonary edema Traube’s sign Flint murmur

4.2. Theoretical questions:

7. Causes and hemodynamics of aortic stenosis.
8. Symptoms and signs of aortic stenosis.
9. Data of additional methods of investigation at patients with aortic stenosis.
10. Causes and hemodynamics of aortic regurgitation.
11. Symptoms and signs of aortic regurgitation.
12. Data of additional methods of investigation at patients with aortic regurgitation.
4.3. Practical task that should be performed during practical training
1. Collecting symptoms at patient with aortic valve diseases
2. Revealing signs of the aortic valve diseases
3. Assessing data of ECG, Echocardiography and X-ray examination of the aortic valve diseases patient

Topic content
Causes of aortic stenosis:
Senile calcification is the commonest
rheumatic fever,
congenital aortic bicuspid valve (associated with coarctation of the aorta),
congenital stenosis of valve cusps,
septic endocarditis.
Hemodynamics of the aortic stenosis is impaired if the aortic opening is decreased from normal
3 sm until 1,00 -0,75 sm2 and less. During systole blood doesn’t go to the aorta completely. Increased
2
left ventricular pressure tries to overcome the resistance of the narrowed valvular opening. The massive
hypertrophy of the left ventricle has being developed. The added workload increases the demand for
oxygen, and diminished cardiac output causes poor coronary artery perfusion, ischemia of the left
ventricle, and left ventricular failure.
Later compensatory ability of the left ventricle has been diminished and its cavity has been
enlarged. It is developed diastolic dysfunction of the left ventricle. Relative mitral regurgitation is
formed and results in increased pulmonary artery pressure, eventually leading to left and right
ventricular failure.
Symptoms and signs of aortic stenosis: Symptoms appear if aortic stenosis has decompensated.
There is dyspnea on exertion, paroxysmal nocturnal dyspnea, fatigue, palpitations, angina pectoris,
headache, dizziness, and syncope.
Dizziness and syncope can be due to insufficiency of the cerebral circulation. The angina occurs
when hypertrophy myocardium of the left ventricle needs more oxygen than coronary arteries can get
because cardiac output is low than normal.
Dyspnoea appears at blood congestion in the pulmonary veins resulting in reduction of the
pulmonary tissue elasticity. At first, dyspnoea appears only on physical effort, later at rest when the
patient is lying and it is relieved if patient sits (orthopnea). At last dyspnea does not disappear even in an
upright position of the patient. Dyspnoea is frequently mixed with difficulty in inspiration and expiration
as well as involvement of the auxiliary respiratory muscles in the act of respiration.
Paroxysmal dyspnea sometimes appears suddenly at night as attack of cardiac asthma with dry
cough or heamoptysis. The most severe complication of this disease is pulmonary oedema.
At the visual examination a pale skin due to low blood filling of peripheral arterioles is observed.
Pulse is low-volume, slow rising with narrow pulse pressure ( ‘parvus and tardus ’). Systolic blood
pressure is decreased and diastolic blood pressure is normal.
Apex beat is heaving, displaced to the left, and resistant. You can obtain systolic trembling of
chest at the base region named “cat purring ”. It is palpation sensation of murmur which appears during
going flow blood through narrowing aortic opening.
The left border of relative heart dullness shifts left due to hypertrophy left ventricle.
On auscultation diminished S1 (muscle component) on the apex, a quiet S2 on the aorta
(sometimes inaudible due to calcified and unmoving valve) are heard. There is rough ejection systolic
murmur heard at the base, left sternal edge and the aortic area, radiates to the carotids and
interscapular region.
Chest X-ray examination: Aortic configuration of the heart at the front position: accentuated
waist of heart and left ventricle enlargement, valvular calcification, post-stenotic dilatation of ascending
aorta, and pulmonary vein congestion are recognized.
ECG: There is left ventricle hypertrophy, chronic coronary insufficiency (depressed ST segment and
negative T-wave in I, II, AVL, V 4-6). Sometimes p-mitrale can be if relative mitral regurgitation has been
developed.
Echocardiography: There is thickened calcified aortic valve and thickened left ventricular wall,
interventricular septum. Reduction of aortic opening square (normal – 3 cm 2) are revealed.
Causes of aortic regurgitation:
Rheumatic fever,
infective endocarditis,
syphilitic aortitis
hypertension,
connective tissue disorders (rheumatoid arthritis, systemic lupus erythematosus, Marfan
syndrome),
congenital (may be associated with other defects, such as ventricular septal defect),
trauma with aortic dissection.
Hemodynamics of the aortic regurgitation: Blood flows back into the left ventricle during
diastole, causing fluid overload in the ventricle, which dilates and hypertrophies. The excess
volume causes fluid overload in the left atrium and, finally, the pulmonary system. Left
ventricular failure and pulmonary edema eventually result.
Pulmonary hypertension augments loading of right ventricle and causes its hypertrophy and
failure.
Symptoms and signs of the aortic regurgitation: Symptoms appear if aortic regurgitation has
decompensated and congestive changes in pulmonary circulation are developed.
The first complains are fatigue, palpitation and heaviness in the heart region which increase in the
reclining position. The characteristic complain is an angina which is caused by worsened coronary
circulation of the hypertrophied left ventricle and low diastolic blood pressure in the aorta.
Dizziness, pulsating headache and syncope can be due to insufficiency of the cerebral circulation.
Dyspnea, cough, cardiac asthma attack occur when cardiac decompensation have been
developed. Finally, heaviness in the right under rib and leg edemas appear as symptoms of the right
ventricle failure.
At the visual examination a pale skin due to low blood filling of peripheral arterioles during
diastole and their reflex spasm is observed. There is carotid pulsation (Corrigan ’s sign), head nodding (de
Musset’s sign), capillary pulsation in nail beds (Quincke ’s sign), pulsatile narrowing and widening pupils,
pulsatile dermography spot. All this signs occur because of quick fluctuation of blood pressure.
Pulse is rapidly rising, collapsing (water-hammer), large, high and frequent ( ‘pulsus celer, altus,
magnus’). Systolic blood pressure is decreased and diastolic blood pressure is normal.
Apex beat is heaving, wide, undisplaced to the left and downward, and resistant.
The left border of relative heart dullness drifts left and downward due to enlarged left ventricle.
On auscultation the weakened S1on the apex (due to hypertrophy and overfilling of the left
ventricle), and weakened S2 at the 2 nd intercostals space near right edge of the sternum (due to absence
of closing the aortic valve) are heard. If the aortic valve has broken significantly S2 over aorta couldn ’t be
heard.
There is high-pitched soft blowing early diastolic murmur at the right 2 nd intercostals space near
sternum. It is heard best in expiration, with patient sitting forward and radiates to the 5 th point of
auscultation.
In severe aortic regurgitation an Austin Flint murmur (due to the fluttering of the anterior mitral
valve cusp caused by regurgitation stream) may be heard.
If relative mitral regurgitation has developed the systolic murmur can be heard on the apex.
There are associated auscultation phenomena: ‘pistol shot ’ sound over femoral arteries
(Traube’s sign) and femoral diastolic murmur as blood flows backwards in diastole (Duroziez ’s sign).
Arterial blood pressure always is changed: systolic is high and diastolic is low → wide pulse
pressure.
Chest X-ray examination: Aortic configuration of the heart at the front position: accentuated
waist of heart and left ventricle enlargement dilated ascending, and pulmonary vein congestion are
recognized.
ECG: There is left ventricle hypertrophy, chronic coronary insufficiency (depressed ST segment and
negative T-wave in I, II, AVL, V 4-6). Sometimes p-mitrale can be if relative mitral regurgitation has been
developed.
Echocardiography: aortic valvular insufficiency, left ventricular enlargement, alteration in mitral
valve movement (indirect indication of aortic valve disease) and mitral enlargement and thickening,
pulmonary hypertension signs are revealed. Doppler echo allow assessing size and sites of regurgitation.
Cardiac catheterization confirms diagnosis (aortic regurgitation, anatomy of aortic root reduction in
arterial diastolic pressures, and increased left ventricular end-diastolic pressure), excludes other valve
disease, assesses coronary artery disease.

Reference source
o Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000 – P.892-895
 Materials for self-control (added)
1. How is the systolic murmur conducted at patient with aortic stenosis?
A. along the right edge of breastbone;
B. to the Botkin-Erb point;
C. to the vessels of neck;
D. to the lift axillary area;
E. not conducted.

2. How is the first sound changed at the patient with aortic stenosis?
A. Amplified;
B. Diminished;
С. Split;
D. not changed;
E. Depend on clinical situation.

3. How is the second sound changed at the patient with aortic stenosis?
A. increased above the aorta
B. increased above the pulmonary artery;
C. diminished above the aorta;
D. diminished above the pulmonary artery;
E. not changed.

4. What are ECG changes at the patients with aortic stenosis?

A. hypertrophy left atrium
B. hypertrophy of right atrium;
C. hypertrophy of right ventricle;
D. hypertrophy of left ventricle;
E. all mentioned above.
5. What border of the relative heart dullness is shift at the patient with aortic stenosis?
A. right is shift right
B. left is shift left and downward;
C. upper is shift upward;
D. upper is shift upward and right is shift right;
E. left is shift left.

6. How is the first sound changed at the patient with aortic regurgitation?
A. Amplified;
B. Diminished;
С. Split;
D. not changed;
E. Depend on clinical situation.
7. What border of the relative heart dullness is shift at the patient with aortic regurgitation?
A. right is shift right
B. left is shift left and downward;
C. upper is shift upward;
D. right answers A, B, and C;
E. borders of the relative heart dullness are not changed.
8. What murmur at the aorta point can be heard at the patient with aortic regurgitation?
A. systolic
B. diastolic;
C. systolic and diastolic;
D. murmur is absent;
E. depend on clinical situation
9. Which area is the murmur at the patient with aortic regurgitation conducted to?
 A. neck vessels
B. axillary region
C. interscapular region
D. Botkin-Erb point
E. is not conducted.
10. What are the symptoms of decompensated aortic stenosis?
A. Dyspnea and fatigue,
B. Palpitation,
C. Chest pain,
D. Faintness
E. All mentioned above
11. What are the symptoms of decompensated aortic regurgitation?
A. Dyspnea and cough,
B. Palpitation, heaviness in the heart region
C. Cardiac asthma attack,
D. Faintness, dizziness
E. All mentioned above
12. What are the main causes of aortic regurgitation?
A. Rheumatic fever,
B. infective endocarditis, syphilitic aortitis
C. connective tissue disorders (rheumatoid arthritis, systemic lupus erythematosus, Marfan
syndrome),
D. congenital (may be associated with other defects, such as ventricular septal defect),
E. all mentioned above
13. What are the main causes of aortic stenosis?
A. Senile calcification is the commonest
B. rheumatic fever,
C. congenital valve diseases
D. septic endocarditis.
E. all mentioned above
14. How is color of skin changed at patients with aortic valve diseases?
A. Became bluish
B. Become reddish
C. Become yellowish
D. Became pale
E. Nothing from above.
15. Capillary pulse is a sign of…
A. Aortic stenosis
B. Mitral stenosis
C. Mitral regurgitation
D. Pulmonary hypertension
E. Aortic regurgitation
16. ‘Carotid dance’ (carotid pulsation) is a sign of …
A. Mitral stenosis
B. Pulmonary hypertension
C. Aortic regurgitation
D. Aortic stenosis
E. Mitral regurgitation
17. How is blood pressure changed at patient with aortic stenosis?
A. Systolic increased, diastolic normal
B. Systolic decreased, diastolic normal
C. Systolic normal, diastolic increased
D. Systolic normal, diastolic decreased
 E. Systolic increased, diastolic decreased
18. What murmur at the aorta point can be heard at the patient with aortic stenosis?
A. systolic
B. diastolic;
C. systolic and diastolic;
D. murmur is absent;
E. depend on clinical situation
19. How is the second sound changed at the patient with aortic regurgitation?
A. increased above the aorta
B. increased above the pulmonary artery;
C. diminished above the aorta;
D. diminished above the pulmonary artery;
E. not changed.
20. Systolic ‘cat purring’ is a sign of…
A. aortic regurgitation
B. mitral regurgitation
C. arterial hypertension
D. aortic stenosis
E. mitral stenosis
 TOPIC 22
Clinical, laboratory and instrumental examinations of patients with essential
hypertension, symptomatic arterial hypertension. Hypertensic crisis
7. Importance of the topic
Arterial hypertension is the most spread cardiovascular disorder. Complications of the arterial
hypertension are the main cause of mortality and disability of the cardiovascular patients. Knowledge
about causes, symptoms and signs of essential and symptomatic hypertensions is a basis of the
cardiovascular diseases.
8. Concrete aims:
To learn and understand causes of development, symptoms, signs, laboratory and instrumental
data at patients with arterial hypertension.
Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart
Normal physiology Principles of the heart working
Histology histological structure of the heart
Propedeutics to Symptoms of the cardiovascular diseases, data of general and local visual
internal diseases inspection, palpation, percussion, auscultation of the heart, main ECG-signs,
Echo-CG signs of arterial hypertension

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

Essential hypertension ‘Malignant' hypertension Hypertonic crisis

Secondary hypertension Dairy BP monitoring Target organs
Isolated systolic Hypertensive retinopathy Hypertensive
hypertension encephalopathy
Boundary isolated Papilloedema Hypertensive
systolic hypertension hephrosclerosis

4.2. Theoretical questions:

13. Definition, classification and risk factors of the arterial hypertension.
14. Symptoms and signs of arterial hypertension.
15. Data of additional methods of investigation at patients with arterial hypertension.
16. Definition and classification of the essential hypertension.
17. Complication of the uncontrolled arterial hypertension.
18. Main symptoms and signs of the hypertonic crisis.
4.3. Practical task that should be performed during practical training
1. Collecting symptoms at patient with arterial hypertension
2. Revealing signs of the arterial hypertension
3. Assessing data of ECG, Echocardiography and laboratory examination of the patient with arterial
hypertension.

Topic content
Hypertension is an intermittent or a sustained elevation in diastolic or systolic blood
pressure (BP).
Hypertension occurs as two major types:
1. Essential (idiopathic, cause unknown) hypertension, the most common (95 %),
 2. Secondary hypertension, which results from kidney disease or another identifiable
cause.
BP should be assessed over a period of time (don't rely on a single reading). The
'observation' period depends on the BP and the presence of other risk factors or end-organ
damage.
Measuring blood pressure
•Use the correct size cuff. The width of the cuff should be at least 40% of the arm
circumference. The bladder should be centered over the brachial artery, and the cuff applied
snugly. Support the arm in a horizontal position at mid-sternal level. Inflate the cuff while
palpating the brachial artery, until the pulse disappears. This provides an estimate of systolic
pressure.
Inflate the cuff until 30mmHg above systolic pressure, then place stethoscope over the
brachial artery. Deflate the cuff at 2mmHg/s.
• Systolic pressure: The appearance of sustained repetitive tapping sounds•Korotkoff I).
• Diastolic pressure: Usually the disappearance of sounds (Korotkoff V). -However, in
some individuals (eg pregnant women) sounds are present until the zero-point. In this case,
the muffling of sounds, Korotkoff IV, should be used.

Arterial hypertension classification according to level of BP (WHO, 1996):

Type Systolic BP (SBP, Diastolic BO (DBP,
mm Hg) mm Hg)
Normal BP <140 <90
I. Mild hypertension 140-159 90-99
- boundary 140-149 90-94
II. Moderate hypertension 160-179 100-109
III. Severe hypertension ≥ 180 ≥ 110
Isolated systolic hypertension > 140 < 90
Boundary isolated systolic hypertension 140-149 < 90

Systolic hypertension in the elderly: The age-related rise in systolic BP was considered part of
the 'normal' ageing process, and isolated systolic hypertension (ISH) in the elderly was largely
ignored. But evidence from 3 major studies indicates, beyond doubt, that benefits of treating
are even greater than treating moderate hypertension in middle-aged patients.
‘Malignant' hypertension: This refers to severe hypertension (eg systolic >200, diastolic
>130mmHg) in conjunction with bilateral retinal haemorrhages and exudates; papilloedema may
or may not be present. Symptoms are common eg headache ± visual disturbance. Alone it
requires urgent treatment. However, it may precipitate acute renal failure, heart failure, or
encephalopathy which are hypertensive emergencies. Untreated, 90% die in 1yr; treated, 70%:
survive 5yrs. Pathological hallmark is fibrinoid necrosis. It is more common in younger patients
and in Blacks. Look hard for any underlying cause.

Risk factors
Family history, race (most common in blacks), stress, obesity, a high intake of saturated fats or
sodium, use of tobacco, sedentary lifestyle, and aging are risk factors for essential
hypertension.
Causes of the secondary hypertension -5% of cases:
1. Renal disease: The most common secondary cause. 3/4 are from intrinsic renal disease:
- glomerulonephritis,
 - polyarteritis nodosa (PAN),
- systemic sclerosis,
- chronic pyelonephritis, or polycystic kidneys.
1/4 are due to renovascular disease:
- most frequently atheromatous (elderly male cigarette smoker; eg with
peripheral vascular disease)
- rarely fibromuscular dysplasia; (young female).
2. Endocrine disease:
- Cushing's syndromes
- Conn's syndromes
- Phaeochromocytoma
- Acromegaly
- Hyperthyreoidism
- Hyperparathyroidism.
3. Coarctation of the aorta
4. Pregnancy;
5. Neurologic disorders;
6. Use of oral contraceptives or other drugs, such as cocaine, epoetin alfa, and cyclosporine,
steroids.
Signs and symptoms
• Cerebral symptoms: headache, dizziness, buzzing in the ears and head, irritation (due to
disorders of vessel tone, their widening is changed spasm. It results in disorders of
cerebral circulation. There is an irritation of the cerebral vessels by increased BP).
• Cardiac symptoms: heart pain, palpitation and interruption of the heart bit
• General symptoms: fatigue, sleep disorders, decreasing work ability
Visual examination: flush of the face and sclera. Pulse is hard, intense.
Apex bit is heaving, undisplaced to the left, and resistant. The left border of relative
heart dullness drifts left due to hypertrophy left ventricle.
On auscultation diminished S1 (muscle component) on the apex, and accented S2 on the
aorta (high pressure) are heard.
Investigations
Serial blood pressure measurements that are greater than 140/90 mm Hg in people under confirm
hypertension
We can use a dairy BP monitoring: measuring BP every 15 min during day and every 30 min during
night with following computer reading.
Ophthalmoscopy reveals arteriovenous nicking and, in hypertensive encephalopathy, papilledema.
Hypertensive retinopathy

I. Tortuous arteries with thick shiny walls (silver or copper wiring)

II. A-V nipping (narrowing where arteries cross veins)

III. Flame haemorrhages and cotton wool spots

IV. Papilloedema.

• Urinalysis: The presence of protein, red blood cells, and white blood cells may indicate
glomerulonephritis.
Only proteinuria means renal complication of hypertension
• Excretory urography: Renal atrophy indicates chronic kidney disease; one kidney that is more
than 5/8 (1.5 cm) shorter than the other suggests unilateral kidney disease.
• Serum potassium: Levels less than 3.5 mEq/L may indicate adrenal dysfunction (primary
hyperaldosteronism).
• Blood urea nitrogen (BUN) and serum creatinine levels: A BUN level that is normal or elevated to
more than 20 mg/dl and a serum creatinine level that is normal or elevated to more than 1.5 mg/dl
suggest kidney disease.
Other tests help detect cardiovascular damage and other complications:
• Electrocardiography may show left ventricular hypertrophy or ischemia (depressed ST
segment and negative T-wave in I, II, AVL, V4-6).
• Chest X-ray may show cardiomegaly.
• Echocardiography may show left ventricular hypertrophy. There are thickened left ventricular
walls, interventricular septum.
• Renal arteriography may show renal artery stenosis.
Classification and clinical presentation of the essential hypertension:
• I stage – episodic elevation of BP with cerebral, cardiac and general symptoms without
any other signs except high BP
• ІІ stage: Permanent symptoms and signs of affect of the target organs without their
failure:
Heart – left ventricle hypertrophy ( sings, ECG, Ehocardiography, X-Ray)
eye grounds- hypertensive retinopathy I-II
Kidney – proteinuria, increased blood creatinine (male 115-133 mcmol/l or 1,3-1,5 mg/dl,
female 107-124 mcmol/l or 1,2-1,4 mcmol/l)
• ІІІ stage - Permanent symptoms and signs of affect of the target organs with their failure
(complicated stage)
Heart – myocardial infartion, heart failure ІІ-ІІІ st.
Brain - cerebrovascular accident, chronic hypertensive encephalopathy ІІІ st. and vassel
dementia
Eye grounds- hypertensive retinopathy III- IV
Kidney – proteinuria, increased blood creatinine (male >133 mcmol/l or >1,5 mg/dl, female
>124 mcmol/l or >1,4 mcmol/l), chronic renal failure
Vassels– aortic dissecting aneurysm
Clinical presentation of the hypertensic crisis
Sudden increasing BP in the patients with hypertension which is accompanied significant
change in the target organs.
There are two types of the hypertensic crisis I type (adrenal crisis) and II type (nor-adrenal
crisis)
І type
• Occur during I or II stage of hypertension
• Fast beginning (several hours)
• SBP > DBP
• Intensive vegetative disorders (headache, trembling, palpitation, flush, frequent
urination)
• Visual examination: flush of the face and sclera
• Duration: several hours, usually complications are absent.
ІІ type
• Occur during II or III stage of hypertension
• Slow developing (dozens hours or several days)
• DBP>SBP
• Continuing dairy
 • Symptoms: disorders of eyesight, limb numbness, nausea, vomiting, headache, nose
bleeding
• There are the target organs complications: brain: cerebrovascular accident, retina:
blindness, heart: myocardial infarction, acute heart failure, pulmonary oedem,kidneys:
proteinuria, edema and renal failure.

Reference source
Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –
Vinnytsya: NOVA KNYHA, 2006. – p. 220-227

Materials for self-control (added)

1. Which level of the blood pressure is corresponded to mild hypertension?
A. > 140/< 90 mm Hg.
B. 140-159/90-99 mm Hg.
C. 160-179/100-109 mm Hg.
D. ≥ 180/≥ 110 mm Hg.
E. ≥155/≥100 mm Hg
2. Risk factors of essential hypertension:
A. Family history, race (blacks), stress, obesity, a high intake of saturated fats or sodium, use of tobacco,
sedentary lifestyle.
B. Family history, stress, obesity, a high intake of saturated fats or sodium, use of tobacco, hepatitis,
sedentary lifestyle.
C. Family history, stress, obesity, a high intake of saturated fats or sodium, cardiac arrhythmia,
sedentary lifestyle.
D. Stress, obesity, a high intake of saturated fats or sodium, use of tobacco, hepatitis, sedentary lifestyle.
E. Family history, race (blacks), cardiac arrhythmia, sedentary lifestyle.
3. What arterial pressure is corresponded to moderate hypertension?
A. > 140/< 90 mm Hg.
B. 140-159/90-99 mm Hg.
C. 160-179/100-109 mm Hg.
D. ≥ 180/≥ 110 mm Hg.
E. ≥155/≥100 mm Hg
4. What are the pulse properties at patients with arterial hypertension?
A. Hard, intense.
B. Hard.
C. Frequent.
D. Intense, frequent.
E. Arrhythmic, slow.
5. What is the commonest symptom at patients with essential hypertension?
A. Sleep disorders.
B. Headache.
C. Myalgia.
D. Arrhythmia.
E. Edemas
6. How are the heart borders displaced at patient with the 2nd stage of essential hypertension?
A. Shift to the right.
B. Shift to the left.
C. Shift to the left and up.
D. Shift to the right, left and up.
E. Not changed.
7. During auscultation of patients with prolonged arterial hypertension you can hear:
A. Diminished S1 at the apex, and accented S2 at the aorta.
B. Loud S1 at the apex, and accented S2 at the aorta.
C. Increased S1 at the apex, and diminished S2 at the aorta.
D. Diminished S1 at the apex and S2 at the aorta.
E. Normal heart sounds
8. ECG sign of the left ventricular hypertrophy:
A. High R at the V3, V4.
B. High R at the V1, V2.
C. High R at the V5, V6.
D. Deep S at the I lead.
E. High R at the III lead.
9. Which organs are considered target at the patients with arterial hypertension?
A. Heart, liver, lungs and brain
B. Liver, brain, kidney, eyes
C. Heart, brain, kidney, eyes, vessels
D. Heart, liver, lungs and kidney
E. Liver, brain, kidney, eyes, heart.
10. Criterions of the ІI stage of essential hypertension:
A. Episodic elevation of BP with cerebral, cardiac and general symptoms without any other signs except
high BP.
B. Permanent symptoms and signs of the target organs affecting without their failure.
C. Permanent symptoms and signs of the target organs affecting with their failure (complicated stage)
D. Frequent hypertonic crisis.
E. Lack of effect of the medication treatment.
11. What blood pressure is corresponded to severe hypertension?
A. > 140/< 90 mm Hg.
B. 140-159/90-99 mm Hg.
C. 160-179/100-109 mm Hg.
D. ≥ 180/|≥ 110 mm Hg.
E. >160/>100 mm Hg.
12. How is color of skin changed at the patient with arterial hypertension?
A. Flush of the face and sclera.
B. Flush of the foot.
C. Flush of the stomach.
D. Flush of the back
E. Flush of the hands
13. What blood pressure is corresponded to isolated systolic hypertension?
A. > 140/< 90 mm Hg.
B. 140-159/90-99 mm Hg.
C. 160-179/100-109 mm Hg.
D. ≥ 180/|≥ 110 mm Hg.
14. How is apex bit changed at patient with prolonged arterial hypertension?
A. Heaving displaced to the right, and resistant.
B. Heaving, displaced to the left, and not resistant.
C. Heaving, displaced to the left, and resistant.
D. Not changed, normal
E. Displaced to the right and not resistant.
15. How are the heart borders displaced at patient with the 1st stage of essential hypertension?
A. Shift to the right.
B. Shift to the left.
C. Shift to the left and up.
D. Shift to the right, left and up.
E. Not changed.
16. During auscultation of patients with hypertonic crisis you can hear:
A. Diminished S1 at the apex, and accented S2 at the aorta.
B. Loud S1 at the apex, and accented S2 at the aorta.
C. Increased S1 at the apex, and diminished S2 at the aorta.
D. Diminished S1 at the apex and S2 at the aorta.
E. Normal heart sounds
17. Which investigation is the most informative for establishing arterial hypertension?
A. Daily BP monitoring.
B. Daily EKG monitoring.
C. Coronarography.
D. Echocardiography
E. Tredmill test.
18. Criterions of the ІIІ stage of essential hypertension:
A. Episodic elevation of BP with cerebral, cardiac and general symptoms without any other signs except
high BP.
B. Permanent symptoms and signs of the target organs affecting without their failure.
C. Permanent symptoms and signs of the target organs affecting with their failure (complicated stage)
D. Frequent hypertonic crisis.
E. Lack of effect of the medication treatment.
19. Which diseases can be accompanied with arterial hypertension?
A. Renal diseases
B. Endocrine disease
C. Coarctation of aorta.
D. Nephropathy of pregnancy
E. all mentioned above
20. EchoCG sign of the left ventricular hypertrophy:
A. Widening of the cavity of left ventricular.
B. Widening of the cavity of right ventricular.
C. Widening of the posterior wall of the left ventricle.
D. Widening of the left atrium cavity.
E. Low ejection fraction.

Control questions:
19. Definition, classification and risk factors of the arterial hypertension.
20. Symptoms and signs of arterial hypertension.
21. Data of additional methods of investigation at patients with arterial hypertension.
22. Definition and classification of the essential hypertension.
23. Complication of the uncontrolled arterial hypertension.
24. Main symptoms and signs of the hypertonic crisis.
Practical skills
1. Collecting symptoms at patient with arterial hypertension
2. Revealing signs of the arterial hypertension
3. Assessing data of ECG, Echocardiography and laboratory examination of the patient with arterial
hypertension.
 TOPIC 23
Clinical, laboratory and instrumental examinations of patients with ischemic
heart disease: angina pectoris and myocardial infarction
1.Importance of the topic
Ischemic heart disease is one of the most spread cardiovascular disorders. It is the main
cause of mortality and disability of the cardiovascular patients. Knowledge about causes,
symptoms and signs of angina pectoris, myocardial infarction and cardiosclerosis is a basis of
the cardiovascular diseases.
2.Concrete aims:
To learn and understand causes of development, symptoms, signs, laboratory and
instrumental data at patients with acute and chronic coronary syndrome.
3.Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart
Normal physiology Principles of the heart working
Histology histological structure of the heart
Propedeutics to Symptoms of the cardiovascular diseases, data of general and local visual
internal diseases inspection, palpation, percussion, auscultation of the heart, main ECG-
signs, Echo-CG signs of coronary ischemia and necrosis of myocardium

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

Coronary ischemia coronarography “scissors” sign

Coronary trombosis Troponin C cardiosclerosis
Angina pectoris creatinphosphokinase Treadmill test
Acute coronary myoglobin Holter monitoring ECG
syndrome

4.2. Theoretical questions:

25. Definition, causes and classification of the ischemic heart disease.
26. Symptoms and signs of angina pectoris.
27. Data of additional methods of investigation at the patients with angina pectoris.
28. Symptoms and signs of myocardial infarction, their dynamics.
29. Data of additional methods of investigation at patients with myocardial infarction, their
dynamic changes.
30. Main symptoms and signs of the cardiosclerosis, additional investigations.
4.3. Practical task that should be performed during practical training
1. Collecting symptoms at patient with angina pectoris and myocardial infarction
2. Revealing ECG-signs of the acute and chronic coronary syndrome
3. Assessing data of laboratory tests at patients with acute myocardial infarction
Topic Content:
Coronary artery disease (CAD) or ischemic heart disease (IHD) is an acute or chronic
dysfunction of myocardium stipulated for inconsistency between coronary circulation and
myocardial tissue needs of oxygen and nutrients.
This disease is near epidemic in the Western world.
 CAD occurs more often in men than in women, in whites, and in middle-aged: elderly people. In
the past, this disorder rarely affected women who were premenopausal; however, that's no
longer the case, perhaps because many women now take oral contraceptives, smoke
cigarettes, and are employed in stressful jobs that used to be held exclusively by men.
Causes Atherosclerosis is the usual cause of CAD. In this form of arteriosclerosis, fatty, fibrous
plaques narrow the lumen of the coronary arteries; reduce the volume of blood that can flow
through them, and lead to myocardial ischemia. Plaque formation also predisposes to
thrombosis, which can provoke myocardial infarction (MI).
Atherosclerosis usually develops in high-flow, high-pressure arteries, such as those in the
heart, brain, kidneys, and aorta, especially at bifurcation points. It has been linked to many risk
factors: family history, hypertension, obesity, smoking, diabetes mellitus, stress, a sedentary
lifestyle, and high serum cholesterol and triglyceride levels.
Uncommon causes of reduced coronary artery blood flow include dissecting aneurysms,
infectious vasculitis, syphilis, and congenital defects in the coronary vascular system. Coronary
artery spasms may also impede blood flow.
Classification of the CAD:
I. Sudden coronary death
II. Angina pectoris:
- Stable angina causes pain that's predictable in frequency and duration and can be
relieved with nitrates and rest.
- Unstable angina causes pain that increases in frequency and duration. It's more easily
induced.
- Prinzmetal ’ s angina causes unpredictable coronary artery spasm.
III. Myocardial infarction (MI):
- acute MI with Q (transmural or large-focal)
- acute MI without Q (small-focal)
- recurrent MI
- repeated MI
IV. Cardiosclerosis
V. Painless form of CAD
Signs and symptoms of angina pectoris
The classic symptom of CAD is angina, the direct result of inadequate flow of oxygen to the
myocardium. Anginal episodes most often follow physical exertion but may also follow
emotional excitement, exposure to cold, or a large meal.
It's usually described as a burning, squeezing, or tight feeling in the substernal or pre-cordial
chest that may radiate to the left arm, neck, jaw, or shoulder blade.
Typically, the patient clenches his fist over his chest or rubs his left arm when describing the
pain, which may be accompanied by nausea, vomiting, fainting, sweating, and cool
extremities. Pain can be relieved by rest, nitroglycerine during 1-5 min.
Patient stands motionless. His skin is pale and extremities are cold.
Severe and prolonged anginal pain generally suggests MI, with potentially fatal arrhythmias
and mechanical failure.
CORONARY ARTERY SPASM
A spontaneous, sustained contraction of one or more coronary arteries causes ischemia and
dysfunction of the heart muscle in coronary artery spasm. This disorder also causes Prinzmetal's
angina and even myocardial infarction in patients with unoccluded coronary arteries.
Cause
Although the cause of coronary artery spasm is unknown, possible contributing factors include:
• intimal hemorrhage into the medial layer of the blood vessel
• hyperventilation
• elevated catecholamine levels
• fatty buildup in the lumen
• cocaine use.
• Signs and symptoms
Angina is the major symptom of coronary artery spasm. But unlike classic angina, this pain often
occurs spontaneously and may not be related to physical exertion or emotional stress; it's also
more severe, usually lasts longer, and may be cyclic, frequently recurring every day at the same
time.
These ischemic episodes may cause arrhythmias, altered heart rate, lower blood pressure
and, occasionally, fainting from diminished cardiac output. Spasm in the left coronary artery
may result in mitral insufficiency, producing a loud systolic murmur and, possibly, pulmonary
edema, with dyspnea, crackles, hemoptysis, or sudden death.
Additional diagnostic measures include the following:
Electrocardiography (ECG) during angina may show ischemia (ST depression; flat or inverted T
waves) or may be normal; it may also show arrhythmias, such as premature ventricular contractions.
The ECG is apt to be normal when the patient is pain-free.
Treadmill or bicycle exercise test may provoke chest pain and ECG signs of myocardial ischemia (ST-
segment depression).
The patient undergoes a graduated, treadmill exercise test, with continuous 12-lead ECG and
blood pressure monitoring.
Indications:
• To help confirm a suspected diagnosis of IHD.
• Assessment of cardiac function and exercise tolerance.
• Prognosis following Ml.
• Evaluation of response to treatment (drugs, angioplasty, coronary artery bypass grafting).
• Assessment of exercise-induced arrhythmias.
Contraindications:
• Unstable angina
• Recent Q wave Ml (<5d)
•Severe aortic stenosis
• Uncontrolled arrhythmia, hypertension, or heart failure.
Be cautious about arranging tests that will be hard to perform or interpret
• Complete heart block, LBBB
• Pacemaker patients
• Osteoarthritis, COPD, stroke, or other limitations to exercise.
Stop the test if
• Chest pain or dyspnoea occurs.
•The patient feels faint, exhausted, or is in danger of falling.
• ST segment elevation/depression >2mm (with or without chest pain).
• Atrial or ventricular arrhythmia (not just ectopics).
• Fall in blood pressure, failure of heart rate or blood pressure to rise with effort, or
excessive rise in blood pressure (systolic >230mmHg).
• Development of AV block or LBBB.
• Maximal or 90% maximal heart rate for age is achieved.
Interpreting the test: A positive test only allows one to assess the probability that the patient has
IHD. 75% with significant coronary artery disease have a positive test, but so do 5% of people
with normal arteries (the false positive rate is even higher in middle-aged women, eg 20%). The
more positive the result, the higher the predictive accuracy. Down-sloping ST depression is
much more significant than up-sloping, eg 1mm J-point depression with down-sloping ST
segment is 99% predictive of 2-3 vessel disease.
Ambulatory ECG monitoring (Holter) - Continuous ECG monitoring for 24h may be used to
detect ST segment depression, either symptomatic (to prove angina), or to reveal 'silent'
ischaemia (predictive of re-infarction or death soon after Ml).

Coronary angiography reveals narrowing or occlusion of the coronary artery, with possible
collateral circulation.
Myocardial perfusion imaging with thallium-201 or cardiolite during treadmill exercise detects
ischemic areas of the myocardium, visualized as "cold spots."
Acute coronary syndromes (ACS) includes unstable angina and evolving myocardial infarction
(MI).
In MI, also known as heart attack, reduced blood flow through one of the coronary arteries results in
myocardial ischemia and necrosis. In cardiovascular disease, the leading cause of death in the
United States and western Europe, death usually results from the cardiac damage or complications
of MI.
Mortality is high when treatment is delayed; almost half of all sudden deaths due to an MI occur
before hospitalization, within 1 hour of the onset of symptoms. The prognosis improves if vigorous
treatment begins immediately.
Causes
Predisposing factors include:
• positive family history
• hypertension
• smoking
• elevated levels of serum triglycerides, total cholesterol, and low-density lipoproteins
• diabetes mellitus
• obesity or excessive intake of saturated fats, carbohydrates, or salt
• sedentary lifestyle
• aging
• stress or a Type A personality (aggressive, ambitious, competitive, addicted to work,
chronically impatient)
• drug use, especially cocaine.
Men and postmenopausal women are more susceptible to MI than pre-menopausal women,
although incidence is rising among females, especially those who smoke and take oral
contraceptives.
The site of the MI depends on the vessels involved. Occlusion of the circumflex branch of the
left coronary artery causes a lateral wall infarction; occlusion of the anterior descending
branch of the left coronary artery, an anterior wall infarction.
True posterior or inferior wall infarctions generally result from occlusion of the right
coronary artery or one of its branches. Right ventricular infarctions can also result from right
coronary artery occlusion, can accompany inferior infarctions, and may cause right heart failure.
In transmural MI, tissue damage extends through all myocardial layers; in subendocardial MI,
only in the innermost and possibly the middle layers.
Signs and symptoms
The cardinal symptom of MI is persistent, crushing substernal pain that may radiate to the left
arm, jaw, neck, or shoulder blades. Such pain is often described as heavy, squeezing, or crushing
and may persist for 12 hours or more. However, in some MI patients— particularly older adults
or diabetics — pain may not occur at all; in others, it may be mild and confused with indi-
gestion.
 In patients with coronary artery disease, angina of increasing frequency, severity, or duration
(especially if not provoked by exertion, a heavy meal, or cold and wind) may signal impending
infarction.
Other features
Other clinical effects include a feeling of impending doom, fatigue, nausea, vomiting, and
shortness of breath. Some patients may have no symptoms. The patient may experience
catecholamine responses, such as coolness in extremities, perspiration, anxiety, and rest-
lessness. Fever is unusual at the onset of an MI, but a low-grade fever may develop during the
next few days. Blood pressure varies; hypotension or hypertension may be present.
Auscultation may reveal diminished heart sounds, gallops and, in papillary dysfunction, the api-
cal systolic murmur of mitral insufficiency over the mitral valve area.
Stage of MI
I-acutest stage – some first hours – 1 day
II – acute stage 2 day till 2 weeks
III – subacute stage till 2-3 months
IV – scarring stage till6 month
Complications
The most common post-MI complications include recurrent or persistent chest pain,
arrhythmias, left ventricular failure (resulting in heart failure or acute pulmonary edema), and
cardiogenic shock. Unusual but potentially lethal complications that may develop soon after
infarction include thromboembolism; papillary muscle dysfunction or rupture, causing mitral
insufficiency; rupture of the ventricular septum, causing ventricular septal defect; rupture of
the myocardium; and ventricular aneurysm.
Up to several months after infarction, Dressler's syndrome may develop (pericarditis, pericardial
friction rub, chest pain, fever, leukocytosis and, possibly, pleurisy or pneumonitis).
Additional diagnostic
ECG:
Classically, hyperacute (tall) T waves, ST elevation or new LBBB occur within hours of acute Q
wave (transmural infarction) (I st.)
T wave inversion and the development of pathological Q waves follow over hours to days ( II
st.)
pathological Q, InvercionT wave and ST isoelectrically till 2-3 month (III st.)
if patient has scar – only pathological Q can be on ECG ( IV st.)
In other ACS: ST-depression, T-wave inversion, non-specific changes, or normal.
–In 20% of MIs, the ECG may be normal initially.
Blood: leucocytosis is being increased till 2-3 day, than it is being decreasing till 7th day.
Urea, electrolytes, creatinine in plasma, glucose increased, lipids decreased, cardiac enzymes (CK,
AST, LDH, troponin) increased, CK is found in myocardial and skeletal muscle. It is raised in: MI; after
trauma (falls, seizures); prolonged exercise; myositis; Afro-Caribbeans; hypothermia;
hypothyroidism. Check CK-MB isoenzyme levels if there is doubt as to the source (norm. CK-MB/CK
ratio <5%).
Troponin C better reflects myocardial damage (peaks 12-24h; elevated for >1wk). If normal >6h
after onset of pain, and ECG normal, risk of missing Ml is tiny (0.3%). Auscultation may reveal
diminished heart sounds, gallops and, in papillary dysfunction, the apical systolic murmur of
mitral insufficiency over the mitral valve area.
Echocardiography: may show ventricular wall motion abnormalities in patients with a
transmural MI.
Scans using I.V technetium 99 can identify acutely damaged muscle by picking up radioactive
nucleotide, which appears as a "hot spot" on the film. They are useful in localizing a recent MI.
REFERENCE:
1. . Murray Longmore et al Oxford Handbook of clinical medicine. Sixth edition – Oxford
University Press. – 2004. – p.98-121
2. Handbook of diseases. – 2nd edition.- Springhouse Corporation, Springhouse, Pennsylvania.
-2000. – p. 245-247, 557-559.
TESTS FOR SELF-CONTROL
1. What usual cause of Coronary artery disease:
A. Atherosclerosis.
B. Hepatitis.
C. Tonsillitis.
D. Low serum cholesterol and triglyceride levels.
E. Ulcer of stomach.
2. What risk factors of development of Coronary artery disease:
A. Hypertension.
B. Smoking.
C. Family history.
D. Obesity.
E. All of them.
3. Angina pectoris may be:
A. Stable.
B. Dangerous.
C. Strong.
D. Delicate.
E. Acute.
4. Pain can be relieved by nitroglycerine during:
A. 1 min.
B. 1-5 min.
C. 15-20 min.
D. 20-30 min.
E. 30-50 min.
5. What electrocardiography changes may show ischemia:
A. Change T waves.
B. Change P.
C. Change Q.
D. Change R.
E. Change S.
6. Duration of pain at a myocardial infarction:
A. 1-3 min.
B. 10-20 min.
C. More then 30 min.
D. Some days.
E. During week.
7. Where will be changes will be defined at a inferior infarction:
A. І, ІІ, AVL.
B. ІІ, ІІІ, AVF.
C. V1, V2.
D. V4.
E. V5, V6.
8. Duration І – acutest stage:
A. Some first hours – 1 day.
B. 2 day till 2 weeks.
C. Till 2-3 months.
D. Till 6 month.
E. 30-60 min.
9. When leucocytosis is being increased:
A. Till 1-2 day.
B. Till 12-24 hours.
C. Till 2-3 day.
D. Till 5-th day.
E. Till 7-th day.
10. Duration ІІІ – subacute stage:
A. Some first hours – 1 day.
B. 2 day till 2 weeks.
C. Till 2-3 months.
D. Till 6 month.
E. 30-60 min.
11. What risk factors of development of Coronary artery disease:
A. High serum cholesterol and triglyceride levels.
B. Sedentary lifestyle.
C. Stress.
D. Diabetes mellitus.
E. All of enumeration.
12. Angina pectoris may be:
A. Delicate.
B. Dangerous.
C. Strong.
D. Unstable.
E. Acute.
13. What electrocardiography changes may show ischemia:
A. Change T waves.
B. Change P.
C. Change Q.
D. Change R.
E. Change S.
14. Duration of pain at the angina pectoris:
A. 1-3 min.
B. 5-20 min.
C. More then 30 min.
D. Some days.
E. During week.
15. Where will be changes will be defined at a anterior infarction:
A. І, ІІ, AVL, V1-V3.
B. ІІ, ІІІ, AVF.
C. V1, V2.
D. V4.
E. V5, V6.
16. Duration ІІ – acute stage:
A. Some first hours – 1 day.
B. 2 day till 2 weeks.
C. Till 2-3 months.
D. Till 6 month.
E. 30-60 min.
17. When leycocytosis is being decreasing:
A. Till 1-2 day.
B. Till 12-24 hours.
C. Till 2-3 day.
D. Till 5-th day.
E. Till 7-th day.
18. What indicator of blood is a myocardial infarction marker:
A. Electrolytes.
B. Glucose.
C. Creatinine.
D. Troponine.
E. Cholesterole.
19. Duration ІV – scarring stage:
A. Some first hours – 1 day.
B. 2 day till 2 weeks.
C. Till 2-3 months.
D. Till 6 month.
E. 30-60 min.
20. Acute coronary syndromes includes unstable angina and:
A. Stable angina.
B. Myocardial infarction.
C. Myocarditis.
D. Pericarditis.
E. Hypertension attack.

Control questions:
1. Definition, causes and classification of the ischemic heart disease.
2. Symptoms and signs of angina pectoris.
3. Data of additional methods of investigation at the patients with angina pectoris.
4. Symptoms and signs of myocardial infarction, their dynamics.
5. Data of additional methods of investigation at patients with myocardial infarction, their
dynamic changes.
6. Main symptoms and signs of the cardiosclerosis, additional investigations.
Practical skills
1. Collecting symptoms at patient with angina pectoris and myocardial infarction
2. Revealing ECG-signs of the acute and chronic coronary syndrome
3. Assessing data of laboratory tests at patients with acute myocardial infarction
 TOPIC 24
Clinical, laboratory and instrumental examinations of patients with heart
failure. Acute and chronic blood circulation insufficiency
1.Importance of the topic
Heart failure (HF) is a common syndrome, 0,4 – 2% of adults suffer from it. Almost 10% of the
people older than 75 has heart failure. Prognosis is poor with 82% of patients dying within 6 years of
diagnose.
It is necessary to recognize heart failure from the very beginning and provide optimal
management of these patients.
2. Concrete aims:
─ To Study main symptoms and signs of the heart failure
─ To Learn instrumental and laboratory examination of patients with HF
─ To Learn classification of heart failure

3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the heart, their blood supply and innervation
Normal physiology Mechanics of cardiac muscle contraction, the Frank – Starling
relationship.
Histology Ontogenesis of the cardiovascular system, histological structure of
the heart and vessels.
Propedeutics to internal Subjective, objective and instrumental examinations of the patients
medicine with cardiovascular disorders.
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Left ventricle failure Excessive preload
Right ventricle failure Excessive afterload
Low – output failure Systolic dysfunction
High – output failure Diastolic dysfunction

4.2. Theoretical questions:

20. Definition of heart failure
21. Causes of heart failure
22. Classification of heart failure
23. Symptoms of left and right ventricle failure
24. Instrumental and laboratory methods of examination of the patients with heart failure.
4.3. Practical task that should be performed during practical training
57. Revealing and assessment of symptoms and signs of the left and right ventricle failure.
58. Revealing and assessment of functional data at patients with heart failure.
Topic content
Heart failure is an incompetence of the heart to provide the requirements of the body organs and
tissues at blood circulation during rest or physical activity. Congestive heart failure should never be
considered a diagnosis. Rather, it is a syndrome resulting from many diseases that interfere with
cardiac function.
Heart failure is not the same blood circulation insufficiency. The last term is wider and it concludes
decreasing the myocardial contractility(e.g. heart failure), abnormalities of vascular tone, volume of
the blood, decrease of the oxyhemoglobin level and changes of its properties and others.
Classification: May be acute (as a direct result of myocardial infarction), but it's generally a chronic
disorder associated with retention of sodium and water by the kidneys.
According to heart part may by left ventricle failure (LVF), right ventricle failure (RVF) or together left
and right ventricle failure as congestive cardiac failure.
Low-output cardiac failure: The heart's output is inadequate (e.g. ejection fraction <0.35), or is only
adequate with high filling pressures.
Causes: Usually ischemia, hypertension, valve disorders, or increased alcohol use.
Pump failure due to:
Heart muscle disease: IHD; cardiomyopathy .
Restricted filling: Constrictive pericarditis, tamponade, restrictive cardiomyopathy. This may be the
mechanism of action of fluid overload: an expanding right heart impinges on the LV, so filling is
restricted by the ungiving pericardium.
Inadequate heart rate: beta-blockers, heart block, post MI
Negatively inotropic drugs: e.g. most antiarrhythmic agents.
Excessive preload: e.g. mitral regurgitation or fluid overload. Fluid overload may cause LVF in a normal
heart if renal excretion is impaired or big volumes are involved (e.g. IV infusion running too fast). More
common if there is simultaneous compromise of cardiac function and in the elderly.
Chronic excessive afterload: e.g. aortic stenosis, hypertension.
High-output failure is rare. Here, output is normal or increased in the face of much increased needs.
Failure occurs when cardiac output fails to meet needs. It will occur with a normal heart, but even
earlier if there is heart disease. Causes: Heart disease with anemia or pregnancy, hyperthyroidism
Paget's disease, arterio-venous malformation, beri- beri. Consequences: Initially features of RVF; later
LVF becomes evident.
Classification of the New York Heart Association :
I Heart disease present, but no undue dyspnea from ordinary activity.
II Comfortable at rest; dyspnea on ordinary activity.
III Less than ordinary activity causes dyspnea, which is limiting.
IV Dyspnea presents at rest; all activity causes discomfort.

Clinical presentation
Symptoms of the LVF
Dyspnea mixed
Orthopnea
Paroxysmal nocturnal dyspnea
Nocturnal cough (± pink frothy sputum)
Wheeze (cardiac «asthma»)
Nocturia
Cold peripheries
Weight loss
Muscle wasting
Palpitations
Arrhythmias

Visual examination
The patient may look ill and exhausted, with cool peripheries, peripheral cyanosis, orthopnea position.
May be «Corvisart’s face» - edematous, pale yellowish with cyanotic tint, the eyes are dull and eyelids
are sticky, always open mouth, cyanotic lips. It occurs if HF due to mitral stenosis.
Palpation
Pulse : resting tachycardia, pulsus alternans.
Systolic BP decreased, narrow pulse pressure.
The apex beat displaced left, it’s narrow, weakend.
Percussion
The left border of relative heart dullness drifts left due to hypertrophy and dilatation of the left
ventricle.
Auscultation of the heart
If patient does not have valve diseases S1 and S2 are dimished. Pulmonic S2 may be accentuated. Third
heart sound (ventricular gallop), which occurs early in diastole, probably is the single most reliable sign
of left heart failure revealed during physical examination. The S3 occurs during rapid filling of the left
ventricle. Increased left atrial pressure (which propels the blood forward with increased force) and non
compliance of the left ventricle are two important factors in the production of this extra sound. It also
may be heard in young, healthy athletes as a normal finding.
Fourth heart sound (S4). Patients in sinus rhythm and heart failure often have an S4 (atrial gallop).
The S4 is produced as left atrial systole propels volume into the ventricle just prior to ventricular systole.
In congestive heart failure, the left ventricle is noncompliant and the S4 probably results from the
reverberation of the blood ejected from the left atrium into the left ventricle.
Murmurs of mitral or aortic valve disease.
Chest
Tachypnea
Bibasal and inspiratory rales
Wheeze (cardiac asthma)
Right – sided pleural effusion
Symptoms of the RVF
Edema of the lower extremities, sacrum, abdominal wall.
Fullness in the right upper quadrant of the abdomen.
Abdominal distension (ascites)
Fatique
Dizziness
Facial engorgement
Pulsation in neck and face, fullness in the neck (tricuspid regurgitation)
Nausea, vomiting, anorexia
Syncope
In addition, patients may be depressed, complain of drug – related side effects.
Visual examination
The patient may look ill and exhausted, with cool peripheries, peripheral cyanosis, peripheral edema
and, probably with ascites.
Palpation
Pulse: resting tachycardia, pulsus altermans.
Systolic BP decreased, narrow pulse pressure. An abnormal pulsation (heave) is felt at the right sternum
border near the fifth intercostals space if the right ventricle is enlarged.
Percussion
The right border of relative heart dullness drifts right from the sternum due to enlarged right ventricle.
Auscultation of the heart
The weakened S1 and S2, S3 gallop, S4 over the right ventricle.
Murmurs of valve disease, systolic murmur of tricuspid regurgitation.
Chest: tachypnea and signs of pleural effusions.
Abdomen : an enlarged and tender liver, pulsatile in tricuspid regurgitation.
Investigations
Chest X-ray:
1.Cardiomegaly (cardiothoracic ratio>50 prominent upper lobe veins (upper
lobe diversion),
2. peribronchial cuffing, diffuse and intersticial or alveolar shadowing.
3. classical perihilar “bat’s wing’’ shadowing, fluid in the fissures,
4. pleural effusions,
5. Kerley B lines (variously attributed to interstitial edema and engorged peripheral lymphatics).
ECG may indicate cause of heart failure (look for evidence of ischemia, MI, or ventricular hypertrophy).
It is rare to get a completely normal ECG in chronic heart failure. ECHOCARDIOGRAPHY is the key
investigation. It may indicate the cause (MI, valvular heart disease) and can confirm the presence or
absence of LV dysfunction. Ejection fraction is used to determinate severity of the LVF: if ejection
fraction > 45% heart failure is absent, ejection fraction = 35-45% - mild LVF, ejection fraction = 25-35% -
moderate LVF, ejection fraction < 25% - severe LVF. If ejection fraction <20% prognosis is poor.
Circulatory collapse is a pathological condition due to losing vessel smooth muscle tone or reducing
blood circulation volume.
Causes of the losing vessel smooth muscle tone are disorder of their innervations, vessels paresis due to
infection or intoxication. Causes of the reducing blood circulation volume are hemorrhage and
dehydration. These causes result in widening arterioles and venues, decreasing BP, slowing down
bloodstream, diminishing blood circulation and blood accumulation in the blood depot. The cardiac
output decreases and the brain circulation becomes insufficient.
Acute circulatory collapse:
Syncope is a sudden short-time loss of consciousness due to brain ischemia.
Shock is a severe life-threatening condition result from influence very strong irritates and accompanying
with progressive disorders of essential functions and critical disorder of hemodynamics.
There are two phases of the shock:
early stage - patient is exciting and inadequately mobile. Pulse is frequent and good filling, BP is
increased, tachypnoea
late stage - restlessness, apprehension, irritability, thirst from decreased cerebral tissue perfusion,
tachycardia, low filling pulse and tachypnea, hypotension, altered level of consciousness, oliguria,
anuria, hypothermia.
Collapse is an abrupt decreasing vessel smooth muscle tone or acute reducing blood circulation volume.
It develops critically. Patient fills visual impairment, buzzing in the ears, weakness and then losses
consciousness.
He has pale skin, cold sweat and extremities, vein collapse, tachypnea, hypotension, thready pulse.
Acute pulmonary edema is a dramatic and life-threatening manifestation of acute left ventricle
failure secondary to sudden onset of pulmonary venous hypertension. A sudden rise in left ventricle
filling pressure to high levels results in rapid movement of plasma fluid through pulmonary capillaries
into the interstitial spaces and alveoli. The patient presents with extreme dyspnea, tachypnea,
hyperpnea, cyanosis, restlessness and anxiety with a sense of suffocation.
The pulse may be thready, and the BP may be high.
Respirations are grunting and labored with inspiration, expiration is prolonged. Rales are widely
dispersed over both lung fields anteriorly and posteriorly.
Reference sources
1. Harrison’s Principles of Internal Medicine – 15 th ed. – ed. E. Braunwald and al.- McGraw – Hill,
2001 – p. 1318 – 1323
2. Medicine/ed. By Allen R. Myers – 3rd ed. (National medical series) – Williams & Wilkins, 1997 –
p. 1-7

Test for self – control

1. Heart failure is an ...
a) Incompetence of the heart to provide the body ’s requirements at blood circulation during
rest
b) Incompetence of the heart to provide the body ’s requirements at blood circulation during
rest and physical activity
c) Incompetence of the heart to provide the body ’s requirements at blood circulation during
physical activity
d) Incompetence of patient to hold stable level of blood pressure and pulse rate.
e) Nothing from above
2. Which symptoms characterize LVF?
a) Nocturia, hepatomegaly, nocturnal cough.
b) Dyspnea, chest pain, dry cough.
c) Dyspnea, orthopnea, nocturnal cough.
d) Edema of the lower extremities, hepatomegaly.
e) All from above.
3. Which symptoms characterize RVF?
 a) Nocturia, hepatomegaly, nocturnal cough.
b) Edema of the lower extremities, hepatomegaly.
c) Edema of the lower extremities, nocturnal cough
d) Dyspnea, chest pain, dry cough.
e) Nothing from above
4. What symptom does not characterize LVF?
a) Dyspnea
b) Orthopnea
c) Cough
d) Nocturia
e) Edema of the lower extremities
5. What symptom does not characterize RVF?
a) Edema of the lower extremities
b) Hydrotorax
c) Hepatomegaly
d) Ascites
e) Dry cough Dyspnea, chest pain, dry cough.
6. What diseases can lead to heart failure?
a) Arterial hypertension
b) Valvular heart disease
c) Myocardial infarction
d) Cardiomyopathies
e) All from above
7. What are percussion findings at the patients with LVF?
a) The left border of relative heart dullness drifts left
b) The right border of relative heart dullness drifts right
c) The right border of relative heart dullness drifts left
d) Nothing from above
e) Depend on clinical situation
8. What are percussion findings at the patients with RVF?
a) The left border of relative heart dullness drifts left
b) The right border of relative heart dullness drifts right
c) The right border of relative heart dullness drifts left
d) Nothing from above
e) Depend on clinical situation
9. What are auscultation findings at the patients with heart failure?
a) Weakened S1 and S2, S3 gallop
b) Weakened S1 and systolic murmur
c) Depend on disease which lead to heart failure
d) Accented S2 over aorta, diastolic murmur
e) Weakened both sounds
10. What are the lung auscultation findings at the patients with heart failure?
a) Vesicular breathing, basal rales
b) Diminished vesicular breathing
c) Diminished vesicular breathing and crepitation
d) Vesicular breathing and pleural friction rub
e) Nothing from above
11. What BP does patient with heart failure have?
a) Systolic BP decreased, narrow pulse pressure
b) Systolic BP increased, wide pulse pressure
c) Systolic BP normal, increased diastolic BP
d) Depend on clinical situation
e) Nothing from above
12. If patient has heart disease, but ordinary activity does not cause dyspnea, he has…
 a) I functional class of HF
b) II functional class of HF
c) III functional class of HF
d) IV functional class of HF
e) Nothing from above
13. If patient has dyspnea on ordinary activity, he has…
a) I functional class of HF
b) II functional class of HF
c) III functional class of HF
d) IV functional class of HF
e) Nothing from above
14. If patient has dyspnea at rest and all activity causes discomfort, he has…
a) I functional class of HF
b) II functional class of HF
c) III functional class of HF
d) IV functional class of HF
e) Nothing from above
15. If less than ordinary activity causes dyspnea at the patient, he hes…
a) I functional class of HF
b) II functional class of HF
c) III functional class of HF
d) IV functional class of HF
e) Nothing from above
16. Ecchocardiography:
a) May indicate the cause of HF
b) Can confirm the presence or absence of LV dysfunction
c) Is the less useful than chest X – ray for recognizing HF
d) a and b
e) All from above
17. Ejection fraction is used to determinate…
a) Cause of the LVF
b) Severity of the LVF
c) Cardiothoracic ratio
d) a and b
e) Nothing from above
18. If patient has ejection fraction 37 % he has…
a) No heart failure
b) Mild LVF
c) Moderate LVF
d) Severe LVF
e) Terminal LVF
19. If patient has ejection fraction 44 % he has…
a) No heart failure
b) Mild LVF
c) Moderate LVF
d) Severe LVF
e) Terminal LVF
20. If patient has ejection fraction 23 % he has…
a) No heart failure
b) Mild LVF
c) Moderate LVF
d) Severe LVF
e) Terminal LVF
 Control questions:
23. What is a heart failure?
24. What are causes of heart failure?
25. What are the main symptoms of LVF?
26. What are the main symptoms of RVF?
27. What are findings of physical examination of patients with HF?
28. What are findings of instrumental investigations of patients with HF?
29. What is a classification of HF?

Practical task
1.Revealing and assessment of symptoms and signs of the left and right ventricle failure.
2. Revealing and assessment of functional data at patients with heart failure.
 Topic 25
Conclusion module control including test-control of the theoretical
training, control of the practical skills, assessment of the instrumental
investigation reports.
1.Importance of the topic
Conclusion module control is very important for strengthening and checking knowledge
obtained during study at the department. It needs for repeating and systematization all learned
theoretical material and training practical skills.
2. Concrete aims:
─ To check students theoretical knowledge
─ To check students practical skills

3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the respiratory and cardiovascular systems
Normal physiology Functions of the respiratory and cardiovascular systems
Histology Ontogenesis of the respiratory and cardiovascular systems.
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine patients with diseases of the respiratory and cardiovascular
systems.
LIST OF QUESTIONS FOR CONCLUSION CONTROL
1. The contribution of prominent clinicists: T. Yankovskiy, V. Obraztsov, M. Kurlov, M.
Gubergrits, M. Stragesko, G. Lang, B. Shklyar to the development of therapeutic school.
2. Basic methods of diagnostics of internal disases.
3. Plan of patient inquiring. Basic structural parts of anamnesis.
4. Sequence of general visual inspection.
5. Types of constitution and their main criteria.
6. Sequence of lymphonodes palpation and characteristics of obtaining findings.
7. Rules of visual inspection of head and neck.
8. Sequence of visual inspection body and extremities.
9. Static visual inspection of the chest, diagnostic importance of basic signs.
10. Dynamic visual inspection of the chest, diagnostic importance of basic signs.
11. Visual inspection of the precardial region, diagnostic importance of basic signs.
12. The main pulse characteristics, the subsequent and rules for their determination.
13. The rules for blood pressure measurement, analysis of obtained results.
14. Palpation of the chest: the subsequent, rules and diagnostic significance.
15. Palpation of the heart region: the subsequent, rules and clinical significance.
16. The consequent of lung percussion, qualities of sounds and diagnostic significance of
obtained results.
17. The main tasks of topographic percussion of the lung, its technique and consequent. The
topographical parameters of the lung in normal and pathological conditions.
18. Percussion of the heart – relative and absolute cardiac dullness, the borders of the
relative cardiac dullness in normal and pathological conditions.
19. Percussion of the heart – displacement of the heart borders accordantly to cardiac and
extracardiac reasons.
20. The width of the vascular bundle, technique of its evaluation by percussion and
diagnostically significance.
21. Auscultation of the lung - the main respiratory sounds, their quantitative and qualitative
changes, conditions for occurs.
22. Auscultation of the lung - additional respiratory sounds, conditions for occurs.
23. Rales, their types and mechanisms of formation and diagnostic significance.
24. Conditions for crepitation and pleural friction sound formation. Differential signs of
adventitious sounds.
25. Determination of vocal fremitus, its diagnostic significance.
26. Auscultation of the heart - mechanism of heart sounds formation and their main
properties. Changers of the tones by strength and timbre.
27. Auscultation of the heart - the notion of heart sounds reduplication and splitting, the
causes of onset and periodic characteristics.
28. Additional heart sounds: "Gallop" and "quails" rhythms.
29. The causes of heart murmurs and their classification.
30. The main characteristics of cardiac murmurs description (timing, intensity, pitch, quality,
configuration, duration, location and radiation, changers depending from body position
and physical load). The notion of functional murmurs and their differences from the
organic one.
31. Diastolic cardiac murmurs: the causes for onset and diagnostic significance.
32. The rules for ECG interpretation. Determination of heart rate end electrical axis of the
heart.
33. ECG signs of altered automatic function.
34. ECG signs of altered excitability function. The main types of premature heart
contraction.
35. ECG signs of altered conductivity. Classification
36. Clinical and ECG signs of atrial and ventricular flutter and fibrillation. The
mechanisms of their onset.
37. Syndrome of focal and lobar consolidation of lung tissue, causes, diagnostic symptoms
and signs.
38. The syndrome of increased airiness of lung tissue: etiology, pathogenesis, clinical,
laboratory and instrumental methods of diagnosis.
39. The syndrome of fluid accumulation in pleural cavity: etiology, pathogenesis, clinical,
laboratory and instrumental methods of diagnosis.
40. The syndrome of air accumulation in pleural cavity: etiology, pathogenesis, clinical,
laboratory and instrumental methods of diagnosis.
41. The syndrome of bronchial obstruction: etiology, pathogenesis, clinical, laboratory and
instrumental methods of diagnosis.
42. The syndrome of the pain in the heart: etiology, pathogenesis, clinical, laboratory and
instrumental methods of diagnosis.
43. The syndrome of cardiovascular incompetence: etiology, pathogenesis, clinical,
laboratory and instrumental methods of diagnosis.
44. Left ventricular heart failure syndrome: etiology, pathogenesis, clinical, laboratory and
instrumental methods of diagnosis.
45. Right ventricular heart failure syndrome: etiology, pathogenesis, clinical, laboratory and
instrumental methods of diagnosis.
46. Vascular failure syndrome: etiology, pathogenesis, clinical, laboratory and instrumental
methods of diagnosis.
47. The syndrome of arterial hypertension: etiology, pathogenesis, clinical, laboratory and
instrumental methods of diagnosis.
48. Chronic obstructive pulmonary diseases: clinical presentation and diagnostics.
49. Bronchial asthma: classification, chief clinical features and diagnosis.
50. Emphysema of the lung: the main factors for development, symptoms and diagnosis.
51. Hospital and extrahospital pneumonia: classification, chief clinical features and
diagnosis.
52. Dry and exudative pleurisies: chief clinical features and diagnosis.
53. Cancer of the lung: main clinical forms, clinical features and diagnosis.
54. Mitral valve defects: etiology, chief clinical features and diagnosis.
55. Aortic valve defects: etiology, chief clinical features and diagnosis.
56. Coronary heart disease: etiology, chief clinical features and diagnosis of angina pectoris.
57. Coronary heart disease: etiology, chief clinical features and diagnosis of acute
myocardial infarction.
58. Essential hypertension: modern classification, etiology, chief clinical features and
diagnosis.
59. Symptomatic arterial hypertension: etiology, classification, chief clinical features,
diagnosis, objective and instrumental examination data that give opportunity to suspect
the secondary character of hypertension.
THE LIST OF PRACTICAL SKILLS
1. To conduct inquiring of the patient. To make conclusion according to the obtained
anamnestic data.
2. To conduct inquiring of the patient with respiratory organs disease. To define the chief
symptoms.
3. To conduct inquiring of the patient with cardiovascular pathology. To define the chief
symptoms.
4. To conduct general examination of the patient. To define the chief symptoms.
5. To carry out examination of the head and neck. To define the clinical significance of
obtained symptoms.
6. To carry out examination of the trunk and extremities. To define the clinical significance
of obtained symptoms.
7. To conduct inspection of the chest in patient with respiratory organs disease. To
evaluate the static signs.
8. To conduct inspection of the chest in patient with respiratory organs disease. To
evaluate the dynamic signs.
9. To carry out inspection of the heart region. To define the clinical significance of obtained
symptoms.
10. To perform palpation of the chest, to define the clinical significance of obtained
symptoms.
11. To carry out palpation of the lymphatic nodes, to evaluate obtained results.
12. To conduct examination of the pulse. To define the clinical significance of obtained
symptoms.
13. To carry out palpation of the heart region. To define the clinical significance of obtained
symptoms.
14. To conduct blood pressure measurement on upper extremities, to analyze obtained
results.
15. To conduct blood pressure measurement on low extremities, to analyze obtained
results.
16. To carry out comparative percussion of the lung. To define the clinical significance of
obtained symptoms.
17. To carry out topographic of the lung. To define the clinical significance of obtained
symptoms.
18. To determine the respiratory excursion of the lower border of the lung. To define the
clinical significance of obtained symptoms.
19. To determine the borders of the relative cardiac dullness by percussion. To make the
clinical evaluation.
20. To determine the borders of the absolute cardiac dullness by percussion. To make the
clinical evaluation.
21. To evaluate the width of the vascular bundle, to assess the obtained results.
22. To conduct auscultation of the lung – to determine the main respiratory sounds their
quantitative and qualitative characteristics, clinical evaluation of obtained results.
23. To conduct auscultation of the lung – to determine the additional respiratory sounds, to
define the clinical significance of obtained data.
24. To carry out bronchophonia, to make clinical evaluation of obtained results.
25. To conduct auscultation of arteries, to define the clinical significance of obtained
symptoms.
26. To conduct auscultation of the heart – to determine the main characteristics of the
heart sounds with clinical evaluation of obtained results.
27. To conduct auscultation of the heart – to determine the presence of cardiac murmurs
with clinical evaluation of obtained results.
28. To analyze results of ECG recording in patient with altered conductivity.
29. To analyze results of ECG recording in patient with altered excitability function. To
differentiate the types of premature heart contractions.
30. To analyze results of ECG recording in patient with altered automaticy function.
31. To analyze results of ECG recording in patient with combinative arrhythmias.
32. To analyze results of US examination at the patient with heart valve defects.
33. To carry out examination of the patient with mitral valve disease. To define the major
symptoms and syndromes.
34. To conduct examination of the patient with aortic valve disease. To identify the major
symptoms and syndromes.
35. To carry out examination of the patient with arterial hypertension. To define the major
symptoms and syndromes.
36. To make inquiring of the patient with coronary heart disease (stable angina pectoris), to
detail the complain pain in the heart, to define the functional class of the patient.
37. To conduct general inspection and objective examination of the patient with acute
myocardial infarction. To identify the major symptoms and syndromes.
38. To evaluate the ECG of the patient with acute myocardial infarction. To define the
character and localization of myocardial damage.
39. To carry out examination of the patient with heart failure. To define the major
symptoms, syndromes and functional class of the patient.
40. To carry out inquiring of the patient with obstructive lung disease. To define the major
symptoms, syndromes, with taking into consideration spirography results determine the
stage of the disease.
41. To conduct palpation, percussion of the chest and auscultation of the lung in the patient
with obstructive lung disease. To define the major symptoms and syndromes.
42. To conduct inquiring and objective examination of the patient with pneumonia. To
identify the major symptoms and syndromes.
43. To carry out inquiring and objective examination of the patient with pleurisies. To
identify the character of pleurisies and chief symptoms and syndromes.

Tests:
1.What are the respiratory symptoms?
A. Chest pain, cough, dyspnea, wheezes, haemoptysis.
B. Pain in the heart region, palpitation, intermissions, oedema
C. Headache, dizziness, dysphagia, nausea, vomiting.
D. Pain in the right subcostal region, bitter taste, brown urine, skin itching, jaundice.
E. Back pain, dysuria, ishuria, eyes oedema, weakness.
2.What feature does pleural pain have?
A. Be caused by physical extension
B. Radiate to the right hand
C. Appears and increases due to cough and deep breathing
D. Radiate to the left hand and scapula
E. Duration under 15 minutes.
3. If patient has laryngitis his cough is characterized with
A. harsh and hoarse sound
B. absent of sputum
C. it is permanent
D. it is loud
E. all mentioned above.
4. Chronic expectorating copious sputum is observed at patient with
A. Acute bronchitis
B. Asthma
C. Atelectasis
D. Emphysema
E. Bronchiectasis
5. Which type of dyspnea is observed at the patients with obstructive syndrome?
A. Expiratory
B. Inspiratory
C. Mixed
D. Changing
E. All mentioned above.
6. Which of the following characteristics is not typical of pleuritic chest pain?
A. Increases with deep breathing
B. Increases with coughing
C. Radiates to the jaw
D. Is located laterally
E. Diminishes with splinting of the affected side
7. Inspiratory dyspnea is –
A. Difficult breathing during exhalation
B. Difficult breathing during inhalation
C. Difficult breathing during exhalation and inhalation
D. Difficult breathing during hyperventilation
E. Northing from above
8. Whistle and noise breathing with feeling breathlessness is named …
A. Dyspnea
B. Respiratory noise
C. Musical breathing
D Wheezing
E. All mentioned above
9. Lung bleeding is a pathological condition when the blood expectorates from airways.
What quantity of the blood is characterized lung bleeding?
A. 15 - 20 ml
B. 30–40 ml
C. 240 - 250 ml
D. All mentioned above
E. Northing from above
10. Mixed dyspnea is –
A. Difficult breathing during exhalation
B. Difficult breathing during inhalation
C. Difficult breathing during exhalation and inhalation
D. Difficult breathing during hyperventilation
E. Northing from above
11. What are the respiratory symptoms?
A. Abdominal pain, nausea, vomiting
B. Heartburning, faint (syncope), palpitation
C. Cough with rusty sputum, chest pain, dyspnea
D. Swelling abdomen, constipation, melena
E. Oedema, dysuria, haematuria
12. What are the cough causes?
A. Irritation of the larynx receptors
B. Irritation of the trachea and bronchus receptors
C. Irritation of the pleural receptors
D. All mentioned above
E. Northing from above
13. If patient has clear, thick sputum it is named
A. Mucoid
B. Purulent
C. Copious
D. Fetid
E. Hemoptysis
14. What is an objective dyspnea?
A. Disorders of the respiratory rate
B. Disorders of the respiratory depth
C. Disorders of the respiratory rhythm
D. Disorders of the respiratory rate, depth, rhythm
E. Northing from above
15. Which types of dyspnea do you know?
A. Mixed
B. Expiratory
C. Inspiratory
D. All mentioned above
E. Northing from above
16. Sputum production that contains pus is described by what term?
A. Purulent
B. Fetid
C. Copious
D. Colored
E. None of the above
17. Which type of pulmonary problem usually causes a breathing pattern with a prolonged
expiratory time?
A. Chronic obstructive pulmonary disease
B. Atelectasis
C. Pulmonary edema
D. Pneumonia
E. Pleural effusion.
18. Expiratory dyspnea is –
A. Difficult breathing during exhalation
B. Difficult breathing during inhalation
C. Difficult breathing during exhalation and inhalation
D. Difficult breathing during hyperventilation
E. Northing from above
19. What quantity of the blood is characterized hemoptysis?
A. 20-50 ml
B. 60 – 70 ml
C. 140 - 250 ml
D. All mentioned above
E. Northing from above
20. Amount of cigarettes that patient smokes in a day multiply to number of smoking years
and divide to 20 (pack/years) use for calculating …
A. Smoking history
B. cigarettes consumption
C. Smoking habit
D. Smoking abuse
E. All mentioned above.
21.If patient’s respiratory rate is 32 per minute he has…
a. Tachypnea
b. Bradypnea
c. Apnea
d. Polypnea
e. Dyspnea
22. What types of breathing does healthy man have in a rest?
a.Abdominal breathing
b.Thoracic breathing
c. Mixed breathing
d. All mentioned above
e. Northing from above
23. Kussmaul ‘s breathing is…
a. Disorder of breathing depth
b. Disorder of the respiratory rate
c. Disorder of the respiratory rhythm
d. Disorder of the respiratory types
e. Hyperventilation syndrome
24.hat is the normal respiratory rite in a rest?
a. 12-14 per 1 minute
b. 16-20 per 1 minute
c. 10-12 per 1 minute
d. 20-24 per 1 minute
e. 24-28 per 1 minute
25. Which of the following condition is associated with asymmetrical diminished vocal
fremitus?
a. Pneumonia
b. Emphysema
c. Bronchial asthma
d. Chronic bronchitis
e. Pleural effusion
26. Which of the following condition is associated with increased chest resistance?
a. acute bronchitis
b. focal pneumonia
c. COPD
d. mild bronchial asthma
e. all mentioned above.
27. What kind of posture is observed at the bronchial obstruction?
a. Upright
b. Sitting position fixing the shoulder girdle
c. Orthopnoea
d. Sitting posture bending forward
e. Knee-elbow posture
28. What shape of the chest can be observed at the patient with chronic tuberculosis?
a. Normosthenic
b. Asthenic
c. Barrel
d. Paralytic
e. "Funnel breast"
29. What kind of posture is observed at the left dry pleurisy?
a. Upright
b. Sitting position fixing the shoulder girdle
c. Orthopnoea
d. On the left side
e. Sitting posture bending forward
30. If patient skin has diffuse bluish tint, it is named:
a. Diffuse cyanosis
b. Diffuse erythema
c. Acrocyanosis
d. Pathological pallid skin
e. Northing mentioned above.
31. If patient doesn’t have respiratory moving his condition is named:
a. Tachypnea
b. Bradypnea
c. Apnea
d. Polypnea
e. Dyspnea
32. Cheyne-Stokes breathing is …
a. Disorder of breathing depth
b. Disorder of the respiratory rate
c. Disorder of the respiratory rhythm
d. Disorder of the respiratory types
e. Hyperventilation syndrome
33. What types of breathing does healthy woman have in a rest?
a. Abdominal breathing
b. Thoracic breathing
c. Mixed breathing
d. All mentioned above
e. Northing from above
34. If patient’s respiratory rate is 10 per minute he has…:
a. Tachypnea
b. Bradypnea
c. Apnea
d. Polypnea
e. Dyspnea
35. Which of the following conditions is associated with increased vocal fremitus?
a. Pneuomonia
b. Emphysema
c. Pneumothorax
d. Pleural effusion
e. Bronchial asthma
36. Which of the following condition is associated with painfulness of the pleural points?
a. Lobar pneumonia
b. Bronchial asthma
c. Pleural effusion
d. Emphysema
e. Chronic bronchitis
37. What does the general inspection start with?
a. Skin
b. Position in bed.
c. General condition
d. Edemas
e. Joints
38. What kind of posture is observed at the right pleural effusion?
a. Orthopnea
b. On the right side
c. Sitting position fixing the shoulder girdle
d. On the left side
e. Sitting posture bending forward
39. What shape of the chest can be observed at the patient with emphysema?
a. Normosthenic
b. Asthenic
c. Barrel
d. Paralytic
e. "Funnel breast"
40. How is the chest shape changed at the left side pneumothorax?
a. Enlarged left part of the chest
b. Reduced left part of the chest
c. Enlarged right part of the chest
d. Reduced right part of the chest
e. Not changed
41. What type of percussion sounds may you hear over health lung?
a. Tympanic
b. Clear lung
c. Dull
d. Stony dull
e. Resonant.
42. When may you hear hyper-resonant percussion sounds over the lung?
f. Emphysema,
g. Pneumothorax,
h. Above the level of pleural effusion
i. Large cavity
j. Everything mentioned above.
43. What pathological condition can produce dull percussion sound?
f. Pneumonia
g. Emphysema
h. Large cavity
i. Bronchitis
j. Pneumothorax.
44. What percussion sound is heard of emphysema?
f. Tympanic
g. Impaired
h. Dull
i. Clear lung
j. Resonant.
45. What percussion sound is heard of pleural effusion?
f. Tympanic
g. Impaired
h. Dull
i. Clear lung
j. Resonant.
46. What percussion sound is heard of the focal pneumonia near root of lung?
f. Tympanitic
g. Impaired
h. Dull
i. Clear lung
j. Resonant.
47. What is the first line along which the lower border of the right lung is determined?
f. Scapular
g. Paravertebral
h. Parasternal
i. Medioclavicular
j. Axilar anterior
48. What is position of the lower border of the left lung along medioclavicular line?
f. 6th interspace
g. 10th interspace
h. Not determine
i. 5th interspace
j. 8th interspace
49. What are the causes of increase height of the lung apex?
f. Pulmonary emphysema
g. Inflammatory infiltration of the lungs
h. Pleural effusion
i. Pleural obliteration
j. Everything mentioned above.
50. What are the causes of upward displacement of the lower border?
f. pulmonary emphysema
g. pneumosclerosis
h. abscess
i. obturation atelectasis
j. everything mentioned above.
51. When may you hear dull percussion sound over lung?
a Thickened pleura.
b Collapse of lung.
c. Consolidation of lung.
d. Fluid in pleural cavity.
e. Everything mentioned above.
52. What percussion sound is heard of the lobular pneumonia?
f. Tympanic
g. Impaired
h. Dull
i. Clear lung
j. Resonant.
53. What percussion sound is heard of acute bronchial asthma?
f. Tympanitic
g. Impaired
h. Dull
i. Clear lung
j. Resonant.
54. What percussion sound is heard of collapse of the lung lobe resulting from obstruction of
the bronchus lumen?
f. Tympanitic
g. Impaired
h. Dull
i. Stony dull
j. Resonant.
55. What is determined on topographic percussion of the lung?
p. Position of the height of the lung apex
q. Lung border mobility
r. Position of the lower border
s. Kronig's fields width
t. All mentioned above
56. What lines is topographic percussion done along?
a. Scapular
b. Paravertebral
c. Parasternal
d. Medioclavicular
e. Everything mentioned above.
57. What is the first line along which the lower border of the left lung is determined?
f. Scapular
g. Paravertebral
h. Parasternal
i. Medioclavicular
j. Axilar anterior
58. What is position of the lower border of the right lung along medioclavicular line?
f. 6th interspace
g. 10th interspace
h. 7th interspace
i. 5th interspace
j. Not determine
59. What is the normal height of the lung apex?
f. 6-8 sm
g. 3-5 sm
h. 8-10 sm
i. 5-7 sm
j. 1-2 sm
60. What are the causes of reduced mobility of the lower border?
f. pulmonary emphysema
g. inflammatory infiltration of the lungs
h. fluid in the pleural cavity
i. pleural obliteration
j. everything mentioned above.
61. Where is bronchial breath sound formed?
a. in larynx
b. in trachea
c. in bronchus
d. in alveoli
e. in pleural cavity
62. Where is vesicular breath sound formed?
a. in the larynx
b. in the trachea
c. in the bronchus
d. in the alveoli
e. in the pleural cavity
63. Which of the following properties is not appropriate to bronchial breath sound?
a. Heard over trachea and major bronchi
b. Loud and rough
c. Heard only during inspiration
d. Sound like “h” heard during inspiration and expiration
e. Formed in the larynx
64. Which of the following properties is not appropriate to vesicular breath sound?
f. Heard over trachea and major bronchi
g. Soft sound
h. Heard during inspiration and one third of expiration
i. Sound like “f” heard during inspiration and expiration
j. Formed in the alveoli
65. When can the weakened vesicular breath sound be heard?
a. 2nd stage of lobar pneumonia
b. Acute bronchitis
c. Large cavity in the lung
d. Emphysema
e. Complete atelectasis
66. When can not the weakened vesicular breath sound be heard?
a. Emphysema
b. Focal pneumonia
c. Dry pleurisy
d. Large cavity in the lung
e. Pneumosclerosis
67. When can the amphoric breath sound be heard?
f. Emphysema
g. lobar pneumonia
h. Dry pleurisy
i. Large cavity in the lung
j. Pneumosclerosis
68. What auscultation phenomenon is heard of the large pleural effusion?
a. Absent of the breath sound
b. Vesicular breath sound with prorogated exhalation
c. Rough vesicular breath sound
d. Bronchial breath sound
e. Weakened vesicular breath sound
69. What auscultation phenomenon is heard of the bronchial asthma?
f. Absent of the breath sound
g. Vesicular breath sound with prorogated exhalation
h. Rough vesicular breath sound
i. Bronchial breath sound
j. Weakened vesicular breath sound
70. What breath sound is heard of the focal pneumonia near root of lung?
f. Normal vesicular breath sound
g. Vesicular breath sound with prorogated exhalation
h. Rough vesicular breath sound
i. Bronchial breath sound
j. Weakened vesicular breath sound
71. How vesicular breath sound is changed in case of pneumotorax?
a. Not change
b. Became weakened
c. Became pathological bronchial
d. Became amphoric
e. Became rough
72. How vesicular breath sound changed is in case of acute bronchitis?
f. Not change
g. Became weakened
h. Became pathological bronchial
i. Became amphoric
j. Became rough
73. How vesicular breath sound is changed in case of the 2nd stage of the lobar pneumonia?
f. Not change
g. Became weakened
h. Became pathological bronchial
i. Became amphoric
j. Became rough
74. How vesicular breath sound is changed in case of emphysema?
f. Not change
g. Became weakened
h. Became pathological bronchial
i. Became amphoric
j. Became rough
75 When can the stridor be heard?
p. Emphysema
q. Atelectasis
r. Pleural effusion
s. Obstruction of the trachea and major bronchi
t. Pneumosclerosis
76. How vesicular breath sound is changed in case of COPD exacerbation?
f. Not change
g. Became weakened
h. Became pathological bronchial
i. Became amphoric
j. Became rough with prorogated exhalation
77. How vesicular breath sound is changed in case of the 1nd and 3rd stage of the lobar
pneumonia?
f. Not change
g. Became weakened
h. Became pathological bronchial
i. Became amphoric
j. Became rough
78. How vesicular breath sound is changed in case of the dry pleurisy?
f. Not change
g. Became weakened
h. Became pathological bronchial
i. Became amphoric
j. Became rough
79. When can bronchophony be heard?
a. pulmonary emphysema
b. lobar infiltration of the lungs
c. fluid in the pleural cavity
d. pleural obliteration
e. Everything mentioned above.
80. What auscultation phenomenon is heard of the complete atelectasis of the lower right
lung lobe?
f. Absent of the breath sound
g. Vesicular breath sound with prorogated exhalation
h. Rough vesicular breath sound
i. Bronchial breath sound
j. Weakened vesicular breath sound
81. Which adventitious lung sound is formed in alveoli?
a. wheeze
b. moist rales
c. pleural frictional rub
d. crepitation
e. nothing mentioned above
82. Where are buzzing dry rales formed?
a. in the larynx
b. in the trachea and big bronchi
c. in the small bronchi
d. in the alveoli
e. in the pleural cavity
83. Where are moist rales formed?
k. In the pleural cavity
l. In the alveoli
m. In the bronchi and lung cavities
n. In the bronchi
o. In the lung cavities
84. What is the main mechanism of the pleural friction rub forming?
k. Swelling mucous membrane of the bronchus
l. Storing viscous secretion in the bronchus
m. Storing viscous secretion over the pleural sheets
n. Infiltration of the alveolar walls and their saturating with exudate that result in their
adhering
o. Storing liquid secretion in the bronchi or lung cavities
85. What is the main mechanism of the moist rales forming?
k. Swelling mucous membrane of the bronchus
l. Storing viscous secretion in the bronchus
m. Storing viscous secretion over the pleural sheets
n. Infiltration of the alveolar walls and their saturating with exudate that result in their
adhering
o. Storing liquid secretion in the bronchi
86. What adventitious lung sounds can be heard at the bronchial asthma?
a. Crepitation
b. Pleural friction rub
c. Wheezes
d. Moist rales
e. Nothing from adventitious lung sounds
87. What adventitious lung sound can be heard at the dry pleurisy?
k. Crepitation
l. Pleural friction rub
m. Wheezes
n. Non-sonorous moist rales
o. Nothing from adventitious lung sounds
88 The sonorous moist rales are signs of…
a. Emphysema
b. Bronchitis
c. Pleural effusion
d. Pneumonia
e. Bronchial asthma
89. Appearance of the pleural friction rub at the patient with exudative pleurisy is sing of …
k. Increasing exudate
l. Obturative atelectasis in the lung collapse region
m. Decreasing exudate
n. Pneumothorax
o. All answers are right depending on clinical situation
90. The sonorous medium bubbling rales can be heard at the patient with…?
f. Emphysema
g. bronchiectasis
h. Acute bronchitis
i. Pleural effusion
j. Obturative atelectasis
91. Where is wheeze formed?
a. in the larynx
b. in the trachea
c. in the small bronchus
d. in the alveoli
e. in the pleural cavity
92. Which phenomena are the adventitious lung sounds?
k. Rales
l. Crepitation
m. Pleural friction rub
n. All mentioned above
o. Northing mentioned above
93. Where is pleural friction rub formed?
a. in the larynx
b. in the trachea and big bronchi
c. in the small bronchi
d. in the alveoli
e. in the pleural cavity
94. What is the main mechanism of the dry rales forming?
k. Swelling mucous membrane of the bronchus
l. Storing viscous secretion in the bronchus
m. Storing viscous secretion over the pleural sheets
n. Infiltration of the alveolar walls and their saturating with exudate that result in their
adhering
o. Storing liquid secretion in the bronchi
95. What is the main mechanism of the crepitation forming?
k. Swelling mucous membrane of the bronchus
l. Storing viscous secretion in the bronchus
m. Storing viscous secretion over the pleural sheets
n. Infiltration of the alveolar walls and their saturating with exudate that result in their
adhering
o. Storing liquid secretion in the bronchi or lung cavities
96. What adventitious lung sound can be heard at the 1st stage of lobar pneumonia?
k. Crepitation
l. Pleural friction rub
m. Wheezes
n. Non-sonorous moist rales
o. Nothing from adventitious lung sounds
97. What adventitious lung sound can be heard at the pulmonary edema?
f. Crepitation
g. Pleural friction rub
h. Wheezes
i. Non-sonorous moist rales
j. Nothing from adventitious lung sounds
98. The buzzing dry rales are sign of…
f. Emphysema
g. Bronchitis
h. Pleural effusion
i. Pneumonia
j. Bronchial asthma
99. The non-sonorous moist rales are sign of …
f. Bronchial asthma
g. Fibrinous pleurisy
h. Lobar pneumonia
i. Exudative pleurisy
j. All answers are wrong
100. The sonorous coarse bubbling rales can be heard at the patient with…
z. Emphysema
aa. Chronic abscess
bb. Pleural effusion
cc. Lobar pneumonia
dd. Compressive atelectasis
101. What is a spirometry?
a. Measuring airflow and lung volumes during a forced expiratory maneuver from full
inspiration
b. Measuring inspiratory volume
c. Measuring tidal volume
d. Measuring airflow
e. All mentioned above
102. Which parameters can be measured with open spirometry?
a. FEV1, FVC
b. TLC, RAV
c. O2 saturation
d. O2 consumption
e. all mentioned above
103. Which types of the ventilation disorders do you know?
a. obstruction
b. restriction
c. mixed
d. all mentioned above
e. northing mentioned above
104. If patient’s FEV1 is low and FVC is normal, he has…
a. Normal lung function
b. Restriction
c. Obstruction
d. mixed disorder
e. Northing mentioned above
105. If patient’s FVC is low and FEV1 is normal, he has…
f. Normal lung function
g. Restriction
h. Obstruction
i. mixed disorder
j. Northing mentioned above
106. What is the lower limit of the normal parameters of lung function?
a. 100% from predicted
b. 90% from predicted
c. 85% from predicted
d. 80% from predicted
e. 70% from predicted
107. Ratio FEV1/FVC is used for diagnostics of
a. Severity of lung function disorders
b. Types of lung function disorders
c. This ratio is obsolete and now is useless
d. Patient’s constitution
e. Northing mentioned above
108. What is a peak flowmetry?
a. Measuring speed of the airflow
b. Measuring expiratory volume
c. Measuring inspiratory volume
d. Measuring vital capacity
e. Measuring minute volume
109. What is pulse oximetry?
a. Non-invasive method of estimation O2 saturation
b. Measuring blood gas (CO2 and O2) pressure
c. Measuring blood O2 concentration
d. Method of measuring pulse and respiratory rate
e. Method of measuring pulse and pulmonary blood pressure
110. What is normal level of the O2 saturation?
a. 75-80%
b. 80-85%
c. 70%
d. 90%
e. 85-90%
111. What is diagnostic indication for bronchoscopy?
a. Suspected lung cancer
b. Slowly resolving pneumonia
c. Interstitial lung disease
d. Pneumonia in the immunosuppressed patients
e. All mentioned above
112. What is therapeutic indication for bronchoscopy?
a. aspiration of mucus plugs causing lobar collapse
b. removal of foreign bodies
c. stopping lung bleeding
d. aspiration purulent copious sputum at the debilitated patient
e. All mentioned above
113. Which radiologic method of lung examination is routinely used?
 a. Computed tomography
b. Magnetic resonance imaging
c. Bronchography
d. X-ray
e. Nothing from above
114. Which radiologic method of lung examination has the highest level of resolution for
distinguishing the smallest lung structures?
f. Computed tomography
g. Magnetic resonance imaging
h. Bronchography
i. X-ray
j. Nothing from above
115 Which method of sputum examination is used for establishing the pathogen of
pneumonia?
a. General macro- and microscopic
b. Cytological
c. histological
d. Cultural
e. Northing from above
116. Which method of sputum examination is used for establishing revealing tuberculosis
mycobacterium?
f. Microscopic with Gram staining
g. Microscopic with Ziehl-Nielsen staining
h. Microscopic with Romanovskiy-Himza staining
i. Microscopic without staining
j. Macroscopic
117. Which method of sputum examination may help to establish lung cancer?
f. General macroscopic
g. Cytological
h. General microscopic
i. Cultural
j. Northing from above
118. How long should be sputum transported to laboratory for bacteriological investigation?
a. Urgent delivery
b. Under 1 hour
c. Under 2 hours
d. Under 24 hours
e. Under 24-72 hours
119. Which property could not transudes have?
a. Light yellow color
b. Protein 60 g/l
c. Negative Rivalt test
d. 1-5 leucocytes
e. 2-3 epitheliocytes
120. Which property could not exudates have?
f. Light yellow color
g. Protein 60 g/l
h. Negative Rivalt test
i. 15-20 leucocytes
j. 5-7 epitheliocytes
121. Syndrome of the focal consolidation of the lung tissue can be if patient has:
k. focal pneumonia;
l. focal pneumofibrosis;
m. focal tuberculosis;
n. lung cancer;
o. all mentioned above.
122. Syndrome of the lobar consolidation of the lung does not reveal at patient with…
k. Lobar pneumonia
l. Infiltrative tuberculosis
m. Pulmonary embolism with infarction-pneumonia
n. COPD
o. Lung cancer
123.At the patient with lobar consolidation at palpation of the chest can be obtained
k. Amplifying vocal fremitus on the affected side
l. Weakened vocal fremitus on the affected side
m. Vocal fremitus does not change
n. Vocal fremitus is absent
o. Amplifying vocal fremitus on the health side
124.At the patient with focal consolidation near the root of lung at palpation of the chest can
be obtained
f. Amplifying vocal fremitus on the affected side
g. Weakened vocal fremitus on the affected side
h. Vocal fremitus does not change
i. Vocal fremitus is absent
j. Amplifying vocal fremitus on the health side
125.Pathological bronchial breathing is heard at patients with:
k. focal consolidation
l. lobar consolidation
m. pleural effusion
n. emphysema
o. acute bronchitis
126.Percussion sound of the lobar consolidation of lung tissue is:
f. tympanic
g. clear
h. resonance
i. dull
j. small dull
127.Auscultation signs of the focal consolidation is:
k. Vesicular breathing with prorogated exhalation and wheeze
l. Absent of the any breath sound
m. Diminished vesicular breathing and sonorous bubbling (moist) rales
n. Unchanged vesicular breathing
o. Pathological bronchial breathing
128.Auscultation signs of the lobar consolidation is:
a. Vesicular breathing with prorogated exhalation and wheeze
b. Absent of the any breath sound
c. Diminished vesicular breathing and sonorous bubbling (moist) rales
d. Unchanged vesicular breathing
e. Pathological bronchial breathing
129. Obstructive atelectasis can be if patient has:
k. Lung cancer;
l. Metastasis into pulmonary lymphonodes;
m. Foreign body of bronchus;
n. Tuberculosis of the pulmonary lymphonodes;
o. all mentioned above.
130. Compressive atelectasis can be if patient has:
f. Pleural tumor (mesotelioma);
g. Massive pleural effesion;
h. Pneumothorax;
i. Deformation of the chest;
j. all mentioned above.
131. Percussion sound over massive pleural effusion:
f. tympanic
g. clear
h. resonance
i. dull
j. small dull
132. Percussion sound over pneumothorax:
f. tympanic
g. clear
h. resonance
i. dull
j. small dull
133. Auscultation signs of pneumothorax:
f. Diminished vesicular breathing and wheeze
g. Diminished vesicular breathing and crackles
h. absent of breath sounds
i. unchanged breath sound
j. Pathological bronchial breathing
134. Auscultation signs of massive pleural effusion:
f. Diminished vesicular breathing and wheeze
g. Diminished vesicular breathing and crackles
h. absent of breath sounds
i. unchanged breath sound
j. Pathological bronchial breathing
135. If patient has massive pleural effusion vocal fremitus is:
f. Absent on the affected side
g. Increased on the affected side
h. Diminished on the affected side
i. Normal
j. Increased on the health side
136. Percussion sound over small pleural effusion:
k. tympanic
l. clear
m. resonance
n. dull
o. small dull
137.If patient has small pleural effusion vocal fremitus is:
f. Absent on the affected side
g. Increased on the affected side
h. Diminished on the affected side
i. Normal
j. Increased on the health side
138. Which properties does transudate have?
a. Light yellow color
b. Protein < 30 g/l
c. Negative Rivalt test
d. 1-5 leucocytes and 2-6 mezoteliocytes
e. All mentioned above
139. Which properties does not exudate have?
f. Comparative density < 1,018
g. Protein > 30 g/l
h. Positive Rivalt test
i. 10-25 leucocytes and 2-6 mezoteliocytes
j. Yellow color
140. Percussion sound of the focal consolidation of lung tissue is:
f. tympanic
g. clear
h. resonance
i. dull
j. small dull
141.What disease does patient have only dry cough and never sputum at?
а) Acute bronchitis;
b) Dry pleurisy;
c) Bronchoectasis;
d) Cavernous tuberculosis;
e) Pneumonia
142. Test of Rivalt needs for:
a) % contents of lymphocytes
b) Determination of fibrin in pleural fluid
c) Differentiation transudates from exudates
d) Determination of hemorrhagic character of exudates
e) Determination of neutrophiles in pleural fluid
143.Auscultation data of lobar pneumonia at resolution is:
a) Bronchial breath sounds
b) Vesicular breath sounds
c) Amphoric breath sounds
d) Saccadic breath sounds
e) crackles
144.Auscultation signs of the focal pneumonia near root of lung is:
a) Wheeze
b) Bronchial breath sounds
c) sonorous bubbling (moist) rales
d) diminished vesicular breath sounds
e) Vesicular breath sounds
145.Percussion data of high point of lobar pneumonia is:
a). small dullness
b) dullness
c) clear
d) resonance
e) small dullness with tympanic tinge.
146. Pneumonia is an inflammatory process that affects:
a) Bronchi and never alveoli or pleura
b) only alveoli and never bronchi
c) only pleura and bronchi
d) alveoli and pleura, can spread from bronchi
e) only interstitial tissue and pleura
147.Which of the following characteristics is not typical of pleuritic chest pain?
a) Increases with deep breathing
b) Radiates to the jaw
c) Is located laterally
d) Diminishes with splinting of the affected side
e) Increases with cough
148. Which of the following may cause an increase in vocal resonance?
a) Emphysema
b) asthma
c) pneumonia
d) atelectasis
e) dry pleurisy
149. Percussion sound over fluid at the patient with massive exudative pleurisy is:
a) Dull
b) Tympanic
c) Resonant
d) Small dull
e) Clear
150. Auscultation data at patient with dry pleurisy:
a) Diminished vesicular breathing and crackles
b) Diminished vesicular breathing and moist rales
c) Bronchial breathing
d) Rough vesicular breathing and dry rales
e) Diminished vesicular breathing and pleural friction rub
151. Auscultation data at patient with high point stage of the lobar CAP is:
a) breathing is absent
b) normal vesicular breathing
c) bronchial breathing
d) diminished vesicular breathing
e) rough vesicular breathing
152.What types of pneumonias do you know?
a) Community-acquired pneumonia
b) Hospital pneumonia
c) Aspiration pneumonia
d) Pneumonia at immunocompromised patients
e) All mentioned above
153.At the patient with focal pneumonia near the root of lung at palpation of the chest can
be obtained
a) Amplifying vocal fremitus on the affected side
b) Weakened vocal fremitus on the affected side
c) Vocal fremitus does not change
d) Vocal fremitus is absent
e) Amplifying vocal fremitus on the health side
154. Which syndrome can develop at the patient with central lung cancer?
a) emphisema;
b) pneumotorax;
c) obstructive atelectasis;
d) lobar consolidation;
e) northing from above.
155. Which syndrome can develop at the patient with peripheral lung cancer?
a) emphisema;
b) pneumotorax;
c) obstructive atelectasis;
d) lobar consolidation;
e) northing from above.
156. Auscultation signs of massive exudative pleurisy:
a. Diminished vesicular breathing and crackles
b. absent of breath sounds
c. unchanged breath sound
d. Pathological bronchial breathing
e. Diminished vesicular breathing and wheeze
157. Which investigation is obligatory for confirming pneumonia?
a. Sputum culture
b. Full blood analysis
c. X-ray examination
d. Bronchoscopy
e. Lung function test
158. Which properties does not transudate have?
a. Light yellow color
b. Protein = 30 g/l
c. Negative Rivalt test
d. 1-5 leucocytes and 2-6 mezoteliocytes
e. All mentioned above
159. Which properties does exudate have?
a. Comparative density > 1,018
b. Protein > 30 g/l
c. Positive Rivalt test
d. 10-25 leucocytes and 2-6 mezoteliocytes
e. All from above
160. Which investigation is the most informative for confirming lung cancer?
a. Sputum culture
b. Full blood analysis
c. X-ray examination
d. Bronchoscopy with biopsy
e. Computered tomography
161. What diseases is the bronchial obstruction syndrome developed at?
a. Bronchial asthma;
b. COPD;
c. Acute obstructive bronchitis;
d. all mentioned above;
e. northing from above.
162. What diseases is the syndrome of increased lung airiness developed at?
a. Lobar pneumonia
b. Emphysema
c. Lung cancer
d. Acute bronchitis
e. Dry pleurisy
163. What diseases is the respiratory failure developed at?
a. Lobar pneumonia
b. Severe COPD
c. Severe exacerbation of the bronchial asthma
d. Massive pleural effusion
e. all mentioned above
164. What symptoms characterize the bronchial obstruction syndrome?
a. Wheezing, dry cough, tightness in the chest
b. Cough with sputum, chest pain, fever
c. Mixed dyspnea, hemoptysis, weakness
d. Dyspnea, chest pain, palpitation
e. Dry cough, chest pain, edema
165. What symptoms don’t characterize the bronchial obstruction syndrome?
a. Wheezing
b. cough
c. tightness in the chest
d. dyspnea
e. purulent sputum
166.What change of vocal fremitus can be at the patient with bronchial obstruction?
a. Amplifying
b. Decreasing
c. Absence
d. Not changed
e. Change depends on clinical situation
167. What change of vocal fremitus can be at the patient with emphysema?
f. Amplifying
g. Decreasing
h. Absence
i. Not changed
j. Change depends on clinical situation
168. What change of vocal fremitus can be at the patient with respiratory failure?
f. Amplifying
g. Decreasing
h. Absence
i. Not changed
j. Change depends on clinical situation
169. What is the main symptom of the respiratory failure?
a. cough;
b. dyspnea;
c. palpitation;
d. wheezing;
e. chest pain.
170. What is the main symptom of the emphysema?
a. cough;
b. expiratory dyspnea;
c. inspiratory dyspnea;
d. wheezing;
e. mixed dyspnea.
171. How is elasticity of the chest changed at the patient with emphysema?
a. increasing
b. decreasing
c. not changed
d. absence
e. depend on clinical situation
172. How is elasticity of the chest changed at the patient with respiratory failure?
a. increasing
b. decreasing
c. not changed
d. absence
e. depend on clinical situation
173. How percussion sound is changed at the patient with bronchial obstruction?
f. unchanged
g. dull
h. small box sound
i. tympanic
j. depend on clinical situation
174. How percussion sound is changed at the patient with emphysema?
f. unchanged
g. dull
h. small box sound
i. tympanic
j. depend on clinical situation
175. How percussion sound is changed at the patient with respiratory failure?
f. unchanged
g. dull
h. small box sound
i. tympanic
j. depend on clinical situation
176. What are auscultation findings at the patient with bronchial obstruction?
a. Vesicular breathing with prorogated expiration, wheezing
b. Diminished vesicular breathing,
c. Diminished vesicular breathing and moist rales
d. Diminished vesicular breathing and crepitation
e. Vesicular breathing and pleural friction rub
177. What are auscultation findings at the patient with emphysema?
f. Vesicular breathing with prorogated expiration, wheezing
g. Diminished vesicular breathing,
h. Diminished vesicular breathing and moist rales
i. Diminished vesicular breathing and crepitation
j. Vesicular breathing and pleural friction rub
178. How is spirometry changed at the patient with bronchial obstruction?
a. Increased FEV1, decreased FVC, FEV1/FVC> 70%
b. Normal FVC, decreased FEV1, FEV1/FVC< 70%
c. Decreased FVC, decreased FEV1, FEV1/FVC <70%
d. Increased FVC, increased FEV1, FEV1/FVC > 100%
e. Normal FVC, normal FEV1, FEV1/FVC< 70%
179. How is spirometry changed at the patient with emphysema?
f. Increased FEV1, decreased FVC, FEV1/FVC> 70%
g. Normal FVC, decreased FEV1, FEV1/FVC< 70%
h. Decreased FVC, decreased FEV1, FEV1/FVC <70%
i. Increased FVC, increased FEV1, FEV1/FVC > 100%
j. Normal FVC, normal FEV1, FEV1/FVC< 70%
180. Which method can help to establish respiratory failure?
a. bronchoscopy
b. X-ray
c. Computer tomography
d. pulsoxymetry
e. spirometry
181. Bronchial asthma is a…
a. Acute inflammatory disease;
b. Acute infective disease;
c. Chonic infective disease;
d. Chonic iinflammatory disease;
e. northing from above.
182. Chronic obstructive pulmonary disease is a…
a. chronic inflammatory of trachea and large bronchus
b. chronic inflammatory of large and medium bronchus
c. chronic inflammatory of medium, small bronchus with involving lung parenchyma and
vessels
d. All from above
e. Northing from above
183. Which symptoms characterize bronchial asthma?
a. Mixed dyspnea, cough with purulent sputum
b. Episodic dry cough, tightness of the chest, wheezing
c. Chest pain with radiation to jaw, inspiratory dyspnea
d. Permanent expiratory dyspnea, cough
e. Episodic hemoptysis and dyspnea due to physical effort
184. Which symptoms characterize COPD?
f. Mixed dyspnea, dry cough, chest pain
g. Episodic dry cough, tightness of the chest, wheezing
h. Chest pain with radiation to jaw, inspiratory dyspnea
i. Permanent expiratory dyspnea, cough, sputum production
j. Episodic hemoptysis and dyspnea due to physical effort
185. What symptom doesn’t characterize bronchial asthma?
a. Wheezing
b. cough
c. tightness in the chest
d. dyspnea
e. purulent sputum
186. What symptom doesn’t characterize COPD?
f. Wheezing
g. cough
h. chest pain
i. dyspnea
j. purulent sputum
187. What change of vocal fremitus can be at the patient with COPD?
a. Amplifying
b. Decreasing
c. Absence
d. Not changed
e. Change depends on clinical situation
188. What change of vocal fremitus can be at the patient with bronchial asthma?
a. Amplifying
b. Decreasing
c. Absence
d. Not changed
e. Change depends on clinical situation
189. If patient has asthma symptoms 1-2 times in a week, 1 night awaking in a mouth, he
has…
a. Intermitend asthma;
b. Mild persistent asthma;
c. Moderate persistent asthma;
d. Severe persistent asthma;
e. depends on clinical situation
190. If patient has asthma symptoms 1-2 times in a day, 1 night awaking in a week, he has…
f. Intermitend asthma;
g. Mild persistent asthma;
h. Moderate persistent asthma;
i. Severe persistent asthma;
j. depends on clinical situation
191. If patient has asthma symptoms 1-2 times in a year, night awaking is absent, he has…
f. Intermitend asthma;
g. Mild persistent asthma;
h. Moderate persistent asthma;
i. Severe persistent asthma;
j. depends on clinical situation
192. If patient has asthma symptoms 8-10 times in a day, every night awaking, he has…
f. Intermitend asthma;
g. Mild persistent asthma;
h. Moderate persistent asthma;
i. Severe persistent asthma;
j. depends on clinical situation
193. How percussion sound is changed at the patient with COPD?
a. unchanged
b. dull
c. small box sound
d. tympanic
e. depend on clinical situation
194. How mobility of the lung border is changed at the patient with COPD?
a. unchanged
b. limited
c. increased
d. became immovable
e. depend on clinical situation
195. How percussion sound is changed at the patient with mild asthma?
a. unchanged
b. dull
c. small box sound
d. tympanic
e. depend on clinical situation
196. What are auscultation findings at the patient with asthma attack?
a. Vesicular rough breathing with prorogated expiration, wheezing
b. Diminished vesicular breathing,
c. Diminished vesicular breathing and moist rales
d. Diminished vesicular breathing and crepitation
e. Vesicular breathing and pleural friction rub
197. What are auscultation findings at the patient with COPD?
a. Vesicular rough breathing
b. Diminished vesicular breathing with prolongated expiration, wheezing
c. Diminished vesicular breathing and moist rales
d. Diminished vesicular breathing and crepitation
e. Vesicular breathing and pleural friction rub
198. How is FEV1 increased after bronchial spasmolytic if patient has reversible obstruction?
a. >12% from initial
b. >20% from initial
c. >25% from initial
d. 30% from initial
e. 10% from initial
199. If patient has permanent expiratory dyspnea during physical effort, FEV1 is 52% from
predicted and FEV1/FVC 55% he has…
a. Mild COPD
b. Moderate COPD
c. Severe COPD
d. Very severe COPD
e. Depend on clinical situation
200. If patient has permanent expiratory dyspnea in a rest, FEV1 is 22% from predicted and
FEV1/FVC 45% he has…
f. Mild COPD
g. Moderate COPD
h. Severe COPD
i. Very severe COPD
j. Depend on clinical situation
201. What are the cardiovascular symptoms?
A. Chest pain, cough, dyspnea, wheezes, haemoptysis.
B. Pain in the heart region, palpitation, intermissions, oedema
C. Headache, dizziness, dysphagia, nausea, vomiting.
D. Pain in the right subcostal region, bitter taste, brown urine, skin itching, jaundice.
E. Back pain, dysuria, ishuria, eyes oedema, weakness.
202. What are the cardiovascular symptoms?
A. Abdominal pain, nausea, vomiting
B. Dyspnea, faint (syncope), palpitation, dry cough
C. Cough with rusty sputum, chest pain, dyspnea
D. Swelling abdomen, constipation, melena
E. Oedema, dysuria, haematuria
203. What feature does the pain at angina pectoris have?
A. Be caused by physical extension
B. Duration under 15 minutes
C. Constricting, feeling of heaviness
D. Radiate to the left hand and scapula
E..All mentioned above
204. What feature does not the pain at myocardial infarction have?
A. Prolonged, continuous > 20-30 min.
B. Severe, tight or burning.
C Relief at rest.
D. Does not respond to nitrates.
E. Radiate to both hands, jaws, neck.
205. If patient has heart failure his cough is characterized with
A. appearing at lying position
B. a lot of rusty sputum
C. it is permanent
D. it is loud
E. all mentioned above.
206. If patient has feeling of solitary beats at various intervals it is named
A. exrtasistole
B. palpitation
C. syncope
D. dizziness
E. heart dyspnea
207. If patient has feeling of accelerated and intensified heart contractions onto the chest
wall it is named
A. exrtasistole
B. palpitation
C. syncope
D. heart dyspnea
E. heart pain
208. If patient has a lot of foamy pink liquid sputum it means he has
A. Pulmonary edema
B. Pulmonary embolism
C. Aortic aneurysm dissection
D. all from above
E. Northing from above
209. Which type of dyspnea is observed at the patients with cardiovascular diseases?
A. Expiratory
B. Inspiratory
C. Mixed
D. Changing
E. All mentioned above.
210. What is feature of dyspnea at patient with cardiac asthma attack?
A. Appear at night
B. Accompanying with dry cough
C. Inspiratory
D. Ortopnea position in the bed
E. all mentioned above
211. Which of the following disorders is not likely to be associated with hemoptysis?
A. Mitral stenosis
B. Pulmonary embolism
C. Pulmonary edema
D. Pericarditis
E. None of the above
212. What characteristics of edema at patient with heart failure?
A. Asymmetrical on the part of body which patient lies on.
B. Firstly on the face than gradually spreads to body down.
C Firstly on the legs than gradually spreads to body up
D. Hear the heart region
E. Only on abdomen and hands
213. What position does a patient with cardiovascular insufficiency occupy?
F. . A forced sitting position with the legs let down.
G. The patient prefers to lie on the affected side.
H. The patient sits upright or resting the hands on the edge of the table of chair.
I. A lying position on the side (lateral recumbent position) with the head thrown back and
the bent legs pulled up to the abdomen.
J. A forced knee-elbow position.
214. What mechanisms are caused by the orthopnoea posture?
F. Tissue oxygen demand reduce at rest, decreased myocardial ischemia
G. Re-distribution of blood into the iow extremities, reducing of circulating blood volume,
H. Decreasing blood volume, decreasing of venous pressure in the lesser circulation,
improvement of gas exchange in the "alveoli-pulmonary capillaries" system, displacement of
ascitis fluid
I. Pericardial layers presses to one another, reduce their movement that decrease
irritation of pain receptors in pericardium
J. Improvement of diastolic cardiac function
215. What kind of posture is observed at angina pectopis?
F. Upright
G. On the right side with high head of the bed
H. Orthopnoea
I. Sitting posture bending forward
J. Knee-elbow posture
216. What kind of posture is observed at acute left ventricular failure?
F. Upright
G. On the right side with high head of the bed
H. Orthopnoea
I. Sitting posture bending forward
J. Knee-elbow posture
217. What cardiovascular disease is characterized with constant pale skin color?
A. Angina pectoris
B. Mitral stenosis
C. aortic valve diseases
D Essential hypertension
E. All mentioned above
218. Which of the following conditions is least to produce jugular venous distention?
A. right heart failure
B. Chronic left heart failure
C. Chronic hypoxemia
D. Liver failure
E. circulation insufficiency
219. What kind of cyanosis is usually observed at patient with cardiovascular diseases?
A. Central, warm
B. peripheral, cold
C. peripheral warm
D. Local (near heart region), cold
E. Diffuse warm
220. Which method can we use for establishing edema
A. Visual inspection
B. Palpation
C. weighing patient
D. measuring leg circumstance
E. All mentioned above.
221. The normal pulse rate is:
A.70 – 80 in a min.
B.50 – 70 in a min.
C. 60 – 80 in a min.
DI. 80 – 100 in a min.
E. 50-90 in a min
222. Arising condition to cardiac '' humpback'':
A. enlargement of the heart chambers in childhood
B. effusion in the pericardium cavity
C. the thrust of the heart apex against chest wall
D. dilation and hypertrophy of the right ventricle
E. adhesion of the parietal and visceral layers of the pericardium
223. Arising condition of pulsated bulging in the jugular fossae:
A. dilation of the ascending part of the aorta
B. hypertrophy and dilation of the right ventricle
C. pulmonary hypertension
D. dilation of the aortic arch
E. left atrium dilatation
224. Arising conditions of pulsation in the II interspace to the right of the sternum edge:
A. dilation of the ascending part of the aorta
B. hypertrophy and dilation of the right ventricle
C. pulmonary hypertension
D. dilation of the aortic arch
E. left atrium dilatation
225. Arising conditions of epigastric pulsation that increases in deep inspiration:
A. dilation of the ascending part of the aorta
B. pulsation of the abdominal aorta
C. pulmonary hypertension
D. dilation of the aortic arch
E. Left ventricle hypertrophy
226. A normal apex beat is found:
A. in the 5th intercostal space in 1-1,5 cm medially from the left midclavicular line
B. in the 6th intercostal space 0-1 cm medially from the left midclavicular line
C. in the 4th intercostal space on the left midclavicular line
D. in the 5th intercostal space in 1-1,5 cm laterally from the left midclavicular line
E. in the 6th intercostal space on the left left midclavicular line
227. If patient has left ventricle hypertrophy his apex beat sift…
A. leftward
B. downward
C. upward
D. rightward
E. unchenged
228. Apex beat properties is:
A. localization, area, height, strenght (or resistence)
B. area, height
C. height, strenght
D. area, exertion, strength
E. localization, height
229. Area of normal apex beat is:
A. near 2 cm2
B. near 3 cm2
C. near 1 cm2
D. near 1,5 cm2
E. near 4,5 cm
230. The normal right border of the relative cardiac dullness is:
A. 4th interspace 1 cm laterally of the right edge of the sternum
B. 4th interspace 1,5 cm laterally of the right edge of the sternum
C. 4th interspace 2 cm laterally of the right edge of the sternum
D. 4th interspace 2,5 cm laterally of the right edge of the sternum
E. 4th interspace near the right edge of the sternum
231. The normal upper border of the relative cardiac dullness is:
A. 3th interspace at the left parasternal line
B.3th interspace at the right parasternal line
C.2th interspace at the left parasternal line
D.2th interspace at the right parasternal line
E. 4th interspace at the left parasternal line
232. The normal left border of the relative cardiac dullness is:
A. 5th interspace 2,5 cm medially of the left midclavicular line
B. 5th interspace 1,5 cm medially of the left midclavicular line
C.5th interspace 2 cm medially of the left midclavicular line
D.5th interspace 3 cm medially of the left midclavicular line
E. 5th interspace on the left midclavicular line
233. Right border of the relative heart dullness is displaced to the right in case of:
A. Dilation and hyper trophy of the left ventricle
B. Dilation of the left atrium
C. Atelectasis of the left lung
D. Dilation and hypertrophy of the right ventricle and/or right atrium
E. Pneumothorax of the right lung
234. Left border of the relative heart dullness is displaced to the left in case of:
A. dilation and hypertrophy of the right ventricle
B. dilation of the right atrium
C. hypertrophy and dilation of the left ventricle
D. dilation of the right ventricle and right atrium
E. dilation of the left atrium
235. The normal right borders of the absolute cardiac dullness:
A. along the left edge of the sternum in 5th interspace
B. along the left edge of the sternum from 4th to 6th rib
C. along the right edge of the sternum from 5th to 6th rib
D. along the right edge of the sternum from 3th interspace
E. along the middle of the sternum between 5th rib
236. The normal upper borders of the absolute cardiac dullness:
A. lower edge of the 3 th rib along left parasternal line
B. lower edge of the 4th rib along left parasternal line
C. lower edge of the 5th rib along left parasternal line
D. lower edge of the 4th rib along right parasternal line
E. lower edge of the 5 th rib along right parasternal line
237. The upper border of the relative heart dullness shift upward in a case of:
A. mitral stenosis
B. aortic stenosis
C. tricuspid regurgitation
D. pulmonary stenosis
E. pulmonary regurgitation
238. Transverse length of the heart in a norm is:
A. 8 – 10 cm
B. 11 – 13 cm
C. 12 – 14 cm
D. 6 – 7 cm
E.15-17 cm
239. The normal width of the vascular bundle is:
A. 4 – 6 cm
B. 5 – 7 cm
C. 6 – 8 cm
DI. 2–3 cm
E. 1,5-2,5 cm
240. The normal range of blood pressure is:
А. 120 – 149/70-99 mm. Hg
В. 90 – 159/60 – 109 mm. Hg
С. 80 – 129/50 – 99mm.Hg
D. 100 – 139/60 – 89 mm. Hg
E. 110-149/40-79 mm Hg
241. Where is the mitral valve on the front chest wall projected?
f. 2nd intercostal space to the left of the sternum
g. On the sternum midway between 3rd left and 5th right costosternal articulation
h. To the left of the sternum at the level of the 3rd costosternal articulation
i. To the left of the sternum at the level of the 4th costosternal articulation
j. On the sternum midway between 3rd left and 3th right costosternal articulation
242. Where is the pulmonary artery valve on the front chest wall projected?
f. 2nd intercostal space to the left of the sternum
g. On the sternum midway between 3rd left and 5th right costosternal articulation
h. To the left of the sternum at the level of the 3rd costosternal articulation
i. To the left of the sternum at the level of the 4th costosternal articulation
j. On the sternum midway between 3rd left and 3th right costosternal articulation
243. Where is listening point for tricuspid valve?
a. heart apex
b. 2nd intercostals space right from the sternum
c. 2nd intercostals space left from the sternum
d. Base of the xiphoid process
e. 3rd intercostals space left from the sternum
244. Where is listening point for aortic valve?
a. heart apex
b. 2nd intercostals space right from the sternum
c. 2nd intercostals space left from the sternum
d. Base of the xiphoid process
e. 3rd intercostals space left from the sternum
245. Which auscultation point coincides with heart valve projection on the chest wall?
f. 1st auscultation point
g. 2nd auscultation point
h. 3rd auscultation point
i. 4th auscultation point
j. 5th auscultation point
246. Which components does the second heart sound consist of?
f. Muscular, valvular and vascular
g. Muscular and valvular
h. Valvular and vascular
i. Valvular, vascular and atrial
j. None of variants
247. What produces the third heart sound?
f. The ventricular systole
g. The closure of the aortic and pulmonary valves
h. The vibration of the ventricular diastole
i. The closure of the bicuspid and tricuspid valves
j. The vibration of the ventricular during passive rapid filling
248. Which auscultation points are used for the first sound assessment?
f. 1st and 2nd auscultation points
g. 2nd and 3rd auscultation points
h. 3rd and 4th auscultation points
i. 1st and 3rd auscultation points
j. 1st and 4th auscultation point
249. Which sound follows the long pause?
a. The 1st heart sound
b. The 2st heart sound
c. The 3st heart sound
d. The 4st heart sound
e. Depends on clinical situation
250. What can not be assessed by heart auscultation?
a.Heart rhythm
b.Cardiac index
c. Heart rate
d.Heart sounds
e. Heart murmurs
251. Where is the tricuspid valve on the front chest wall projected?
f. 2nd intercostal space to the left of the sternum
g. On the sternum midway between 3rd left and 5th right costosternal articulation
h. To the left of the sternum at the level of the 3rd costosternal articulation
i. To the left of the sternum at the level of the 4th costosternal articulation
j. On the sternum midway between 3rd left and 3th right costosternal articulation
252. Where is the aortic valve on the front chest wall projected?
a. 2nd intercostal space to the left of the sternum
b. On the sternum midway between 3rd left and 5th right costosternal articulation
c. To the left of the sternum at the level of the 3rd costosternal articulation
d. To the left of the sternum at the level of the 4th costosternal articulation
e. On the sternum midway between 3rd left and 3th right costosternal articulation
253. Where is listening point for mitral valve?
a. heart apex
b. 2nd intercostals space right from the sternum
c. 2nd intercostals space left from the sternum
d. Base of the xiphoid process
e. 3rd intercostals space left from the sternum
254. Where is listening point for pulmonary artery valve?
a. heart apex
b. 2nd intercostals space right from the sternum
c. 2nd intercostals space left from the sternum
d. Base of the xiphoid process
e. 3rd intercostals space left from the sternum
255. Where is placed Botkin-Erb’s listening point?
f. 2nd intercostal space to the right of the sternum
g. 2nd – 3rd intercostal space to the left of the sternum
h. 3rd – 4th intercostal space to the left of the sternum
i. 4th – 5th intercostal space to the left of the sternum
j. 3rd – 4th intercostal space to the right of the sternum
256. From which components consists the first heart sound?
f. Muscular, valvular and vascular
g. Valvular, vascular and atrial
h. Valvular and vascular
i. Muscular, valvular, vascular and atrial
j. None of variants
257. When can the forth heart sound be listened?
a. At the beginning of the ventricular systole
b. At the end of the ventricular systole
c. At the beginning of the ventricular diastole
d. At the end of the ventricular diastole
e. At the beginning of the precordial systole
258. Which auscultation points are used for the second sound assessment?
f. 1st and 2nd auscultation points
g. 2nd and 3rd auscultation points
h. 3rd and 4th auscultation points
i. 1st and 3rd auscultation points
j. 1st and 4th auscultation point
259. Which sound follows the short pause?
f. The 1st heart sound
g. The 2st heart sound
h. The 3st heart sound
i. The 4st heart sound
j. Depends on clinical situation
260. What can be assessed by heart auscultation?
a. Heart rhythm
b. Heart rate
c. Heart sounds
d. Heart murmurs
e. All mentioned above
261. Loud first sound in the cardiac apex is auscultated in case of:
E. Myocardial infarction
F. Myocarditis
G.Myocardial sclerosis
H. Synchronic systole of atriums and ventricles in case of full atrioventricular blockade
I. Mitral regurgitation
262. Weakening of both heart sounds is auscultated in case of:
E. Myocardial infarction
F. Myocarditis
G.Emphysema
H.Myocardiosclerosis
I. All mentioned cases
263. Loud second sound over pulmonary artery is auscultated in case of:
A. Aortic stenosis
B. Mitral stenosis
C. Essential hypertension
D.Aortic insufficiency
E. Regurgitation of the pulmonary artery
264. Loud both heart sounds are heard in case of:
E. Lungs shrinkage
F. Posterior mediastinum tumors
G.Forward inclination of body
H.Fever
I. All mentioned reasons
265. ‘Quail’ rhythm is:
A. The loud ‘flapping’ first sound
B. The loud ‘flapping’ first sound, second sound, opening snap of mitral valve
C. Opening snap of mitral valve
D.The first sound, click and second sound
E. Northing from above
 266. Ground of the second sound accent appearance over the pulmonary artery is:
E. High pressure in greater circulation
F. High pressure in the pulmonary circulation
G.High pressure in cava veins
H.All above mentioned
I. Northing from above
267. ‘Gallop’ rhythm can appear in case of:
A. Diffuse myocarditis
B. Myocardial infarction
C. Dilatational cardiomyopathy
D.Heart failure
E. All mentioned variants
268 Splitting of the first sound appears in case of:
F. Asynchronous right and left ventricle contraction
G.Right bundle branch block
H.Bisystolia (systole in 2 portions)
I. All mentioned variants
J. Northing from above
269. Splitting of second sound in pulmonary artery is connected with:
F. High pressure in lesser circulation
G. Asynchronous aortic and pulmonary artery valve closing
H. Breathing
I. All mentioned is true
J. No right answer
270. Presystolic ‘gallop’ rhythm is auscultated in case of:
F. Mitral stenosis
G. Tricuspid insufficiency
H. Myocardial infarction
I. Pulmonary insufficiency
J. All above mentioned cases
271. Weakening of the first sound in the cardiac apex is auscultated with:
E. Stenosis of mitral orifice
F. Insufficiency of mitral valve
G.Synchronic systole of atriums and ventricles in case of full atrioventricular blockade
H.Extrasystole
I. Northing from above
272. The Loud second sound over aorta is auscultated in case of:
E. Insufficiency of aortic valve
F. Aortic stenosis
G.Essential hypertension
H.Mitral stenosis
I. Mitral regurgitation
273. The loud first sound over the cardiac apex is auscultated in case of:
F. Mitral stenosis
G.Ciliary arrhythmia
H.Full atrioventricular blockade
I. All mentioned cases
J. No right answer
274. The loud second sound over pulmonary artery is auscultated in case of:
F. Emphysema of lungs
G.Chronic obstructive lung disease
H.Pneumosclerosis
I. All mentioned reasons
J. No right answer
275. The loud ‘flapping’ first sound over heart apex is auscultated in case of:
A. Mitral stenosis
B. Mitral insufficiency
C. Aortic stenosis
D. aortic insufficiency
E. Pulmonary artery stenosis
276. Ground of the second sound accent above aorta is:
E. High pressure in greater circulation
F. High pressure in pulmonary circulation
G.High pressure in pulmonary veins
H.All above mentioned
I. Northing from above
277. The first sound in case of ‘gallop’ rhythm is:
F. Intensified
G.Bifurcated
H.Weakened
I. All variants are right
J. No right answer
278. Splitting of the second sound appears more often over:
E. Aorta
F. Pulmonary artery
G.Apex
H.Near xiphoid process
I. All mentioned variants
279. Protodiastolic ‘gallop’ rhythm is commonly auscultated in case of:
F. Severe heart failure
G.Essential hypertension
H.Chronic nephritis with hypertensive syndrome
I. Myocardial infraction
J. All above mentioned cases
280. Embryocardia or pendular rhythm appears in case of:
F. High fever
G.Paroxysmal tachycardia
H.Heart failure
I. Severe cardiomyopathy with prolonged systole
J. All mentioned variants
281 What heart diseases listed below can you find organic systolic cardiac murmurs at?
A. mitral stenosis
B. Aortic stenosis
C. Aortic regurgitation
D. Pulmonary regurgitation
E. Tricuspid stenosis
282. The best point for hearing the systolic murmurs at aortic stenosis is
A. The heart apex
B. The Botkin – Erb point
C. The second intercostal space, to the right from the breastbone
D. The second intercostal space, to the left from the breastbone
E. On the middle of the breastbone on the level of third rib
283. Anaemic functional murmur is more often:
A. Systolic
B. Diastolic
C. Protodiastolic
D. Presystolic
E. Systola-diastolic
284. Haemodinamical functional murmurs can be auscultated at
A. Thyrotoxicosis
B. Mitral stenosis
C. Myocarditis
D. Cardiosclerosis
E. Hypertension disease
285. The pericardial friction pub is better heard
A. On the heart apex
B. on the Botkin-Erb point
C. Above the absolute heart’s dullness zone
D. On heart’s base
E. Near the xiphoid process
286. The pericardial friction rub differs from organic murmurs in that it is
A. More delicate
B. Heard like far away
C. Heard near the ear
D. Always coincide with systole
E. Well radiate to other auscultatic zones
287. Which of the following does not characterized the pericardial friction rub?
A. Never gives any tactile fillings
B. Becomes stronger if patient bends forward
C. Coincidance with systola and diastola
D. Well irradiate to other auscultatic zones
E. Loud
288 Which organic murmur gives the filling of “cat purr” in the second intercostal space right
from the breastbone?
A. Systolic murmur of mitral regurgitation
B. Diastolic murmur of mitral stenosis
C. Systolic murmur of aortic stenosis
D. Diastolic murmur of aortic regurgitation
E. Systolic murmur of tricuspid regurgitation
289. Systolic murmur of aortic stenosis irradiates
A. To the heart apex and to Botkin’s point
B. To the left axillary region
C. To the second left intercostal space
D. To the area of xiphoid process
E. To the carotid and subclavical arteries
290. Which functional murmur can be heard at mitral stenosis?
A. Systolic hydremic
B. Systolic hemodynamic
C. Systolic muscular
D. Kumbs’ murmur
E. Graham-Steel murmur
291. What heart diseases listed below can you find organic diastolic cardiac murmurs at?
A. Stenosis of mitral foramen
B. Stenosis of orifice of aorta
C. Mitral valve deficiency
D. Stenosis of lung arteries orifice
E. Tricuspid valve deficiency
292. The best point for hearing the diastolic murmurs at aortic regurgitation is
A. The heart apex
B. The Botkin – Erb point
C. The second intercostal space, to the right from the breastbone
D. The second intercostal space, to the left from the breastbone
E. On the middle of the breastbone on the level of third rib
293. Anaemic murmur is heard better
A. Above the lung artery
B. At Bodkin’s point
C. Above all valve orifices
D. On the apex of the heart
E. Above the aorta
294. How is functional systolic murmur differed from organic one?
A. It is not ruled by periods of breathing
B. Loud, harsh, prolonged
C. Do not change during exercises
D. Do not have irradiative zones
E. Often supported by feeling of systolic “cat purr”
295. The pericardial friction rub usually appears at
A. Uremia
B. Hydropericardium
C. Cardiomegaly
D. Angina pectoris
E. Adhesion of pericardium and pleura
296. Which of the following is not a differential sign between pericardial friction rub from
organic murmur?
A. Become stronger during pressing the chest
B. Becomes weaker if patient bends forward
C. Heard above zones, projections and places of the best auscultation of heart ’s vavles
D. Do not coincidance with cardiac periods
E. Never gives tactile sings
297. Which organic murmur gives the filling of “cat purr” on the heart apex?
A. Systolic murmur of mitral regurgitation
B. Diastolic murmur of mitral stenosis
C. Systolic murmur of aortic stenosis
D. Diastolic murmur of aortic regurgitation
E. Systolic murmur of tricuspid regurgitation
298. Which cardiac murmur gives tactile filling above absolute cardiac dullness that becomes
stronger while bending the body forward?
 A. Systolic murmur of mitral regurgitation
B. Diastolic murmur of mitral stenosis
C. Systolic murmur of aortic stenosis
D. Diastolic murmur of aortic regurgitation
E. Systole-diastolic pericardial friction rub.
299. Which functional murmur can be heard at aortic regurgitation?
A. Systolic hydremic
B. Systolic hemodynamic
C. Flint’s murmur
D. Coombs’ murmur
E. Graham-Steel murmur
300. What are the reasons for Flint’s murmur in aorta valve deficiency
A. Relative mitral regurgitation
B. Relative mitral stenosis
C. Relative aortic stenosis
D. Relative tricuspid regurgitation
E. Relative pulmonary stenosis
301. Which pathological conditions can be confirmed by 2-dimenshional echocardiography?
f. congenital heart disease,
g. left ventricular aneurysm
h. mural thrombus
i. Valve heart diseases
j. All mentioned above
302 .Normal value of ejection fraction is …
f. 60-66%
g. 45-50%
h. 50-55%
i. 66-75%
j. 40-45%
303. If patient has diastolic dysfunction which echocardiographic parameter can confirm it?
f. End systolic volume
g. End diastolic volume
h. Stroke volume
i. Ejection fraction
j. Minute volume
304. Indications for exercise ECG testing are:
f. confirming a suspected diagnosis of IHD
g. Assessment of cardiac function and exercise tolerance
h. Prognosis following myocardial infarction
i. Evaluation of response to treatment
j. All mentioned above
305. Indication for dairy ECG monitoring
f. Symptoms could be related with rhythm disorders
g. Diseases with high risk of fatal arrhythmias and sudden death
h. Assessing circadian variability of the sinus rhythm at patient with myocardial infarction,
heart failure, obstructive sleep apnea syndrome
i. Revealing of ischemic disorders (ischemic heart disease)
j. All mentioned above
i. Doppler echocardiography used for revealing …
 f. flow and gradients across valves and septal defects
g. left ventricular hypertrophy
h. ejection fraction
i. stroke volume
j. northing from above
ii.Normal value of posterior wall thickness in diastole is …
f. 0,8-1,1 sm
g. 0,6-0,7 sm
h. 1,3-1,4 sm
i. 0,4-0,5 sm
j. 1,5-1,6 sm
308.If patient has left ventricular hypertrophy which parameters are changed?
f. Posterior wall thickness
g. Ejection fraction
h. End diastolic volume
i. Diameter of the interventricular septum
j. a and d.
309.Contraindication for exercise ECG testing:
f. Unstable angina
g. Recent Q wave myocardial infarction (<5day)
h. Severe aortic stenosis
i. Uncontrolled arrhythmia, hypertension, or heart failure
j. All mentioned above
310.Indication for dairy blood pressure monitoring:
f. Diagnostics of the ‘white coat’ hypertension,
g. Diagnostics of the border hypertension,
h. Diagnostics of the symptomatic hypertension
i. Control of antihypertensive therapy.
j. All mentioned above
311. How is the first sound changed at the patient with mitral stenosis?
A. Amplified;
B. Diminished;
С. Split;
D. not changed;
E. Depend on clinical situation.
312. How is the second sound changed at the patient with mitral stenosis?
A. increased above the aorta
B. increased above the pulmonary artery;
C. diminished above the aorta;
D. diminished above the pulmonary artery;
E. not changed.
313. What murmur can be heard at the patient with mitral stenosis?
A. pansystolic
B. presystolic;
C. systolic and diastolic;
D. murmur is absent;
E. short systolic
314. What are ECG changes at the patients with mitral stenosis?
A. hypertrophy left atrium
B. hypertrophy of right atrium;
C. hypertrophy of right ventricle;
D. hypertrophy of left ventricle;
E. all mentioned above.
315. What border of the relative heart dullness is shift at the patient with mitral stenosis?
A. right is shift right
B. left is shift left and downward;
C. upper is shift upward;
D. upper is shift upward and right is shift right;
E. borders of the relative heart dullness are not changed.
316. How is the first sound changed at the patient with mitral regurgitation?
A. Amplified;
B. Diminished;
С. Split;
D. not changed;
E. Depend on clinical situation.
317. What border of the relative heart dullness is shift at the patient with mitral
regurgitation?
A. right is shift right
B. left is shift left and downward;
C. upper is shift upward;
D. right answers A, B, and C;
E. borders of the relative heart dullness are not changed.
318. What murmur at the heart apex can be heard at the patient with mitral regurgitation?
A. systolic
B. diastolic;
C. systolic and diastolic;
D. murmur is absent;
E. depend on clinical situation
319. Which area does the systolic murmur at the patient with mitral regurgitation conduct
to?
A. neck vessels
B. axillary region
C. interscapular region
D. Botkin-Erb point
E. does not conduct.
320. What are the symptoms of decompensated mitral stenosis?
F. Dyspnea and fatigue,
G. palpitation,
H. chest pain,
I. heamoptysis
J. All mentioned above
321What are the main causes of aortic regurgitation?
F. Rheumatic fever,
G. infective endocarditis, syphilitic aortitis
H. connective tissue disorders (rheumatoid arthritis, systemic lupus erythematosus,
Marfan syndrome),
I. congenital (may be associated with other defects, such as ventricular septal defect),
J. all mentioned above
322.What are the symptoms of decompensated aortic stenosis?
F. Dyspnea and fatigue,
G. Palpitation,
H. Chest pain,
I. Faintness
J. All mentioned above
323.How is color of skin changed at patients with aortic valve diseases?
F. Became bluish
G. Become reddish
H. Become yellowish
I. Became pale
J. Nothing from above.
324. Capillary pulse is a sign of…
F. Aortic stenosis
G. Mitral stenosis
H. Mitral regurgitation
I. Pulmonary hypertension
J. Aortic regurgitation
325. How is blood pressure changed at patient with aortic stenosis?
F. Systolic increased, diastolic normal
G. Systolic decreased, diastolic normal
H. Systolic normal, diastolic increased
I. Systolic normal, diastolic decreased
J. Systolic increased, diastolic decreased
326. What border of the relative heart dullness is shift at the patient with aortic
regurgitation?
A. right is shift right
B. left is shift left and downward;
C. upper is shift upward;
D. right answers A, B, and C;
E. borders of the relative heart dullness are not changed.
327. How is the first sound changed at the patient with aortic stenosis?
A. Amplified;
B. Diminished;
С. Split;
D. not changed;
E. Depend on clinical situation.
328. How is the second sound changed at the patient with aortic regurgitation?
A. increased above the aorta
B. increased above the pulmonary artery;
C. diminished above the aorta;
D. diminished above the pulmonary artery;
E. not changed.
329.What murmur at the aorta point can be heard at the patient with aortic stenosis?
A. systolic
B. diastolic;
C. systolic and diastolic;
D. murmur is absent;
E. depend on clinical situation
330.Which area is the murmur at the patient with aortic regurgitation conducted to?
A. neck vessels
B. axillary region
C. interscapular region
D. Botkin-Erb point
E. is not conducted.
331.What are the main causes of aortic stenosis?
F. Senile calcification is the commonest
G. rheumatic fever,
H. congenital valve diseases
I. septic endocarditis.
J. all mentioned above
332.What are the symptoms of decompensated aortic regurgitation?
F. Dyspnea and cough,
G. Palpitation, heaviness in the heart region
H. Cardiac asthma attack,
I. Faintness, dizziness
J. All mentioned above
333.Carotid dance’ (carotid pulsation) is a sign of …
F. Mitral stenosis
G. Pulmonary hypertension
H. Aortic regurgitation
I. Aortic stenosis
J. Mitral regurgitation
334.Systolic ‘cat purring’ is a sign of…
A. aortic regurgitation
B. mitral regurgitation
C. arterial hypertension
D. aortic stenosis
E. mitral stenosis
335.What border of the relative heart dullness is shift at the patient with aortic stenosis?
A. right is shift right
B. left is shift left and downward;
C. upper is shift upward;
D. upper is shift upward and right is shift right;
E. left is shift left.
336.How is the first sound changed at the patient with aortic regurgitation?
A. Amplified;
B. Diminished;
С. Split;
D. not changed;
E. Depend on clinical situation.
337.How is the second sound changed at the patient with aortic stenosis?
A. increased above the aorta
B. increased above the pulmonary artery;
C. diminished above the aorta;
D. diminished above the pulmonary artery;
E. not changed.
338.What murmur at the aorta point can be heard at the patient with aortic regurgitation?
A. systolic
B. diastolic;
C. systolic and diastolic;
D. murmur is absent;
E. depend on clinical situation
339.How is the systolic murmur conducted at patient with aortic stenosis?
A. along the right edge of breastbone;
B. to the Botkin-Erb point;
C. to the vessels of neck;
D. to the lift axillary area;
E. not conducted.
340.What are ECG changes at the patients with aortic stenosis?
A. hypertrophy left atrium
B. hypertrophy of right atrium;
C. hypertrophy of right ventricle;
D. hypertrophy of left ventricle;
E. all mentioned above.
341. Which level of the blood pressure is corresponded to mild hypertension?
A. > 140/< 90 mm Hg.
B. 140-159/90-99 mm Hg.
C. 160-179/100-109 mm Hg.
D. ≥ 180/≥ 110 mm Hg.
E. ≥155/≥100 mm Hg
342. Risk factors of essential hypertension:
F. Family history, race (blacks), stress, obesity, a high intake of saturated fats or sodium, use
of tobacco, sedentary lifestyle.
G. Family history, stress, obesity, a high intake of saturated fats or sodium, use of tobacco,
hepatitis, sedentary lifestyle.
H. Family history, stress, obesity, a high intake of saturated fats or sodium, cardiac
arrhythmia, sedentary lifestyle.
I. Stress, obesity, a high intake of saturated fats or sodium, use of tobacco, hepatitis,
sedentary lifestyle.
J. Family history, race (blacks), cardiac arrhythmia, sedentary lifestyle.
343. What arterial pressure is corresponded to moderate hypertension?
A. > 140/< 90 mm Hg.
B. 140-159/90-99 mm Hg.
C. 160-179/100-109 mm Hg.
D. ≥ 180/≥ 110 mm Hg.
E. ≥155/≥100 mm Hg
344. What are the pulse properties at patients with arterial hypertension?
A. Hard, intense.
B. Hard.
C. Frequent.
D. Intense, frequent.
E. Arrhythmic, slow.
345. What is the commonest symptom at patients with essential hypertension?
A. Sleep disorders.
B. Headache.
C. Myalgia.
D. Arrhythmia.
E. Edemas
346. How are the heart borders displaced at patient with the 2nd stage of essential
hypertension?
A. Shift to the right.
B. Shift to the left.
C. Shift to the left and up.
D. Shift to the right, left and up.
E. Not changed.
347. During auscultation of patients with prolonged arterial hypertension you can hear:
A. Diminished S1 at the apex, and accented S2 at the aorta.
B. Loud S1 at the apex, and accented S2 at the aorta.
C. Increased S1 at the apex, and diminished S2 at the aorta.
D. Diminished S1 at the apex and S2 at the aorta.
E. Normal heart sounds
348. ECG sign of the left ventricular hypertrophy:
A. High R at the V3, V4.
B. High R at the V1, V2.
C. High R at the V5, V6.
D. Deep S at the I lead.
E. High R at the III lead.
349. Which organs are considered target at the patients with arterial hypertension?
A. Heart, liver, lungs and brain
B. Liver, brain, kidney, eyes
C. Heart, brain, kidney, eyes, vessels
D. Heart, liver, lungs and kidney
E. Liver, brain, kidney, eyes, heart.
350. Criterions of the ІI stage of essential hypertension:
A. Episodic elevation of BP with cerebral, cardiac and general symptoms without any other
signs except high BP.
B. Permanent symptoms and signs of the target organs affecting without their failure.
C. Permanent symptoms and signs of the target organs affecting with their failure (complicated
stage)
D. Frequent hypertonic crisis.
E. Lack of effect of the medication treatment.
351. What blood pressure is corresponded to severe hypertension?
A. > 140/< 90 mm Hg.
B. 140-159/90-99 mm Hg.
C. 160-179/100-109 mm Hg.
D. ≥ 180/|≥ 110 mm Hg.
E. >160/>100 mm Hg.
352. How is color of skin changed at the patient with arterial hypertension?
A. Flush of the face and sclera.
B. Flush of the foot.
C. Flush of the stomach.
D. Flush of the back
E. Flush of the hands
353. What blood pressure is corresponded to isolated systolic hypertension?
A. > 140/< 90 mm Hg.
B. 140-159/90-99 mm Hg.
C. 160-179/100-109 mm Hg.
D. ≥ 180/|≥ 110 mm Hg.
354. How is apex bit changed at patient with prolonged arterial hypertension?
A. Heaving displaced to the right, and resistant.
B. Heaving, displaced to the left, and not resistant.
C. Heaving, displaced to the left, and resistant.
D. Not changed, normal
E. Displaced to the right and not resistant.
355. How are the heart borders displaced at patient with the 1st stage of essential
hypertension?
A. Shift to the right.
B. Shift to the left.
C. Shift to the left and up.
D. Shift to the right, left and up.
E. Not changed.
356. During auscultation of patients with hypertonic crisis you can hear:
A. Diminished S1 at the apex, and accented S2 at the aorta.
B. Loud S1 at the apex, and accented S2 at the aorta.
C. Increased S1 at the apex, and diminished S2 at the aorta.
D. Diminished S1 at the apex and S2 at the aorta.
E. Normal heart sounds
357. Which investigation is the most informative for establishing arterial hypertension?
A. Daily BP monitoring.
B. Daily EKG monitoring.
C. Coronarography.
D. Echocardiography
E. Tredmill test.
358. Criterions of the ІIІ stage of essential hypertension:
A. Episodic elevation of BP with cerebral, cardiac and general symptoms without any other
signs except high BP.
B. Permanent symptoms and signs of the target organs affecting without their failure.
C. Permanent symptoms and signs of the target organs affecting with their failure (complicated
stage)
D. Frequent hypertonic crisis.
E. Lack of effect of the medication treatment.
359. Which diseases can be accompanied with arterial hypertension?
A. Renal diseases
B. Endocrine disease
C. Coarctation of aorta.
D. Nephropathy of pregnancy
E. all mentioned above
360. EchoCG sign of the left ventricular hypertrophy:
A. Widening of the cavity of left ventricular.
B. Widening of the cavity of right ventricular.
C. Widening of the posterior wall of the left ventricle.
D. Widening of the left atrium cavity.
E. Low ejection fraction.
361. What is usual cause of Coronary artery disease?
A. Atherosclerosis.
B. Hepatitis.
C. Tonsillitis.
D. Low serum cholesterol and triglyceride levels.
E. Ulcer of stomach.
362. What are risk factors of development of Coronary artery disease?
A. Hypertension.
B. Smoking.
C. Family history.
D. Obesity.
E. All mentioned above.
363. Angina pectoris may be:
A. Stable.
B. Dangerous.
C. Strong.
D. Delicate.
E. Acute.
364. Pain can be relieved by nitroglycerine during:
A. 1 min.
B. 1-5 min.
C. 15-20 min.
D. 20-30 min.
E. 30-50 min.
365. What electrocardiography changes may show ischemia?
A. Change of T wave.
B. Change of P wave.
C. Change of Q wave.
D. Change of R wave.
E. Change of S wave.
366. Duration of pain at myocardial infarction is…
A. 1-3 min.
B. 10-20 min.
C. More then 30 min.
D. Some days.
E. During week.
367. Where are changes localized at the inferior infarction?
A. І, ІІ, AVL.
B. ІІ, ІІІ, AVF.
C. V1, V2.
D. V4.
E. V5, V6.
368. Duration of the first (acutest stage) of myocardial infarction is…
A. Some first hours – 1 day.
B. 2 day till 2 weeks.
C. Till 2-3 months.
D. Till 6 month.
E. 30-60 min.
369. How long is leukocytosis being increased?
A. Till 1-2 day.
B. Till 12-24 hours.
C. Till 2-3 day.
D. Till 5-th day.
E. Till 7-th day.
370. Duration of the third (subacute stage) of myocardial infarction is…
A. Some first hours – 1 day.
B. 2 day till 2 weeks.
C. Till 2-3 months.
D. Till 6 month.
E. 30-60 min.
371. What are risk factors of the Coronary artery disease developing?
A. High serum cholesterol and triglyceride levels.
B. Sedentary lifestyle.
C. Stress.
D. Diabetes mellitus.
E. All of enumeration.
372. Angina pectoris may be …
A. Delicate.
B. Dangerous.
C. Strong.
D. Unstable.
E. Acute.
373. Which wave is changed in the necrotic zone of myocardial infarction?
A. Change T waves.
B. Change P.
C. Change Q.
D. Change R.
E. Change S.
374. Duration of pain at the angina pectoris:
A. 1-3 min.
B. 5-20 min.
C. More then 30 min.
D. Some days.
E. During week.
375. Where are changes localized at the anterior infarction?
A. І, ІІ, AVL, V1-V3.
B. ІІ, ІІІ, AVF.
C. V1, V2.
D. V4.
E. V5, V6.
376. Duration of the second (acute stage) of myocardial infarction is…
A. Some first hours – 1 day.
B. 2 day till 2 weeks.
C. Till 2-3 months.
D. Till 6 month.
E. 30-60 min.
377. How long is leukocytosis being decreased?
A. Till 1-2 day.
B. Till 12-24 hours.
C. Till 2-3 day.
D. Till 5-th day.
E. Till 7-th day.
378. What chemical parameter is the most informative myocardial infarction marker?
A. Electrolytes.
B. Glucose.
C. Creatinine.
D. Troponine.
E. Cholesterole.
379. Duration of the forth (scarring stage) of myocardial infarction is:
A. Some first hours – 1 day.
B. 2 day till 2 weeks.
C. Till 2-3 months.
D. Till 6 month.
E. 30-60 min.
380. Acute coronary syndromes includes unstable angina and:
A. Stable angina.
B. Myocardial infarction.
C. Myocarditis.
D. Pericarditis.
E. Hypertension attack.
381. Heart failure is an ...
f) Incompetence of the heart to provide the body’s requirements at blood circulation
during rest
g) Incompetence of the heart to provide the body’s requirements at blood circulation
during rest and physical activity
h) Incompetence of the heart to provide the body’s requirements at blood circulation
during physical activity
i) Incompetence of patient to hold stable level of blood pressure and pulse rate.
j) Nothing from above
382. Which symptoms characterize RVF?
f) Nocturia, hepatomegaly, nocturnal cough.
g) Edema of the lower extremities, hepatomegaly.
h) Edema of the lower extremities, nocturnal cough
i) Dyspnea, chest pain, dry cough.
j) Nothing from above.
383. What symptom does not characterize LVF?
f) Dyspnea
g) Orthopnea
h) Cough
i) Nocturia
j) Edema of the lower extremities
384. What are percussion findings at the patients with LVF?
f) The left border of relative heart dullness drifts left
g) The right border of relative heart dullness drifts right
h) The right border of relative heart dullness drifts left
i) Nothing from above
j) Depend on clinical situation
385 What are auscultation findings at the patients with heart failure?
f) Weakened S1 and S2, S3 gallop
g) Weakened S1 and systolic murmur
h) Depend on disease which lead to heart failure
i) Accented S2 over aorta, diastolic murmur
j) Weakened both sounds
386. What BP does patient with heart failure have?
f) Systolic BP decreased, narrow pulse pressure
g) Systolic BP increased, wide pulse pressure
h) Systolic BP normal, increased diastolic BP
i) Depend on clinical situation
j) Nothing from above
387. If patient has dyspnea on ordinary activity, he has…
f) I functional class of HF
g) II functional class of HF
h) III functional class of HF
i) IV functional class of HF
j) Nothing from above
388. If less than ordinary activity causes dyspnea at the patient, he hes…
f) I functional class of HF
g) II functional class of HF
h) III functional class of HF
i) IV functional class of HF
j) Nothing from above
389. Ejection fraction is used to determinate…
f) Cause of the LVF
g) Severity of the LVF
h) Cardiothoracic ratio
i) a and b
j) Nothing from above
400. If patient has ejection fraction 44 % he has…
f) No heart failure
g) Mild LVF
h) Moderate LVF
i) Severe LVF
j) Terminal LVF
401. Which symptoms characterize LVF?
f) Nocturia, hepatomegaly, nocturnal cough.
g) Dyspnea, chest pain, dry cough.
h) Dyspnea, orthopnea, nocturnal cough.
i) Edema of the lower extremities, hepatomegaly.
j) All from above.
402. What symptom does not characterize RVF?
f) Edema of the lower extremities
g) Hydrotorax
h) Hepatomegaly
i) Ascites
j) Dry cough Dyspnea, chest pain, dry cough.
403. What diseases can lead to heart failure?
f) Arterial hypertension
g) Valvular heart disease
h) Myocardial infarction
i) Cardiomyopathies
j) All from above
404. What are percussion findings at the patients with RVF?
f) The left border of relative heart dullness drifts left
g) The right border of relative heart dullness drifts right
h) The right border of relative heart dullness drifts left
i) Nothing from above
j) Depend on clinical situation
405. What are the lung auscultation findings at the patients with heart failure?
f) Vesicular breathing, basal rales
g) Diminished vesicular breathing
h) Diminished vesicular breathing and crepitation
i) Vesicular breathing and pleural friction rub
j) Nothing from above
406. If patient has heart disease, but ordinary activity does not cause dyspnea, he has…
f) I functional class of HF
g) II functional class of HF
h) III functional class of HF
i) IV functional class of HF
j) Nothing from above
407. If patient has dyspnea at rest and all activity causes discomfort, he has…
f) I functional class of HF
g) II functional class of HF
h) III functional class of HF
i) IV functional class of HF
j) Nothing from above
408. Ecchocardiography:
f) May indicate the cause of HF
g) Can confirm the presence or absence of LV dysfunction
h) Is the less useful than chest X – ray for recognizing HF
i) a and b
j) All from above
409. If patient has ejection fraction 37 % he has…
f) No heart failure
g) Mild LVF
h) Moderate LVF
i) Severe LVF
j) Terminal LVF
410. If patient has ejection fraction 23 % he has…
f) No heart failure
g) Mild LVF
h) Moderate LVF
i) Severe LVF
j) Terminal LVF
 Topic 26
Taking history and visual inspection patients with gastrointestinal pathology.
Visual inspection and superficial palpation of the abdomen
1.Importance of the topic
Inquiring patients is the basic, informative method of examination. It is the first
interaction between the patient and doctor. If it has been done correctly, it provides
valuable information that cannot be obtained in any other way. It allows recognizing
symptoms of disease and points, in the most cases, diagnostic search on the right way.
If patient suffers from the gastrointestinal diseases he has a lot of specific and general
symptoms that must be reveal and rightly assess. It is very important part of the
diagnostic process.
Visual inspection and superficial palpation of the abdomen is the very important part
of patient examination, because they help to reveal some specific signs of
gastrointestinal diseases what required for correct care of patient.

2. Concrete aims:
─ asking about main gastrointestinal symptoms
─ refinement gastointestinal symptoms
─ taking medical history and assessment of the obtained data
─ to perform visual inspection of the abdomen and assess changes
─ to perform superficial palpation and to assess pathological changes

3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the gastrointestinal system and topographic
regions of the abdomen
Normal physiology Functions of the different gastrointestinal organs
Histology Ontogenesis, histological structure of the different
gastrointestinal organs
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Definition
dyspepsia Disorders of digestion
dysphagia Sensation of “sticking” or obstruction of the passage of food through the
mouth, pharynx, or esophagus
odynophagia Painful swallowing
heartburn Specific burning sensation behind the sternum associated with regurgitation of
gastric contents into the inferior portion of the esophagus
ascites Collecting fluid in the abdominal cavity
meteorism Collecting gas in the bowel

4.2. Theoretical questions:

64. Rules of the interviewing gastrointestinal patient.
65. Main gastrointestinal symptoms
66. What is stomach dyspepsia?
67. What is biliary dyspepsia?
 68. What is intestine dyspepsia?
69. Features of the abdominal pain, its refinement.
70. Rules for visual inspection of the abdomen, main pathological changes that can be found
using this method.
71. Rules for superficial palpation of the abdomen, main pathological changes that can be
found using this method.

4.3. Practical task that should be performed during practical training

59. Inquiring patient about gastrointestinal symptoms
60. Refinement of the gastrointestinal symptoms
61. Taking history of the gastrointestinal patient
62. Performing and assessing visual inspection of the abdomen
63. Performing and assessing superficial palpation of the abdomen

Topic content
At patients with pathology of gastrointestinal system two groups of symptoms take place:
1. Abdominal pain
2. dyspepsia (syndrome of disorder of digestion)

Abdominal pain
Mechanism of development:
1. irritation of pain receptors due to spasm of organ
2. irritation of pain receptors due to tension of organ
3. irritation of pain receptors by directly (непосредственно) a pathological process (it was
swollen, defect of shell, growth of tumor, food, gastric juice)

Refinement of pain:
 localization (shows the organ of defeat)
 communication with eating (early, late)
 character
 intensity
 duration
 irradiation
 effect from preparations

FEATURES OF DYSPEPTICAL SYNDROME depends on an organ which is staggered.

esophageal dyspepsia
 disordering of swallowing) (dysphagia)
 heartburn
 vomiting
 bleeding from the veins of gullet
Gastric dyspepsia
 disorders of appetite (decline or increase of appetite)
 nausea
 vomiting
 belch, regurgitation
 heaviness in an epigastrial region
 heartburn
Duodenal dyspepsia
  heartburn
 vomiting sour
 increase of appetite
Intestinal dyspepsia
 diarrhea
 rumbling of intestine
 motion of intestine
 flatulence, sense of the intestine
 constipation
 tenesmes (pains during defecation)
 alternation of episodes of diarrheas and constipations
Biliary dyspepsia
 bitter, dry, metalic taste in to the mouth
 alternation of diarrhea and constipation
 vomiting with a bile
 syndrome of predmestrual tension at women
Pancreatic dyspepsy
 permanent nausea
 vomiting (sometimes indomitable)
 citophobia - patients prefer not to meal, to eliminate pain
 malabsorption
 maldigestion
General visual inspection helps to find at patients with gastrointestinal diseases:
 increase of abdomen (accumulation of free liquid in an abdominal region or gas in
intestine)
 edema
 pallor (sign of anaemia)
 jaundice – yellow skin (defeat of liver)
 gain and loss in weight
Visual inspection of oral cavity
 Cavity of mouth (color, humidity, state of teeth, gums, tongs is clean, moist, dry, whith
whitish fur, the state of papillae is atrophy, hypertrophy)
 Visual inspection of the abdomen
1. form (in a volume, diminished in a volume)
2. symmetry (symmetric, asymmetric in relation to a white line)
3. participation in the act of breathing (both halves symmetric participate in the act
of breathing, lag of one half in the act of breathing from other takes place)
4. estimation of all visible changes on the front wall of stomach (growth of hairs,
scars, striae, veins, hernia, metastases, pigmentations, depigmentations)

An abdomen can be enlarged in a volume diffusely at:

 pregnancy
 obesity
 flatulence (accumulation of gases in an intestine)
 ascites (accumulation of liquid in an abdominal region)

An abdomen can be diminished in a volume diffusely at:

 loss of weight (alimentary)
 endocrine pathology
 neurotic pathology
  oncologic pathology

An abdomen can be enlarged in a volume locally at the isolated increase of organ

(hyperplasia, tumor, cyst)
A stomach can be diminished in a volume locally at:
 sclerotic processes in an abdominal region
 joints of abdominal region
 atrophy of organs
 after operative treatment (resection, amputation)
Superficial palpation of abdomen (it can be 2 types - reference and comparative)
Purpose –
 to study the painless of abdomen
 to study tone of front wall of abdomen (resistance, tension - defans)
 to study the state of front wall of abdomen (it can be swollen, accumulation of fat, hernia,
scars, metastases, hypodermic emphysema)
 to estimate the symptoms of Mendel and Schetkyn-Blyumberg
Rules of superficial palpation of abdomen
 A patient lies on a bed, the region of abdomen is free of clothes (from a processes xyfoid
sprout to pubis)
 The doctor’s hands must be warm, nails are shortly cut
 Beginning of palpation from a left inguinal region, anticlockwise direction to the right
inguinal region
 It is necessary to conduct palpation on the arc of large radius, on the arc of small radius
and comparative palpation in relation to the white line of abdomen
 A stomach is palpated on the depth of to 1 cm
 The symptom of Mendel is estimated on the symmetric regions of abdomen by the
percussion strike by one finger. It can be (+) – at appearance of pain during percussion
(the affected organ is in the area of appearance of pain). His intensity is estimated in
pluses from + (minimum degree) to ++++ (maximal degree)
 The Schetkyn-Blyumberg Symptom (symptom of irritation of peritoneum) – is
estimated on all surface of abdomen by slow immersion in an abdominal region and
sharp tearing off of fingers. In a norm it (-), in pathology it (+) is origin of abdomen-ache
at the sharp tearing off of fingers - exposes the presence of local or diffuse peritonitis.
Resistens of the front abdominal wall - it is the increase of tone, is not accompanied by pain,
is disappeared at the distraction of attention of patient, reveals the presence of the affected
organ in the place of resistance
Muscles’ tension (defans) of front abdominal wall - it is the increase of tone, hard consistency
(wooden belly), is accompanied by pain, does not disappear at the distraction of attention of
patient, reveals the presence of peritonitis

Materials for self-control (added)

7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –

Vinnytsya: NOVA KNYHA, 2006. – p. 309-338.
 Test for self-control
1. What are the gastrointestinal symptoms?
A. Chest pain, cough, dyspnea, wheezes, haemoptysis.
B. Pain in the heart region, palpitation, intermissions, oedema
C. Headache, dizziness, dysphagia, nausea, vomiting.
D. Pain in the right subcostal region, bitter taste, brown urine, skin itching, jaundice.
E. Back pain, dysuria, ishuria, eyes oedema, weakness.
2. Which symptoms appear in case of intestinal disorders?
A. Dysphagia, odynophagia, heartburn, chest pain, hematemesis
B. Nausea, vomiting, epigastric pain, hematemesis, early satiety
C. Diarrhea, constipation, abdominal swelling
D. Heaviness in the right subcostal region, nausea, bitter taste, vomiting
E..Northing from mentioned above
3. Which symptoms appear in case of esophageal disorders?
A. Dysphagia, odynophagia, heartburn, chest pain, hematemesis
B. Nausea, vomiting, epigastric pain, hematemesis, early satiety
C. Diarrhea, constipation, abdominal swelling
D. Heaviness in the right subcostal region, nausea, bitter taste, vomiting
E..Northing from mentioned above
4. Which symptoms appear in case of stomachic disorders?
A. Dysphagia, odynophagia, heartburn, chest pain, hematemesis
B. Nausea, vomiting, epigastric pain, hematemesis, early satiety
C. Diarrhea, constipation, abdominal swelling
D. Heaviness in the right subcostal region, nausea, bitter taste, vomiting
E..Northing from mentioned above
5. What are causes of organic dysphagia?
A. Cancer
B. Foreign body in esophagus
C. compression from outside by an aortic aneurism
D. Cicatricial stenosis of esophagus
E. All mentioned above.
6. What are causes of functional dysphagia?
A. Muscular spasm due to reflex disorders
B. Cancer
C. Foreign body in esophagus
D. compression from outside by an aortic aneurism
E. Cicatricial stenosis of esophagus
7. What diseases can be a cause of heartburn?
A. Gasrtroesophgeal reflux disease
B. Chronic gastritis
C Peptic ulcer diseases
D. Hiatus hernia
E. All mentioned above.
8. Which diseases are the causes of central vomiting?
A. Stroke
B. Peptic ulcer disease
C. Liver failure
D. Myocardial infarction
E. Pancreatitis
9. Which diseases are the causes of toxic vomiting?
A. Stroke
B. Peptic ulcer disease
C. Liver failure
D. Myocardial infarction
E. Pancreatitis
10. If patient has abdominal pain you should ask him about…
A. Location
B. Character
C. Connection with meal
 D. reliving factors
E. all mentioned above
11. What are visual characteristics of the obesity abdomen?
A. Oval shape, symmetrical, anterior abdominal wall take part in the breathing
B. Protuberant, abdominal wall is thick, umbilicus is sunken.
C Round shape, distention, visible peristalsis
D. Round shape, distention, does not change shape in different positions (standing, lying)
E. Protuberant, distention, changes shape in different positions (standing, lying)
12. What are visual characteristics of the normal abdomen?
A. Oval shape, symmetrical, anterior abdominal wall take part in the breathing
B. Protuberant, abdominal wall is thick, umbilicus is sunken.
C Round shape, distention, visible peristalsis
D. Round shape, distention, does not change shape in different positions (standing, lying)
E. Protuberant, distention, changes shape in different positions (standing, lying)
13. What are visual characteristics of the abdomen at the patient with meteorism?
A. Oval shape, symmetrical, anterior abdominal wall take part in the breathing
B. Protuberant, abdominal wall is thick, umbilicus is sunken.
C Round shape, distention, visible peristalsis
D. Round shape, distention, does not change shape in different positions (standing, lying)
E. Protuberant, distention, changes shape in different positions (standing, lying).
14. What are visual characteristics of the abdomen at the patient with tumor?
A. Oval shape, symmetrical, anterior abdominal wall take part in the breathing
B. Protuberant, abdominal wall is thick, umbilicus is sunken.
C Round shape, distention, visible peristalsis
D. Round shape, distention, does not change shape in different positions (standing, lying)
E. Protuberant, distention, changes shape in different positions (standing, lying).
15. What are visual characteristics of the abdomen at the patient with ascitis?
A. Oval shape, symmetrical, anterior abdominal wall take part in the breathing
B. Protuberant, abdominal wall is thick, umbilicus is sunken.
C Round shape, distention, visible peristalsis
D. Round shape, distention, does not change shape in different positions (standing, lying)
E. Protuberant, distention, changes shape in different positions (standing, lying).
16. What are visual characteristics of the abdomen at the patient with umbilical hernia?
A. Protuberant, abdominal wall is thick, umbilicus is sunken.
B Round shape, distention, visible peristalsis
C. Round shape, distention, does not change shape in different positions (standing, lying)
D. Protuberant, distention, changes shape in different positions (standing, lying).
E. Symmetrical, protruded and enlarged umbilicus, visible peristalsis in umbilicus
17. Which topographic abdominal region we use for starting superficial palpation?
A. suprapubical
B. right iliac
C. left iliac
D left inguinal
E. right hypohondrium
18. Which signs can be revealed by superficial palpation?
A. Muscular resistance
B. Abdominal tenderness
C. Involuntary rigidity of the abdominal wall.
D. Fluctuation.
E. All mentioned above
19. What are characteristics of the normal abdominal wall received by superficial palpation?
A. soft
B. painless
C. diastasis recti is absent
D. fluctuation symptom is negative
E. all mentioned above
20. The Shchetkin-Blumberg symptom indicates …
A. position of the vermiform process
B. enlarged gall bladder
 C. localization of duodenum ulcer
D. irritation of the peritoneum
E. northing from above.

Control questions
25. Rules of the interviewing gastrointestinal patient.
26. Main gastrointestinal symptoms
27. What is stomach dyspepsia?
28. What is biliary dyspepsia?
29. What is intestine dyspepsia?
30. Features of the abdominal pain, its refinement.
31. Rules for visual inspection of the abdomen, main pathological changes that can be found
using this method.
32. Rules for superficial palpation of the abdomen, main pathological changes that can be
found using this method.

Practical tasks
1. Inquiring patient about gastrointestinal symptoms
2. Refinement of the gastrointestinal symptoms
3. Taking history of the gastrointestinal patient
4. Performing and assessing visual inspection of the abdomen
5.Performing and assessing superficial palpation of the abdomen
 Topic 27
Deep, sliding, methodic palpation of the intestine parts and stomach

1.Importance of the topic

Deep palpation of the abdomen is one of the important methods of examination. It
helps to assess properties of organs of the abdominal cavity, reveal pathological
changes of them and direct to diagnostic search. Obtaining and improving practical
skills of deep palpation is need for every doctors and student who will treat patients
with internal diseases.
2. Concrete aims:
To learn rules of the deep palpation of the abdomen
─ Master deep palpation of the sigmoid and caecum
─ Master deep palpation of the ascending and descending
─ Performing and assessing position of the lower border of the stomach
─ Master deep palpation of the transverse colon and assessment its properties
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the large intestine
Normal physiology Function of the large intestine
Histology Ontogenesis, histological structure of the large intestine
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Peristaltic rumbling Deep sliding systematic palpation
Tubercular surface “Splash noise” method
Passive mobility Percussion-auscultation method

4.2. Theoretical questions:

1. Name the sequence of deep palpation of abdomen?
2. Name the basic rules of deep palpation of abdomen?
3. What purpose of conducting of deep palpation of abdomen?
4. What characteristics are been by sigmoid in a norm?
5. What pathological states can normal properties of sigmoid change at?
6. Where is the low border of stomach situated in a norm?
7. What pathological states can displace the low border of stomach downward?
8. What methods of determination of position of lower border of stomach do you know?

4.3. Practical task that should be performed during practical training

64. Palpation and assessing properties of the sigmoid
65. Palpation and assessing properties of the caecum
66. Palpation and assessing properties of the ascending colon
67. Palpation and assessing properties of the descending colon
68. To find lower border of the stomach
69. Palpation and assessing properties of the transverse colon

Topic content
 Deep sliding systematic palpation of the abdomen according to Obraztsov and
Strazhesko
Deep palpation can give you full information about the condition of the abdominal cavity and
its organs, as well as their topography. It’s named DEEP because palpation of organs to the back
surface of abdominal region, SLIDING – at palpation the doctor’s fingers slide on an organ or
organ under fingers, SYSTEMATIC (METHODICAL) –palpation performed with a same method
from 4 stages:
1. Setting of fingers
2. Formation of fold
3. Immersion in an abdominal region
4. Sliding
TOPOGRAPHICAL – we palpate for the topographies of organs, which are most often affecting
1. Sygmoid (is palpated in 90-100% patients), it is the most affected
2. Caecum (is palpated in 90-80% patients
3. Ascending colon (is palpated in 80-70% patients)
4. Descending colon (is palpated in 70-60% patients)
5. Stomach (large curvature) (is palpated in 50-60% patients)
6. Transverse colon (is palpated in 50% patient)
7. Liver (50%)
8. Spleen
9. Pancreas (1-2%)
10. Kedneys
PURPOSE – to define…
 Is organ palpated or not?
 Where is organ palpated?
 Form
 Sickliness (painless)
 Consistency (closeness)
 Mobility
 State of surface
 Rumbling for an intestine
SIGMOID.
Properties in a norm –
 Is palpated at 90-100% of patients
 In a left iliac region
 As a cylinder wideness 2-3 cm
 Unpainful
 Mobile 2-3 cm
 Surface smooth
 Consistency is densely-elastic
 Does not rumble
It is affected at:
 Sigmoiditis
 Cancer
 Dysentery
 Shigellosis
 Unspecific ulcerous colitis
 Specific granulematosis colitis (illness of Crohn’s)
 Dolychosigmoid (anomaly of development)
  Megacolon (anomaly of development)
CAECUM
Properties in a norm –
 Is palpated at 80-90% of patients
 In a right iliac region
 As a cylinder wideness 2-3 cm
 painfulness or sensible at palpation
 Mobile 2-3-4 cm
 Surface smooth
 Consistency is softly-elastic
 Rumbles (poorly)
It is affected at:
 Typhus, paratyphoid
 Salmonellosis
 Tuberculosis of intestine
 Irritable bowel syndrome (disorders of function, related to disorders of vegetative
innervation)
 Cancer
 Unspecific ulcerous colitis (proksymal form)
 illness of Crohn’s (proximal form)
ASCENDING COLON
Properties in a norm –
 Is palpated at 70-80% of patients
 In the right lateral region of abdomen
 As a cylinder wideness 2-3 cm
 Unpainful or sensible at palpation
 Immobile
 Surface smooth
 Consistency is softly-elastic
 Rumbles (poorly)
It is affected at:
 Typhus, paratyphoid
 Salmonellosis
 Tuberculosis of intestine
 Irritable bowel syndrome (disorders of function, related to disordering of vegetative
innervation)
 Cancer
 Unspecific ulcerous colitis (proksymal form)
 illness of Crohn’s (proximal form)
DESCENDING COLON
Properties in a norm –
 Is palpated at 60-70% of patients
 In the left lateral region of abdomen
 As a cylinder wideness 2-3 cm
 painfulness
 Immobile
 Surface is smooth
 Consistency is densely-elastic
 Does not rumble
It is affected at:
 Sigmoiditis
 Cancer
 Dysentery
 Shigellosis
 Unspecific ulcerous colitis
 Specific granulematosis colitis (illness of Crohn’s)
 Dolychosigmoid (anomaly of development)
 Megacolon (anomaly of development)
TRANSVERSE COLON
Properties in a norm –
 Is palpated at 50% of patients
 In overhead part of abdomen, 2 cm lower than positions of large curvature of stomach
of patient
 As a cylinder wideness 2-3 cm
 painfulness
 Mobile 2-3 cm
 Surface smooth
 Consistency is densely-elastic
 Does not rumble
It is affected at:
 Cancer
 Unspecific ulcerous colitis
 Specific granulematosis colitis (illness of Crohn’s)
 Tuberculosis of intestine
 Megacolon (anomaly of development)
 Irritable bowel syndrome (disorders of function, related to disorders of vegetative
innervation)
METHODS OF DETERMINATION OF STATUTE OF LOW BOUND OF STOMACH
1. Percussion method (above a stomach the percussion sound is low timpanic sound,
above an intestine is high timpanic sound. The place of transition of low timpanic sound
in high timpanic – is the the position of the lower boder of stomach)
2. Palpation method – the narrow cylinder is palpated in the place which was
determinated by percussion
3. Percussion-auscultation method (Doctor puts the phonendoscope on the epigastric
region nearer to the left costal arc, and performs easy percussion strike from a xifoid
process on the white line of abdomen downward . Above a stomach sounds in
phonendoscope are audible. In area of lower than border of stomach sounds disappear)
4. Percussion-palpation method (“splash noise”) - patient must drink at 300-400 ml
liquids on an empty stomach, a doctor puts a left hand in a low part of sternum, by a
right hand executes motions (shoves) – “sucussio”. Above a stomach the « splash noise
» is heard, at the level of large curvature the « splash noise» disappears.
In a norm the lower border of stomach is located at men – on 3-4 cm higher than umbilicus, at
women – on 1-2 cm higher than umbilicus.
There can be displacement of lower border of stomach downward in pathology:
 At gastroptosis (prolapsus of stomach)
 At expansion of stomach (ecstasy)
 At decompensated stenosis of pylorus
 Materials for self-control (added)

7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –

Vinnytsya: NOVA KNYHA, 2006. – p. 338-342.
 Test for self-control

Control questions
1. Name the sequence of deep palpation of abdomen?
2. Name the basic rules of deep palpation of abdomen?
3. What purpose of conducting of deep palpation of abdomen?
4. What characteristics are been by sigmoid in a norm?
5. What pathological states can normal properties of sigmoid change at?
6. Where is the low border of stomach situated in a norm?
7. What pathological states can displace the low border of stomach downward?
8. What methods of determination of position of lower border of stomach do you know?

Practical tasks
70. Palpation and assessing properties of the sigmoid
71. Palpation and assessing properties of the caecum
72. Palpation and assessing properties of the ascending colon
73. Palpation and assessing properties of the descending colon
74. To find lower border of the stomach
75. Palpation and assessing properties of the transverse colon
 TOPIC 28
Deep, sliding, methodic palpation of the of the liver, spleen, and pancreas

1.Importance of the topic

Deep palpation of the abdomen is one of the important methods of examination. It
helps to assess properties of organs of the abdominal cavity, reveal pathological
changes of them and direct to diagnostic search. Obtaining and improving practical
skills of deep palpation is need for every doctors and student who will treat patients
with internal diseases.
2. Concrete aims:
To learn rules of the deep palpation of the abdomen
─ Master percussion and deep palpation of the liver
─ Master deep palpation of the spleen
─ Performing and assessing position of the points and zones of the pancreas affecting
─ Master deep palpation of the pancreas
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the liver, spleen, pancreas
Normal physiology Function of the liver, spleen, pancreas
Histology Ontogenesis, histological structure of the liver, spleen, pancreas
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
hepatomegaly DeGarden point
splenomrgaly Gubergrits point
hepatoptosis Meyo-Robson point

4.2. Theoretical questions:

9. Rules to percussion of the liver according to M.G. Kurlov
10. Normal sizes of the liver.
11. Palpation of the lower edge of liver.
12. Characteristics of the lower edge of liver in a norm and changes in pathology.
13. Rules to palpation of the spleen, assessing in a norm and changes in pathology.
14. Characteristics of points and zones that reflect affecting of different parts of pancreas.
15. Rules to palpation of the pancreas.

4.3. Practical task that should be performed during practical training

76. Percussion and assessing the liver by M.G. Kurlov
77. Palpation and assessing properties of the lower edge of liver
78. Palpation and assessing properties of the spleen
79. Palpation and assessing points and zones that reflect affecting of different parts of pancreas

Topic content
Basic rules of palpation of liver
 The lower edge of liver is palpated only
 The edge of liver is palpated on all topographical lines
  At the beginning of palpation the lower border of liver is determined by the method
of percussion
 A liver is palpated in 4 stages:
1. Setting of fingers
2. Formation of fold
3. Immersion in an abdominal region in the expiration (right subcostal region)
4. Sliding in the inspiration (the edge of liver moves under fingers)
Properties of normal edge of liver
 Can palpated at 50% of healthy patients
 Even
 Thin
 Smooth
 Elastic (softly-elastic)
 Painless
 Mobile (easily moves under fingers at palpation)
Edge of liver at hepatitis
 A liver is enlarged, is palpated always
 Sharp
 Uneven
 Smooth
 Sickly, painful
 Dense
 Immobile
Edge of liver at congestive liver
 A liver is enlarged, is palpated always
 Round
 Even
 Smooth
 Sickly
 Dense
 Immobile
Edge of liver at cirrhosis
 A liver is enlarged, is palpated always
 Sharp
 Uneven
 Surface uneven
 Painless
 Dense
 Immobile
Edge of liver at the cancer
 A liver is enlarged, is palpated always
 Uneven
 A surface is uneven
 Sharp sickly
 Dense (like stone)
 Immobile
Reasons of hepatomegaly
 Disorders of blood circulation, lymph and bile
 1. constructive pericarditis
2. insufficiency of the right heart
3. biliry cirrhosis of liver
 Development of connective tissue (fibrosis and cirrhosis of liver)
 Inflammatory infiltration of liver (hepatitis)
 Granulematosis of liver (tuberculosis, Syphilis, lymphogranulematosis, sarcoidosis)
 Illnesses of metabolic disturbance (diabetes, amyloidosis)
 Abscesses of liver
 hepatic hydatid (cyst)
 Cancer of liver
 Chronic myeloid and lymphoid leukemia
Basic rules of palpation of spleen
 A patient must lie on the right side, a right leg must be bended, left - is line
 1-2 cm lower than level of middle of left costal arc we execute palpation of spleen in 4
stages
Estimate:
 Is palpated or not?
 Where is it palpated?
 Degree of increase of spleen (how many cm comes forward from under a costal arc)
 Form
 density
 Relief of surface (smoothness, unevenness)
 Mobility
 Sickliness
In a norm a spleen isn’t palpated, not enlarged, region of its palpation is painfulness.
There can be 2 degrees of increasing spleen in pathology (splenomegaly):
1. moderate (the edge of spleen comes forward to 2-8 cm from under a left costal arc)
2. expressed (the edge of spleen comes forward more than on 8 cm from under a left
costal arc)
Reasons of moderate splenomegaly:
1. Infectious diseases (typhus - an abdominal, recurrent, rash, paratyphoid, malaria, sepsis,
syphilis, tuberculosis)
2. Infarction of spleen due to septic endocarditis
3. Illnesses of the system of blood (В-12-deficies-anaemia, gemolitic anaemias,
poltcitaemia, lymphogranulematosis, acute leukemia, chronic lymph leucosis)
4. Hepatolienal syndrome at a liver cirrhosis and portal hypertention
Reasons of expressed splenomegalyy:
1. Chronic myeloleukois
2. Amyloidosis of spleen
3. The Goshe Illness
4. leishmaniasis
5. Chronic malaria
6. Thrombosis of splenic vein
7. Cysts of spleen (echinococcosis)
8. Cancer of spleen
9. Abscesses of spleen
PALPATION OF PANCREAS
It can be superficial or deep. At the beginning – superficial (reference) palpation must be done.
Thus on the front wall of abdomen we must perform the palpation the next structure:
  The Shoffar zone (region of localization of 4 organs – duodenum, head of pancreas,
pylorus, vesica fellia) is a triangle which is formed by the white line of abdomen, by a
right costal arc and bisector of right direct corner
 The Gubergryts-Skulskiy zone (a symmetric region on the left is the triangle formed by
the white line of stomach, by a left costal arc and bisector of left direct corner) - it is the
region of localization of pancreas body.
 The DeGarden Point – in the Shoffar zone, on 5-6 cm from a umbilicus on the line
conducted from a umbilicus to the right subaxillar region
 The Gubergryts Point - in the Gubergyts-Skulskiy zone, on 5-6 cm from a umbilicus on
the line conducted from a umbilicus to the left subaxillar region
 Front Meyo-Robson Point – on 1 sm the middles of left costal arc are below
(projection of tail of pancreas at the front surface)
 Back Meyo-Robson Point – in a left costal-vertebral corner (place of fixing of a 12 left
rib to the spine (projection of tail of pancreas at the back surface)
At the revealing of sickliness or increase of tone in these anatomic places – deep palpation of
pancreas in 4 stages is executed.
1. Setting of fingers in the place of projection of pancreas (a pancreas is located in
the place of localization of low border of stomach). Therefore, at the beginning
it is necessary to define position of large curvature of stomach and set fingers in
this place
2. Formation of fold
3. Immersion in an abdominal region
4. Sliding on an organ
In a norm a pancreas isn’t palpated, not enlarged, place of its projection painfulness
In pathology a pancreas can be enlarged and can be palpated, if
1. it is enlarged in sizes (cysts, tumor, hyperplasia)
2. it is become more the dense due to fibrosis, sclerosis, pancreatitis
Estimate:
localisation
sizes (length, width) – megascopic, not megascopic
closeness
state of surface (smooth, uneven)
sickliness
pulsation
presence of by volumes additional structures (cyst, tumour)
a pancreas is always immobile

Materials for self-control (added)

7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –

Vinnytsya: NOVA KNYHA, 2006. – p. 338-342.

Lecturer Konstantinovich T.V., Professor assistant Demchuk H.V.

 Test for self-control
1. At palpation the normal properties of lower edge of liver are
1. Thin
2. Even
3. Smooth
4. Painless
5. All answers are correct
6. All answers are wrong
2. At palpation the lower edge of liver at congestion in the greater circulation becomes
1. Even
2. Thick
3. Painfull
4. Smooth
5. All answers are correct
6. All answers are wrong
3. At palpation of lower edge of liver at hepatitis determines
1. Even
2. Sharp
3. Painfull
4. Dense
5. All answers are wrong
6. All answers are correct
4. At palpation of low edge of liver at the cirrhosis of liver determines
1. Uneven
2. Painless
3. Dense
4. Immobile
5. All answers are correct
6. All answers are wrong
5. At palpation of lower edge of liver it is possible to define at the cirrhosis of liver
1. Sharp edge
2. Round edge
3. Uneven edge
4. Flat edge
5. All answers are correct
6. Depends on a clinical situation
6. What size has a liver on a right midclavicular line in a norm
1. 10-12 sm
2. 9-11 sm
3. 8-10 sm
4. 7-9 sm
5. 11-13 sm
7. What is the left oblique size of liver in a norm
1. 10-12 sm
2. 9-11 sm
3. 8-10 sm
4. 7-9 sm
5. 11-13 sm
8. Reasons which can cause the displacement of low border of liver downwards are
1. Hypertrophy cirrhosis of liver
2. Atrophy cirrhosis of liver
3. Atelectasis of lung
4. Resection of lung
5. High standing of diaphragm
9. Write the normal sizes of absolute dullness of liver on Kurlov in sm
1. On a right midclavicular line –
2. On a anterior middle line –
3. Left oblique size –
10. Name reasons which can cause splenomegaly
1. Malaria
2. Leucosis
3. Cirrhosis of liver
4. Thrombosis of splenic vein
5. Sepsis
6. All answers are correct
7. All answers are wrong
11. At palpation the normal properties of lower edge of liver are
1. Round
2. Dense
3. Uneven
4. Painfull
5. All answers are correct
6. All answers are wrong
12. At palpation the lower edge of liver at congestion in the greater circulation becomes
1. Sharp
2. Uneven
3. Painless
4. All answers are correct
5. All answers are wrong
13. At palpation of lower edge of liver at hepatitis doesn’t determine
1. Soft edge
2. Painfull edge
3. Uneven edge
4. Immobile edge
5. All answers are correct
14. At palpation of lower edge of liver at the cirrhosis determines
1. Even
2. Soft
3. Painless
4. Mobile
5. All answers are correct
6. All answers are wrong
15. At the cancer of liver the lower edge of liver becomes
1. Uneven
2. “Stone” density
3. Painfull
4. Immobile
5. All answers are wrong
6. Depends on a clinical situation
16. What size has a liver on a anterior middle line in a norm
1. 10-12 sm
2. 9-11 sm
3. 8-10 sm
4. 7-9 sm
5. 11-13 sm
17. Next reasons can cause veritable hepatomegaly
1. Fybrosis of liver
2. Cirrhosis of liver
3. Abscess of liver
4. Cancer of liver
5. All answers are correct
6. All answers are wrong
18. Displacement of low border of liver upwards can be at
1. Atrophy cirrhosis of liver
2. Ascites
3. Flatulence
4. To hernia of white line of abdomen
5. All answers are correct
19. In a norm during palpation of spleen
1. The spleen is palpated about 2 sm below than left costal arc
2. A spleen is palpated about 1 sm below than left costal arc
3. A spleen is not palpated
4. A spleen is palpated about 0,5 sm. below than left costal arc
5. Depends on a clinical situation
20. Pancreas in a norm
1. Is palpated at men
2. Is palpated at women
3. Is palpated at children
4. Is not palpated
5. All answers are correct
6. All answers are wrong
Control questions
1. Rules to percussion of the liver according to M.G. Kurlov
2. Normal sizes of the liver.
3. Palpation of the lower edge of liver.
4. Characteristics of the lower edge of liver in a norm and changes in pathology.
5. Rules to palpation of the spleen, assessing in a norm and changes in pathology.
6. Characteristics of points and zones that reflect affecting of different parts of
pancreas.
7. Rules to palpation of the pancreas.

Practical tasks
1. Percussion and assessing the liver by M.G. Kurlov
2. Palpation and assessing properties of the lower edge of liver
3. Palpation and assessing properties of the spleen
4. Palpation and assessing points and zones that reflect affecting of different parts of
pancreas
 TOPIC 29
Clinic, instrumental and laboratory examinations of the patients with chronic
gastritis, stomach, and duodenum ulcers. Basic symptoms and syndromes .
9. Importance of the topic
Modern instrumental investigations of the gastrointestinal system play very important role
in diagnostic process today. These methods allow revealing and establishing different severe
and difficult in diagnostics stomach, intestine, liver and pancreas diseases. They help to assess
severity of diseases, property of their treatment and correct therapy in time. Thanks to using
instrumental investigations, medical care gastrointestinal patients have become more qualified.
10. Concrete aims:
-to study main principles and methods of the abdominal sonography
-to learn the most important ultrasonographic parameters of the lever, gallbladder,
spleen and pancreas
-to study main principles of pH-metry, gastric intubation
- to study main principles of duodenal intubation, bile examination
- to study main principles of fibrogastroscopy, colonoscopy
- to learn main biochemical tests of blood, feces, gastric juice, its diagnostic value

Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the gastrointestinal system
Normal physiology Functions of the different gastrointestinal organs
Histology Histological structure of the different gastrointestinal organs
Biochemistry Principles of different products metabolism

4. Task for self-depending preparation to practical training

4.1. List of the main terms that should know student preparing practical training

echocardiography End diastolic diameter Daily ECG monitoring

Doppler principles End systolic diameter Daily BP monitoring
End diastolic volume Stroke volume Coronorography
End systolic volume Ejection fraction Treadmill

4.2. Theoretical questions:

18. What is abdominal sonography, its main principles?
19. The normal value of the main ultrasonographic parameters of the lever,
gallbladder, spleen and pancreas? Their diagnostic value.
20. What are main principles of of pH-metry, gastric intubation?
21. What are main principles of duodenal intubation, bile examination? Its diagnostic
importance.
22. What purpose do we use daily blood pressure monitoring with? Its diagnostic
importance.
23. What are main principles of fibrogastroscopy, colonoscopy? Their diagnostic
importance.
24. What are main biochemical tests of blood, feces, gastric juice? Their diagnostic
value
4.3. Practical task that should be performed during practical training
1. Assessing abdominal ultrasonographic conclusion
2. Assessing results of biochemical tests of blood, feces, gastric juice, bile
3. Assessing results of pH-metry, fibrogastroscopy, colonoscopy
Topic content
Ultrasound examination (ultrasonography). Ultrasound examination of the liver is safe,
cheap, and accurate in experienced hands. Abscesses appear as black transonic areas surrounded
by high-intensity echoes, whilst cysts have black transonic areas surrounded by a thin echogenic
rim. Neo-plasia produces areas of discontinuity in the homogeneous pattern of the liver. Most
commonly, the echo amplitude is less than that of the surrounding liver, but some metastases,
particularly from the colon, produce high-intensity echoes. Direct ultrasonography of the liver
exposed at surgery may show lesions not visible by the normal transcutaneous technique.
Cirrhosis produces a higher amplitude of echoes than does the normal liver and a large portal
vein may be demonstrated. Colour-flow Doppler can help to differentiate hemangiomas from
other neoplasms and is invaluable in the assessment of the portal and hepatic veins. Diagnostic
biopsy of liver tumors is greatly facilitated by ultrasound control.
High-definition sector scanners provide an excellent real-time image of the gallbladder, and the
intrahepatic and extrahepatic bile ducts. The small probe can be used between the ribs and
allows scanning with the patient erect. The accuracy in detecting gallstones is similar to that of
oral cholecystography with the added advantage that the bile ducts may be examined at the
same time. Ultrasooography has replaced oral cholecystography as the method of choice for
detecting biliary tract calculi and as the initial investigation for suspected gallbladder disease. A
thickened gallbladder wall is sometimes seen in acute cholecystitis. Dilated hepatic and
common bile ducts may be identified and, if the bowel is relatively free from gas, intraductal calculi
or an enlarged head of pancreas may be identified.
Ultrasonography allows the measurement of size and the visualization of parenchyma of the
pancreas. Acute pancreatitis, neoplasms, and pseudocysts may be identified and, if a neoplasm is
diagnosed, it may be biopsied using a Chiba needle guided by ultrasound. Ultrasound is often used
to investigate epigastric masses with the advantage that other organs in the region of the pancreas
including the aorta, paraaortic lymph nodes, and adrenal glands may be seen. Peroperative
ultrasonography may identify insulinomas not identified by other techniques. Ultrasound may be
used to measure splenic size and in identifying splenic cysts.
Normal values of ultrasonic inspection of gall-bladder
Area – 10-15 sm2
Length – 7-10 sm
Width (depth) – 3-5 sm
Thickness of cystic wall - < 4 sm
Diameter of visible part of ductus choledochus - 5-7 mm
Retractive ability on introduction of irritant (magnesia, sorbit, 2 yolks) – 30% from
initial
Endoscopy
Endoscopy not only provides the ability to visualize the esophagus, stomach, duodenum, and
colon directly but also allows biopsy specimens and cytological samples to be taken.
Endoscopy is the investigation of choice for gastroduodenal disease. Gastritis (acute, chronic,
superficial, atrophic), the presence of erosions is readily recognized and biopsy specimens can be
obtained for histological diagnosis. This has become particularly important since the association
between Helicobacter pylori and gastritis and ulcer disease has been recognized. All gastric ulcers,
even if they appear benign, require biopsy and cytological brushing to exclude malignancy.
Endoscopy is also essential for symptomatic patients who have had previous gastric surgery, as the
postoperative stomach is notoriously difficult to examine radiologically.
Duodenal disease is always better assessed by endoscopy rather than by radiography,
although the endoscopist can miss duodenal ulcers if they are just behind the rim of the pylorus.
Distal duodenal biopsy specimens are being increasingly used for the diagnosis of coeliac disease.
Colonoscopy is being increasingly used for the diagnosis of colonic disease in preference to a
double-contrast barium enema.
 Visualization of the pancreatic duct by direct endoscopic cannulation should be done when
pancreatic tumors or chronic pancreatitis are suspected. This procedure, together with ultrasound or
a computerized tomographic scan and possibly a pancreatic function test, will give maximal
diagnostic information.
Endoscopic visualization of the biliary tree is now the best diagnostic procedure for stones,
tumors, and strictures of the bile duct and is the only reliable means of diagnosing primary
sclerosing cholangitis. Furthermore, it offers the therapeutic procedures of sphincterotomy,
stone withdrawal, and the insertion of stents across strictures.
Study of the gastric secretion
Study of the gastric secretion allows assessing fasting stomach function, secretory, partially
evacuatory, and also acid-secretory function of the stomach.
Fractional method
Study is done in two periods: examination of nonstimulated secretion (basal secretion), and
examination of stimulated secretion (after stimulants are given).
The amount of pure gastric juice aspirated during 1 h is called "hour strain" of secretion.
Fasting sample collecting (Normally 5-40 ml)
Basal secretion (Normally 50-100 ml) during 1 hour
Histamin or pentagastrin administration
Stimulated secretion (Normally 100-150 ml) during 1 hour
Study of the gastric content includes assessing of its physical, chemical rroperties,
and microscopic studies.
Physical study
The following physical properties are determined: amount, color, consistency, and
admixtures.
Amount Normally, after night fast the stomach contains from 5 to 40 ml, basal secretion is
from 50 to 100 ml, and stimulated secretion is from 100 to 150 ml.
Changes of the gastric contents amount are of great diagnostic significance, and allow
assess secretory and partially evacuatory function of the stomach.
Increased fasting gastric juice amount suggests constant gastric secretion
(gastrochronorrhea) in high activity of parasympathetic system, in long-standing smoking abuse,
ulcer disease, meal delay in the stomach, etc. Elevated "hour strain" of secretion usually
suggests hypersecretion or delayed evacuation from the stomach; decreased "hour strain" -
hyposecretion or accelarate evacuation.
Color. Normally, the gastric juice is colorless. In the presence of bile that may be belched
into the stomach from the duodenum the juice is yellow or green. In the presence of blood, the
gastric juice is red or more frequently brownish-black. In the presence of large amount of
unaltered scarlet blood the procedure should be finished immediately.
Consistency, Normally, gastric juice is liquid; in the presence of mucus - tenacious and it is
sometimes difficult to separate a portion from the whole mass of the juice taken.
Admixtures of bile, blood, and mucus can be present in the gastric juice. Ample mucus
may suggest gastritis; supernatant mucus originates from the airways. Presence of the
residues of food taken before indicates motor dysfunction of the stomach.
Chemical study
Study of the chemical properties allows assess acid-secreting function and include
measurement of acidity, unbound hydrochloric acid, bound hydrochloric and lactic acid.
Total acidity is summary acidity of all acidic factors of gastric contents in physiological and
pathological conditions (unbound, bound hydrochloric acid, organic acids and acid phosphates).
Total acidity level depends mainly on unbound hydrochloric acid level.
Unbound (free) hydrochloric acid is that part of acid, which are contained in the stomach in a
form of dissociated hydrogen and chlorine ions.
Bound hydrochloric acid is that part of acid, which is contained in the stomach in a form of non-
dissociated molecules, chemically bound with proteins.
Measurement of basal and stimulated gastric secretion is used in the clinical assessment of
patients with some gastrointestinal diseases. The range of values for normal subjects is extremely
broad.
Study of the gastric secretion
Fasting stomach content
Amount 5-40 ml
Total acidity Not more than 20-30 mmol/1
Unbound hydrochloric acid To 15 mmol/1
Basal secretion
Total amount collected by four portion in 1 hour after aspiration of
fasting portion 50-100 ml
Total acidity 40-60 mmol/1
Unbound hydrochloric acid 20-40 mmol/1
Bound hydrochloric acid 10-15 mmol/1
1-h total hydrochloric acid output 1.5-5.5mmol/h
1-h unbound hydrochloric acid output 1. 0-4.0 mmol/h
Histamine stimulated secretion
Total amount 100-1 50 ml
Total acidity 80-100 mmol/1
Unbound hydrochloric acid 65-85 mmol/1
Bound hydrochloric acid 10-1 5 mmol/1
1-h total hydrochloric acid output 8-14 mmol/h
1-h unbound hydrochloric acid output 6.5-12 mmol/h
Normally, fasting stomach contains usually no free hydrochloric acid. In can be present, but its
contents should not be exceed 15 mmol/1. Presence of unbound hydrochloric acid in the fasting
stomach, especially in high concentration (50-80 mmol/1) indicates duodenum ulcer or "irritated"
stomach.
Basal unbound hydrochloric acid secretion is 20-40 mmol/1, total acidity is 40-60 mmol/1
normally.
Stimulated secretion of unbound hydrochloric acid is 65-85 mmol/1, total acidity is 80-100
mmol/1 in normal subjects.
In pathology can be observed hyperacidity (in the patients with peptic ulcer, chronic gastritis
with acid hypersecretion), hypoacidity (in the patients with chronic gastritis with hyposecretion), and
unacidity or achlorhydria -complete absence of hydrochloric acid after maximum dose of stimulator
(atrophic gastritis associated with pernicious anemia, tumor).
To obtain more detailed information about gastric secretion function 1-h gastric acid output is
measured.
Gastric output is absolute amount of hydrochloric acid secreted in certain period, and is
calculated by formula or by nomogram in laboratory. Such calculations are done for each portion of
the gastric juice. Then 1-h acid output is measured.
1-h acid output is absolute amount of unbound hydrochloric acid secreted in one hour, and is
calculated by formula. 1-h basal acid output (BAO), stimulate submaximal acid output (SAO) or
stimulate maximal acid output (MAO) are measured. 1 -h acid output allows determining either HC1
concentration, and amount of secreted gastric juice; and reflects true level of unbound HC1 secretion.
1-h HC1 output more authentically than concentration reflects condition and dynamic of acid
secretion function of the stomach, especially in pathology.
Lactic acid. Gastric juice in physiological conditions contains insignificant amount of lactic acid
that practically is undeterminable. In pathology it is produced as a result of vital activity of the
lactobacillus in congested gastric contents in the absence of hydrochloric acid. In malignant tumor
lactic acid can be produced as a product of tumor cells metabolism.
Endogastric pH-metry.
This method has advantages over routine fractional study of the gastric contents. Acidity
measurement directly in the stomach is more physiological, as aspiration itself altered normal acid
secretion. Furthermore, endogastric pH-metry allows studying acidity in the separate regions of
the stomach: antrum, body, and cardia. Measurement of pH on separate levels has great
diagnostic significance, especially in chronic gastritis. Registration is done in each 15 min before
and after stimulation.
Assessing ofthepH-metry results (according to U. Linar).
Secretion pH
Fasting
Greatly acid 0.9-1.9
Medium acid 2.0-2.9
Moderate acid 3.0-4.9
Poor acid 5.0-6.9
Alkaline 7.0-8.9
Basal
Hyperacidity Less than 1.5
Normal acidity 1.6-2.0
Hypoacidity 2.1-5.9
Unacidity More than 6.0
Stimulated
Hyperacidic reaction Less than 1 .2
Normoacidic reaction 1.2-2.0
Hypoacidic reaction 2.1-3.0
Decreased reaction 3.1-5.0
Unacidic reaction 5.0 and more

Endogastric pH-metry allows obtaining more precise data concerning dynamic of gastric
secretion in basal conditions and after stimulation. It is possible to assess duration and
ending of secretion in response to stimulation.
Duodenal intubation with bile examination (6-staging chromatic duodenal intubation)
6-staging chromatic duodenal intubation is used for assessment bile secretion
1 stage is the basal secretion of bile (duration 20-25 minutes, amount 20-25 ml)
2 stage is the stage of hold-up of biliary excretion due to closed Oddi’s sphincter (duration 2-7
minutes, amount – 0 ml)
3 stage is the stage of closed Lyutkens’s and opened Oddi’s sphincter, excretion bile from bile
duct( duration – 3-6 minutes, amount 3-6 ml is portion A)
4 stage is a cystic bile, excretion bile from gall-bladder (duration 20-30 minutes, amount 30-60
ml is portion B)
5 stage is a intrahepatic bile, excretion bile from common hepatic duct, secreting during
examination in liver (duration 20-25 minutes, amount 20-25 ml is portion C)
6 stage is a remaining cystic bile, final contraction of gall bladder in 2-2,5 hours of examination
(duration – 10-15 minutes, amount 10-15 ml).
Cystic bile (portion B) examination– in a norm:
 amount 40-70 ml, time of selection 20-30 minutes
 specific gravity of bile norm value– 1016 ±1
 pH of bile– 7,3 ± 0,1
 concentration of cholesterol in a cystic bile 8,04 ± 0,72 mmol/l
 cholato-cholesterol coefficient - 29 ± 2
 concentration of bilirubin - 3,8 ± 0,38 mmol/l
 concentration of sialic acids - 130 ± 12 units
 negative C-reactive protein (norm is negative
  bile is sterile

Materials for self-control (added)

Reference source
o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. – Vinnytsya: NOVA KNYHA,
2006. – p. 347-367.
 Materials for self-control (added)
Control questions:
1. What is abdominal sonography, its main principles?
2. The normal value of the main ultrasonographic parameters of the lever,
gallbladder, spleen and pancreas? Their diagnostic value.
3. What are main principles of of pH-metry, gastric intubation?
4. What are main principles of duodenal intubation, bile examination? Its diagnostic
importance.
5. What purpose do we use daily blood pressure monitoring with? Its diagnostic
importance.
6. What are main principles of fibrogastroscopy, colonoscopy? Their diagnostic
importance.
7. What are main biochemical tests of blood, feces, gastric juice? Their diagnostic
value
Practical task that should be performed during practical training
1. Assessing abdominal ultrasonographic conclusion
2. Assessing results of biochemical tests of blood, feces, gastric juice, bile
3. Assessing results of pH-metry, fibrogastroscopy, colonoscopy.
 Topic 30
Clinic, instrumental and laboratory examinations of the patients with chronic
gastritis, stomach, and duodenum ulcers. Basic symptoms and syndromes
1.Importance of the topic
Chronic gastritis, peptic stomach and duodenum ulcers are widely spread diseases of
the gastrointestinal tract. They produce serious problems with health. Ability to
recognizing gastritis, peptic ulcers is very important for every doctor or student,
because sometimes these diseases cause emergency life-threatened complications
that should be resolved immediately, usually by sugary intervention.

2. Concrete aims:
─ To study main symptoms and signs of the chronic gastritis, stomach and
duodenum peptic ulcers
─ To learn main instrumental methods that can help to establish chronic gastritis,
stomach and duodenum peptic ulcers
─ To learn laboratory features of the gastric juice at patients with hyper- and
hyposecretion
─ To study complications of the peptic ulcer
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the stomach, duodenum, their blood supply and
innervation
Normal physiology Digestion in the stomach and duodenum
Histology Ontogenesis of the stomach and duodenum, histological
structure of them
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine gastrointestinal patients
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Hyposecretion achylia
hypersecretion achlorhydria
Computer pH-metry Bilious dyspepsia
penetration perforation

4.2. Theoretical questions:

25. Definition and classification of the chronic gastritis
26. Main syndromes of the chronic gastritis
27. Clinical presentation of the gastritis A
28. Clinical presentation of the gastritis B
29. Instrumental and laboratory methods of examination of patients with chronic gastritis
and peptic ulcers
30. Methods of the revealing H.pylori infection
31. Clinical presentation of the gastric peptic ulcer
32. Clinical presentation of the duodenum peptic ulcer
33. Complications of the peptic ulcers
 4.3. Practical task that should be performed during practical training
80. Revealing and assessment of symptoms and signs of chronic gastritis
81. Revealing and assessment of symptoms and signs of peptic ulcers
82. Revealing and assessment of instrumental and laboratory data at patients with chronic
gastritis, peptic ulcers.
Topic content
Diagnostics of chronic gastritis, peptic gastric and duodenal ulcers
Complications of peptic ulcer

Chronic gastritis is the chronic inflammatory process of mucous membrane of stomach, which
is accompanied with the changes of cellular regeneration, progressive atrophy of glandular
epithelium, disorders of secretory, motor and incretory functions of stomach.
Functions of stomach
1. Secretory
a. Synthesis of acid
b. Synthesis of pepsin
2. Motor and evacuation
3. Incretory (synthesis of prostoglandines and gastrointestinal hormones)
4. Mucus production
5. Absorption
6. Exretory

Types of chronic gastritis

 Chronic gastritis type A (autoimmune, atrophy)
 Chronic gastritis type B (bacterial)
 Chronic gastritis type C (chemical, reflux-gastritis)
 Chronic gastritis of the mixed type

Reasons of development of chronic gastritis

 Autoimmune inflammation
 Bacterial infection (H. pylori)
 Reflux of duodenal content into a stomach
 Use of medicines (steroid and nonsteroid anti-inflammatory drugs), irritating substances
(alcohol, cigarette smoke, and environmental agents).
 Pathological hypersecretion (gastrinoma, hypercalciaemia)
 Combination of the mentioned causes.

Main syndromes of chronic gastritis

1. Pain (early pain, connected with meal, in an epigastric region)
2. Gastric dyspepsia (disorders of appetite, nausea, vomiting, belch, heaviness in an
epigastric region, heartburning)
3. Intestinal dyspepsia (diarrhea, constipation depending on the type of secretion)
4. Asthenoneurotic (vegetative) – (weakness, fatigue, bad sleep, disorders of mood,
irritability, vegetative disorders)

Features of the chronic gastritis type A

 Develops more frequent at the young patients
 More frequent at men
 Affects cardial part and body of stomach
  Formation of autoantibodies to the glandular cells of stomach
 Diffuse and deep atrophy process with development of severe secretory insufficiency of
stomach (hyposecretion, hypoaciditas, anaciditas, achylia, histamine refractory
achlorhydria)
 Combination with В12- deficiency anemia
 Combination with polyposis of stomach
 Combination with other immune diseases (rheumatoid arthritis, thyroiditis, vitiligo,
connective tissue diseases)
Clinical presentation:
Pain is a dull, boring, and early with sensation of stomach overfilling and heaviness even if
patient has eaten small portion of food. Patient complains of a chronic nausea, belch with
rotten eggs odor, sometimes vomiting relieving pain and gastric heaviness, frequent diarrhea,
diminished or absent appetite. Patient loses weight and has a lot of aesthetic symptoms.
Vitamin deficiency signs (gingival hemorrhage, angular cheilosis, hyperkeratosis, nail fragility,
hear loss and smooth bright crimson tongue), pale skin are observed at visual inspection.
Superficial palpation reveals moderate painfulness at the epigastric region.
Features of chronic gastritis type B
 Develops in any age
 It can be at the persons of any sex
 The prepyloric (antrum) part of stomach is affected
 Absence of formation of autoantibidies to the gastric cells
 Related to the H. pylori infection
 The secretion of stomach is normal or increased (normosecretion, normaciditas,
hypersecretion, hyperaciditas)
 Does not combine with anemia, polyposis of stomach, immune diseases
Clinical presentation:
Pain is a boring and sometimes burning, with sensation of heaviness. Hunger pain may
be relieved by small meal. Patient complains of nausea; belch with acid odor,
heartburning, acid taste in mouth, sometimes vomiting relieving pain and gastric
heaviness, frequent constipation, increased appetite. Patient has normal or over weigh.
Superficial palpation reveals moderate painfulness at the pyloric region.

Methods of verification (confirmation) of chronic gastritis

1. General clinical (anamnesis, general visual examination, palpation, percussion,
auscultation)
2. Fibrogastroduodenoscopy (atrophy processes of mucous membrane of stomach
in different departments, polyposis of stomach)
3. Biopsy is histological and cytological research of tissue sample for confirming and
specifying gastritis type and severity. It should be taken from 5 different places
of stomach (cardia, fundus, small curve, greater curve, pylorus).
4. Methods of the H. Pylori revealing:
 Serology tests
 Histological assessment of H.pylori presentation if tissue sample
 Cytological assessment of H.pylori presentation in smear from stomach
 Cultural investigation
 Acute ureasa test (using medicine that rapidly reveals ureasa production by
H. pylori)
 Fecal antigen test
 13
С-urea breath tests
 5. Revealing of autoantibodies to the glandular cells of stomach
6. Endogastric pH-metry (in norm the pH in stomach is 1,6-2,2)
7. Fractional investigation of the gastric secretion
8. X-Ray examination of stomach

PEPTIC ULCER is inflammation of mucous membrane of gastroduodenal area with

forming of local erosive damage of mainly infectious or noninfectious origin in reply to
disorders of endogenous balance between the local agents of «aggression» and «protection».

Types of peptic ulcer –

 Peptic gastric ulcer
 Peptic duodenum ulcer

Syndromes of peptic ulcer

1. Pain
2. Dyspeptic syndrome (gastric dyspepsia, duodenal dyspepsia)
3. Intestinal dyspepsia (diarrhea, constipation, flatulence)
4. Asthenoneurotic (vegetative) syndrome
5. Syndrome of complications
 Bleeding
 Perforation
 Penetration
 Malignization
 Stenosis of pylorus

Features of peptic gastric ulcer

 Pain is related to eating, early (10 min - 1 hour), in an epigastric region, intensive,
periodic, seasonal is intensification in spring and in autumn.
 Gastric dyspepsia
 Intestinal dyspepsia (diarrhea, flatulence)
 Type of secretion – hyposecretion is more frequent, rarer – normal or hypersecretion

Features of duodenum peptic ulcer

 Pain is late after meal (1,5-2 hours), night, fasting, intensive, burning, acute, periodic,
seasonal.
 Dyspepsia of duodenal type (nausea, vomiting, belch, heartburning, bloating)
 Intestinal dyspepsia (constipations)
 Type of secretion – always hypersecretion

Methods of verification (confirmation) of peptic ulcer.

1. General clinical (anamnesis, general visual examination, palpation, percussion,

auscultation)
2. Fibrogastroduodenoscopy (ulcerative defect of mucous membrane of different parts in
stomach and duodenum, features of bleeding)
2. Biopsy (histological and cytological investigation of tissue samples from stomach or
duodenum, brash-biopsy smear)
3. Methods of the H. Pylori revealing:
 Serology tests
 Histological assessment of H.pylori presentation if tissue sample
 Cytological assessment of H.pylori presentation in smear from stomach
 Cultural investigation
 Acute ureasa test (using medicine that rapidly reveals ureasa production
by H. pylori)
 Fecal antigen test
 13С-urea breath tests
4. Endogastric pH-metry (in a norm the pH in stomach is 1,6-2,2)
5. Fractional investigation of the gastric secretion
6. X-Ray barium contrasting examination of stomach and duodenum (recess symptom)

COMPLICATIONS OF PEPTICAL ULCER

Acute Gastrointestinal Bleeding occurs due to injury of gastrointestinal vessel by ulcerative

process. Main symptoms and signs:
 Vomiting with maintenance of bright red blood or “coffee-grounds” - Haematemesis
 Melena mean black motions, often like tar (signifying altered blood, which has a
characteristic smell)
 Symptoms of collapses (palpitation, pallor, tachycardia, low blood pressure)
 Posthemorrhagic anemia

Perforation is a rapture of ulcer into abdominal cavity

 “Dagger” pain
 Forced position in a bed with feet claps to abdomen
 The Grekov’s Symptom - bradycardia in the first hour after the perforation
 Wooden belly, abdomen does not participate in breathing
 Symptoms of irritation of peritoneum (pneumoperitoneum, peritonitis)
 The Klarka’s Symptom is disappearance of hepatic dullness at percussion
 Leukocitosis
 “Sickle” symptom is air under the right cupula of diaphragm at the X-ray film of
abdomen
Penetration is a rapture of ulcer into neighboring organ (liver, gallbladder, pancreas,
transversum)
 Change of typical rhythm of pain, it becomes more gnawing.
 Pain is resistant to treatment
 Appearance of pain irradiation
 Leykotcitosis
 Specific symptoms depend on organ where ulcer penetrated.

Stenosis of Pylorus is narrowing of pylorus or beginning part of duodenum due to scarry

deformation after repeated ulcers.
 Belch with rotten eggs odor
 Vomiting, including by the food used the day before
 Weight loss
 Prolonged ulcerous anamnesis
 Visible antiperistaltics in an epigastric region
  Positive Vasylenko symptom (noise of splash at tapping the wall of abdomen near
the stomach in 7-8 hours after a meal)
 Downward displacement of the lower stomach border.

Malignization is a transformation of ulcerative defect to tumor.

Usually long-term gastric ulcer transforms. We can suppose tumor if pain has become less
intensive, but permanent, loss seasonable. Patient suddenly lost weight and appetite or
changes of taste and favour products.

Reference source
o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –
Vinnytsya: NOVA KNYHA, 2006. – p. 318-319, 327-328,341-342, 347-349,351-357.
o Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000.

Test for self-control

1. What types of the chronic gastritis do you know?
A. Autoimmune (types A).
B. Bacterial (Type B)
C. Alcohol, toxic (type T)
D. Answers A and B
E. Answers B and C
2. What types of the chronic gastritis do you know?
A. Mixed types
B. Bacterial (Type B)
C. Chemical (type C)
D. Answers A and B
E. Answers A, B and C
3. What features does pain in epigastria have at patient with chronic atrophic gastritis?
A. boring, hunger and burning, accompanied with heartburn, belch with acid odor
B. boring, dull, and early accompanied with nausea, vomiting, epigastric pain, belch with
rotten eggs odor
C. periodic, intensive, unbearable, early accompanied with abdominal swelling, diarrhea
D. periodic, intensive, night, fasting, acute accompanied with acid taste, vomiting,
constipation
E. Dagger, intensive, unbearable.
4. What features does pain in epigastria have at patient with chronic bacterial gastritis?
A. boring, hunger and burning, accompanied with heartburn, belch with acid odor
B. boring, dull, and early accompanied with nausea, vomiting, epigastric pain, belch with
rotten eggs odor
C. periodic, intensive, unbearable, early accompanied with abdominal swelling, diarrhea
D. periodic, intensive, night, fasting, acute accompanied with acid taste, vomiting
E. Dagger, intensive, unbearable.
5. What dyspeptic symptoms can be at patient with bacterial gastritis?
A. Vomiting, nausea, stomach overfilling, diarrhea.
B. Vomiting, nausea, belch with bile, diarrhea and constipation.
C. Heartburning, vomiting, nausea, acid taste, constipation
D. Vomiting, dysphagia, odynophagia, regurgitation, constipation
E. Northing from above.
6. What dyspeptic symptoms can be at patient with autoimmune gastritis?
A. Vomiting, nausea, stomach overfilling, diarrhea.
B. Vomiting, nausea, belch with bile, diarrhea and constipation.
C. Heartburning, vomiting, nausea, acid taste, constipation
D. Vomiting, dysphagia, odynophagia, regurgitation
E. Northing from above.
7. Visual inspection of a patient with autoimmune gastritis reveals …
A. Blush cheek, normal weight, good muscle developing
B. Pale skin, gingival hemorrhage, nails fragility, bright crimson tongue
C Normal skin color, normal or over weight, white tongue with hypertrophied lingual
papillas
D. Jaundice, weight loss, scratching on skin, spider naevi.
E. Pale, dry skin, bruises, rush, oedema.
8. Visual inspection of a patient with bacterial gastritis reveals …
A. Blush cheek, normal weight, good muscle developing
B. Pale skin, gingival hemorrhage, nails fragility, bright crimson tongue
C Normal skin color, normal or over weight, white tongue with hypertrophied lingual
papillas
D. Jaundice, weight loss, scratching on skin, spider naevi.
E. Pale, dry skin, bruises, rush, oedema.
9. Which investigation is the best for confirming chronic gastritis?
A. Serological with determination of autoantibodies to stomach cells
B. Cultural with obtaining H.pylori
C. Fibrogastroscopy with biopsy
D. Endogastric pH-metry
E. X-ray examination of stomach
10. The most popular and accurate examination for H.pylori revealing is…
A. Serology tests
B. Histological tests
C. Cytological tests
D. 13C-urea breath tests
E. Cultural investigation
11. Peptic ulcers have…
A. inflammatory origin
B. neoplastic origin
C anatomy abnormal origin
D. all mentioned above
E. northing from above
12. What pathogen can cause peptic ulcer?
A. H. pylori
B. Candida albicans
C Herpes zoster
D. Shigella spp.
E. All mentioned above
13. What features does pain in epigastria have at patient with Stomach Peptic Ulcer?
A. boring, hunger and burning, accompanied with heartburn, belch with acid odor
B. boring, dull, and early accompanied with nausea, vomiting, epigastric pain, belch with
rotten eggs odor
C. periodic, intensive, unbearable, early accompanied with abdominal swelling, diarrhea
D. periodic, intensive, night, fasting, acute accompanied with acid taste, vomiting,
constipation
E. Dagger, intensive, unbearable.
14. What features does pain in epigastria have at patient with duodenum peptic ulcer?
A. boring, hunger and burning, accompanied with heartburn, belch with acid odor
B. boring, dull, and early accompanied with nausea, vomiting, epigastric pain, belch with
rotten eggs odor
C. periodic, intensive, unbearable, early accompanied with abdominal swelling, diarrhea
D. periodic, intensive, night, fasting, acute accompanied with acid taste, vomiting,
constipation
E. Dagger, intensive, unbearable.
15. What syndromes are developed at patients with peptic ulcers?
A. Abdominal pain
B. Stomach dyspepsia
C Intestinal dyspepsia
D. Vegetative
E. all mentioned above
16. What method is the best for confirming peptic ulcer?
A. Fibrogastroscopy
B. X-ray examination of stomach
C. Fractional investigation of the gastric secretion
D. Endogastric pH-metry
E. All mentioned above.
17. Rapture of ulcer into neighboring organ is named…
A. perforation
B. acute gastrointestinal bleeding
C. penetration
D. malignization
E. pylorostenosis
18. Rapture of ulcer into abdominal cavity is named…
A. perforation
B. acute gastrointestinal bleeding
C. penetration
D. malignization
E. pylorostenosis
19. If patient has belch with rotten eggs odor, vomit with the food used the day before,
weight loss, prolonged ulcerous anamnesis, visible antiperistaltics in an epigastric region
he suffers from …
A. perforation
B. acute gastrointestinal bleeding
C. penetration
D. malignization
E. pylorostenosis
20. If patient has vomiting with “coffee-grounds”, melena, collapses, ulcerous anamnesis
he suffers from
A. perforation
B. acute gastrointestinal bleeding
C. penetration
D. malignization
E. pylorostenosis
Control questions:
1. Definition and classification of the chronic gastritis
2. Main syndromes of the chronic gastritis
3. Clinical presentation of the gastritis A
4. Clinical presentation of the gastritis B
5. Instrumental and laboratory methods of examination of patients with chronic gastritis
and peptic ulcers
6. Methods of the revealing H.pylori infection
7. Clinical presentation of the gastric peptic ulcer
8. Clinical presentation of the duodenum peptic ulcer
9. Complications of the peptic ulcers
Practical task
1. Revealing and assessment of symptoms and signs of chronic gastritis
2. Revealing and assessment of symptoms and signs of peptic ulcers
3. Revealing and assessment of instrumental and laboratory data at patients with chronic
gastritis, peptic ulcers.
 TOPIC 31
Diagnostics of the gall-bladder and biliary tract diseases. Clinical
presentation of the chronic cholecystitis, gallstones
1.Importance of the topic
Gall-bladder and biliary tract diseases are widely spread diseases of the
gastrointestinal tract. They produce serious problems with health. Ability to
recognizing gallstones, chronic cholecystitis and cholangitis is very important for every
doctor or student, because sometimes these diseases appear with emergency life-
threatened condition that should be resolved immediately, usually by sugary
intervention.

2. Concrete aims:
─ Study main symptoms and signs of the biliary tract diseases
─ Learn main instrumental methods that can help to establish chronic cholecystitis
and cholangitis
─ Learn laboratory features of the bile at patients with gallstones
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the biliary tract, their blood supply and innervation
Normal physiology Mechanics of bile formation and extraction
Histology Ontogenesis of the biliary tract, histological structure of the
bale ducts and gall-bladder
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine gastrointestinal patients
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Hepatic or biliary colic 6-staging chromatic duodenal intubation
Gallstones Biliary tract dyskinesia
Gall-bladder signs Bilious dyspepsia

4.2. Theoretical questions:

34. Main syndromes at biliary tract affecting
35. Data of the objective examination of the patients with biliary tract diseases
36. Provocative symptoms of the gall-bladder affecting
37. Main principles and purposes of the 6-staging chromatic duodenal intubation. It’s
diagnostic importance.
38. Instrumental and laboratory methods of examination of patients with gall-bladder and
billiary tract diseases.
39. Definition of chronic cholecystitis, its causes, main symptoms and signs.
40. Definition of the cholelitiasis, its causes, main symptoms and signs.
4.3. Practical task that should be performed during practical training
83. Revealing and assessment of symptoms and signs of chronic cholecystitis
84. Revealing and assessment of symptoms and signs of Hepatic colic
85. Revealing and assessment of instrumental and laboratory data at patients with gallstones
Topic content
Main syndromes
1. Pain syndrome (depends on the type of dyskinesia)
 Localizes in the right subcostal region, in point of projection of the bottom of
gall-bladder (the Makenzy point). It arises up after fat and fried food, in 3-5
hours later eating, irradiates into the right shoulder, under the right
subscapularic region, in the region of heart (Botkyn’ symptom or cholecysto-
cardial symptom)
 It can be the severe, sharp brief or dull aching, required emergency care
 Mechanism of pain appearence:
 increase of internal pressure in the gall-bladder,
 spasm of the gall-bladder muscles,
 expansion walls of gall-bladder,
 increasing pressure in extra- and intrahepatic and biliary channels (compression
by the stones in the area of large duodenal papilla).
2. Biliary dyspepsy - bitter taste in the mouth at mornings, vomiting with bile without relief,
intolerance of fat and fried food, regurgitation (belching) by air, nausea, heartburn.
3. Intestinal dyspepsy - related to the unstable selection of bile - alternation of diarrheas
with constipations, flatulence, abdominal swelling.
4. Syndrome of premenstrual tension at women – biliary diskinesia symptoms appear last
week before menses
5. Astheno-neurotic (vegetative) syndrome – bed mood, irritation, nervousness,
weakness, fatigue

Data of physical examination

 Jaundice -yellowish skin and mucous, tracks from scratching due to skin itch (sign of
intrahepatic holestasis, calculesis)
 Pigmentation in right subcostal region (tracks from a hot-water bottle)
 At general examination a gall-bladder is not determinated and can be visible at
examination and palpation if patient has:
1. gallstones
2. gall-bladder cancer
3. hydropsy of gall-bladder
4. empiema (abscess) of gall-bladder
5. cancer of pancreas head (the Kurvuasie’s symptom)

Provocative symptoms allow exposing pathology of gall-bladder

 the Kerr’s sign (pain at deep palpation of gall-bladder bottom)
 the Ortner’s sign (pain at percussion over the right costal arch
 the Lepene-Vasylenko’s sign (pain at percussion on the front wall of stomach on the
right parallel to the right costal arch)
 the Mussy-Georgyevskiy’s sign (frenicus) - pain at deep palpation between the legs of
right m.sternocleidomastoideus
 the Merphy’s sign (pain and breaking (stop) of inspiration during deep palpation of
projection point of the gall-bladder bottom)

Investigations:
Full blood analysis (leukocytosis, shift to the left at leukocytal formula, increasing ERS)
Duodenal intubation with bile examination (6-staging chromatic duodenal intubation)
  6-staging chromatic duodenal intubation
 1 stage is the basal secretion of bile (duration 20-25 minutes, amount 20-25 ml)
 2 stage is the stage of hold-up of biliary excretion due to closed Oddi’s sphincter
(duration 2-7 minutes, amount – 0 ml)
 3 stage is the stage of closed Lyutkens’s and opened Oddi’s sphincter, excretion bile
from bile duct( duration – 3-6 minutes, amount 3-6 ml is portion A)
 4 stage is a cystic bile, excretion bile from gal bladder (duration 20-30 minutes,
amount 30-60 ml is portion B)
 5 stage is a intrahepatic bile, excretion bile from common hepatic duct, secreting
during examination in liver (duration 20-25 minutes, amount 20-25 ml is portion C)
 6 stage is a remaining cystic bile, final contraction of gall bladder in 2-2,5 hours of
examination (duration – 10-15 minutes, amount 10-15 ml).
Ultrasound examination of the lever, bile ducts and gall bladder in a rest and after bile-expelling
breakfast.
Radiologic investigation
oPlain abdominal X-ray examination(it is possible to see stone in a gall-bladder and bile
ducts)
o Oral cholecystography - oral contrasting X-Ray examination (patient accepts the
contrasting material in pills)
o IV cholecyatography - infusion intravenous contrasting X-Ray examination (the
contrasting material is entered intravenously)
o Retrograde duodenocholecystocholangiopancreatography (a contrast is entered
through a catheter entered by fybrogastroduodenoscope)

CHRONIC CHOLECYSTITIS is the chronic inflammatory disease of gall-bladder related with

functional disorders (dyskynesia and dyscholia)

DIAGNOSTICS
 Clinical symptoms (see upper)
 positive provocative symptoms of palpation (6 symptoms mentioned above)
Duodenal intubation - the change of time and amount of 4 stages of cystic bile (portion B) – in
a norm: amount 40-70 ml, time of selection 20-30 minutes.
1. decline of specific gravity of bile (norm value– 1016 ±1)
2. change of pH of bile into sour reaction (norm value – 7,3 ± 0,1)
3. decline of maintenance of bile acids in a cystic bile
4. increase of concentration of cholesterol in a cystic bile (norm value 8,04 ± 0,72
mmol/l)
5. decline of cholato-cholesterol coefficient (norm value - 29 ± 2)
6. increase of concentration of bilirubin (norm value 3,8 ± 0,38 mmol/l)
7. increase of concentration of sialic acids (norm value 130 ± 12 units)
8. determination of the C-reactive protein (norm is negative)
9. (+) bacteriological culture of cystic bile (in a norm a bile is sterile)
Results of ultrasound examination:
1. increasing thickness of gall-bladder wall more than 4 mm (< 4 mm in a norm)
2. (+) sonografic Merphy’s sign
3. increasing gall-bladder sizes more than 5 sm is higher than upper boder of norm
for this age
4. presence of shade from the gall-bladder walls
presence of paravisceral echo-negative shade (exudate)
 Gall-Stone Disease or Cholelithiasis

Risk factors is “sign of 5 “F” – Female, Forty age, Fertile, Fat (obesity) Fair (complexion)

Reasons of development
 infection
 stagnation of bile in a gall-bladder
 anomalies of development
 features of food
 heredity
 adynamy, decreased physical activity

A main pathological sign is forming of stones in the gall bladder (calcium, cholesterol, bilirubin,
mixed)
Stones can be silent (if they are located in a body and bottom of gall bladder) and active (if they
are located in the bladder neck and ducts).
The clinical signs appear only if stones become active. A main symptom (syndrome) is a hepatic
(biliary) colic.

Symptoms and signs of biliary colic:

 intensive increased pain in right subcostal region, with a tendency to distribution
 a reason of appearing - use of fat, fried food, alcohol, after physical exercise, jolting
jorney
 the pain is appeared in 3-4 hours after eating (more frequent in a night-time)
 irradiation – upwards, in a right shoulder, in a right clavicula, in a right subscapular
region, sometimes – in the region of heart (the Botkin’s symptom) lake as angina
pectoris
 vomiting with bile does not relief patient’s condition
 fever, chill, trembling, anxiety,
 vegetative storm (diarrhea, constipation, swelling of stomach)
 Jaundice
Investigation of gallstones:
1. Ultrasonography reflects stones in the gall bladder with 96% accuracy.
2. Endoscopic retrograde cholangiopancreatography
3. Plain abdominal X-ray identify calcified but not cholesterol stones with 15% accuracy.
4. Oral cholecystography shows stones in the gallbladder and biliary duct obstruction.
7. Reference source

o Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000 – P.197-200.

 Test for self-control
1. The pain due to gall-bladder and biliary ducts diseases appear after meal in:
p. ½ -1 hours;
q. 1-2 hours;
r. 7-8 hours;
s. 3-4 hours;
t. 2-6 hours.
2. What kinds of foods can cause the pain due to biliary disorders?
p. Milk porridge
q. Fried potatoes
r. Boiled vegetables
s. Boiled fish
t. Apple pie
3. Where does the pain radiate due to biliary disorders?
p. Umbilicus region
q. Epigastric region
r. Left subcostal region
s. Right subscapularic region
t. Pubic region
4. If pain in the heart region appears at patient with biliary tract disorder it names …
k. Angina pectoris
l. Vegetative cardialgia
m. Cholecystocardil symptom
n. Stomach cardialgia
o. Northing from above
5. What syndromes may be at patient with biliary tract disorders?
p. Pain syndrome
q. Asthenovegitative symdromes
r. Biliary dyspepsia
s. Syndrome of premenstrual tension
t. All mentioned above
6. What syndromes cannot be at patient with biliary tract disorders?
a. Pain syndrome
b. Asthenovegitative symdromes
c. Nephrotic syndrome
d. Syndrome of premenstrual tension
e. Biliary dyspepsia
7. What symptoms characterize biliary dyspepsia?
a. Dysphagia, odynophagia, heartburn, hematemesis
b. Nausea, vomiting, hematemesis, early satiety
c. Diarrhea, constipation, abdominal swelling
d. Heaviness in the right subcostal region, nausea, bitter taste, vomiting
e. Northing from mentioned above
8. What symptoms characterize intestinal dyspepsia?
a. Dysphagia, odynophagia, heartburn, hematemesis
b. Nausea, vomiting, hematemesis, early satiety
c. Diarrhea, constipation, abdominal swelling
d. Heaviness in the right subcostal region, nausea, bitter taste, vomiting
e. E.Northing from mentioned above
 9. If patient has biliary tract or gall-bladder disease during visual inspection you can
find…
p. Weight loss, pale skin;
q. Yellowish skin and mucous, tracks from scratching due to skin itch;
r. Hyperemia of abdomen and chest, overweight;
s. Diffuse cyanosis, visible peristaltic;
t. Northing from mentioned above
10. If patient has biliary tract or gall-bladder disease during visual inspection you can
find…
a. Anasarca, pale skin, swelled abdomen;
b. Pigmentation in right subcostal region (tracks from a hot-water bottle);
c. Hyperemia of abdomen and chest, overweight;
d.Diffuse cyanosis, visible peristaltic;
e.All mentioned above
11. When may gall-bladder be palpated?
a. Gallstones
b. gall-bladder cancer
c. hydropsy, empiema (abscess) of gall-bladder
d. cancer of pancreas head (the Kurvuasie’s symptom)
e. all mentioned above
12. When cannot gall-bladder be palpated?
a. Gallstones
b. gall-bladder cancer
c. in a norm
d. hydropsy, empiema (abscess) of gall-bladder
cancer of pancreas head (the Kurvuasie’s symptom)
13. What provocative sign named Merphys?
k. pain at deep palpation of gall-bladder bottom
l. pain at deep palpation between the legs of right m.sternocleidomastoideus
m. pain and breaking inspiration during deep palpation of projection point of the
gall-bladder bottom
n. pain at percussion over the right costal arch
o. pain at percussion on the front wall of abdomen on the right parallel to the
right costal arch
14. What provocative sign named Ortner’s?
a. pain at deep palpation of gall-bladder bottom
b. pain at deep palpation between the legs of right m.sternocleidomastoideus
c. pain and breaking inspiration during deep palpation of projection point of the gall-
bladder bottom
d. pain at percussion over the right costal arch
e. pain at percussion on the front wall of abdomen on the right parallel to the right costal
arch
15. Duodenal intubation is used for …
k. assessment shape and size of the gall-bladder
l. Function of the gall-bladder and biliary tract
m. Disintoxication function of the liver
n. Assessment shape and size of the biliary tract
o. All mentioned above
16. The cystic bile during duodenal intubation is received at …
a. the 1 stage
b. the 3 stage
c. the 2 stage
d. the 5 stage
e. the 4 stage
17. Ultrasound examination of the abdomen is used for …
a. assessment shape and size of the gall-bladder
b. Function of the gall-bladder and biliary tract
c. Assessment structure, shape and size of the liver
d. Assessment shape and size of the biliary tract
e. All mentioned above
18. If patient has cholecystitis what changes if his bile may be found?
a. specific gravity of bile is 1016
b. pH of bile is 7,3
c. C-reactive protein
d. Bilirubin is 3,5 mmol/l
e. cholato-cholesterol coefficient 27

19. Ultrasound signs of chronic cholecystitis are…

a. increasing thickness of gall-bladder wall more than 4 mm
b. (+) sonografic Merphy’s sign
c. increasing gall-bladder sizes more than 5 cm is higher than upper boder of norm
d. presence of shade from the gall-bladder walls
e. all mentioned above
20. What investigation is the most accurate for revealing gallstones?
a. Ultrasonography of the gall bladder and the liver
b. Endoscopic retrograde cholangiopancreatography
c. Plain abdominal X-ray
d. Oral cholecystography shows stones in the gallbladder and biliary duct obstruction
e. All mentioned above

Control questions:
1. Main syndromes at biliary tract affecting
2. Data of the objective examination of the patients with biliary tract diseases
3. Provocative symptoms of the gall-bladder affecting
4. Main principles and purposes of the 6-staging chromatic duodenal intubation. It’s
diagnostic importance.
5. Instrumental and laboratory methods of examination of patients with gall-bladder and
billiary tract diseases.
6. Definition of chronic cholecystitis, its causes, main symptoms and signs.
7. Definition of the cholelitiasis, its causes, main symptoms and signs.
Practical task that should be performed during practical training
1. Revealing and assessment of symptoms and signs of chronic cholecystitis
2. Revealing and assessment of symptoms and signs of Hepatic colic
3. Revealing and assessment of instrumental and laboratory data at patients with
gallstones
 TOPIC 32
Main symptoms and syndromes at the liver diseases: jaundice, cytolysis and
mesenchymal inflammation
5. Importance of the topic
Liver diseases usually are very dangerous and severe conditions. They gradually
destroyed liver with loss its function and development of the liver cirrhosis.
Knowledge about causes, mechanism, symptoms and signs of the jaundice,
hepatocytes cytolysis and inflammation is very important for physicians of every
specialty, because liver pathology influence on the course and treatment of majority
of the human diseases.

2. Concrete aims:
─ To study, types, causes, main symptoms and signs of jaundice
─ To study, causes, degrees, main symptoms and signs of hepatocytes cytolysis
─ To study, causes, main symptoms and signs of mesenchymal inflamation
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the liver and biliary tract, their blood supply and
innervation
Normal physiology Liver functions in the metabolism
Histology Ontogenesis and histological structure of the liver and biliary
tract
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine gastrointestinal patients
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Pre-hepatic jaundicec cytolysis
Hepatocellular jaundice cholestasis
Cholestatic (obstructive) jandice Immunoinflammatory syndrome

4.2. Theoretical questions:

41. Main liver functions
42. Jaundice classification
43. Causes, symptoms and signs of the pre-hepatic jaundice
44. Causes, symptoms and signs of the hepatocellular jaundice
45. Causes, symptoms and signs of the cholestatic jaundice
46. Definition, causes, signs and degrees of cytolysis syndrome
47. Definition, causes and signs of immunoinflammatory syndrome
4.3. Practical task that should be performed during practical training
86. Revealing and assessment of symptoms and signs of jaundice
87. Revealing and assessment of signs and level of cytolysis syndrome
88. Revealing and assessment of signs of immunoinflammatory syndrome
Topic content
Liver functions
Liver takes part in different metabolism systems of the body.
 Pigment metabolism
Liver maintains normal level of bilirubin in blood:
Total bilirubin - 8.5-20.5 mkmol/l,
Conjugated bilirubin - 2.2-5.1 mkmol/l,
unconjugated bilirubin - 6.3-15.4 mkmol/l.
Protein metabolism
Liver maintains normal level of total protein and its fraction in the blood serum. Normally,
the total protein content in the blood serum is 70-90 g/l. Total protein consists of three
fractions: albumins, globulins and fibrinogen. Total protein contains 55.5-65.5 % of albumins,
32.5-42.5 % of globulins, 0.7-2% of fibrinogen/
Globulins are subdivided into four fractions: α1-globulins (2.5-5 %), α2-globulins (5.1-9.2 %),
β-globulins (8.1-12.2 %), and γ-globulins (12.8-19.0 %).
Thymol test - is so-called protein sedimentation test that reflects shift of albumin-globulin
fractions. Normally, thymol test is 0-5 Units. The test is always positive in virus hepatitis, toxic
hepatitis, chronic hepatitis, chronic cholecyctitis, and liver cirrhosis. It is negative in obstructive
jaundice.
Coagulation system
Liver produces prothrombin and other coagulation system components. We evaluate this
function using protrombin index (normal level 90-105%) and other coagulation factors.
Lipid metabolism
Liver produces and metabolizes cholesterol and other lipids Total cholesterol content in
the blood is less than 5.2 mmol/l.
Normal β-lipoprotein content in the blood serum is less than 4.9 mmol/l.
Liver enzymes
To assess functional condition of the liver, content of enzymes in the blood serum is
measured.
Alanine aminotransferases (ALT) normal level is 0.1-0.68 mmol/hxl. Increasing of ALT blood
level are revealed in necrosis of the liver cells, acute and chronic hepatitis, cholangitis, fatty
hepatic dystrophy, liver cirrhosis, obstructive jaundice, liver tumor, hemolytic conditions.
Aspartate aminotransferases (AST) normal content is 0.1-0.45 mmol/hxl. Increased AST
blood levels occur in necrosis of liver cells, obstructive jaundice, acute and chronic hepatitis,
fatty dystrophy of the liver.
Alkaline phosphatase normal level is 0.5-1.3 mmol/hxl according Bodanovsky or 1-3
mmol/hxl according Becey-Lauri. Increased level of alkaline phosphatase is especially
pronounced in obstructive jaundice, and can also be observed in cholangitis, tumor of the bile
bladder, chronic hepatitis, liver abscess, tumor and cirrhosis.
Increased activity of ALT, AST, alkaline phosphatase suggests hepatocytes lysis and release
of these enzymes in the blood.
Lactate dehydrogenase (LDG) normal blood serum content is to 3.2 mkmol/sxl. Increased
LDS level in the blood is determined in hepatitis and liver tumor.
Cholinesterase level normally is 160-340 mmol/hxl. Decreased cholinesterase content is
detected in hepatitis, liver cirrhosis, liver tumor, and congestive liver.
Sorbitol dehydrogenase (SDG) normal level is 0-5.6 nmol/sxl. Elevated SDG level is found in
grave damage of the liver parenchyma (acute infectious hepatitis, toxic hepatitis, liver cirrhosis,
liver tumor).
Ceruloplasmin normal content is 1.52-3.31 mkmol/1. increased level occur in liver
cirrhosis, hepatitis, obstructive jaundice; decreased - in grave liver diseases, in Konovalov-
Wilson disease (congenital disease characterized by decreased synthesis in the liver of
ceruloplasmin, the copper transport protein and its increased deposition in tissues).
 Cytolytic syndrome is developed due to destroying hepatocytes.
Causes of cytolytic syndrome:
 Acute and chronic hepatitis,
 necrotic damage of the liver (hepatocytolysis, liver necrosis) due to trauma or toxic
influences
Signs of the cytolysis syndrome':
• Increased activity of ALT, AST, LDG, SDG, aldolaza
• hyperbilirubunemia with predominance of bound fraction.
Degrees of activity:
1 degree (mild) – increased level of the ALT in 3-5 times from normal;
2 degree (moderate) – increased level of the ALT activity in 5-10 times from normal;
3 degree (severe) - increased level of the ALT activity in more than 10 times from normal.
Immunoinflammatory syndrome reflects specific long term autoimmune inflammation in
liver that is developed as a reaction on the different damaging factors (viruses, parasites,
bacteria, toxins and others).
Signs:
• Increased γ-globulins level
• hyperproteinemia,
• elevated thymol test
• Increased specific immunoglobulins G and M to the hepatosytes components
Jaundice (icterus) refers to a yellow pigmentation of skin, sclerae, and mucosa due to a raised
plasma bilirubin (visible at >35µrnol/L). Jaundice may be classified by the site of the problem
(pre-hepatic, hepatocellular, or choleste: obstructive). Bilirubin metabolism: Bilirubin is formed
from the breakdow of haemoglobin. It is conjugated with glucuronic acid by hepatocytes,
making it water soluble. Conjugated bilirubin is secreted into the bile and passes out into the
gut. Some is taken up again by the liver (enterohepatic circulation) and the rest is converted to
urobilinogen by gut bacteria. Urobilinogen is either reabsorbed and excreted by the kidneys, or
converted to stercobilin, which colours faeces brown.
Pre-hepatic jaundice If there is excess bilirubin production (haemolysis, decreased liver uptake
or decreased conjugation), unconjugated bilirubin enters the blood. It is water insoluble, it
does not enter urine resulting in an unconjugated (acholuric) hyperbilirubinaemia
Causes:
 Physiological (neonatal);
 Haemolysis;
 dyserythropoiesis;
 glucuronyl transferase deficiency.
Clinical features:
 Pale lemon-yellow pigmentation of skin.
 Dark brown faeces due to increased level of the stercobilin.
 Dark yellow urine due increased level of urobilin.
 Enlargement liver and spleen
 In blood: increased level of total bilirubin due to unbounded (unconjugated) fraction,
 Anemia, increased reticulocytes, positive direct and indirect Coomb ’s tests, autoimmune
antibody to erythrocytes, pathological shapes of erythrocytes.
Hepatocellular jaundice There is hepatocyte damage may be with or without some cholestasis.
Causes:
 Viruses: hepatitis ( A, B, C, etc.), cytomegalovirus, Epstein-Barr virus;
  Drugs: paracetamol overdose, anti-TB (isoniazid, rifampicin, pyrazinamide), statins,
monoamioxidase inhibitors
 alcoholic hepatitis;
 cirrhosis;
 liver metastases/abscess;
 haemochromatosis;
 autoimmune hepatitis;
 septicaemia;
 leptospirosis; α1- antitrypsin deficiency;
 Budd-Chiari and Wilson's disease
 failure to excrete conjugated bilirubin (Dubin-Johnson and Rotor syndromes);
 right heart failure;
 toxins, eg carbon tetrachloride;
 funfi (Amanita phalloides).
Clinical features:
 Redish-yellow pigmentation of skin.
 Dark brown urine due to increased level of the direct bilirubin.
 Light yellow faeces due to decreased production of the stercobilin
 In blood: increased level of total bilirubin due to both unbounded (unconjugated) and
bounded (conjugated) fractions,
 Signs of cytolysis (increased ALT, AST, LDG, SDG and other hypatocytes components)
 Sometimes signs of cholestasis (increased activity of alkaline phosphotase in
combination with hyperbilirubunemia, hypercholesterolemia, and β-lipoproteinemia)
Cholestatic (obstructive) jaundice If the common bile duct is blocked, conjugated bilirubin
overspills into the blood causing a conjugated hyperbilirubinaemia. Being water soluble, it is
excreted in urine, making it dark. Less conjugated bilirubin enters the bowel and the faeces
become pale.
Cause:
 Gallstones in the common bile duct;
 pancreatic cancer;
 lymph nodes at the porta hepatis;
 drugs (antibiotics: flucloxacillin, fusidic acid, co-amoxiclav, nitrofurantoin; anabolic
steroids, oral contraceptives, sulfonylureas, gold);
 cholangiocarcinoma;
 sclerosing cholangitis;
 primary biliary cirrhosis;
 choledochal cyst;
 biliary atresia.
Clinical features:
Dryness, metallic and bile taste in the mouth
Olive-colored jaundice
Biliary pruritus (itch) with scratches on the skin
Palpable gall bladder, and positive gall-bladder symptoms (extrahepatic cholestasis)
Ultrasound signs of gallstones, tumor of pancreas, enlargement lymphonodes and others.
Signs of cholestasis (increased activity of alkaline phosphotase in combination with
hyperbilirubunemia, hypercholesterolemia, and β-lipoproteinemia)
 7. Reference source

o Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –

Vinnytsya: NOVA KNYHA, 2006. – p. 364-367.
Control questions:
1. Main liver functions
2. Jaundice classification
3. Causes, symptoms and signs of the pre-hepatic jaundice
4. Causes, symptoms and signs of the hepatocellular jaundice
5. Causes, symptoms and signs of the cholestatic jaundice
6. Definition, causes, signs and degrees of cytolysis syndrome
7. Definition, causes and signs of immunoinflammatory syndrome
Practical task
1. Revealing and assessment of symptoms and signs of jaundice
2. Revealing and assessment of signs and level of cytolysis syndrome
3. Revealing and assessment of signs of immunoinflammatory syndrome
 TOPIC 33
Symptoms and syndromes of the liver diseases: portal hypertension, hepatic-
cellular failure and shunting of liver syndromes
6. Importance of the topic
Liver diseases usually are very dangerous and severe conditions. They gradually
destroy liver with its function loss and development of the liver cirrhosis. Knowledge
about causes, mechanism, symptoms and signs of the portal hypertension and
hepatic-cellular failure is very important for physicians of every specialty, because liver
pathology influence the course and treatment of majority of the human diseases.

2. Concrete aims:
─ To study causes, main symptoms, signs and stages of portal hypertension
─ To study causes, main symptoms, signs and stages of hepatic-cellular failure
─ To study features of the hepatic coma
─ To study clinical presentation of the liver cirrhosis
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the liver and biliary tract, their blood supply and
innervation
Normal physiology Liver functions in the metabolism
Histology Ontogenesis and histological structure of the liver and biliary
tract
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine patients with liver disorders
4. Task for self-study preparation for practical training
4.1. List of the main terms a student should know preparing for practical training

Term Term
Portal hypertension Hepatic coma
Hepatic-cellular failure Fetor hepaticus
Asterixis Hepatic encephalopathy

4.2. Theoretical questions:

48. Main liver functions
49. Portal hypertension classification
50. Clinical presentation of the portal hypertension
51. Causes, symptoms and signs of the hepatic-cellular failure
52. Classification of the liver failure
53. Definition, causes, clinical presentation and classification of the chronic hepatitis
54. Definition, causes, clinical presentation and classification of the liver cirrhosis
4.3. Practical task that should be performed during practical training:
89. Revealing and assessment of symptoms and signs of portal hypertension
90. Revealing and assessment of symptoms and signs of hepatic-cellular failure
91. Revealing and assessment of symptoms and signs of liver cirrhosis and chronic hepatitis
Topic content
Liver functions
Liver takes part in different metabolism systems of the body.
 Pigment metabolism
Liver maintains normal level of bilirubin in blood:
Total bilirubin - 8.5-20.5 mkmol/l,
Conjugated bilirubin - 2.2-5.1 mkmol/l,
unconjugated bilirubin - 6.3-15.4 mkmol/l.
Protein metabolism
Liver maintains normal level of total protein and its fraction in the blood serum. Normally,
the total protein content in the blood serum is 70-90 g/l. Total protein consists of three
fractions: albumins, globulins and fibrinogen. Total protein contains 55.5-65.5 % of albumins,
32.5-42.5 % of globulins, 0.7-2% of fibrinogen/
Globulins are subdivided into four fractions: α1-globulins (2.5-5 %), α2-globulins (5.1-9.2 %),
β-globulins (8.1-12.2 %), and γ-globulins (12.8-19.0 %).
Thymol test - is so-called protein sedimentation test that reflects shift of albumin-globulin
fractions. Normally, thymol test is 0-5 Units. The test is always positive in virus hepatitis, toxic
hepatitis, chronic hepatitis, chronic cholecyctitis, and liver cirrhosis. It is negative in obstructive
jaundice.
Coagulation system
Liver produces prothrombin and other coagulation system components. We evaluate this
function using protrombin index (normal level 90-105%) and other coagulation factors.
Lipid metabolism
Liver produces and metabolizes cholesterol and other lipids Total cholesterol content in
the blood is less than 5.2 mmol/l.
Normal β-lipoprotein content in the blood serum is less than 4.9 mmol/l.
Liver enzymes
To assess functional condition of the liver, content of enzymes in the blood serum is
measured.
Alanine aminotransferases (ALT) normal level is 0.1-0.68 mmol/hxl. An increase of ALT
blood level are revealed in necrosis of the liver cells, acute and chronic hepatitis, cholangitis,
fatty hepatic dystrophy, liver cirrhosis, obstructive jaundice, liver tumor, hemolytic conditions.
Aspartate aminotransferases (AST) normal content is 0.1-0.45 mmol/hxl. Increased AST
blood levels occur in necrosis of liver cells, obstructive jaundice, acute and chronic hepatitis,
fatty dystrophy of the liver.
Alkaline phosphatase normal level is 0.5-1.3 mmol/hxl according Bodanovsky or 1-3
mmol/hxl according Becey-Lauri. Increased level of alkaline phosphatase is especially
pronounced in obstructive jaundice, and can also be observed in cholangitis, tumor of the bile
bladder, chronic hepatitis, liver abscess, tumor and cirrhosis.
Increased activity of ALT, AST, alkaline phosphatase suggests hepatocytes lysis and release
of these enzymes in the blood.
Lactate dehydrogenase (LDG) normal blood serum content is to 3.2 mkmol/sxl. Increased
LDS level in the blood is determined in hepatitis and liver tumor.
Cholinesterase level normally is 160-340 mmol/hxl. Decreased cholinesterase content is
detected in hepatitis, liver cirrhosis, liver tumor, and congestive liver.
Sorbitol dehydrogenase (SDG) normal level is 0-5.6 nmol/sxl. Elevated SDG level is found in
grave damage of the liver parenchyma (acute infectious hepatitis, toxic hepatitis, liver cirrhosis,
liver tumor).
Ceruloplasmin normal content is 1.52-3.31 mcmol/l. Increased level occurs in liver
cirrhosis, hepatitis, obstructive jaundice; decreased - in grave liver diseases, in Konovalov-
Wilson disease (congenital disease characterized by decreased synthesis in the liver of
ceruloplasmin, the copper transport protein and its increased deposition in tissues).
Portal hypertension is an increased pressure in the portal vein system due to disorders in the
liver vein circulation. There are three types of the portal hypertension:
1. Under-hepatic hypertension, when disorder of circulation occurs before coming portal
vein to the liver due to thrombosis, compression by tumor, lymphonodes, aneurysm of
the hepatic artery and others.
2. Intra-hepatic hypertension, when disorder of circulation occurs in the liver.
3. Supra-hepatic hypertension when obstacle to blood flow from liver to vein cava is
developed due to thrombosis, Budd-Chiari syndrome, veno-occlusive disease and
others.
In case of the chronic liver diseases the intra-hepatic hypertension is developed due to process
of regeneration and fibrosis of the liver tissue, reconstruction of the liver and obliteration of the
vena porta branching. It results in increase of the portal vein pressure more than 10 mm Hg.
Stages of the portal hypertension:
1. Subclinical – without any clinical symptoms and signs, only increased portal pressure
more than 5 mm Hg and speed of the blood stream through main vessels of the portal
system that can be measured by Doppler ultrasound examination.
2. Clinical initial (I) – increased portal pressure more than 20 mm Hg, diarrhea, swelling
abdomen, pain at the epigastric region and normal liver tests.
3. Clinical full-scaled (II) – increased portal pressure 25-30 mm Hg, enlargement superficial
abdominal veins (caput medusa), hemorrhoid veins, esophagus veins, splenomegaly
(enlargement spleen), hepatomegaly
4. Clinical terminal (III) – hepatomegaly, splenomegaly, hypersplenism (increased spleen
functions of destroying blood cells results in anemia, thrombocytopenia with
hemorrhage syndrome, leucopenia with frequent flu and other infections), bleeding
from enlargement esophagus veins, hemorrhoid veins, ascites, edema, porto-systemic
encephalopathy.
Hepatic-cellular failure is a symptomocomplex that is formed due to depression of the main
liver functions.
Causes: Infections: viral hepatitis, yellow fever, leptospirosis
Drugs: paracetamol overdose, halothane, izoniazid
Toxins: Ammanita phalloides mushrooms, carbon tetrachloride
Vascular: Budd-Chiari syndrome, veno-occlusive disease.
Other: secondary cirrhosis and primary biliary cirrhosis, haemochromatosis,
autoimmune hepatitis,α1-antitripsin deficiency, malignancy
Mild – compensatory
Any clinical symptoms and signs of liver insufficiency are absent. There is dysproteinemia and
disorders of the absorbing and eliminating functions of the liver.
Moderate
There is mild peripheral oedema, weakness, undue fatiguability, psychology attrition,
changeable appetite, headache, bruises, spider nevi, palmar erythema, jaundice, fetor hepatic
(smells like pear drops), muscular atrophy, gynecomastia, loss of the chest and axillary hair,
testicular atrophy, menstrual irregularities, loss of libido, sterility. There is hypoalbuminemia,
dysproteinemia, decreased synthesis of the blood clotting factors and increased cholinesterase
activity.
Severe
It is presented by the above mentioned symptoms and signs but they decreased more than 50%
from norm and hyperbilirubinemia. There are symptoms and signs of the hepatic
encephalopathy. It is developed when only 1 kg of the live hepatic tissue works.
Hepatic encephalopathy
It develops as a result of rising blood ammonia levels. Factors cause these levels to rise:
Improper shunting of blood – when portal blood enters into the systemic circulation by the
portacaval shunts without neutralization in the liver.
Excessive protein intake,
Sepsis
Excessive accumulation of nitrogenous body wastes (from constipation or gastrointestinal
hemorrhage)
Clinical features of the hepatic encephalopathy
Grade I Altered mood or behavior
Grade II Increasing drowsiness, confusion, slurred speech
Grade III Stupor, incoherence, restlessness, significant confusion, liver flap (asterixis)
Grade IV Coma
Investigations:
Liver function tests (bilirubin, ALT, AST), Clotting (low protrombin), glucose, full blood
analysis, hepatitis serology
Abdominal ultrasound, Doppler flow studies of the portal vein and hepatic vein
Neurophysiological studies: EEG may show high-voltage slow waveforms.
Cirrhosis is a final stage of the all chronic diseases and demerges of the liver characterized
by diffuse destruction, fibrotic regeneration of hepatic cells and structural reconstruction of the
liver with following portal hypertension and hepatic failure.
Causes
Hepatocellular disease: Postnecrotic cirrhosis account for 10% to 30% of patients and
stems from various types of hepatitis (such as types A, B, C, D viral hepatitis) or toxic exposures.
Laennec s cirrhosis, also called portal, nutritional, or alcoholic cirrhosis, is the most common
type and is primarily caused by hepatitis C. Liver damage results from malnutrition (especially
dietary protein) and chronic alcohol indegestion. Fibrous tissue forms in portal areas and
around central veins.
Autoimmune disease, such as sarcoidosis and chronic inflammatory bowel disease, may result
in cirrhosis.
Cholestatic diseases
This group includes diseases of the biliary tree (biliary cirrhosis resulting from bile duct diseases
suppressing bile flow) and sclerosing cholangitis.
Metabolic diseases
This group includes disorders such as Wilson's disease, alpha rantitrypsin deficiency, and
hemochromatosis (pigment cirrhosis).
Other types of cirrhosis
Other types of cirrhosis include Budd-Chiari syndrome, cardiac cirrhosis, and cryptogenic
cirrhosis. Cardiac cirrhosis is rare; the liver damage results from right-sided heart failure.
Cryptogenic refers to cirrhosis of unknown cause.

Signs and symptoms

Clinical manifestations of cirrhosis and fibrosis are similar for all types, regardless of cause.
Early indications are insidious and vague but usually include weakness, fatigue, muscle cramps,
weight loss, GI symptoms (anorexia, indigestion, nausea, vomiting, constipation, diarrhea), and
abdominal pain (which may be attributed to an enlarged liver).
Major and late symptoms develop as a result of hepatic insufficiency and portal hypertension
and include the following:
• respiratory — pleural effusion and limited thoracic expansion because of abdominal ascites,
interfering with efficient gas exchange and leading to hypoxia
• central nervous system—progressive symptoms of hepatic encephalopathy: lethargy, mental
changes, slurred speech, asterixis (flapping tremor), peripheral neuritis, paranoia,
hallucinations, extreme obtundation, and coma
• hematologic—bleeding tendencies (nosebleeds, easy bruising, bleeding gums), anemia, and
hematemesis
• endocrine—testicular atrophy, menstrual irregularities, gynecomastia, loss of chest and
axillary hair, loss of libido, and sterility
• skin—severe pruritus, extreme dryness, poor tissue turgor, abnormal pigmentation, spider
nevi (on upper half of body), palmar erythema, jaundice, and peripheral edema
• hepatic—jaundice, hepatomegaly, ascites, edema of the legs, hepatic encephalopathy, and
hepatorenal syndrome constitute the other major effects of full-fledged cirrhosis
• miscellaneous — musty breath, enlarged superficial abdominal veins, muscle atrophy, pain in
the right upper abdominal quadrant that worsens when the patient sits up or leans forward,
splenomegaly, and wasting appearance of chronic illness. Fever may be present and usually
associated with portal hepatitis, spontaneous bacterial peritonitis, or cholangitis. Bleeding from
esophageal and rectal varices results from portal hypertension.
Investigations
A liver biopsy, the definitive test for cirrhosis, detects destruction and fibrosis of hepatic tissue.
A liver scan shows abnormal thickening and, possibly, a liver mass.
Plain films of the abdomen may reveal hepatic or splenic enlargement. Ultrasonography can
assess liver size and detect ascites or hepatic enlargement. Doppler ultrasonography is used to
evaluate patency of the splenic, portal, and hepatic veins. Computed tomography with IV
contrast or magnetic resonance imaging with serum alpha-fetoprotein levels can further
assess liver nodules. Suspicious liver nodules or masses can be biopsied to assess for cancer.
Esophagogastroscopy can detect causes of bleeding in the esophagus, stomach, and proximal
duodenum to confirm the presence of varices.
The following laboratory findings are characteristic of cirrhosis:
• decreased platelet count and hematocrit and decreased levels of hemoglobin, albumin,
electrolytes (sodium, potassium, chloride, and magnesium), and folate.
• elevated levels of globulin, serum ammonia, total bilirubin, alkaline phosphatase, serum
aspartate aminotransferase, serum alanine aminotransferase, and lactate dehydrogenase and
increased thymol turbidity
• coagulation abnormalities characterized by prolonged prothrombin and partial
thromboplastin times.
Classification of the cirrhosis severity grade by Child-Pugh
Sign A (1 score) B (2 score) C (3 score)
Bilirubin(mcmol/l) <35 35-55 >55
Albumin (g/l) >35 30-35 <30
Ascites none curable resistant
Encephalopathy latent 1-2 grade 3-4 grade
Prothrombin ratio (seconds > normal) 1-3 4-6 >6
Class A – 5-6 scores – compensated cirrhosis
Class B – 7-10 scores- sub-compensated cirrhosis
Class C >10 scores – decompensated cirrhosis
7. Reference source
Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000

Control questions:
1. Main liver functions
2. Portal hypertension classification
 3. Clinical presentation of the portal hypertension
4. Causes, symptoms and signs of the hepatic-cellular failure
5. Classification of the liver failure
6. Definition, causes, clinical presentation and classification of the chronic hepatitis
7. Definition, causes, clinical presentation and classification of the liver cirrhosis
Practical task:
1. Revealing and assessment of symptoms and signs of portal hypertension
2. Revealing and assessment of symptoms and signs of hepatic-cellular failure
3. Revealing and assessment of symptoms and signs of liver cirrhosis and chronic hepatitis
 TOPIC 34
Symptoms and syndromes of the pancreas and bowels diseases

7. Importance of the topic

Bowel and pancreas diseases usually are very dangerous and severe conditions. They
are the main cause of digestion insufficiency, weight loss and poor quality of life.
Knowledge about causes, mechanism, symptoms and signs of the chronic diarrhea,
constipation and pancreatitis is very important for physicians of every specialty,
because poor digestion influences the course and treatment of majority of the human
diseases.

2. Concrete aims:
─ To study causes, classification, main symptoms and signs and stages of chronic
diarrhea
─ To study causes, main symptoms, signs and stages of chronic constipation
─ To study main syndromes of chronic pancreatitis
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the bowel, pancreas
Normal physiology Functions of the bowel and pancreas
Histology Ontogenesis and histological structure of the bowel and
pancreas
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine patients with bowel and pancreas disorders
4. Task for self-study preparation for practical training
4.1. List of the main terms a student should know preparing for practical training

Term Term
Intestine dyspepsia steatorrhea
maldigestion creatorrhea
malabsorption amilorrhea

4.2. Theoretical questions:

55. Definition, classification of the chronic diarrhea.
56. Characteristics of the different types of chronic diarrhea
57. Definition, classification of the chronic constipation.
58. Causes, symptoms and signs of the different types of chronic constipation
59. The main syndromes of the pancreas affection
60. Instrumental and laboratory investigation patients with intestinal and pancreas
disorders
4.3. Practical task that should be performed during practical training:
92. Revealing and assessment of symptoms and signs of chronic diarrhea
93. Revealing and assessment of symptoms and signs of chronic constipation
94. Revealing and assessment of symptoms and signs of chronic pancreatitis
Topic content
Chronic diarrhea
 More than 4 weeks,
  defecation more than 2 times per days,
 liquid excrements (stool, feces),
 amount of excrements more than 250 g/day.
Classification: osmotic, secretory, motor, inflammatory.
OSMOTIC (in a 72 o'clock of starvation (fasting) (water is settled) diarrhea diminishes or
disappears, osmotic fall in an excrement more than a 100 Osm/kg excrement ’s masses)
It can be at:
 lactase insufficiency,
 disacharidase insufficiency,
 at using purgative (sorbitol, laktuloza, normaze)
 overdosing antiacid,
 at the syndrome of malabsorption (chronic pancreatitis, celiacia)
 unbearable of cereals
 the SPRU illness.
SECRETORY (does not diminish in a 72 hours of starvation, consistency is the water painted out
by an excrement, osmotic fall less than 50).
It can be at:
 cholera,
 neuroendocrinal tumours (gastrinoma, VIPoma, medulla cancer of thyroid, cartcinoid)
 microscopic colitis,
 using purgative (bisacodil)
 connective tissue diseases (sclerodermia).
MOTOR (alternations of diarrheas and constipations, always flatulence, the considerable
admixture of mucus in an excrement, pain and defecation are synchronous, facilitation after the
act of defecation, increasing of diarrhea at emotional stress)
It can be at:
 irritable colon syndrome,
 after the resection of stomach,
 after vagotomia,
 after the resection of ileo-caecum corner,
 at heavy diabetes mellitus due to enteropathy, neuropathy.
INFLAMMATORY (combination with fever, with the loss of body mass, pain feelings at the
defecation, imperative urges to defecation (tebesmes), presents the of blood and mucus in an
excrements, at a microscopy is leukocytosis of excrement)
It can be at:
 unspesific ulcerous colitis,
 Crohn's disease (specific granulematosis colitis),
 infectious diseases (salmonellosis, typhus, dysentery),
 tumors of colon.
Plan of examination of patient with chronic diarrhea
1. Feces occult blood test,
2. leucocytes, parasite infection,
3. maintenance of neutral fat,
4. osmotic failure (fall),
5. pH of excrement,
6. ultrasonic research of abdomen,
7. fibrocolonoscopy,
8. RectoRomanoScopy,
9. enterography,
 10. biopsy of mucous of colon

CHRONIC CONSTIPATION
 More than 6 weeks,
 defecation less than 3 times per a week,
 «sheep excrement»,
 Amount of feces less than 100 g in a day
 tension act more than 25% from all act of defecation
Classification of constipation
by PATHOGENIS –
 disorder of defecation act (finger research, RRS, FCS, bulb fibrocolonoscopy),
 disorder of transit feces in a colon (at disorder of motility and at presence of mechanical
obstaction of colon) – FCS, irrigoscopy.
by CAUSES -
 PRIMARY – develops due to presence of pathology of intestine.
А) Organic (crack of rectum, proctitis, tumors of colon, narrowing of rectum, anomalies of
development – dolichosigmoid, megacolon)
Б) Functional –
 anorectal (pathology of ampoule and sphincter due to atony at old patients)
 cologenic (at slow motion on an intestine) is irritable colon syndrome.
 SECONDARY – unconnected with the defeat of intestine.
Can be at:
- endocrine pathology (diabetes, hypotireosis)
- metabolic pathology (frequent using of psychotropic and diuretic medicines)
- muscles’ pathology (myasthenia, myopathy)
- neurogenic pathology (heavy diseases central nervous system, spinal cord, illness of
Parkinson, myopaty)
- reflex (how concomitant to other pathology - peptic ulcer, gallbladder-stone disease)
SYMPTOMS AND SYNDROMES OF PANCREATIC DISORDERS
1. Abdominal pain
Features of pain syndrome
 localization - an epigastric region
 a reason - the reception of fat, fried food, alcohol, eggs, chocolate, candies, ice-cream,
dough
 time of appearing – 5-6 hours after eating
 irradiation – in the back on a type «belts» or «semibelts»
 equivalents of pain - kidney colic, intestinal colic, combination with an icterus
 facilitation - application of cold
2. panсreatic dyspepsy
 permanent nausea
 vomiting (sometimes indomitable)
 citophobia - patients prefer not to meal, to eliminate pain
 malabsorption
 maldigestion
3. syndrome of exocrine (extrasecretory) insufficiency
4. syndrome of endocrine insufficiency (diabetes mellitus)
 5. syndrome of byliaric hypertention (verden-icterus, itch (pruritis) of skin, urine has
colors of beer, colorless excrement, scratching tract on a skin, increase of total and
direct bilirubin, increase of levels of enzymes of cholestasis)

MALDIGESTION SYNDROME - is disordering of digestion due to deficiency of pancreatic

enzymes of pancreas
 a pancreatic feces - there is diarrhea, large, liquid, more than 500 ml in a day
 flatulence, swelling of stomach
 periodic stomach pain (in area of umbilicus and during motion of intestine) decreased
after defecation or gassing
 pains at palpation in area of umbilicus (the Porges’s area)
 rumbling in area of caecum
 “noise of splash” at palpation of caecum
MALABSORBTION SYNDROME - is disordering of absorbtion of proteins, fats, carbohydrates,
vitamins because of deficit of pancreatic enzymes –
Disorders of all types of metabolism are characterised with
Proteins metabolism – hyproproteinemia, edema, fatty dystrophy of liver
Lipid metabolism - loss of weight, hypocholesterolemia, steatorrhea (fatty feces), deficit of the
А (blindness), D (osteoporosis), Е vitamins (disorders of sexual function)
Carbohydrate metabolism - hypoglycemia states
Methods of the investigation of patients with pathology of pancreas
1. VISUAL EXAMINATION
 The Grott’ Symptom - atrophy of hypodermic fatty layer in the area of projection of
pancreas
 The Tuzhylyn’ («symptom of bloody dew») Symptom - the red shallow point rises in
the area of projection of pancreas
 Loss of weight
 Dryness of skin
 Phenomena of avitaminosis
2. PALPATION
o Superficial (the Shoffar’and Gubergryts-Skulskiy zone, the DeGardena,
Gubergrytsa, Meyo-Robsona front and back points)
o Deep (on Obraztsov’, on Grott’)
Diagnostic value: the pancreas can be accessible to palpation and to be painful at:
 Sclerosis of body, tail, head
 Pancreatitis fibrosis (indurative)
 Cancer of head
 Cysts and pseudocysts of pancreas
3. ADDITIONAL METHODS OF RESEARCH
А) Laboratory - determination of activity of enzymes (amylase, lypase, tripsin,
bicarbonates) in biological liquids (urine, blood, excrement, duodenal juice, pancreatic juice)
A «gold standard» is determination of amount of elastase in feces.
Diastase of urine – (urine amylase) is the simplest method – in a norm 64-128 units by
Volgemut.
Coprological study reveal coprological signs:
 Amylorrhea (insufficiency of amylasa) – more than 2-3 starch grains in field of vision
are identified in feces
 Steatorrhea (insufficiency of lypase) – more than 2-3 drops of neutral fat in in field
of vision are identified in feces
  Creatorrhea (insufficiency of trypsyn) – more than 10 undigested muscle fibres in
field of vision are identified in feces
Instrumental methods
1. Ultrasonic research (estimates sizes, contour, density of pancreas, length and diameter
of general bilious channel and pancreatic channel)
ULTRASONIC-sign of pancreatitis:
 Increase of one or all sizes of pancreas
 Uneven contour
 Increase of closeness of fabric of gland
 Increase of diameter of general bilious channel (cholestasis)
 Diminishment of diameter of pancreatic channel
2. Roentgenologic research (X-Ray examination)
4. Duodenography
5. Computer tomography
6. Retrograde choletsystopancreatography
7. Selective angiography
8. Puncture biopsy of pancreas
7. Reference source
Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine, Part 1. –
Vinnytsya: NOVA KNYHA, 2006. – p. 357-364.
Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000

Control questions:
61. Definition, classification of the chronic diarrhea.
62. Characteristics of the different types of chronic diarrhea
63. Definition, classification of the chronic constipation.
64. Causes, symptoms and signs of the different types of chronic constipation
65. The main syndromes of the pancreas affection
66. Instrumental and laboratory investigation patients with intestinal and pancreas
disorders
4.3. Practical task that should be performed during practical training:
95. Revealing and assessment of symptoms and signs of chronic diarrhea
96. Revealing and assessment of symptoms and signs of chronic constipation
97. Revealing and assessment of symptoms and signs of chronic pancreatitis
 TOPIC 35
Symptoms and syndromes of the renal diseases (chronic and acute
glomerulonephritis and pyelonephritis): urinary, nephritic, nephrotic
syndromes
1.Importance of the topic
Renal diseases usually have latent and progressing course. They gradually destroyed
kidney with developing chronic renal failure. It is very severe difficulty treated
condition that eventually results in death. The most specific signs of the renal diseases
may be received by urine and blood chemistry investigations. Knowledge about
causes, mechanism, symptoms and signs of the urinary, nephrotic syndromes is very
important for physicians of every specialty, because kidney pathology influences on
the course and treatment of majority of the human diseases.

2. Concrete aims:
─ To study mains parameters of urine analysis
─ To study main signs of urinary syndrome
─ To study main symptoms, signs of nephrotic syndrome
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the kidney and urinary tract, their blood supply
and innervation
Normal physiology Kidney functions in the metabolism
Histology Ontogenesis and histological structure of the kidney and
urinary tract
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine patients with kidney disorders
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
proteinuria Renal edema
hematuria casturia
leukocituria Specific gravity of urine

4.2. Theoretical questions:

67. What parameters are investigated by urinalysis?
68. What is a proteinuria, main types, causes?
69. What is a leucocyturia, main types, causes?
70. What is a hematuria, types, causes?
71. What is a casturia, types, causes?
72. What is nephrotic syndrome, main causes?
73. Definition, causes, clinical presentation of the acute and chronic glomerulonephritis.
74. Definition, causes, clinical presentation of the acute and chronic pyelonephritis
4.3. Practical task that should be performed during practical training
98. Revealing and assessment of urinary syndrome signs
99. Revealing and assessment of nephrotic syndrome signs
100. Revealing and assessment of nephritic syndrome signs
 Topic content
Urine analysis
Clinical urine analysis includes: macroscopic (physical properties), chemical, microscopic,
bacteriological and bacterioscopic studies.
Macroscopic study
Macroscopic study includes assessment of physical properties of the urine: amount, color,
cloudiness, smell, and specific gravity.
Physical properties of the urine
Amount of the urine. In healthy adult the normal amount of excreted urine is between 1000 ml
and 2000 ml in 24 h (diurnal diuresis).
Polyuria is defined as a production by an adult of more than 2000 ml of urine/24h.
Olyguria is defined as a production by an adult of less than 500 ml of urine/24h.
Color of the urine depends on the presence of physiologic pigments (urochromes,
urobilinoids, uroerythrin, etc) and on its concentration. The color of the normal urine varies from
straw yellow to orange-yellow. Different pathological conditions of the urinary organs can cause
peculiar changes of the urine color.
Clinical significance of urine color changes.
Color Pathological condition Cause
Dark yellow Congestive kidney, edema, burns, High concentration of urochrome
diarrhea, vomiting
Pale, water-like Diabetes mellitus, diabetes Low concentration of urochrome
Dark insipidus
Hemolytic anemia Urobilinogenuria
Dark, Acute hemolytic kidney Hemoglobinuria
almost
black
Red Renal colic, renal infarction Hematuria (unaltered blood)
Appearance Acute glomerulonephritis Hematuria (altered blood)
of "meat
wastes"
Greenish- Parenchymatous jaundice Bilirubinuria, urobilinuria
brown (beer-
like)
Greenish- Obstructive jaundice Bilirubinuria
yellow
Whitish Fatty degeneration and decomposition Lipuria
of the renal tissue
Milky Renal lymphostasis Hyluria

Cloudiness of the urine. Normal, freshly excreted urine is clear. Cloudiness of the urine can be
cause by the presence of salts, cellular elements (leucocytes, erythrocytes, epithelium cells),
bacteria, mucus, and fats.
Smell of the urine. Normally, the urine has not strong specific smell. In bacterial
decomposition on air or in urinary ducts (severe cystitis, degradation of malignant tumor) urine
smells of ammonia. Peculiar "fruity" or "apple" odor of the urine is characteristic of diabetic coma or
diabetes mellitus in decompensation stage. Such specific odor of the urine is a result of ketone
bodies presence.
Specific gravity of the urine is proportional to concentration of dissolved in it substances: urea,
uric acid, various salts, and depends not only on amount but mainly on their molecular weight.
 Specific gravity is measured by urometer, normally it varies from 1.015 to 1.025. In health there is
diurnal variation of the specific gravity; in morning, the most concentrated portion of the urine, it
can be to 1.020-1.026.
Assessment of the specific gravity of the urine is of great diagnostic significance, because these
parameter gives information about concentrating ability of the kidneys. The specific gravity can also
be depends on the volume of urine excreted.

Clinical significance of specific gravity.

Specifi Extrarenal causes Renal causes
c Physiological Pathological
Low Polyuria Diuretics taking Alimentary dystrophy Diabetes Renal failure
High Oliguria insipidus
Fluid accumulation in cavities and tissues (edema, Renal glucosuria Renal
ascitis, hydrothorax, etc) Profuse vomiting, diarrhea amyloidosis with high
Diabetes mellitus proteinuria

Zimnitsky's test characterize condition of renal concentrating and excretory ability. In order to
correct measure urinary concentrating ability, the patient must avoid taking much fluid.
Urine samples are collected each 3 hours in separate container with designation of time - 8
portions during 24 hours. Volume and specific gravity of the urine is measured in each portion.
The advantages of this method are:
• Possibility to measure diurnal diuresis and to detect presence of polyuria or oliguria;
• Possibility to measure separately daily and nightly diuresis and to detect presence of nycturia;
• Possibility to determine diurnal variation of the specific gravity and its maximal value.
Normally, diurnal diuresis is 1000-2000 ml, amount of urine in each portion can vary from
50 to 250 ml, daily diuresis exceeds nocturnal, and specific gravity vary from 1.010 to 1.025. If
the maximal mean of specific gravity in Zimnitsky's test exceeds 1.020, renal concentrating ability
is considered to be normal.
Low specific gravity in all portions is typical to renal failure.
Isosthenuria is defined as condition when osmotic concentration of urine is equal to
osmotic concentration of blood plasma. Maximal osmotic concentration of urine in isosthenuria
is 270-330 mmol/1, and maximal specific gravity- 1.010-1.012.
Hyposthenuria is defined as condition when maximal osmotic concentration of urine is less
than osmotic concentration of blood plasma. Maximal osmotic concentration of urine in
hyposthenuria is 200-250 mmol/1, and specific gravity of urine - 1.005-1.008.
Extrarenal causes of urine specific gravity changes
In diabetes mellitus, polyuria and high specific gravity of the urine (to 1.026-1.050) due to
glucosuria is determined.
Diabetes insipidus and pituitary insufficiency are characterized by polyuria and low specific
gravity of the urine.
Renal causes of urine specific gravity changes
In acute glomerulonephritis, nephrotic syndrome, and in congestive kidney in heart
failure osmotic concentration of urine is elevated to 1200 mmol/1, specific gravity of the urine
- to 1.031-1.035, that accompanied by oliguria. Hyposthenuria in normal diurnal diuresis and
nicturia observe in patients with chronic glomerulonephritis, chronic pyelonephritis, and
nephrosclerosis. Isosthenuria suggests complete absence of renal concentrating ability. Long
standing excretion of urine with low specific gravity, monotonous means in combination with
oliguria are the signs of severe chronic renal failure with unfavorable prognosis.
Chemical study
Chemical study includes assessment of reaction of the urine (urine pH), protein, glucose,
ketone bodies, and bile pigments.
Reaction of the urine - urine pH may vary from pH 5.0 to 7.0 - neutral or feebly acid reaction.
Urine pH can be changed in both physiological and pathological conditions.
Acid: Physiological conditions: much meat food intake. Pathological conditions: diabetes mellitus,
severe renal failure, acute nephritis, congestive kidney, tuberculosis of the kidneys, acidosis,
hypokaliemic alkalosis
Neutral Feebly acid –norm.
Alkaline: Physiological conditions: vegetable diet, at the height of digestion, ample alkaline fluid
intake Pathological conditions: Vomiting, diarrhea, chronic infections of the urinary tracts.
Protein. The normal amount of protein excreted in the urine per 24 hours is 25-75 mg that
cannot be detected by routine tests. More than half of this amount consists of small molecular
weight proteins or protein fragments, although albumin is the largest single component.
Proteinuria is the appearance of protein in the urine in concentration determinable by
qualitative methods.
The protein content of the urine of normal individuals can rise to about 150 mg/1 when the
urine is concentrated.
Selective and non-selective proteinuria is distinguished. Selective proteinuria is
characterized by the presence in the urine of low molecular weight proteins - albumin,
ceruloplasmin, and transferrin. In non-selective proteinuria high molecular weight proteins -
globulins are detected. Moreover, Bence-Jones proteins - low molecular weight proteins, can
be revealed in the urine. In some pathological conditions, hemoglobin, hemosiderin, myoglobin,
and Tamm-Harsfall proteins are present in the urine.
Depend on protein- amount in the urine, microalbuminuria - 30-300 mg/24h, and
proteinuria (macroalbuminuria) — more than 300 mg/24h are distinguished.
Proteinuria can be functional and organic. Functional proteinuria observed in subjects
without renal diseases, has transitory character, does not exceeds 1 g/24h, and are not
accompanied by the other urine abnormalities. Postural (orthostatic), effort, and cold
proteinuria are differentiated. Healthy adults are found to have proteinuria when up and
about, but not after a period of horizontal rest. Standing position can induce significant
proteinuria in a substantial proportion of people who do not otherwise show it. Proteinuria can
also be observed in subjects without renal diseases after severe exercise, in fever, or on
exposure to extremes of cold or heat. These findings do not imply the presence of renal disease
and do not require further investigation.
Organic proteinuria can came about in three ways:
1. The glomerular filter becomes more permeable to proteins of large molecular size, as well
as permitting those of small molecular weight to pass - 'glomerular' proteinuria. This is by
far the commonest cause of proteinuria in clinical practice.
2. There is a marked rise in the plasma concentration of protein in circulation, so that amount
filtered exceeds the reabsorptive capacity of the proximal tubule - 'overflow' proteinuria.
3. The proximal tubule is damaged so that normally reabsorbed proteins, principally of low
molecular weight, pass into the urine - 'tubular' proteinuria.
4. Extrarenal proteinuria is usually caused by protein admixtures (inflammatory exudates,
degradated cells) in the diseases of urinary and sex ducts. Such proteinuria usually does not exceed
lg/1.
Glucose. Excretion of glucose with urine is called glycosuria. If the plasma glucose
concentration rises above the threshold level (around 10 mmol/1 in man) the unreabsorbed glucose
will appear in the urine, and this occurs in uncontrolled diabetes mellitus, the commonest clinical
cause of glycosuria.
Ketone bodies (acetone, acetoacetic and β-oxybutyric acid) are normally absent in the urine.
Ketonuria is defined as a presence of ketone bodies in the urine. They usually occur in diabetes
mellitus, carbohydrate deficit: fasting, grave toxicities, longstanding intestinal disorders, dysentery,
and in postoperative period. Ketonuria is important laboratory sign of decompensation of diabetes
mellitus with transformation to diabetic coma.
Bilirubin. Normal urine contains minimal quantity of the bilirubin. Increased excretion of
bilirubin is pathological condition and is called - bilirubinuria. Bilirubinuria occurs in increased blood
level of bound bilirubin more than 0.01-0.02 g/1 ("renal threshold of bilirubin") in parenchymatous
jaundice (acute virus, toxic, toxico-allergic hepatitis, liver cirrhosis), sub-hepatic jaundice (altered
permeability of bile ducts due to inflammation, obstruction by stones, by tumor, or by scars).
Urobilinoids: urobilin (urobilinogens, urobilins) and stercobilin (stercobilinogens,
stercobilins) are derivates of bilirubin. They are not determined separately. A large quantity of
urobilinoids in urine is called urobilinogenuria. It occurs mainly in: parenchymatous affection of
the liver (hepatitis, cirrhosis), hemolytic processes (hemolytic anemia); and in intestinal diseases
(enteritis, constipation, etc).
Microscopic study
Erythrocytes. The urine of healthy person contains single erythrocytes. The presence of
erythrocytes in the urine is called hematuria. Determination of erythrocytes in microscope
vision area (<50 cells) is defined as microhematuria; the color of the urine is unchanged in such
cases. If erythrocytes amount is >50cells in vision area, the urine is of red color that is defined as
macrohematuria.
Hematuria can be true (from the kidneys and urinary tract) and false (in man in prostatitis,
tuberculosis and tumor of prostate, in woman of genitalia origin).
Erythrocytes in the urine can be altered and unaltered depend on their origin
Glomerular origin - Altered erythrocytes:
• Acute nephritis (macrohematuria)
• Chronic glomerulonephritis (more pronounced during aggravation)
• Renal infarction (macrohematuria)
• Hypernephroma (periodic macro- and microhematuria)
• Renal tuberculosis (constant microhematuria)
• Congestive kidney (congestive microhematuria)
N.B. In the presence of glomerular hematuria, the urine usually contains much protein - so-
called protein-erythrocyte dissociation
Non glomerular origin - Unaltered erythrocytes observes more frequently in urinary tract
diseases:
• Stones in the pelves, urinary bladder, ureters
• Acute cystitis
• Malignant tumors
• Tuberculosis of urinary bladder or pelves
• Hypertrophy of prostate.

Leucocytes are observed mainly in a form of neutrophils, and sometimes eosinophils and
lymphocytes are present. Urine of healthy individuals contains small amount of leucocytes (1-2 in
vision area). Leucocyturia is defined as elevated amount (from 5-6 to 20 cells in vision area) of
leucocytes in the urine. Pyuria is said to be present when amount of leucocytes increases to 60-100
cells in vision field, and they are seen macroscopically.
Epithelium cells
Tubular (renal) epithelium cells are absent normally in the urine. Their presence indicates
acute or chronic affection of the kidneys. They can also be detected in fever, toxicities, and in
infectious diseases.
Transitional epithelium cells presence in the urine suggests inflammatory processes in the
pelves or bladder.
Squamous epithelium cells originate from genitalia and urethra, and diagnostic their
significance is low.
Cylinders (casts). These are cylindrical bodies formed in the lumen of the distal tubule,
particularly the collecting tubule. Casts are protein copies of tubules. Appearance of cylinders in
urine sediment is called cylinduria -the sign of organic renal diseases.
Hyaline casts are occasionally seen in the urine of normal people, particularly when it is
concentrated, or after exercise. Hyaline casts appear in the urine during secondary proteinuria:
febrile, congestive, orthostatic, toxic, and after administration of loop diuretics. Constant hyaline
casts presence suggests proteinuria of renal genesis: glomerulonephritis, pyelonephritis, and
nephropathy.
Granular casts occur in much the same situations as hyaline casts and have similar
significance. They are found in the urine of normal subjects after exercise. They appear in many
 types of renal disease but are particularly characteristic of chronic proliferative or membranous
glomerulonephritis, diabetic nephropathy, and amyloidosis.
Waxy casts presence in the urine indicates chronic diseases of the kidneys.
Erythrocytes (unaltered) casts are pathognomic of renal bleeding: nephrolithiasis,
tuberculosis and rumor of the kidneys; acute process in the kidneys: acute glomerulonephritis.
Erythrocytes (altered) casts are seen in chronic glomerulonephritis.
Leucocytes casts may appear in considerable numbers during an episode of acute
pyelonephritis; a few may be found in the urine in chronic pyelonephritis.
Nechiporenko’ s method allows counting formed elements in 1 ml of urine, normally:
• Leucocytes - to 4000;
• Erythrocytes-to 1000;
• Casts-to 200.
Crystals. Cystine crystals may be found in freshly passed urine but are found more consistently
if a concentrated sample is acidified and cooled in i refrigerator, their presence is diagnostic of
cystinuria. Oxalate crystals are common in urine from normal individuals when it has stood for an
hour or two. When present in freshly passed urine, in large numbers or aggregates, they may
indicate an increased liability to form oxalate stones, but firm conclusions can only be drawn if the
urine is kept at 37 °C until examined on a warm-stage microscope.
Mucus. The normal urine practically contains no mucus. Commonly mucus appears in diseases
of the urinary tract: urethritis, prostatitis, cystitis, and in stones presence.
It must be emphasized that although urinalysis and microscopy yield valuable information, it is
possible for significant renal disease to be present without anything abnormal being detected in the
urine.
Bacterioscopic study
Bacteriuria is defined as presence of bacteria in the urine. In quantity not more than 50 000 in
1 ml they may occur in the urine of healthy person. In the presence of bacteriuria, it is important to
determine its degree and microorganism sensitivity to various antibiotics.
Nephrotic syndrome (NS)is characterized by marked proteinuria (>3 g/24h), hypoalbuminemia
(<30g/L), hyperlipemia, and oedema. Although NS isn't a disease itself, it results from a specific
glomerular defect and indicates renal damage. The prognosis is highly variable, depending on the
underlying cause. Some forms may progress to end-stage renal failure.
Causes
About 75% of NS cases result from primary (idiopathic) glomerulonephritis. Classifications include
the following:
• In lipid nephrosis (nil lesions)—the main cause of NS in children — the glomerali appear normal
by light microscopy. Some tubules may contain increased lipid deposits.
• Membraneous glomerulonephritis— the most common lesion in adult idiopathic NS — is
characterized by uniform thickening of the glomerular basement membrane containing dense
deposits. It can eventually progress to renal failure.
• Focal glomerulosclerosis can develop spontaneously at any age, follow kidney transplantation, or
result from heroin abuse. Reported incidence of this condition is 10% in children with NS and up to
20% in adults. Lesions initially affect the deeper glomerali, causing hyaline sclerosis, with later
involvement of the superficial glomerali. These lesions generally cause slowly progressive
deterioration in renal function. Remissions occur occasionally.
• In membranoproliferative glomerulonephritis, slowly progressive lesions develop in the
subendomelial region of the basement membrane. These lesions may follow infection, particularly
streptococcal infection. This disease occurs primarily in children and young adults.
Other causes of NS include metabolic diseases such as diabetes mellitus; collagen-vascular disorders,
such as systemic lupus erythematosus, Henoch-Schenlein purpura and polyarteritis nodosa;
amyloidosis; circulatory diseases, such as heart failure and sickle-cell anemia; nephrotoxins, such as
mercury, gold, and nonsteroidal anti-inflammatory drags (NSAIDs); allergic reactions; infections, such
as tuberculosis or hepatitis B; preeclampsia toxemia; hereditary nephritis; multiple myeloma; and
other neoplastic diseases. These diseases increase glomerular protein permeability, leading to the
increased urinary excretion of protein, especially albumin, and subsequent hypoalbuminemia.
Signs and symptoms
Taking history patient should be asked about acute or chronic infections, nephrotoxic drugs,
allergies and systemic symptoms.
The dominant clinical feature of nephrotic syndrome is mild to severe dependent oedema of the
ankles or sacrum, facial or periorbital oedema, especially in children (anasarca). Such oedema may
lead to ascites (see abdomen examination), pleural effusion (see respiratory syndromes), and
swollen external genitalia.
Accompanying symptoms may include orthostatic hypotension, lethargy, anorexia, depression,
pallor, xanthelasma, xanthomata, hypertension, and hepatomegaly.
Major complications are
 malnutrition infections (pneumonia, peritonitis);
 coagulation disorders with thromboembolic vascular occlusion (10-40% ): deep vein
thromboflebitis, pulmonary embolism, renal vein thrombosis;
 hyperlipidaemia with accelerated atherosclerosis;
 acute renal failure.
Tests
Urine: Consistent proteinuria in excess 3,5 g/24 hours strongly suggests NS examination of urine
also reveals an increased number of hyaline, granular and waxy, fatty casts, and haematuria.
Blood: Serum values that support the diagnosis are increased cholesterol, phospholipids, and
triglycerides levels. Albumin level is decreased but γ-globulins levels are increased.
Histologic identification of the lesion requires kidney biopsy.
7. Reference source
Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine Part 1. – Vinnytsya:
NOVA KNYHA, 2006. – p. 371-384, 388-401
Control questions:
75. What parameters are investigated by urinalysis?
76. What is a proteinuria, main types, causes?
77. What is a leucocyturia, main types, causes?
78. What is a hematuria, types, causes?
79. What is a casturia, types, causes?
80. What is nephrotic syndrome, main causes?
81. Definition, causes, clinical presentation of the acute and chronic glomerulonephritis.
82. Definition, causes, clinical presentation of the acute and chronic pyelonephritis
Practical task
101. Revealing and assessment urinary syndrome signs
102. Revealing and assessment nephrotic syndrome signs
103. Revealing and assessment nephritic syndrome signs
 TOPIC 36
Symptoms and syndromes of the renal diseases (chronic and acute
glomerulonephritis and pyelonephritis): hypertension, eclampsia, chronic
renal failure
1.Importance of the topic
Renal diseases usually have latent and progressing course. They gradually destroyed
kidney with developing chronic renal failure. It is very severe difficulty treated
condition that eventually results in death. Renal arterial hypertension and eclampsia is
insidious conditions which has latent symptoms and very severe and life-threatening
complication as acute and chronic renal failure. Knowledge about causes, mechanism,
symptoms and signs of the renal arterial hypertension, eclampsia, chronic renal failure
is very important for physicians of every specialty, because kidney pathology
influences on the course and treatment of majority of the human diseases.

2. Concrete aims:
─ To study features of the renal hypertension
─ To study main symptoms and signs of eclampsia
─ To study main symptoms, signs of chronic renal failure
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the kidney and urinary tract, their blood supply
and innervation
Normal physiology Kidney functions in the metabolism
Histology Ontogenesis and histological structure of the kidney and
urinary tract
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine patients with kidney disorders
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
proteinuria Renal edema
hematuria casturia
leukocituria Specific gravity of urine

4.2. Theoretical questions:

83. What are the causes of the renal arterial hypertension?
84. What are the clinical features of the renal arterial hypertension?
85. What is an eclampsia? Causes, pathogenesis, clinical presentation, complication.
86. Definition of the chronic renal failure, its causes.
87. Classification of the chronic renal failure.
88. Clinical symptoms and signs of affecting different systems at the patients with chronic
renal failure.
89. Instrumental and laboratory examination patient with chronic renal failure.
4.3. Practical task that should be performed during practical training
104. Revealing and assessment of the renal hypertension symptoms and signs
105. Revealing and assessment of the eclampsia symptoms and signs
106. Revealing and assessment of chronic renal failure symptoms and signs.

Topic content
Renal hypertension features
All typical symptoms, signs, according to different stages, and complications of arterial hypertension
can be revealed at patient with renal diseases (see syndrome of arterial hypertension).
Causes: diabetic nephropathy, chronic glomerulonephritis, chronic interstitial nephritis; polycystic
kidneys, renovascular diseases, chronic pyelonephritis, Nephrolithiasis, hypo- or dysplasia of kidney,
renal tuberculosis, renal tumor, chronic renal failure, systemic diseases, amyloidosis.
Symptoms: frequently asymptomatic hypertension, but sometimes patients can feel typical
symptoms of the high level of blood pressure: headache, dizziness, palpitation, heart pain, nausea,
vomiting, and dyspnea.
Signs: blood pressure is high and stable, especially diastolic. Level of the high blood pressure doesn’t
decrease during night (“non-dipper” curve at the daily pressure monitoring).
Other symptoms and signs of the kidney affecting can be obtained during examination.

Eclampsia is an outburst of the tonoclonic spasms that is caused by decreased glomerular filtration,
retention of sodium and water. It results in increasing intracranial pressure, brain oedema, and
cerebral angiospasm.
Eclampsia may develop at patients with the acute or exacerbation of the chronic glomerulonephritis,
and nephropathy of pregnancy.
Before eclampsia patient feels headache, sleepiness, languor, vomiting, short-time loss of sight,
speechlessness, transitory palsy, sudden increasing blood pressure, and black-out.
Eclampsia attack begins from tonic, then clonic spasms. The consciousness is soporous. The face is
cyanotic with swelling the neck veins, and foaming at the mouth. The tongue is bit. The pupils are
wide and don’t react to light. The pulse is intense, rare. The blood pressure is increased. The body
temperature is increased too. Sometimes can be involuntary defecation and micturition. The attack
duration is 10-15 min.
Complication: hemorrhagic stroke, acute left ventricular failure, temporary disorders of sight, speech,
amnesia.

Chronic renal failure

Chronic renal failure is usually the result of a gradually progressive loss of renal function. It
occasionally results from a rapidly progressive disease of sudden onset. Few symptoms develop
until after more than 75% of glomerular filtration is lost; then, the remaining normal
parenchyma deteriorates progressively, and symptoms worsen as renal function decreases.
If this condition continues unchecked, uremic toxins accumulate and produce potentially fatal
physiologic changes in all major organ systems.
Causes
Chronic renal failure may result from:
• chronic glomerular disease such as glomeralonephritis
• chronic infections, such as chronic pyelonephritis or tuberculosis
• congenital anomalies such as polycystic kidneys
• vascular diseases, such as renal nephrosclerosis or hypertension
• obstructive processes such as calculi
• collagen diseases such as systemic lupus erythematosus
• nephrotoxic agents such as long-term aminoglycoside therapy
• endocrine diseases such as diabetic neuropathy.
Such conditions gradually destroy the nephrons and eventually cause irreversible renal
failure. Similarly, acute renal failure that fails to respond to treatment becomes chronic renal
failure.
Classification
Chronic renal failure may progress through the following stages:
I stage – initial (glomerular filtration rate [GFR] 90 to 60 ml/minute, blood creatinin 0,176-
0,352mmol/l, blood urea < 10 mmol/l, Hb 119-135 g/l. Electrolytes are in a norm)
II stage - evident (GFR 60 to 30 ml/minute, blood creatinin 0,352-0,701 mmol/l, blood urea 10-
17 mmol/l, Hb 89-118 g/l. Na and K are decreased but Mg, Ca, Cl, P are in a norm, polyuria,
hypoisostenuria)
III stage – severe (GFR 30 to 15 ml/minute, blood creatinin 0,701-1,055 mmol/l, blood urea
17-25 mmol/l, Hb 66-88 g/l. Na and K are decreased or in a norm but Mg↑, Ca↓, Cl in norm or
↓, P ↑, polyuria or pseudonormal diuresis, hypoisostenuria, subcompensated acidosis)
IV stage – terminal (GFR < 15 ml/minute, blood creatinin >1,055 mmol/l, blood urea >25
mmol/l, Hb < 66 g/l. Na is decreased or in a norm, K is increased, Mg↑, Ca↓, Cl in a norm or ↓,
P ↑, oligouria, anuria, decompensated acidosis).

Signs and symptoms

Chronic renal failure produces major changes in all body systems.

Renal and urologic changes

Initially, salt-wasting and consequent hyponatremia produce hypotension, dry mouth, and loss
of skin turgor, listlessness, fatigue, and nausea. Later, somnolence and confusion develop.
As the number of functioning nephrons decreases, so does the kidneys' capacity to excrete
sodium, resulting in salt retention and overload. Accumulation of potassium causes muscle
irritability, then muscle weakness as the potassium level continues to rise.
Fluid overload and metabolic acidosis also occur. Urine output decreases: urine is very dilute
and contains casts and crystals.

Cardiovascular changes
Renal failure leads to hypertension and arrhythmias, including life-threatening ventricular
tachycardia or fibrillation. Other effects include cardiomyopathy, uremic pericarditis, pericardial
effusion with possible cardiac tamponade, heart failure, and peripheral edema.

Respiratory changes
Pulmonary changes include reduced pulmonary macrophage activity with increased
susceptibility to infection, pulmonary edema, pleuritic pain, pleural friction rub and effusions,
and uremic pleuritis and uremic lung (or uremic pneumonitis). Dyspnea from heart failure also
occurs, as do Kussmaul's respirations as a result of acidosis.

GI changes
Inflammation and ulceration of GI mucosa cause stomatitis, gum ulceration and bleeding and,
possibly, parotitis, esophagitis, gastritis, duodenal ulcers, lesions on the small and large bowel,
uremic colitis, pancreatitis, and proctitis. Other GI symptoms include a metallic taste in the mouth,
uremic fetor (ammonia smell to breath), anorexia, nausea, and vomiting.

Cutaneous changes
Typically, the skin is pallid, yellowish bronze, dry, and scaly. Other cutaneous symptoms include severe
itching; purpura; ecchymoses; petechiae; uremic frost (most often in critically ill or terminal
patients); thin, brittle fingernails with characteristic lines; and dry, brittle hair that may change color
and fall out easily.

Neurologic changes
Restless leg syndrome, one of the first signs of peripheral neuropathy, causes pain, burning, and
itching in the legs and feet, which may be relieved by voluntarily shaking, moving, or rocking them.
Eventually, this condition progresses to paresthesia and motor nerve dysfunction (usually bilateral
foot drop) unless dialysis is initiated.
Other signs and symptoms include muscle cramping and twitching, shortened memory and
attention span, apathy, drowsiness, irritability, confusion, coma, and seizures. Electroencephalogram
changes indicate metabolic encephalopathy.

Endocrine changes
Common endocrine abnormalities include stunted growth patterns in children (even with elevated
growth hormone levels), infertility and decreased libido in both sexes, amenorrhea and cessation of
menses in women, and impotence and decreased sperm production in men. Other changes include
increased aldosterone secretion (related to increased renin production) and impaired carbohydrate
metabolism (caus ing increased blood glucose levels similar to those found in diabetes mellitus).

Hematopoietic changes
Anemia, decreased red blood cell (RBC) survival time, blood loss from dialysis and GI bleeding, mild
thrombocytopenia, and platelet defects occur. Other problems include increased bleeding and
clotting disorders, demonstrated by purpura, hemorrhage from body orifices, easy bruising,
ecchymoses, and petechiae.

Skeletal changes
Calcium-phosphorus imbalance and consequent parathyroid hormone imbalances cause muscle
and bone pain, skeletal demineralization, pathologic fractures, and calcifications in the brain, eyes,
gums, joints, myocardium, and blood vessels. Arterial calcification may produce coronary artery
disease.
Diagnosis
Clinical assessment, a history of chronic progressive debilitation, and gradual deterioration of renal
function as determined by creatinine clearance tests lead to a diagnosis of chronic renal failure.
The following laboratory findings also aid in diagnosis:
• Blood studies show elevated blood urea nitrogen, serum creatinine, and potassium levels;
decreased arterial pH and bicarbonate; and low hemoglobin (Hb) and hematocrit (HCT).
• Urine specific gravity becomes fixed at 1.010; urinalysis may show proteinuria, glycosuria,
erythrocytes, leukocytes, and casts, depending on the etiology.
• X-ray studies include kidney-ureter-bladder radiography, excretory urography, nephrotomography,
renal scan, and renal arteriography.
• Kidney biopsy allows histologic identification of underlying pathology.
Material for the self-control (added)

7. Reference source
Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine Part 1. – Vinnytsya:
NOVA KNYHA, 2006. – p. 371-384, 388-401

Professor assistant Demchuk A.V.

Control questions:
 Theoretical questions:
1. What are the causes of the renal arterial hypertension?
2. What are the clinical features of the renal arterial hypertension?
3. What is an eclampsia? Causes, pathogenesis, clinical presentation, complication.
4. Definition of the chronic renal failure, its causes.
5. Classification of the chronic renal failure.
6. Clinical symptoms and signs of affecting different systems at the patients with chronic
renal failure.
7. Instrumental and laboratory examination patient with chronic renal failure.
4.3. Practical tasks
1. Revealing and assessment of the renal hypertension symptoms and signs
2. Revealing and assessment of the eclampsia symptoms and signs
3. Revealing and assessment of chronic renal failure symptoms and signs
 TOPIC 37
Management of patient. Writing the case history

8. Importance of the topic

Management of patient is the basic part of the physician’s working. Practical skills of
taking history, physical examination, recognizing main symptoms and signs of disease,
joint them into syndrome and formulating primary diagnosis are very important for
physicians of every specialty. Every doctor must correctly assess patient ’s state and
perform him laboratory and instrumental investigations for confirming diagnosis and
prescribing properly treatment. All doctor’s actions must be completely reflected in
case history of patient.

2. Concrete aims:
─ To master and train skills of taking history
─ To master and train skills of physical examination of patient
─ To master and train skills of administering appropriate instrumental and
laboratory investigation
─ To write a case history of patient
3. Basic training level

Previous subject Obtained skill

Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine patients with respiratory, cardiovascular, gastrointestinal and
kidney disorders
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Case history Anamnesis vitae
Taking history palpation
Anamnesis morbi percussion
auscultation Visual inspection
Laboratory tests Instrumental examination
Substantiation of diagnosis Clinical diagnosis

4.2. Theoretical questions:

90. Guidelines for clinical examination of patient
91. Guidelines writing case history
4.3. Practical task that should be performed during practical training
1. training skills of taking history
2. training skills of physical examination of patient
3. training skills of administering appropriate instrumental and laboratory
investigation
4. writing a case history of patient
Topic content
Guidelines for clinical examination of patient and writing case history
Interviewing
Passport part:
First and family name
Age
Gender
Occupation and job place
Home address
Admitting date
Present complaints:
Enumerate main complaints are that disturb patient most of all and have made him to visit
doctor.
Enumerate general complaints: weight loss, night sweating, fatigue, sleeping pattern, appetite,
fever, itch
Refinement of the main complains: if patient has pain you should ask about localization,
intensity, character, course, duration, frequency, radiation, associated symptoms, cause of
onset, aggravating factors, and relieving factors.
Additional inquiring about affected systems
Additional inquiring about other systems and refinement of all complaints which have been
obtained.
Inquiring about respiratory system:
1. Breathing free or difficult, throat pain, voice characteristics;
2. Chest pain
3. Breathlessness or dyspnea
4. Asthma attack
5. Wheeze
6. Cough dry or with sputum production and characteristics of sputum
7. Haemoptysis
Inquiring about cardiovascular system:
1. Heart pain
2. Palpitation
3. Intermissions
4. Dyspnea
5. Oedema
6. Cough
7. Haemoptysis
8. Syncope (faint)
9. Heaviness at the right subcostal region
Inquiring about gastrointestinal system
1. Abdominal pain (constant or colicky, sharp or dull; site; radiation; duration; onset;
severity; relationship to eating and bowel action; alleviating/exacerbating or associated
features)
2. Dryness in mouth
3. Swallowing (dysphagia, odynophagia, aphagia)
4. Beaching (with air, “rotten eggs”, soil or bitter liquid)
5. Heartburn
6. Nausea
7. Vomiting
8. Abdomen swelling
9. Diarrhea
10. Hematemesis
11. Constipation
12. tenesmus
 13. Stool: colour, consistency, blood, slime
Genitourinary system:
1. Loins pain
2. Dysuria (painful micturition)
3. Haematuria
4. Nocturia
5. Polyuria
6. Frequent micturition
7. Ishuria
8. Hesitancy (difficulty starting micturition)
9. Vaginal discharge
10. Menses: frequency, regularity, heavy or light, duration, painful, number of pregnancy
11. Menarche, menopause.
Endocrinology system
General complaints (weight loss or gait, muscle pain, fatigue, sleeping pattern, changed
appetite, thirst and amount of the drinking liquid)
Musculoskeletal system
1. Pain
2. Stiffness
3. Swelling of joints
4. Joint movement and deformation
5. Muscular straight
Nervous system
1. Patient character
2. Headache
3. Dizziness
4. Memory
5. Emotions
6. Hallucinations
7. Convulsions
8. vision
9. hearing
10. smelling
Anamnesis Morbi
1. The time of disease onset (acute or gradual)
2. The cause
3. The first symptoms and their character
4. Previous examinations, treatments and their results
5. Exacerbations and remissions, their duration
6. The cause of the present hospitalization.
Anamnesis Vitae (Past medical history)
Biographical data: place of the birth, the age of the parents, living conditions in childhood,
education, profession.
Past diseases: in childhood, adolescent, and adult (tuberculosis, cardiovascular, nervous,
psychiatric, endocrine diseases, etc), possible traumas or operation.
Occupational history: occupation, labor conditions, exprosure to hazard, e.g. chemicals,
mechanical (noise, vibration, high or low temperature, etc), foreign travels, and accidents.
Social history: type of home, size, owned or rented, illumination, hygienic conditions, etc;
nutrition: regularity, quantity (under eating, overeating), character of food (vegetables, fruit,
meat, fatty food, salt).
Family history: hereditary diseases in family (parents, sisters, brothers).
Harmful habits: smoking cigarettes, drinking alcohol and drug abuse. Smoking history:
packs/year= amount of cigarettes in a day*amount of smoking years/20.
Allergological history: allergic reactions to food products, cosmetics, odor, drug, dust, plants
etc; Types of allergic reaction: rhinitis, conjunctivitis, Quinke ’s oedema, anaphylactic shock,
asthma attack etc.
Assessment of the anamnesis data
4. Highlight the main complaints indicated injured system.
5. Note the character of disease (chronic, acute, subacute).
6. Indicate the most likely causes of the disease development.
Objective examination
General visual examination
General patient’s condition: satisfactory, moderate, grave, extremely grave.
Consciousness: clear, depressed (stupor, spoor, coma), excited (irritative disorder, delirium).
Posture of the patient: active, passive, forced.
Patient’s gait: firm, free, and straight (healthy); pathologic: spastic, paretic, hemiplegic, puppet,
peroneal, cerebellar, “proud”.
Habitus: body-build, height and body weight.
Skin: color, eruption, turgor, elasticity,moisture, temperature. Oedema: localization, exposure.
Nails characteristics.
Subcutaneus fat.
Face of the patient: shape, expression, symmetry, color of skin, eyes, ears, nose, lips, hear.
Cavity of the mouth: color of the mucosa, gum, gingival, tongue: shape and size, fur, surface.
Neck: shape, size, symmetry, skin color, scars, visible pulsation, lymph nodes and thyroid gland.
Muscular system: the level of development, sex and age correspondence, tenderness, muscular
tonus, cramps.
Joins system: symmetrical joints, shape, configuration, swelling, hyperemia, movements.
Assessment of the anamnesis and visual examination data
1. Highlight pathological signs obtained by visual inspection
2. Indicate connection between anamnesis data and visual inspection data.
3. Suggest which system or organ could be affected according to get data.
Examination of the respiratory system
Visual inspection of the chest
Shape must be described (normosthenic, asthenic, hypersthenic; pathological:
emphysematous, paralytic, rachitic, funnel, foveated, scoliotic, kyphotic, kyphoscoliotic.
Pattern of breathing: type of respiration, participation of the chest wall in breathing act,
respiration rate, depth and rhythm, participation of the accessory muscles in breathing.
Palpation of the chest
Identification of the tender areas
Assessment of the elasticity of the chest
Assessment of the vocal fremitus
Potenzher’s symptom
Percussion of the lungs
1. Comparative percussion of the lungs: character of the percussion sound over different parts
of the lungs.
2. Topographic percussion of the lungs:
 - determination of the upper borders of the lungs (posterior and anterior positions of
the apex),
- determination of the lower borders of the lungs (along topographic lines: right from
parasternal till paraspinal, left from axillary anterior till paraspinal),
- determination of the excursion of the lower borders of the lungs (scapular and
midaxillary lines).
Auscultation of the lungs:
1. Listening the sounds generated by breathing – breath sound (vesicular or bronchial);
2. Listening adventitious sounds (rales (wheezes, dry, moist), crepitation, pleural friction
rubs).
Assessment of the respiratory system examination
1. Highlight pathological signs obtained by examination
2. Indicate connection between different obtained signs.
3. Suggestion about possible syndrome of the respiratory disease.
Examination of the cardiovascular system
Visual examination of the precordial area
Note cardiac hump, pathological pulsation and skin change on this area
Palpation of the apical pulse
Note location, area, height, resistance. Epigastric pulsation can be produced by the
abdominal aorta or liver.
Pulsation of the right ventricle is seen directly under the xiphoid process, increases on
breathing in, drawing in is more prominent that sticking out.
Percussion. Borders of relative and absolute cardiac dullness
The heart percussion allows determining its size, shape as well as the size of the vascular
band.
The area of the heart not covered by the lungs, which produces the dull sound on
percussion, is termed absolute heart dullness. The portion of the heart covered with the lungs
produces a deadened sound termed relative dullness.
Before percussion it is necessary to determine the level of the diaphragm as the changes
in the position of the diaphragm influence the location of the heart in the chest and the borders
of the heart dullness. With this purpose, the location of the lower border of the right lung
(normally in the 6th intercostal space) is determined along the right medioclavicular line.
Percussion is started from the 1 st intercostal space along the intercostal spaces from a clear to
dull sound.
After determining the position of the diaphragm the plessimeter finger is shifted one
intercostal space upper (or two ribs, in the 4 th intercostal space) placing it parallel to the right
border of the heart. Making taps using medium force, the plessimeter finger is moved along the
intercostal space to the heart until deadened sound appears. The right border of the heart is
noted along the external border of the plessimeter pointing to the clear sound. The right border
is formed by the right atrium and is normally in the 4 th intercostal space 1—1.5 cm outer (to the
right) the right sternal line. To determine the upper border of the heart the plessimeter finger is
placed in the first intercostal space фдщтп the left parasternal line and is shifted downwards
making taps using medium force until a deadened sound appears. The upper border of relative
heart dullness is formed by the auricle of the left atrium and the trunk of the pulmonary artery
and is normally located in the 3 rd intercostal space. The left border of the relative dullness is
determined in the same intercostal space, where apical pulse is located, usually in the 5 th
intercostal space. Percussion is performed in the 5 th intercostal space from the left anterior
axillary line towards the sternum. Normally, it is formed by the left ventricle and is in the 5 th
intercostal space 1-2 cm inner the left medioclavicular line and coincides with the apical thrust.
 Then the borders of absolute heart dulness (the area of the heart which is not covered
with the lungs and adjoins the breastbone) are determined. Light percussion is used for this
purpose. The percussion of this area produces a dull sound. To determine the right border of
absolute heart dulness after determining the border of relative dulness in the 4 th intercostal
space, the plessimeter finger is placed parallel the sternum and then is moved inward until dull
sound appears. Normally the right border of absolute heart dullness is noted along the left edge
of the breastbone. To determine the upper border of absolute heart dullness, the plessimeter
finger is placed in the 3rd intercostal space parallel the ribs, the percussion is performed
downward the intercostal spaces until a dull sound appears. This is normally located in the 4 th
intercostal space. To determine the left border of absolute heart dullness percussion is done
along the 5th intercostal space from the border of relative heart dullness until a dull sound
appears. This is normally 1—2 cm inner the left border of relative dullness.
Auscultation of the heart
Auscultation is performed at quiet respiration, when the patients does not breathe, at
the height of the expiration and inspiration, in a lying and upright position, on the left side, and
after dosed physical load.
The consequence of listening is determined by the incidence of the diseases of the
respective structures: most frequent are the affections of the left ventricle, mitral valve, aortic
valve, right ventricle, tricuspid valve and pulmonary artery valve. When necessary, other
regions can be listened to, e.g. the place of sound conduction, but this is done after the
standard auscultation.
Points of heart auscultation:
a) Point 1 - at the area of the heart apex - mitral valve;
b) Point 2 - at the 2 interspace on the right near the edge of the breastbone - aortic
valve;
c) Point 3 - at the 2 nd interspace on the left near the edge of the breastbone -
pulmonary artery valve;
d) Point 4 – at place of xiphoid process origin - tricuspid valve.
e) Point 5 (Botkin-Erb) is listened at the 3rd intercostal space at the left edge of the
breastbone. These positions are associated with the projection of the aortic
valve on the precordial area. It is the place where acoustic phenomena
developing at the beginning of diastole, especially when the cusps of the aortic
valves are not closed (diastolic sound of blood regurgitation), are well heard.
In healthy adults the heart melody consists of two sounds (first and second), this is
divided by two pauses (systolic and diastolic).
Heart sounds are short acoustic phenomena resulting from tissue vibration, which occur
at vibrations of strained muscles of the ventricles and valve cusps. The first sound (systolic) is
heard at the beginning of systole, the second heart sound (diastolic) is heard at the beginning of
diastole.
The first sound consists of three components: muscular, valvate, and vascular.
The second sound consists of two components: valvate and vascular.
The first and second sounds are heard over the whole precardiac area, but the cardiac
melody differs in different auscultation points: the first sound is better heard in points 1 and 4,
the second one in points 2, 3, 5. There are other features which allow to distinguish the first
and second heart sounds: the first sound is longer, the frequency of vibrations is lower.
The first sound is heard at the beginning of a short pause (systole), it coincides with the
apical pulse and pulsation of the carotid arteries.
Heart murmurs
 Heart murmurs are prolonged acoustic phenomena produced by the working heart.
They are divided into two groups: extracardiac and intracardiac.
Extracardiac murmurs are pericardial friction rub and cardiopulmonary murmurs.
Intracardiac murmurs develop inside the heart and large vessels. Depending on the cause the
murmurs are divided into organic (valvate), functional and organ-functional (muscular).
The following properties of the murmur have diagnostic significance:
- association of the murmur with the phase of the cardiac cycle (systolic, diastolic);
- the area where it is heard best (heart apex, 2 nd intercostal space to the right and left of
the sternum, basis of the xiphoid process);
- direction of the murmur radiation (axillary area, cervical vessels, subscapular area);
- loudness, duration of the murmur;
- the timber of the murmur (blowing, sawing, scratching, musical);
- relation of the murmur and the sound after which it is heard (merges with the sound,
separated from it);
- if the murmur increases or decreases during the pause;
- influence of the position, physical exercise, phases of respiration.
Investigation of the pulse and arterial pressure
Periodic, simultaneous with the work of the heart vibrations of the arterial walls are
called arterial pulse. The most frequent place to study the pulse is the radial artery as it is
located superficially under the skin between the styloid process and the tendon of the inner
radial muscle. The topography of the radial artery allows to press the vessel to the bone, which
facilitates the study of the pulse. The hand of the patient is held with the physician's right hand
in the area of the radioulnar joint, the thumb of the physician should be on the elbow side, the
fingers on the radial side. After the artery is felt it is pressed with the point and middle fingers.
When the wave passes the artery, the physician feels dilation of the artery, that is the pulse.
First, it is necessary to study the properties of the radial artery. The fingers of the physician
should glide along the artery in transverse and longitudinal direction. The normal sensation is
that of a thin, soft, even, elastic, pulsating tube.
Then it is necessary to determine whether the pulses are equal on the both hands.
Normally they are equal. If the pulses are unequal, this is called pulsus differens.
After comparison of the pulse on the both hands, it is necessary to study the properties
the pulse on one hand. If the pulse is different on the both hands, it is studied on the hand
where it is more intensive.
The following properties are to be determined.
Pulse rate , the number of pulse beats per minute. In healthy individuals pulse rate is 60-
80 beats per minute.
Rhythm of the pulse, the beats follow with equal intervals and are equal, i.e. regular
pulse (pulsus regularis). In disturbances of the heart function, this regularity changes, it
becomes arrhythmical, irregular, an irregular pulse (pulsus irregularis).
If the pulse is arrhythmical, it is necessary to determine if the number of the pulse
waves corresponds to the number of the heart contractions. The difference between the
number of the heart contractions and pulse waves per one minute is termed pulse deficiency,
the pulse is called a deficiency pulse (pulsus deficiens).
Pulse tension is the pressure of the blood exercised on the wall of the artery. It is
determined by the force, which should be exercised to compress the artery completely in order
to arrest the blood flow in it. This property of the pulse gives the information about the state of
the vascular system and the arterial pressure. In healthy persons the pulse tension is
satisfactory.
 Pulse filling is the amount of blood in the vessel. This property is most difficult to
determine, namely according to the maximum and minimum volume of the vessel (how the
diameter of the vessel changes in the period of dilation and collapse). To do this, proximal
fingers on the radial artery should press the vessel gradually, the distal finger determines its
maximum filling. In healthy persons the pulse is satisfactory.
Pulse value is a collective concept, uniting such properties as filling and tension. It
depends of the degree of the artery widening during systole and its collapse during diastole. In
healthy persons the pulse is sufficient.
The shape or rate of the pulse is the rate of dilation and the following contraction of the
artery. This property depends of the rate of the pressure changes in the arterial system during
systole and diastole. In aortic valve incompetence, an abrupt pulse (pulsus celer) or a bouncing
pulse (pulsus silens) as well as pulsus altus: the stroke blood volume and systolic blood pressure
are increased, during diastole the pressure drops quickly as the blood returns from the aorta to
the left ventricle can be present.
Slow pulse (pulsus tardus) is opposite to an abrupt pulse. This is associated with slow
increase of the blood pressure in thearterial system and its small fluctuations during a cardiac
cycle. This is observed of aortic stenosis.
Dicrotic pulse (pulsus dicroticus) is a second additional wave after reduction of a normal
pulse wave. In healthy subjects it is not pulpated but registered on sphygmogram. A dicrotic
pulse is present in reduced tone of the peripheral arteries (fever, infections, severe pneumonia,
fig. 47a).
An alternating pulse (pulsus alterans) is alterations of large and small pulse waves when
the pulse is rhythmical (severe affection of the myocardium, i.e. myocarditis, cardiomyopathy,
fig. 47b).
A paradoxical pulse (pulsus paradoxus) is reduction of the pulse waves during breathing
in (in adhesion of the pericardium layers due to compression of the large veins and reduction of
the heart filling during expiration (Fig. 47c).
Arterial blood pressure and methods to measure it
Arterial pressure is the stress exerted by the blood on the walls of the vessels (lateral
pressure) and the column of the blood from the site of the pressure to periphery (end
pressure).
During left ventricle systole, blood pressure in the arteries is the highest, this is systolic
or maximal blood pressure. During diastole it is the lowest, minimum or diastolic pressure. The
difference between maximum and minimum pressure is termed pulse pressure.
Investigation technique The most practical is an auscultation method proposed by N. S.
Korotkoff in 1905. The pressure is usually measured on the brachial artery. The cuff is wrapped
and fastened around the bare upper arm of the patient. The cuff should be tightened to allow
only one finger between it and the patient's skin. The edge of the cuff with the rubber tube
should face downward. The zero level of the apparatus, the artery and the patient's heart
should be at the same level. The patient's arm should rest comfortably with the palm upright
and the muscles relaxed. Than the valve of the apparatus is turned off and the cuff is inflated
with air until the pressure in it exceeds the 30 mm the level when pulsation of the brachial and
radial artery is not felt. After that the valve is turned on and the air is allowed to escape slowly
from the cuff. When the pressure in the cuff is a little lower than systolic pressure, sounds
simultaneous with the heartbeat are heard with a phonendoscope over the brachial artery.
When the sound appears, the values noticed correspond to systolic pressure. When the
pressure in the cuff equals diastolic pressure, the obstacle to the blood flow disappears, the
vibrations decrease sharply. This moment is characterized by evident weakening and
disappearing sounds and corresponds to diastolic pressure.
 Arterial pressure is measured in millimeters mercury. Normal systolic pressure ranges
within 100—140 mm Hg (13—18 kPa), diastolic pressure 60 —90 mm Hg (8 —11 kPa).
Assessment of the cardiovascular system examination
1. Highlight pathological signs obtained by examination
2. Indicate connection between different obtained signs.
3. Suggestion about possible syndrome of the cardiovascular disease.
Examination of the abdomen
Inspection of the abdomen: assess shape, size, symmetry, participation in the breathing,
umbilicus position, expression of the subcutaneous veins, scars, eruptions, scratches, visible
pulsation, peristalsis, teleangioectasia.
Palpation of the abdomen
Superficial tentative oriental palpation
identify muscular resistance, abdominal tenderness, diastesis recti, fluctuation symptom,
Shchetkin-Blumberg symptom, Mendel symptom.
Deep palpation:
Characteristics of the abdominal organs: localization, diameter, density, the condition of
surface (smooth, tubercular), tenderness, mobility, rumbling sounds.
Sequence: the sigmoid, the caecum, the ascending, the descending colons, the stomach, the
transverse colon, the liver, the pancreas, the spleen.
Percussion of the liver according to M.G. Kurlov, Merphy, Kera, Vasilenko, frenicus symptoms.
Assessment of the abdomen examination
1. Highlight pathological signs obtained by examination
2. Indicate connection between different obtained signs.
3. Suggestion about possible syndrome of the gastrointestinal disease.
Formulating suggested (primary) diagnosis.
Plan of the laboratory and instrumental examination
1. Blood investigations (Full blood analysis/ count; biochemical, bacteriological)
2. Urine investigations.
3. Sputum investigations
4. Feces investigation
5. ECG
6. Ultrasound examination of the heart
7. Ultrasound examination of the heart
8. X-ray examination and etc (all for confirm your suggested diagnosis)
Data of the laboratory and instrumental examination
Found and form clinical diagnosis according to classification.
Add patient’s temperature chart.
7. Reference source
Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine Part 1. – Vinnytsya:
NOVA KNYHA, 2006.
Control questions
1. Guidelines for clinical examination of patient
2. Guidelines writing case history
Practical task that should be performed during practical training
1. training skills of taking history
2. training skills of physical examination of patient
3. training skills of administering appropriate instrumental and laboratory
investigation
4. writing a case history of patient
 TOPIC 38
Symptoms and syndromes of anaemias. Full blood analysis
9. Importance of the topic
Full blood test is the commonest test of patient’s examination. Its changes reflect
activity of inflammatory process, disorders of the hematopoietic system, immune
system, malignant process. Anemias are the most prevalent diseases of hematopoietic
system influencing to course and treatment different diseases of internal organs.
Knowledge about anemias, normal and changed full blood test is very important for
physicians of every specialty.

2. Concrete aims:
─ To study mains parameters of full blood test
─ To study main symptoms and signs of anemic syndrome
─ To study classification and clinical features of the different anemias
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the bone marrow and hematopoietic system
Normal physiology Function of the blood cells, hemopoiesis
Histology Ontogenesis and histological structure of the bone marrow and
hematopoietic system
Biochemistry Hemoglobin and iron metabolism
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
Erythremia Eosinophylia
Leukopenia Lymphocytosis
Leukocytosis Hemolysis

4.2. Theoretical questions:

92. What parameters are investigated by full blood test?
93. Normal value of hemoglobin and erythrocytes, changes in pathology.
94. Normal value of leukocytes, changes in pathology
95. Anemia, definition, classification.
96. Clinical presentation of the iron-deficiency anemia
97. Clinical presentation of the pernicious anemia
98. Clinical presentation of the hemolytic anemia
99. Clinical presentation of the post hemorrhagic anemia
100. 4.3. Practical task that should be performed during practical training
107. Assessment of full blood test
108. Revealing and assessment of different anemias

Topic content
Full blood test
Red blood (breathing function is executed (oxygen is carried)
Haemoglobin – 120-160 g/l
Erythrocytes – 3,5-5,5 x 1012 / l
Color index of blood– 0,8 – 1,05
Reticulocytes – 2-12 0/00
Haemoglobin and erythrocytes – reduced at anaemias, increase at polycythemia vera (primary)
secondary - chronic pathology of lungs due to chronic hypoxia, tumors of kidney, liver, ovary,
uterus due to increase erythropoietin and others.
The coloured index is reduced at iron-deficiency anaemia, is increased – at В12-deficiency
anaemia
Reticuloctes – their level is reduced at iron-deficiency anaemia and В12-deficiency anaemia,
increassed – at acute posthaemorragic anaemia and hemolytic anaemias.
White blood (function of defence is executed)
Leucocytes – 4-9 x 109 /l
bond neutrophil– 1-6%
Segmented neutrophil – 47-72%
Eosinophils – 1-5%
Basophils – 0-1%
Lymphocytes – 19-37%
Monocytes – 3-11%
Erythrocyte sedimentation rate (ESR) – 2-10 mm/h (at men), 2-15 mm/h (at women)
Physiological leucocytosis:
 After eating
 After the physical exercise
 After hot or cold water procedures
 During a 2-d half of pregnancy
 During delivery
Pathological leucocytosis:
 Leukosises
 Acute infectious diseases
 General and local infectious processes (pathology of internal organs, surgical and
gynaecological pathology)
 Sepsis
 Streptocooccus skin inflammation
 Cerebrospinal meningitis
 Tumour of marrow (haematosarcoma)
 After loss blood
 Myocardial infarction
 Burns
 Tumours
 Lymphogranulomatosis
 Agony
Leucopenia (distruction leucocytes and depression of the marrow by somethings)
 Action of radiation (radiation illness)
 Typhoid
 Flu
 Pox
 Measles
 Miliary tuberculosis
 Heavy sepsis
 Action of toxic poisons
 The Biermer’s anaemia
  Chronic splenomegaly
 Aplastic anaemias
 sulphanilamid preparations, amidopyryn, butadion using
Basophilia (take part in formation and accumulation of heparin)
 Myeloid leucosis (bazophilic-eosinophilic association)
Eosinophilia:
 Intestinal worm invasion
 Tumor of liver (cysts)
 Tumor of spleen (cysts)
 Allergic illnesses
 Increase of activity of parasimpatic department of the vegetative nervous system)
 Chronic myeloleucosis (bazophilic-eosinophilic association)
Eosinopenia:
 Acute infectious diseases
 Typhoid
 Acute leukosis
 The Biermer's anaemia
Lymphocytosis:
 Typhoid
 The Biermer's anaemia
 Flu
 Chronic splenomegaly
 Endocrine diseases
 Avitaminosises
 Starvation (голодание)
 In the period of recovery after acute infections
 Chronic tuberculosis
 Chronic syphilis
 Mononucleosis infectious
 Lympholeucosis
Lymphopenia:
 Chronic myeloleucosis
 Sepsis
 Heavy infections
 Measles
 Destruction of lymphoid tissue (sarcoma, cancer, tuberculosis of lymphatic nodes)
Monoсytosis (function of moving and phagocytosis, formation of antibodies):
 In the period of recovery after acute infections
 After the attack of recurrent typhus
 During the attack of malaria
 At a chronic malaria
 Intestinal worm invasion
 Chronic infections (syphilis, tuberculosis, chronic sepsis)
 Chronic septic endocarditis
 Monocytic acute tonsillitis (infectious mononucleosis)
Monocytopenia:
 Heavy sepsis
 Myeloleucosis
  Lympholeucosis
Myelogram
The puncture of breastbone is executed by the Kassyrsky needle, preparation of smears,
their staining by Oppengeym or Romanovskiy.
Conduct the count 1000 myelokaryotcytes (nuclear), whereupon the following indexes
are determined:
1. Cytosis of marrow (can be rich, poor) – in a norm 2 million cells in a 1 mcL of marrow
content
2. Count of amount of blasts cells (the cells of 1-4 classes consider). In the norm of them
to 2,5%.
Diagnostic value:
Less than 5% - revival of blood formation,
5-10% is suspicion of acute leucosis,
more than 10% is acute leucosis.
3. Estimation of myeloid (myelokaryocytic) sprout (myeloblastes, promyelocytes,
myelocytes, young, stab, segmented neutrophils) – in the norm of them 50-70% (50-180
х 109/л depending on breeding of marrow content), among which the old cells must
make 2/3, youths – 1/3.
Diagnostic value:
 The increase of cells of myeloid sprout – at the leucosises,
 Diminishment – at the agranulotsytosis.
4. Index of ripening of neutrophils is calculated on a formula:
(promyelocytes + myelocytes + metamyelocytes):(stab neutrophils + segmented
neutrophils).
In a norm it makes to 1.
5. Red (erythroid) sprout (from erythroblasts to acidophilic normocytes) – in a norm make 20-
25%, repressing majority from them hemoglobincontent cells (20%), 5% are
hemoglobinuncontenc cells.
6. Index of ripening of red corpuscles is calculated on a formula:
(acidophilic normocytes + polychromatophilic normocytes):(all cells of erythroid row).
In a norm it makes 0,8-0,9.
7. Correlation beetwen myelokaryocytic and erythroid sprout
In the norm it must be as 4:1 or 3:1.
8. Megakaryocytic sprout – in the norm of them 50-150 in 1 mcL (count in the Goryaev
chamber), in painting – 6-10 in one preparation.
Diagnostic value:
 The increase of their amount at immaturity of cellular structures and rich marrow
testifies to the Verlgof illness.
9. Monocytes +Lymphocytes + Plasmacytes (Plasma cells) – in a norm 6-10%.
Diagnostic value:
 Plasma cells in a norm to 2,5%, their increase of a to 15% diagnostic value does not
have (can testify to the infectious process), at their increase more 15%-20% shows the
plasma cells reaction on a cancer, myelomic illness.
Lymphocytes in a norm 8-12%, their increase of number more than 15% at poor marrow
shows the aplastic of marrow, more than 30% at rich marrow - the chronic lympholeucosis.

Syndrome of anaemia – it is clinic-laboratory symptomocomplex, which is related to hypoxia

(oxygen starvation) of organs and tissues due to decline of hemoglobin and red corpuscles in
unit of blood volume.
Anaemic complaints
 Cardial: pain, palpitation, interruptions, breathlessness
 Cerebral: pain, dizziness, syncopal states (syncope), appearance of sparkles before eyes,
buzzing in the ears
 General: weakness, rapid fatigue, myalgias (pain in the muscles)
Objective data at anaemic syndrome
 Pallor of skin and mucous membranes,
 Becoming thin, weight loss
 Languor of muscles, unsteady gait
 Tachycardia, tachyarrhythmia, blood pressure low, a pulse is small, soft, frequent,
expansion of borders of cardiac dullness, weakening of 1 heart sound on an apex, on the
Botkyn’s point, weakening of 2 heart sound on the aorta and the pulmonary artery (in
heavy cases simultaneous weakening 1 and 2 heart sounds), functional systole noise
above all points of auscultation, „noise of top” on a v. Jugularis
Instrumental researches at the syndrome of anaemia
 ECG - tachycardia, tachyarrhythmia, disorders of excitability, decline of voltage (height)
of waves , change of eventual part of ventricle complex (depression or elevation ST,
pathological T)
 Echocardiography - decline of ejection fraction (in the norm 62-67%)
Acute posthemorrhagic anemia is the pathological state developed due to of rapid loss (during
1 day) more than 1 liter of blood
Etiology
1. Pulmonary bleeding
2. Gastro-intestinal bleeding
3. Traumas of thorax, abdominal region, breaks of liver, spleen
4. Hemorrhagic diathesis
5. Gynecological bleeding
According to the time after development of the blood-losing this type of anemia can has
3 phases. There are:
 The reflex phase of compensation (first 1-2 hours after hemorrhage (loss of blood))
is the symptoms of basic disease + tachycardia, tachyarrhythmia, pallor, the Full
blood analyses (FBA) indexes in a norm.
 Hydremic phase (from a 2 o'clock of to 2 days after hemorrhage (loss of blood))
– clinically syndrome of anaemia + changes in full blood test: ↓ Hb, ↓
erythrocytes (red (blood) cells), color index in a norm, reticulocytes, platelets,
leukocytes (white blood cells) and their formula – in a norm, erythrocyte
sedimentation rate (ESR) in norm.
 Bone-cerebral phase (from 2 days and > hemorrhage (loss of blood)) – clinically
there is the improvement of the state + in changes in FBA: ↓ Hb, ↓ erythrocytes
(red (blood) cells), color index in a norm, ↑↑reticulocytes, ↑↑ platelets,
↑↑leukocytes (white blood cells) and shift formula to the left, ↑↑erythrocyte
sedimentation rate (ESR)
Iron-deficiency anemia
Is the polyetyologycal disease with the development of the deficit of iron in a body and
formation of the disorders of synthesis of hemoglobin and development of trophy changes in
different tissues.
Etiology
1. Chronic hemorrhage (loss of blood)
2. Promoted necessity in a iron (pregnancy, lactation)
 3. Diminishment of receipt of iron with a meal (starvation)
4. Decline of iron absorption in gastro-intestinal system
5. Disorders of iron transport
Clinical syndromes:
а) anaemic,
б) sideropenic (iron-deficiency syndrome) - disorders of skin and its appendages,
muscular, muscle defeats, the gastro-intestinal defeats, changes of sense of smell, central
nervous system)
 Search source of bleeding (fybrogastroduodenoscopy, rectoromanoscopy,
fybrocolonoscopy, x-ray examination of the gastro-intestinal system, analysis of
excrement occult blood, gynaecological inspection)
 Decline of serum iron (n = 12-30 mcмoll/l)
Picture of peripheral blood
 Hypochromia of erythrocytes
 Anisocytosis
 Poikylocytosis
 Shysocytosis
 Polychromatophylia
Pernicious anaemia (В12 - deficiency anaemia) –
Is the polyetyologycal disease with the development of the deficit of vitamin B 12 in an organism
and formation of the disorders of synthesis of desoxyribonucleic acid of the nucleus of the
erythrocytes (dna) and development of changes in different tissues and systems.
Etiology
1. Disorders of absorption of the vitamin в12
2. Сompetition absorption of the vitamin в12 (intestinal worm invasion, dysbaсteriosis)
3. Disorders of receipt of the vitamin в12 with a meal (starvation)
4. Disorders of transport of the vitamin в12

Clinical syndromes
А) anaemic,
Б) gastro-intestinal syndrome (atrophy of mucous along all tract) defeat,
В) neurological syndrome (funicular myelosis – syndrome of defeat of back and lateral posts
of spinal cord)
Diminishment of maintenance of the vitamin в12 in the whey of blood
(in a norm = 0,4-0,9 мкг%)
Common blood analysis – anaemia, hyperchromia of erythrocytes, hyporegeneration,
ovalomacrocytosis, megalocytosis, basophilic pigmentation of red corpuscles, the Kebbot ’s
ring, Golly’s bodies, hypersegmentation of neutrophils, trombocytopenia
Sternal biopsy - advantage of basophilic forms – „dark blue marrow”
Hemolytic anemia - are the group of the pathological states with the development of
predominance of blood destruction above blood formation due to action of hemolytic poisons,
increase of the activity reticulo-endotelial system (res), and also there is the result of innate or
acquired erythropathy. Hemolytic anemia may be congenital and acquired

Microsferotcytosis (the Mynkovskiy-Shoffara illness) – inherited disease related to formation

of inferior membrane of red corpuscles and synthesis of red corpuscles of less than in the norm
of size (less than 6 microns)
 Clinical symptoms are anaemia, icterus, splenomegaly
  Haematological symptoms are anaemia + decline of osmotic resistance of erythrocytes,
mycrocytosis, reticulocytosis
 Biochemical indexes – hyperbilirubinemia, increase of the level of urobilin in urine,
increase of the level of sterkobilin in an excrement
Acquired hemolytic anaemias
 Clinical symptoms are anaemia, icterus, splenomegaly
 Haematological symptoms are anaemia + normal osmotic resistens of red corpuscles,
normal form and diameter of red corpuscles, reticulocytosis
 Biochemical indexes - hyperbilirubinemia, increase of the level of urobilin in urine,
increase of the level of sterkobilin in an excrement
 Positive tests on red anticorpuscles antibodies
7. Reference source
Olga Kovalyova, Tetyana Ashcheulova Propedeutics to internal medicine part 1. – Vinnytsya: Nova
knyha, 2006. – p. 407-417.
Control questions:
1. What parameters are investigated by full blood test?
2. Normal value of hemoglobin and erythrocytes, changes in pathology.
3. Normal value of leukocytes, changes in pathology
4. Anemia, definition, classification.
5. Clinical presentation of the iron-deficiency anemia
6. Clinical presentation of the pernicious anemia
7. Clinical presentation of the hemolytic anemia
8. Clinical presentation of the post hemorrhagic anemia
Practical task
1. Assessment of full blood test
2. Revealing and assessment of different anemias
 Topic 39
Hemorrhagic syndrome and disorders of coagulation. Disseminated
intravascular coagulation syndrome
1.Importance of the topic
Hemorrhagic syndrome usually is developed due to disorders of coagulation system. It
may accompany a lot of different internal diseases and frequently is developed after
surgical and obstetrical interventions. Underestimation of possible risk of coagulation
disorders and clinical symptoms and signs of the syndromes result in life-threatening
conditions which are treated very difficulty. Knowledge about manifestations of the
hemorrhagic syndrome and understanding mechanisms of development of the
clotting disorders is very important for physicians of every specialty.

2. Concrete aims:
─ To study types of hemorrhagic diathesis
─ To study laboratory tests of the hemostatic system
─ To study main symptoms and signs of hemophilia
─ To study main symptoms and signs of thrombocytopenia
─ To study main symptoms and signs of vascular wall disorders
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the hematopoietic system
Normal physiology Principles of blood coagulation
Histology Ontogenesis and histological structure of the bone marrow and
hematopoietic system
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
hematoma petechiae
ecchymoses telangiectasia
purpura bleeding time
partial thromboplastin time prothrombin time

4.2. Theoretical questions:

101. What types of hemorrhagic diathesis do you know?
102. What laboratory tests are used for assessment of the primary hemostasis?
103. How is the plasma coagulation function assessed?
104. Hemophilia, definition, classification.
105. Clinical presentation of the hemophilia.
106. Clinical presentation of the thrombocytopena
107. Clinical presentation of the Henoch-Schonlein purpura
4.3. Practical task that should be performed during practical training
109. To assess types of hemorrhagic diathesis
110. To assess results of coagulation system tests

Topic content
Normal mechanism of hemostasis:
Vasoconstriction following by a vascular injury
Primary hemostasis – formation of the platelet plug at the site on injury
Secondary hemostasis – reaction of the plasma coagulation system that results in fibrin
formation
Types of hemorrhagic diathesis
1. Hematomas are large painful, deep and palpable subcutaneous, intramuscular collections
of blood. Bleeding into body cavities, the retroperitoneum, or joints is a common
manifestation of plasma coagulation defects. Repeated joint bleeding may cause synovial
thickening, chronic inflammation, and fluid collections and may erode articular cartilage and
lead to chronic joint deformity and limited mobility. Joint deformities are particularly
common in patients with deficiencies of factors VIII and IX, the two sex-linked coagulation
disorders referred to as the hemophilias. For unclear reasons, hemarthroses are much less
common in patients with other plasma coagulation defects. Blood collections in various
body cavities or soft tissues can cause secondary necrosis of tissues or nerve compression.
Retroperitoneal hematomas can cause femoral nerve compression, and large collections of
poorly coagulated blood in soft tissues occasionally mimic malignant growths —the
pseudotumor syndrome. Two of the most life-threatening sites of bleeding are in the
oropharynx, where bleeding can compromise the airway, and in the central nervous system.
Intracerebral hemorrhage is one of the leading causes of death in patients with severe
coagulation disorders.
2. Collections of blood in the skin are called purpura and may be subdivided on the basis of
the site of bleeding in the skin. Small pinpoint hemorrhages into the dermis due to the
leakage of red cells through capillaries are called petechiae and are characteristic of platelet
disorders—in particular, severe thrombocytopenia.
3. Larger subcutaneous collections of blood due to leakage of blood from small arterioles and
venules are called ecchymoses (common bruises). They are also common in patients with
platelet defects and result from minor trauma.
4. Dilated capillaries, or telangiectasia, may cause bleeding without any hemostatic defect. In
addition, the loss of connective tissue support for capillaries and small veins that
accompanies aging increases the fragility of superficial vessels, such as those on the dorsum
of the hand, leading to extravasation of blood into subcutaneous tissue—senile purpura.
Laboratory tests of the hemostatic system
The most important screening tests of the primary hemostatic system are
1)a bleeding time (a sensitive measure of platelet function),
2) a platelet count.
The normal platelet count is 150,000 to 450*109/L of blood. As long as the count is
>100,000*109/L, patients are usually asymptomatic and the bleeding time remains normal.
Platelet counts of 50,000 to 100,000*10 9/L cause mild prolongation of the bleeding time;
bleeding occurs only from severe trauma or other stress. Patients with platelet counts
<50,000*109/L have easy bruising, manifested are characteristic of platelet disorders —in
particular, severe thrombocytopenia. Patients with a platelet count <20,000*10 9/L have an
appreciable incidence of spontaneous bleeding, usually have petechiae and may have
intracranial or other spontaneous internal bleeding.
Patients with qualitative platelet abnormalities have a normal platelet count and a prolonged
bleeding time. The bleeding time is ascertained by making a small, superficial skin incision and
timing the duration of blood flow from the wounded area. With careful standardization,
bleeding time is a reliable and sensitive test of platelet function.
Any patient with a bleeding time >10 min has an increased risk of bleeding, but the risk does
not become great until the bleeding time is >15 or 20 min.
Plasma coagulation function is readily assessed with
1. the partial thromboplastin time (PTT),
2. prothrombin time (PT),
3. thrombin time (TT), and
4. quantitative fibrinogen determination.
The PTT screens the intrinsic limb of the coagulation system and tests for the adequacy of
factors XII, HMWK, PK, XI, IX, and VIII. The PT screens the extrinsic or tissue factor –dependent
pathway. Both tests also evaluate the common coagulation pathway involving all the reactions
that occur after the activation of factor X. Prolongation of the PT and PTT that does not resolve
after the addition of normal plasma suggests a coagulation inhibitor. A specific test for the
conversion of fibrinogen to fibrin is needed when both the PTT and PT are prolonged —either a
TT or a clottable fibrinogen level can be employed. When abnormalities are noted in any of the
screening tests, more specific coagulation factor assays can be ordered to determine the nature
of the defect.
HEMOPHILIA
A hereditary bleeding disorder, hemophilia results from the deficiency of specific clotting factors.
Hemophilia A (classic hemophilia), which affects more than 80% of all hemophiliacs, results from
a deficiency of factor VIII; hemophilia В (Christmas disease), which affects 15% of hemophiliacs,
results from a deficiency of factor IX.
The severity and prognosis of bleeding disorders vary with the degree of deficiency and the
site of bleeding. The overall prognosis is best in mild hemophilia, which doesn't cause spontaneous
bleeding and joint deformities.
Advances in treatment have greatly improved the prognosis, and many hemophiliacs live
normal life spans. Surgical procedures can be done safely at special treatment centers for
hemophiliacs under the guidance of a hematologist.
Causes
Hemophilia A and hemophilia В are inherited as X-linked recessive traits. This means that female
carriers have a 50% chance of transmitting the gene to each daughter, who would then be a
carrier, and a 50% chance of transmitting the gene to each son, who would be born with
hemophilia.
Incidence
Hemophilia is the most common X-linked genetic disease, occurring in about 1.25 in 10,000
live male births. Hemophilia A is five times more common than hemophilia B. Hemophilia
causes abnormal bleeding because of a specific clotting factor malfunction. After a person with
hemophilia forms a platelet plug at a bleeding site, clotting factor deficiency impairs the capacity
to form a stable fibrin clot.
Signs and symptoms
Hemophilia produces abnormal bleeding, which may be mild, moderate, or severe, depending on
the degree of factor deficiency.
Mild hemophilia
The mild form of hemophilia frequently goes undiagnosed until adulthood because the patient
with a mild deficiency doesn't bleed spontaneously or after minor trauma but has prolonged
bleeding if challenged by major trauma or surgery. Postoperative bleeding continues as slow
ooze or ceases and starts again up to 8 days after surgery.
Moderate and severe hemophilia
Moderate hemophilia causes symptoms similar to those of severe hemophilia but produces only
occasional spontaneous bleeding episodes.
 Severe hemophilia causes spontaneous bleeding. The first sign of severe hemophilia usually is
excessive bleeding after circumcision. Later, spontaneous bleeding or severe bleeding after
minor trauma may produce large subcutaneous and deep intramuscular hematomas.
Bleeding into joints and muscles causes pain, swelling, extreme tendeness and, possibly,
permanent deformity. Bleeding near peripheral nerves may cause peripheral neuropathies,
pain, paresthesia, and muscle atrophy.
If bleeding impairs blood flow through a major vessel, it can cause ischemia and gangrene.
Pharyngeal, lingual, intracardial, intracerebral, and intracranial bleeding may lead to shock and
death.
Diagnosis
A history of prolonged bleeding after trauma or surgery (including dental extractions) or of
episodes of spontaneous bleeding into muscles or joints usually indicates some defect in the
hemostatic mechanism.
Specific coagulation factor assays can diagnose the type and severity of hemophilia. A positive
family history can also help diagnose hemophilia, but 20% of all cases have no family history.
Characteristic findings in hemophilia A include:
• factor VIII assay 0% to 30% of normal
• prolonged activated partial thromboplastin time (APTT)
• normal platelet count and function, bleeding time, and prothrombin time.
Characteristics of hemophilia В include:
• deficient factor IX-C
• baseline coagulation results similar to those in hemophilia A, with normal factor VIII.
In hemophilia A or hemophilia B, the degree of factor deficiency determines severity:
 mild hemophilia—factor levels 5% to 40% of normal
 moderate hemophilia—factor levels 1% to 5% of normal
 severe hemophilia — factor levels < 1% of normal.
THROMBOCYTOPENIA
The most common cause of hemorrhagic disorders, thrombocytopenia is characterized by
deficiency of circulating platelets. Because platelets play a vital role in coagulation, this
disease poses a serious threat to hemostasis.
Causes
Thrombocytopenia may be congenital or acquired; the acquired form is more common. In
either case, it usually results from the following:
• decreased or defective production of platelets in the marrow (such as occurs in leukemia,
aplastic anemia, or toxicity with certain drugs)
• increased destruction outside the marrow caused by an underlying disorder (such as cirrhosis
of the liver, disseminated intravascular coagulation, or severe infection)
• less commonly, sequestration (hypersplenism, hypothermia) or platelet loss.
Acquired thrombocytopenia may result from certain drugs, such as non-steroidal anti-
inflammatory agents, sulfonamides, histamine blockers, alkylating agents, or antibiotic
chemotherapeutic agents.
An idiopathic form of thrombocytopenia commonly occurs in children. A transient form may
follow viral infections (Epstein-Barr or infectious mononucleosis).
Signs and symptoms
Most adults present with a more indolent form of thrombocytopenia that may persist for
many years and is referred to as chronic idiopatic trombocytopenic purpura. Women age 20 to
40 are afflicted most commonly and outnumber men by a ratio of 3:1. They may present with
an abrupt fall in platelet count and bleeding into any mucous membrane. More often they have a
prior history of easy bruising (petechiae or ecchymoses) or menometrorrhagia. Nearly all patients
are otherwise asymptomatic, although some may complain of malaise, fatigue, and general weakness.
Splenomegaly is usually revealing at palpation of the abdomen.
In adults, large blood-filled. bullae characteristically appear in the mouth. In severe
thrombocytopenia, hemorrhage may lead to tachycardia, shortness of breath, loss of
consciousness, and death.
Diagnosis
To diagnose thrombocytopenia, obtain a patient history (especially a drug history), a physical
examination, and the following laboratory tests:
• Coagulation tests reveal a decreased platelet count (in adults, < 100,000/mcl), prolonged bleeding
time, and normal prothrombin time and partial thromboplastin time.
• If increased destruction of platelets is causing thrombocytopenia, bone marrow studies will reveal a
greater number of megakaryocytes (platelet precursors) and shortened platelet survival (several
hours or days rather than the usual 7 to 10 days).
VESSEL WALL DISORDERS
Bleeding from vascular disorders (nonthrombocytopenic purpura) is usually mild and confined
to the skin and mucous membranes. The pathogenesis of bleeding is poorly defined in many of
the syndromes, and classic tests of hemostasis, including the bleeding time and tests of platelet
function, are usually normal. Vascular purpura arises from damage to capillary endothelium,
abnormalities in the vascular subendothelial matrix or extravascular connective tissues that
support blood vessels, or from the formation of abnormal blood vessels. Several idiopathic
disorders involve the vessel wall and can cause more severe bleeding and organ dysfunction.
HENOCH-SCHONLEIN PURPURA
Henoch-Schonlein, or anaphylactoid, purpura is a distinct, self-limited type of vasculitis
that occurs in children and young adults. Patients have an acute inflammatory reaction in
capillaries, mesangial tissues, and small arterioles that leads to increased vascular permeability,
exudation, and hemorrhage. Vessel lesions contain IgA and complement components. The
syndrome may be preceded by an upper respiratory infection or streptococcal pharyngitis or be
associated with food or drug allergies. Patients develop a purpuric or urticarial rash on the
extensor surfaces of the arms and legs and on the buttocks (purpura simplex) as well as
polyarthralgias or arthritis (purpura rheumatic), colicky abdominal pain (purpura abdominalis),
and hematuria from focal glomerulonephritis (purpura renalis), or cerebral hemorrhage
(purpura cerebralis). Despite the hemorrhagic features, all coagulation tests are normal. A small
number of patients may develop fatal acute renal failure, and 5 to 10% develop chronic
nephritis.
7. Reference source
Olga kovalyova, tetyana ashcheulova propedeutics to internal medicine part 1. – vinnytsya: nova
knyha, 2006. – p. 407-417.
Control questions:
1. What types of hemorrhagic diathesis do you know?
2. What laboratory tests are used for assessment of the primary hemostasis?
3. How is the plasma coagulation function assessed?
4. Hemophilia, definition, classification.
5. Clinical presentation of the hemophilia.
6. Clinical presentation of the thrombocytopena
7. Clinical presentation of the Henoch-Schonlein purpura
Practical task that should be performed during practical training
1. To assess types of hemorrhagic diathesis
2. To assess results of coagulation system tests
 TOPIC 40
Symptoms and syndromes of leukemia, chronic myeloid leukemia, chronic
lymphocytic leukemia
1.Importance of the topic
The leukemias are a heterogeneous group of diseases characterized by
infiltration of the blood, bone marrow, and other tissues by neoplastic cells of the
hematopoietic system. The leukemias comprise a spectrum of malignancies that,
untreated, range from rapidly fatal to slowly growing. Based on their untreated course,
the myeloid leukemias have traditionally been designated acute or chronic. The diseases
usually have long time latent course and unspecific clinical presentation. But every
doctor must remember about them and know symptoms, objective and hematologic
signs of the acute and chronic leucosis, because they are fatal diseases affecting young
and old people.

2. Concrete aims:
─ To study symptoms and signs of acute leucosis
─ To study symptoms and signs of chronic myeloid leucosis
─ To study symptoms and signs of chronic lymphoid leucosis
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the bone marrow and hematopoietic system
Normal physiology Function of the blood cells, hemopoiesis
Histology Ontogenesis and histological structure of the bone marrow and
hematopoietic system
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
ossalgia Leukemic gap
sternalgia blasts
chloroma Eosinophilic basophilic dissociation

4.2. Theoretical questions:

108. What is hyperplastic syndrome?
109. The main clinical symptoms and signs of the hyperplastic syndrome.
110. What is acute leukemia? Symptoms and signs according to stages, blood test changes
and features of myelogram.
111. Clinical presentation of the chronic myeloid leukemia.
112. Clinical presentation of the chronic lymphoid leukemia.
4.3. Practical task that should be performed during practical training
111. To assess blood test at patients with the acute leukemia
112. To assess blood test at patients with the chronic myeloid leukemia
113. To assess blood test at patients with the chronic lymphoid leukemia
Topic content
Hyperplastic syndrome is a hyperproduction of tumor hematopoietic tissue and its
dissemination into extramedullar hematosis loci. Its clinical presentation:
 Ossalgia, sternalgia (spontaneous, percussion)
  Hepatomegaly
 splenomegaly
 lymphoadenopathy
 Syndrome of replacement of the normal marrow with pathologic leukemic clone:
─ Anemia (depressing of erythrocytes hematosis)
─ Hemorrhagic syndrome (depressing of thrombocytes hematosis)
─ Intoxication syndrome - (depressing of leucocytes hematosis, agranulocytosis)- ulcer-
necrotic and trophy changes of skin and mucosa
• Leukemia is malignant affection of blood cells with primary affecting marrow and
entrance of the pathologic clone into peripheral blood
Acute leukemia is disease characterized with a malignant proliferation of white blood cell
precursors (blasts) in bone marrow or lymph tissue and their accumulation in peripheral blood,
bone marrow, and body tissue. The diagnosis of AL is established by the presence of 20%
myeloblasts in blood and/or bone marrow according to the World Health Organization (WHO)
classification. Hematosis is stopped at the forth class of the blood cell differentiation.
Clinical presentation of the acute leukemia
Main syndromes: anemia, hemorrhage, hyperplastic, intoxication, replacement normal
bone marrow with pathologic clone.
Stages:
initial – mild unspecific clinical symptoms, changes in full blood test and myelogram
(myeloblasts).
full-scaled - complete developing all clinical syndromes, in full blood test anemia,
thrombocytopenia, ↑ ESR
terminal – severe bleeding, infections, exhausted patient, severe anemia,
thrombocytopenia, „leukemic gap” – 10-90% blasts
Patients with acute leukemia most often present with nonspecific symptoms that begin
gradually or abruptly and are the consequence of anemia, leukocytosis, leukopenia or leukocyte
dysfunction, or thrombocytopenia. Nearly half have had symptoms for 3 months before the
leukemia was diagnosed. Half mention fatigue as the first symptom, but most complain of
fatigue or weakness at the time of diagnosis. Anorexia and weight loss are common. Fever with
or without an identifiable infection is the initial symptom in _10% of patients. Signs of abnormal
hemostasis (bleeding, easy bruising) are noted first in 5% of patients. On occasion, bone pain,
lymphadenopathy, nonspecific cough, headache, or diaphoresis is the presenting symptom.
Rarely patients may present with symptoms from a mass lesion located in the soft tissues,
breast, uterus, ovary, cranial or spinal dura, gastrointestinal tract, lung, mediastinum, prostate,
bone, or other organs. The mass lesion represents a tumor of leukemic cells and is called a
granulocytic sarcoma, or chloroma.
Physical Findings Fever, splenomegaly, hepatomegaly, lymphadenopathy, sternal
tenderness, and evidence of infection and hemorrhage are often found at diagnosis.
Hematologic Findings Anemia is usually present at diagnosis and can be severe. The
degree varies considerably irrespective of other hematologic findings, splenomegaly, or the
duration of symptoms. The anemia is usually normochromic normocytic. Decreased
erythropoiesis often results in a reduced reticulocyte count, and erythrocyte survival is
decreased by accelerated destruction. Active blood loss also contributes to the anemia.
Changes of the white blood cells: Leucocytosis more than 50*10 9/l leucocytes is named
leukemia, leucocytosis 10-50*109/l - subleukemia, normal or less than normal level of the white
blood cells – aleukemia. Acute leukemia is characterized with „leukemic gap ” – 10-90% blasts
and lower level of mature blood cells without transitional forms of leucocytes.
Platelet counts <100*109/l are found at diagnosis in 75% of patients, and about 25% have
counts <25*109/l. Both morphologic and functional platelet abnormalities can be observed,
including large and bizarre shapes with abnormal granulation and inability of platelets to
aggregate or adhere normally to one another.
ESR always is elevated.
myelogram – increasing cells in marrow and myeloblasts – 30% and more
Chronic granulocytic (myelocytic) leukemia is disease characterized by the abnormal
overgrowth of granulocytic precursors (myeloblasts, promyelocytes, metamyelocytes, and
myelocytes) in bone marrow, peripheral blood and body tissues
Syndromes:
anemia,
hemorrhage syndrome (thrombocytopatia, retinal hemorrhage, ecchymoses, hematuria,
melena, bleeding gums, nosebleeds and easy bruising)
Intoxication
Hyperplastic syndrome
Lymphoadenopaty moderate
Cardiovascular system – myocardiophaty and heart failure
Respiratory system – infectional complications
GIT– significant increasing lever and spleen – “meeting” symptom between them
Skin myeloid sarcomas
Kidney – proteinuria, hematuria, renal failure, calculi
gouty arthritis
Signs and symptoms
The clinical onset of the chronic phase is generally insidious. Accordingly, some patients
are diagnosed while still asymptomatic, during health screening tests; other patients present
with fatigue, malaise, and weight loss or have symptoms resulting from splenic enlargement,
such as early satiety and left upper quadrant pain or mass. Less common are features related to
granulocyte or platelet dysfunction, such as infections, thrombosis, or bleeding. Occasionally,
patients present with leukostatic manifestations due to severe leukocytosis or thrombosis such
as vasoocclusive disease, cerebrovascular accidents, myocardial infarction, venous thrombosis,
visual disturbances, and pulmonary insufficiency.
Progression of chronic myeloleukosis is associated with worsening symptoms. Unexplained
fever, significant weight loss, increasing dose requirement of the drugs controlling the disease,
bone and joint pain, bleeding, thrombosis, and infections suggest transformation into
accelerated or blastic phases. Fewer than 10 to 15% of newly diagnosed patients present with
accelerated disease or with de novo blastic phase chronic myeloleukosis.
Physical Findings In most patients the abnormal finding on physical examination at diagnosis is
minimal to moderate splenomegaly; mild hepatomegaly is found occasionally. Persistent
splenomegaly despite continued therapy is a sign of disease acceleration. Lymphadenopathy
and myeloid sarcomas are unusual except late in the course of the disease; when they are
present, the prognosis is poor.
Hematologic Findings Elevated white blood cell counts, with various degrees of immaturity of
the granulocytic series, are present at diagnosis. Usually <5% circulating blasts and <10% blasts
and promyelocytes are noted. Cycling of the counts may be observed in patients followed
without treatment.
Platelet counts are almost always elevated at diagnosis, and a mild degree of normochromic
normocytic anemia is present. Leukocyte alkaline phosphatase is characteristically low in
chronic myeloleukosis cells. „basophyl-eosinophylic dissociation” is observed in full blood test.
ESR always is elevated.
Serum levels of vitamin B12 and vitamin B12–binding proteins are generally elevated.
Phagocytic functions are usually normal at diagnosis and remain normal during the chronic
phase. Histamine production secondary to basophilia is increased in later stages, causing
pruritus, diarrhea, and flushing.
At diagnosis, bone marrow cellularity, primarily of the myeloid and megakaryocytic lineages,
with a greatly altered myeloid to erythroid ratio, is increased in almost all patients with chronic
myeloleukosis. The marrow blast percentage is generally normal or slightly elevated. Marrow or
blood basophilia, eosinophilia, and monocytosis may be present. While collagen fibrosis in the
marrow is unusual at presentation, significant degrees of reticulin stain–measured fibrosis are
noted in about half of the patients.
Disease acceleration is defined by the development of increasing degrees of anemia
unaccounted for by bleeding or chemotherapy; cytogenetic clonal evolution; or blood or
marrow blasts between 10 and 20%, blood or marrow basophils 20%, or platelet count
<100*109/l. Blast crisis is defined as acute leukemia, with blood or marrow blasts 20%.
Hyposegmented neutrophils may appear (Pelger-Huet anomaly). Blast cells can be classified as
myeloid, lymphoid, erythroid, or undifferentiated, based on morphologic, cytochemical, and
immunologic features. About half the cases are myeloid, one-third lymphoid, 10% erythroid,
and the rest are undifferentiated.
Chronic lymphocytic leukemia is malignant hyperplasia of the lymphoid tissue,
manifested by lymphoid hyperplasia of bone marrow, lymphoadenopaty and
hepatoslenomegalia
Signs and symptoms
• anemia
• General increasing lymphenodes (symmetrical)
• Moderate hepatolienal syndrome
• Respiratory tract infection
• Heart failure
• Asthenia
• Hemorrhage syndromes
Neuroleykemia (limphoid infiltration of the nerves– Herpes Zoster, deafness)
• Bone tenderness and oedema due disorders of lymstream
Laboratory diagnostics
• Full blood analysis – anemia, thrombocytopenia, different account leucocytes
(aleukemia, subleukemia, leukemia), absolute 90-98% lymphocytes, ↑ ESR
• Myelogram – hypercellular, characteristically shows bone marrow infiltration by
significantly increased number of lymphoid elements, lymphocytosis – mature
lymphocytes more 30% (normal 8-12%)
• Lymph nodes aspiration – specific proliferation.
7. Reference source
Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000.
Control questions:
1. What is hyperplastic syndrome?
2. The main clinical symptoms and signs of the hyperplastic syndrome.
3. What is acute leukemia? Symptoms and signs according to stages, blood test
changes and features of myelogram.
4. Clinical presentation of the chronic myeloid leukemia.
5. Clinical presentation of the chronic lymphoid leukemia.
Practical task
1. To assess blood test at patients with the acute leukemia
2. To assess blood test at patients with the chronic myeloid leukemia
3. To assess blood test at patients with the chronic lymphoid leukemia
 Topic 41
Symptoms and syndromes of the diabetes mellitus
1.Importance of the topic
Diabetes mellitus is widely spread disease. It produces serious problems with health
due to affecting most of the internal organs and systems. Diabetes mellitus influences
on course of all chronic and acute diseases and may produce serious and life-
threatening complication. Ability to recognizing major and minor symptoms of
diabetes mellitus is very important for every doctor or student.

2. Concrete aims:
─ To study main symptoms and signs of the different types of diabetes mellitus
─ To learn laboratory tests for revealing diabetes mellitus
─ To study complication of the diabetes mellitus
─ To study symptoms and signs of ketoacidosis and hypoglycemia, hypoglycemic
and hyperglycemic coma
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the pancreas
Normal physiology Insulin functions
Histology Ontogenesis, histological structure of the pancreas and its β-
cells
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
hypoglycemia Diabetic neuropathy
hyperglycemia Diabetic angiopathy
ketoacidosis Diabetic hepatosis
Diabetic nephropathy Test tolerance glucose

4.2. Theoretical questions:

113. Definition and classification of the diabetes mellitus.
114. Major and minor diabetes symptoms.
115. Laboratory test for revealing diabetes mellitus
116. Complications of the diabetes mellitus
117. Symptoms and signs of ketoacidosis and hyperglycemic coma
118. Symptoms and signs of hypoglycemia and hypoglycemic coma
4.3. Practical task that should be performed during practical training
114. Revealing and assessment of symptoms and signs of diabetes mellitus
115. Revealing and assessment of symptoms and signs hypogycemia
116. Revealing and assessment of hyperglycemia and ketoacidodsis.
Topic content
Diabetes mellitus - Systemic heterogenic disease results from a lack (or diminished
effectiveness) of endogenous insulin which is accompanied with disorders of metabolism and
function of all body systems
Types of the diabetes mellitus
• DM type 1 – insulin-dependent
• DM type 1 – insulin-independent
 • Gestational DM
• Other specific types of DM (genetic defect of β-cells, genetic defects of the insulin
action, pancreatic disorders, endocrinopathy, such as acromegaly, Cushing syndrome,
thyrotoxicosis and others, induced by medications or chemicals, cytomegalovirus
infections)
DM symptoms
Major symptoms
• Polyuria
• Polydipsia (thirst)
• Increased appetite - polyphagia
• Progressive weight loss (DM type 1)
• Increased weight (DM type 2)
• Increasing fatigue, weakness, decreasing work ability
Minor symptoms:
 pustular diseases (furunculosis, carbunculosis, acne, fungous diseases)
 bad wound and ulcer scarring,
 progressing caries,
 falling of teeth,
 conjunctivitis,
 stomatitis,
 paradontosis,
 skin and genitals inch,
 abortion.
DM signs
• loss or gain in weight (according to DM type)
• Cheek hyperemia (diabetes rubeosis)
• Skin is dry, thin with maceration, increased epitelium loss, palm xantomatosis
• Younger appearance of patients
• Respiratory system – chronic inflamotory respiratory disease, tuberculosis
• Cardiovascular system –myocardiopathy, progressive coronary atherosclerosis and
painless myocardium ischemia, myocardial infarction
• Gastrointestinal system – fatty liver dystrophy
• Bone pain, osteoporosis (protein bone catabolism), spontaneous fracture
• Central and peripheral nervous system – polyneuropathy (extremities paresthesia, pain
in legs during night, convulsions).
Laboratory diagnostics of DM
• Qualitative sign of glucose in urine (express-diagnostics of glucosuria)
• Glycemia in a norm (fasting):
(3,3-5,5 mmol/l (ortotuloidin test) or
4,4-6,6 mmol/l (by Hagedorn-Yensen test))
• Test tolerance glucose
If patient has diabetes mellitus his fasting hyperglicemia > 6,1 mmol/l, after 2 hours > 10,0
mmol/l.
• Glycemic profile - measuring blood glucose 3 time in a day for assessment its level
change
• Glucasuria profile - measuring urine glucose 4 time in a day for assessment its level
change
DM complications
• Diabetes foot – necrotic ulcer, osteoartropathy, neuropathy leg oedema.
 • Diabetes angiopathy (mycro and macropathy) – early atherosclerosis, disorders of
retina, nervous, skin, kidney vessels result in loss sight, its loss, headache, oedema, renal
syndrome, leg cooling, skin disorders.
• Affecting other system – diabetes liver hepatosis, dermatopathy, enteropathy,
cataracts.
• Acute exacerbations (ketonemic(ketoacidosis, hiperglicemia), hypoglicemic,
hyperosmotic, hyperlactacemia)
Symptoms and signs of the hyperglycemic ketoacidotic coma
• Age – any, frequently young.
• History – onset diabetes, violations of nutrition rules, wrong insulin dose, infection,
stress, pregnancy, delivery, alcohol use
• Precursor of coma – fatigue, nausea, thirst, vomiting, dryness in mouth, polyuria,
gradual losing of consciousness from lethargy to coma.
• Coma developing – gradual, 2-3 days.
• Skin – dry, diabetes rubeosis, diminished turgor, scratching, maceration, infected
trophic injuries, dehydration signs, chaps of lips angles.
• Muscles, reflex – diminished tone
• Eye balls – soft, diminished tone
• Respiratory system – tachypnoe, hyperventilation (Kussmaul breathing), ketotic on
breath, pneumonia.
• Cardiovascular system – hypotonia, tachycardia, minor, soft, filiform pulse.
• Gastrointestinal system – dry, shaggy tongue with dirty brown covering, swelling
abdomen, may be intense, like “acute abdomen”, vomit with coffee grounds,
hepatomegaly, painful liver.
• Renal system – pallakiuria, polyuria, then – oligouria, anuria.
Investigations of the hyperglycemic ketoacidotic coma
• Laboratory diagnostics – high hyperglycemia, glucosuria, ketonuria, increased ketones in
blood (normal ketones 0,08-0,43 mmol/l), increased creatinines and urea in blood,
hypokaliemia, acidosis, increasing blood osmolarity, significantly decreased reserve
alkaline blood balance (in a norm 50-60 volume%).
• Treatment principle – fractional entering simple insulin
Symptoms and signs of the hypoglycemic coma
• Age – any, frequently older.
• History – insulin overdosing, physical overloading, starvation, sulfanilamide or β-
blockers use.
• Precursors of coma– filling hungry, fatigue and suddenly weakness, trembling, worrying,
diplopia, palpitation, facial and tongue numbness, headache, hallucinations, sweating,
exiting that very fast results in coma, clonic convulsions.
• Coma developing – fast, some minutes.
• Skin – pale or pink, significantly wet, profuse sweat, hyperhydration signs, normal
turgor.
• Muscle and reflex – increased tone.
• Eye balls – normal tone.
• Respiratory system – normal breathing, mild tachypnoe.
• Cardiovascular system – normal blood pressure, tachycardia, satisfactory pulse.
• Gastrointestinal system – without pathologic signs
Renal system – without pathologic signs
Investigations of the hypoglycemic coma
 • Laboratory diagnostics – low glycemia, absent of glucosuria and normal ketones in
blood and urine, normal blood creatinin and urea , potassium, рН, osmolarity.
• Treatment principle – IV 40% glucose solution.

Reference source
o Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000.

Test for self-control

Control questions:
1. Definition and classification of the diabetes mellitus.
2. Major and minor diabetes symptoms.
3. Laboratory test for revealing diabetes mellitus
4. Complications of the diabetes mellitus
5. Symptoms and signs of ketoacidosis and hyperglycemic coma
6. Symptoms and signs of hypoglycemia and hypoglycemic coma
Practical tasks
1. Revealing and assessment of symptoms and signs of diabetes mellitus
2. Revealing and assessment of symptoms and signs hypogycemia
3. Revealing and assessment of hyperglycemia and ketoacidodsis
 TOPIC 42
Symptoms and syndromes of thyroid disorders
1.Importance of the topic
Thyroid disorders are widely spread disease especially during last 20 years. They
produce serious problems with health due to affecting most of the internal organs and
systems. Thyrotoxicosis and hypothyroidism influence on course of all chronic and
acute diseases and may produce serious and life-threatening complication. Ability to
recognizing symptoms of thyroid disorders is very important for every doctor or
student.

2. Concrete aims:
─ To study main symptoms and signs of the thyrotoxicosis
─ To study main symptoms and signs of the hypothyroidism
─ To study laboratory tests for confirming thyroid disorders
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the thyroid gland
Normal physiology Metabolism and functions of thyroid hormones
Histology Ontogenesis, histological structure of the thyroid gland
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
thyrotoxicosis myxedema
hypothyroidism goiter
Graves' disease Thyroid ophtalmopathy

4.2. Theoretical questions:

119. Definition and causes of hypothyroidism.
120. Symptoms and signs of hypothyroidism.
121. Definition and causes of thyrotoxicosis
122. Symptoms and signs of thyrotoxicosis
123. Laboratory tests for revealing thyroid disorders
124. Ophthalmic signs at the patients with thyrotoxicosis
4.3. Practical task that should be performed during practical training
117. Revealing and assessment of symptoms and signs of hypothyroidism
118. Revealing and assessment of symptoms and signs thyrotoxicosis
119. Revealing and assessment of laboratory test at patients with thyroid disorders.
Topic content
Hypothyroidism in adults
Hypothyroidism, a state of low serum thyroid hormone, results from hypothalamic, pituitary,
or thyroid insufficiency. The disorder can progress to life-threatening myxedema coma.
Hypothyroidism is more prevalent in women than in men.
Causes
Hypothyroidism results from inadequate production of thyroid hormone, usually because of
dysfunction of the thyroid gland due to surgery (thyroidectomy), radiation therapy (particularly
with 131I), inflammation, chronic autoimmune thyroiditis (Hashimoto's disease) or, rarely, conditions
such as amyloidosis and sarcoidosis. It may also result from pituitary failure to produce thyroid-
stimulating hormone (TSH), hypothalamic failure to produce thyrotropin-releasing hormone,
inborn errors of thyroid hormone synthesis, inability to synthesize thyroid hormone because of
iodine deficiency (usually dietary), or the use of antithyroid medications such as propyl-thiouracil.
In patients with hypothyroidism, infection, exposure to cold, and sedatives may precipitate
myxedema coma.
Signs and symptoms
Typically, the early clinical features of hypothyroidism are vague: fatigue, forgetfulness,
sensitivity to cold, unexplained weight gain, and constipation. As the disorder progresses,
characteristic myxedematous signs and symptoms appear: decreasing mental stability; dry,
flaky, inelastic skin; puffy face, hands, and feet; hoarseness; periorbital edema; upper eyelid
droop; dry, sparse hair; and thick, brittle nails.
Cardiovascular involvement leads to decreased cardiac output, slow pulse rate, signs of poor
peripheral circulation and, occasionally, an enlarged heart. Other common effects include
anorexia, abdominal distention, menorrhagia, decreased libido, infertility, ataxia, and nystagmus.
Reflexes show delayed relaxation time (especially in the Achilles tendon).
Progression to myxedema coma is usually gradual, but when stress aggravates severe or
prolonged hypothyroidism, coma may develop abruptly. Clinical effects include progressive
stupor, hypoventilation, hypoglycemia, hyponatremia, hypotension, and hypothermia.
Diagnosis
Radioimmunoassay confirms hypothyroidism with low triiodothyronine (T3) and thyroxine (T4)
levels.
Supportive laboratory findings include:
• increased TSH level when hypothyroidism is due to thyroid insufficiency; decreased TSH
level when hypothyroidism is due to hypothalamic or pituitary insufficiency
• elevated levels of serum cholesterol, alkaline phosphatase, and triglycerides
• normocytic, normochromic anemia.
In myxedema coma, laboratory tests may also show low serum sodium levels as well as
decreased pH and increased partial pressure of carbon dioxide, indicating respiratory acidosis.
Thyrotoxicosis
Thyrotoxicosis is a metabolic imbalance that results from thyroid hormone overproduction or
thyroid hormone over release from the gland. The most common form of thyrotoxicosis is
Graves' disease, which increases thyroxine production, enlarges the thyroid gland (goiter), and
causes multiple system changes.
Incidence of Graves' disease is highest between ages 30 and 40, especially in people with family
histories of thyroid abnormalities only 5% of patients with thyrotoxicosis are younger than age 15.
With treatment, most patients can lead normal lives. However, thyroid storm—an acute, severe
exacerbation of thyrotoxicosis — is a medical emergency that may lead to life-threatening cardiac,
hepatic, or renal consequences.
Varied forms of thyrotoxicosis may include the following.

Toxic adenoma

This small, benign nodule in the thyroid gland that secretes thyroid hormone is a common
cause of thyrotoxicosis. The cause of toxic adenoma is unknown. Clinical effects are essentially
similar to those of Graves' disease, except that toxic adenoma doesn't induce
ophthalmopathy, pretibial myxedema, or acropachy.

Presence of adenoma is confirmed by iodine 131 (131I) uptake and a thyroid scan, which show a
single hyperfunctioning nodule suppressing the rest of the gland.
Toxic multinodular goiter
Common in the elderly, this form of thyrotoxicosis involves overproduction of thyroid hormone
by one or more autonomously functioning nodules within a diffusely enlarged gland.
Thyrotoxicosis factitia
This form of thyrotoxicosis results from a chronic ingestion of thyroid hormone for thyrotropin
suppression in patients with thyroid carcinoma, or from thyroid hormone abuse by persons who
are trying to lose weight.
Functioning metastatic thyroid carcinoma
This rare disease causes excess production of thyroid hormone.
TSH-secreting pituitary tumor
A pituitary tumor that secretes thyroid-stimulating hormone (TSH) causes overproduction of
thyroid hormone.

Subacute thyroiditis
This is a virus-induced granulomatous inflammation of the thyroid, producing transient
thyrotoxicosis associated with fever, pain, pharyngitis, and tenderness in the thyroid gland.
Silent thyroiditis
Self-limiting, silent thyroiditis is a transient form of thyrotoxicosis, with histologic thyroiditis but
no inflammatory symptoms.

Causes
Thyrotoxicosis may result from genetic and immunologic factors.
• An increased incidence of this disorder in monozygotic twins points to an inherited factor,
probably an autosomal recessive gene.
• This disease occasionally coexists with other endocrine abnormalities, such as diabetes
mellitus, thyroiditis, and hyperparathyroidism.
• Thyrotoxicosis may also be caused by the production of autoantibodies (thyroid-
stimulating immunoglobulin and thyroid-stimulating hormone [TSH]-binding inhibitory
immunoglobulin), possibly because of a defect in suppressor-T-lymphocyte function
that al lows the formation of autoantibodies.
• In latent thyrotoxicosis, excessive dietary intake of iodine and, possibly, stress can
precipitate clinical thyrotoxicosis.

Signs and symptoms

The classic features of Graves' disease are an enlarged thyroid (goiter), nervousness, heat
intolerance, weight loss despite increased appetite, sweating, frequent bowel movements,
tremor, and palpitations. Exophthalmos is considered most characteristic but is absent in many
patients with thyrotoxicosis.
Many other signs and symptoms are common because thyrotoxicosis profoundly affects virtually
every body system:
Central nervous system: difficulty in concentrating because increased thyroxine secretion
accelerates cerebral function; excitability or nervousness due to increased basal metabolic
rate; fine tremor, shaky handwriting, and clumsiness from increased activity in the spinal cord
area that controls muscle tone; emotional instability and mood swings, ranging from occasional
outbursts to overt psychosis.
Skin, hair, and nails: smooth, warm, flushed skin (patient sleeps with minimal covers and little
clothing); fine, soft hair; premature graying and increased hair loss in both sexes; friable nails and
onycholysis (distal nail separated from the bed); pretibial myxedema (dermopathy), producing
thickened skin; and accentuated hair follicles, raised red patches of skin that are itchy and
sometimes painful, with occasional nodule formnation. Microscopic examination shows
increased mucin deposits.
Cardiovascular system: tachycardia; full, bounding pulse; wide pulse pressure; cardiomegaly;
increased cardiac output and blood volume; visible point of maximal impulse; paroxysmal supra-
ventricular tachycardia and atrial fibrillation (especially in elderly people); and, occasionally, a
systolic murmur at the left sternal border
• Respiratory system: dyspnea on exertion and at rest, possibly from cardiac
decompensation and increased cellular oxygen utilization
• GI system: excessive oral intake with weight loss; nausea and vomiting due to
increased GI motility and peristalsis; increased defecation; soft stools or, with severe
disease, diarrhea; and liver enlargement
• Musculoskeletal system: weakness (especially in proximal muscles), fatigue, and
muscle atrophy; rare coexistence with myasthenia gravis; possibly generalized or
localized paralysis associated with hypokalemia; and occasional acropachy (soft-tissue
swelling, accompanied by underlying bone changes where new bone formation
occurs)
• Reproductive system: in females, oligomenorrhea or amenorrhea, decreased
fertility, higher incidence of spontaneous abortions; in males, gynecomastia due to
increased estrogen levels; in both sexes, diminished libido
• Eyes: exophthalmos (produced by the combined effects of accumulation of
mucopolysaccharides and fluids in the retroorbital tissues that force the eyeball
outward, and of lid retraction that produces the characteristic staring gaze); occasional
inflammation of conjunctivae, corneas, or eye muscles; diplopia; and increased
tearing.
When thyrotoxicosis escalates to thyroid storm, these symptoms can be accompanied by
extreme irritability, hypertension, tachycardia, vomiting, temperature up to 41.1° C, delirium, and
coma.
In elderly patients, consider apathetic thyrotoxicosis in patients who exhibit atrial fibrillation or
depression.

Diagnosis

The diagnosis of thyrotoxicosis usually is straightforward and depends on a careful clinical

history and physical examination, a high index of suspicion, and routine hormone
determinations.
The following tests confirm the disorder:
• Radioimmunoassay shows increased serum thyroxine (T4) and triiodothyronine (T3)
concentrations.
• Thyroid scan reveals increased uptake of radioactive iodine 131 ( 131 I) in Graves' disease,
and usually in toxic multinodular goiter and toxic adenoma. Radioactive uptake is low in
thyroiditis and thyrotoxic factitia. This test is contraindicated if the patient is pregnant.
• TSH levels are decreased.
• Thyroid-releasing hormone (TRH) stimulation test indicates thyrotoxicosis if the TSH
level fails to rise within 30 minutes after the administration of TRH. TRH testing is rarely
necessary and is currently done to highly sensitive TSH assays.
• Ultrasonography for assessing size, shape and pathologic nodes in thyroid gland.

Reference source
o Handbook of diseases.-.2nd ed.- Springhouse Corporation, 2000.
 Test for self-control
Control questions:
1. Definition and causes of hypothyroidism.
2. Symptoms and signs of hypothyroidism.
3. Definition and causes of thyrotoxicosis
4. Symptoms and signs of thyrotoxicosis
5. Laboratory tests for revealing thyroid disorders
6. Ophthalmic signs at the patients with thyrotoxicosis
Practical tasks
1. Revealing and assessment of symptoms and signs of hypothyroidism
2. Revealing and assessment of symptoms and signs thyrotoxicosis
3. Revealing and assessment of laboratory test at patients with thyroid disorders.
 TOPIC 43
Clinical, laboratory and instrumental examinations of the patients with
articular syndrome: rheumatoid arthritis, rheumatic polyartritis, osteoarthritis,
gout
1.Importance of the topic
Articular syndrome is one of the widely spread disorders. It may develop at different
diseases and usually is difficulty, long time treated. Ability to recognizing symptoms
and signs of articular syndrome is very important for every doctor or student.

2. Concrete aims:
─ To study main symptoms of articular syndrome
─ To study main signs of articular syndrome
─ To study laboratory tests for confirming articular syndrome
─ To study symptoms, signs of the rheumatoid arthritis, rheumatic polyartritis,
osteoarthritis, gout
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the muscular skeleton system
Histology Ontogenesis, histological structure of the muscular skeleton system
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
gout ankylosing
osteoarthritis Heberden's nodes
degenerative arthropathy Oligoarticular disorders

4.2. Theoretical questions:

125. What types of origin can rheumatological and related diseases have?
126. Symptoms and signs of inflammatory origin of articular syndrome.
127. Laboratory investigation of patients with articular syndrome.
128. Symptoms, signs and laboratory tests of rheumatoid arthritis
129. Symptoms, signs and laboratory tests of rheumatic polyartritis
130. Symptoms, signs and laboratory tests of osteoarthritis
131. Symptoms, signs and laboratory tests of gout
4.3. Practical task that should be performed during practical training
120. Revealing and assessment of symptoms and signs of rheumatoid arthritis, osteoarthritis
121. Revealing and assessment of symptoms and signs rheumatic polyartritis, gout
122. Revealing and assessment of laboratory test at patients with articular syndrome.
Topic content
Rheumatological and related diseases can have
-inflammatory origin (rheumatoid arthritis, rheumatic fever, systemic lupus erythematosus
(SLE), systemic sclerosis and others);
-degenerative arthropathy (osteoarthritis, spondyloarthritides);
-extrajoint rheumatic fever with effecting muscle, fascias, tendons and others.
-joint diseases due to metabolism disorders (gout, osteoporosis)
Individuals with musculoskeletal complaints should be evaluated in a uniform, logical manner
by means of a thorough history, a comprehensive physical examination, and, if appropriate,
laboratory testing. The goals of the initial encounter are to determine whether the
musculoskeletal complaint is (1) articular or nonarticular in origin, (2) inflammatory or
noninflammatory in nature, (3) acute or chronic in duration, and (4) localized or widespread
(systemic) in distribution.
With such an approach and an understanding of the pathophysiologic processes that underlie
musculoskeletal complaints, an adequate diagnosis can be made in the vast majority of
individuals. However, some patients will not fit immediately into an established diagnostic
category. Many musculoskeletal disorders resemble each other at the outset, and some take
weeks or months to evolve into a readily recognizable diagnostic entity. This consideration
should temper the desire always to establish a definitive diagnosis at the first encounter.
ARTICULAR VERSUS NONARTICULAR
The musculoskeletal evaluation must discriminate the anatomic site(s) of origin of the patient's
complaint. Pain from nonarticular structures may mimic true articular pain because of their
proximity to the joint. Distinguishing between articular and nonarticular disease requires a
careful and detailed examination. Articular disorders may be characterized by deep or diffuse
joint pain, limited range of motion on active and passive movement, swelling caused by
synovial proliferation or effusion or bony enlargement, crepitation, instability, locking, or
deformity. By contrast, nonarticular disorders tend to be painful on active but not passive
range of motion, demonstrate point or focal tenderness in regions distinct from articular
structures, and have physical findings remote from the joint capsule. Moreover, nonarticular
disorders seldom demonstrate crepitus, instability, deformity, or swelling.
INFLAMMATORY VERSUS NONINFLAMMATORY
Inflammatory disorders may be infectious (infection with Neisseria gonorrhoea or
Mycobacterium tuberculosis), crystal-induced (gout, pseudogout), immune-related
[rheumatoid arthritis (RA), systemic lupus erythematosus (SLE)], reactive (rheumatic fever,
Reiter's syndrome), or idiopathic. Inflammatory disorders may be identified by the presence of
some or all of the four cardinal signs of inflammation (erythema, warmth, pain, and swelling),
by systemic symptoms (prolonged morning stiffness, fatigue, fever, weight loss), or by
laboratory evidence of inflammation (elevated erythrocyte sedimentation rate or C-reactive
protein level, thrombocytosis, anemia of chronic disease, or hypoalbuminemia). Articular
stiffness is common in chronic musculoskeletal disorders. However, the chronology and
magnitude of stiffness may be diagnostically important. Morning stiffness related to
inflammatory disorders (such as RA) is precipitated by prolonged rest, often lasts several hours,
and may improve with activity and anti-inflammatory medications. By contrast, intermittent
stiffness associated with noninflammatory conditions, such as osteoarthritis, is precipitated by
brief periods of rest, usually lasts less than 60 min, and is exacerbated by activity.
Noninflammatory disorders may be related to trauma (rotator cuff tear), ineffective repair
(osteoarthritis), cellular overgrowth (pigmented villonodular synovitis), or pain amplification
(fibromyalgia). They are often characterized by pain without swelling or warmth, the absence
of inflammatory or systemic features, little or no morning stiffness, and normal laboratory
findings.
CLINICAL HISTORY
When evaluating patients with musculoskeletal complaints, the clinician should always
consider the most common conditions (e.g., low back pain, osteoarthritis) seen in the general
population. Aspects of the patient profile, including age, sex, race, and family history, can
provide important information. Certain diagnoses are more frequent in specific age groups.
SLE, rheumatic fever, and Reiter's syndrome are more common in the young, whereas
fibromyalgia and RA are most common in middle age, and osteoarthritis and polymyalgia
rheumatica in the elderly. Some diseases are more common in a particular gender or race.
Gout and the spondyloarthropathies (e.g., ankylosing spondylitis, Reiter's syndrome) are more
common in men, whereas SLE, RA, and fibromyalgia are more common in women. Polymyalgia
rheumatica, giant cell arteritis, and Wegener's granulomatosis preferentially affect whites,
whereas sarcoidosis and SLE are more common in blacks. Familial aggregation occurs in some
disorders, such as ankylosing spondylitis, gout, RA, and Heberden's nodes of osteoarthritis.

The chronology of the complaint (onset, evolution, and duration) is an important diagnostic
feature. The onset of disorders such as septic arthritis and gout tends to be abrupt, whereas
osteoarthritis, RA, and fibromyalgia may develop more indolently. In terms of evolution,
disorders are classified as acute (e.g., septic arthritis), chronic (e.g., osteoarthritis), intermittent
(e.g., gout), migratory (e.g., rheumatic fever, gonococcal or viral arthritis), or additive (e.g., RA,
Reiter's syndrome). Musculoskeletal disorders typically are called acute if they last less than 6
weeks and chronic if they last longer. Acute and intermittent arthropathies tend to be
infectious, crystal-induced, or reactive. Noninflammatory and immune-related arthritides, such
as osteoarthritis and RA, respectively, are often chronic. The duration of the patient's
complaints may alter the diagnostic considerations. For example, the musculoskeletal signs and
symptoms of hepatitis B virus infection may be identical with those of early RA at the onset but
rarely persist beyond 3 weeks.
The number and distribution of involved articulations should be noted. Articular disorders are
classified as monarticular (one joint involved), oligoarticular or pauciarticular (two to three
joints involved), or polyarticular (more than three joints involved). Nonarticular disorders can
be classified as either focal or widespread. Complaints secondary to trauma and gout are
typically focal or monarticular, whereas polymyositis, RA, and fibromyalgia are more diffuse or
polyarticular. Joint involvement tends to be symmetric in RA but is often asymmetric in the
spondyloarthropathies and in gout. The upper extremities are frequently involved in RA,
whereas lower extremity arthritis is characteristic of Reiter's syndrome and gout at their onset.
Involvement of the axial skeleton is common in osteoarthritis and ankylosing spondylitis but
infrequent in RA, with the notable exception of the cervical spine.
The clinical history should also identify precipitating events, such as trauma, drug
administration, or antecedent or intercurrent illnesses, that may have contributed to the
patient's complaint. Last, a thorough rheumatic review of systems may disclose associated
features outside the musculoskeletal system and provide useful diagnostic information. A
variety of musculoskeletal disorders may be associated with systemic features such as fever
(SLE, infection), rash (SLE, Reiter's syndrome, dermatomyositis), myalgias, weakness
(polymyositis, polymyalgia rheumatica), and morning stiffness (inflammatory arthritis). In
addition, some conditions are associated with involvement of other organ systems, including
the eyes (sarcoidosis, Reiter's syndrome), gastrointestinal tract (scleroderma, inflammatory
bowel disease), genitourinary tract (Reiter's syndrome, gonococcemia), and nervous system
(Lyme disease, SLE, vasculitis).
PHYSICAL EXAMINATION
Examination of involved and uninvolved joints will determine whether warmth, erythema, or
swelling is present. The examination should distinguish true articular swelling caused by
synovial effusion or synovial proliferation from nonarticular or periarticular involvement, which
usually extends beyond the normal joint margins or the full extent of the synovial space.
Synovial effusion can be distinguished from synovial hypertrophy or bony hypertrophy by
palpation or specific maneuvers. For example, small to moderate knee effusions may be
identified by the "bulge sign" or "ballottement of the patella." Bursal effusions (e.g., effusions
of the olecranon or prepatellar bursa) overlie bony prominences and are fluctuant with sharply
defined borders. Joint stability can be assessed by palpation and by the application of manual
stress to assess displacement in different planes. Subluxation or dislocation, which may be
secondary to traumatic, mechanical, or inflammatory causes, can be assessed by inspection
and palpation. Joint volume can be assessed by palpation. Distention of the articular capsule
usually causes pain. The patient will attempt to minimize the pain by keeping the joint in the
position of least intraarticular pressure and greatest volume, usually partial flexion. Clinically,
joint distention may be detected as obvious swelling, voluntary or fixed flexion deformities, or
diminished range of motionѕespecially on extension, which decreases joint volume. Active and
passive range of motion should be assessed in all planes, with contralateral comparison. Serial
evaluations of joint motion may be made using a goniometer to quantify the arc of movement.
Each joint should be passively manipulated through its full range of motion (including, as
appropriate, flexion, extension, rotation, abduction, adduction, inversion, eversion, supination,
pronation, and medial or lateral deviation or bending). Limitation of motion is frequently
caused by effusion, pain, deformity, or contracture. Contractures may reflect antecedent
synovial inflammation or trauma. Joint crepitus may be felt during palpation or maneuvers and
may be prominent or coarse in osteoarthritis. Joint deformity usually indicates a long-standing
or aggressive pathologic process. Deformities may result from ligamentous destruction, soft
tissue contracture, bony enlargement, ankylosis, erosive disease, or subluxation. Examination
of the musculature will permit assessment of strength and reveal atrophy, pain, or spasm. The
examiner should look carefully for nonarticular or periarticular involvement, especially when
articular complaints are not supported by objective findings referable to the joint capsule.
LABORATORY INVESTIGATIONS
Laboratory tests should be used to confirm a specific clinical diagnosis and not be used as a tool
to screen or evaluate patients with vague rheumatic complaints. Indiscriminate use of broad
batteries of diagnostic tests and radiographic procedures are rarely useful or cost-effective.

Besides a complete blood count, including a white blood cell (WBC) and differential count, the
routine evaluation should include determination of an acute-phase indicator, such as the
erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP), which can be useful in
discriminating inflammatory from noninflammatory musculoskeletal disorders. Both tests are
inexpensive and easily performed; the resulting values may be elevated with infections,
inflammatory arthritis, autoimmune disorders, neoplasia, pregnancy, and advanced age. Serum
uric acid determinations are only useful when gout has been diagnosed and therapy
contemplated.
Serologic tests for rheumatoid factor, antinuclear antibodies (ANA), complement levels, Lyme
disease antibodies, or antistreptolysin O (ASO) titer should be carried out only when there is
substantive clinical evidence suggesting a relevant associated diagnosis, as these tests have
poor predictive value when used in a screening fashion, especially when the pretest probability
is low. They should not be performed arbitrarily in patients with minimal or nonspecific
musculoskeletal complaints.
Aspiration and analysis of synovial fluid are always indicated in acute monarthritis or when an
infectious or crystal-induced arthropathy is suspected. Synovial fluid analysis may be crucial in
distinguishing between noninflammatory and inflammatory processes. This distinction can be
made on the basis of the appearance, viscosity, and cell count of the synovial fluid. Tests for
synovial fluid glucose, protein, lactate dehydrogenase, lactic acid, or autoantibodies are not
recommended, as they are insensitive or have little discriminatory value. Normal synovial fluid
is clear or a pale straw color and is viscous, primarily because of the high levels of hyaluronate.
Noninflammatory synovial fluid is clear, viscous, and amber-colored, with a WBC count of
<2000/uL and a predominance of mononuclear cells. The viscosity of synovial fluid is assessed
by expressing fluid from the syringe one drop at a time. Normally there is a stringing effect,
with a long tail behind each drop. Effusions due to osteoarthritis or trauma usually have normal
viscosity. Inflammatory fluid is turbid and yellow, with an increased WBC (2000 to 50,000/uL)
and a predominance of polymorphonuclear leukocytes. Inflammatory fluid has a reduced
viscosity, diminished hyaluronate, and little or no tail following each drop of synovial fluid. Such
effusions are found in RA, gout, other inflammatory arthritides, and septic arthritis. Infectious
fluid is turbid and opaque, with a WBC count usually >50,000/uL, a predominance of
polymorphonuclear leukocytes (>75%), and low viscosity. Such effusions are typical of septic
arthritis, but they occur rarely with sterile inflammatory arthritides such as RA or gout. In
addition, hemorrhagic synovial fluid may be seen with trauma, hemarthrosis, or neuropathic
arthritis.
Synovial fluid should be analyzed immediately for appearance, viscosity, and cell count.
Cellularity and the presence of crystals may be assessed by light or polarizing microscopy,
respectively. Monosodium urate crystals, seen in gouty effusions, are long, needle-shaped,
negatively birefringent, and usually intracellular, whereas calcium pyrophosphate dihydrate
crystals, found in chondrocalcinosis and pseudogout, are usually short, rhomboid-shaped, and
positively birefringent. Whenever infection is suspected, synovial fluid should be Gram-stained
and cultured appropriately. If gonococcal arthritis is suspected, immediate plating of the fluid
on appropriate culture medium is indicated. Synovial fluid from chronic monarthritis patients
should also be cultured for M. tuberculosis and fungi. Last, it should be noted that crystal-
induced arthritis and infection occasionally occur together in the same joint.
DIAGNOSTIC IMAGING IN JOINT DISEASES
Conventional radiography has been a valuable tool in the diagnosis and staging of articular
disorders. Plain x-rays are most appropriate when there is a history of trauma, suspected
chronic infection, progressive disability, or monarticular involvement; when therapeutic
alterations are considered; or when a baseline assessment is desired for what appears to be a
chronic process. However, in most inflammatory disorders, early radiography is rarely helpful in
establishing a diagnosis and may only reveal soft tissue swelling or juxtaarticular
demineralization. As the disease progresses, calcification (of soft tissues, cartilage, or bone),
joint space narrowing, erosions, bony ankylosis, new bone formation (sclerosis, osteophyte
formation, or periostitis), or subchondral cysts may develop and suggest specific clinical entities
Ultrasonography is useful in the detection of soft tissue abnormalities that cannot be
appreciated fully by clinical examination. Radionuclide scintigraphy provides useful information
regarding the metabolic status of bone and, along with radiography, is well suited for total-
body assessment of the extent and distribution of musculoskeletal involvement. It is a very
sensitive but poorly specific means of detecting inflammatory or metabolic alterations in bone
or periarticular soft tissue structures.
Computed tomography (CT) provides rapid reconstruction of sagittal, coronal, and axial images
and thus of the spatial relationships among anatomic structures. It has proved most useful in
the assessment of the axial skeleton because of its ability to visualize in the axial plane.
Articulations that are difficult to visualize by conventional radiography, such as the
zygapophyseal, sacroiliac, sternoclavicular, and hip joints, can be evaluated effectively using CT.
CT has been demonstrated to be useful in the diagnosis of low back pain syndromes, sacroiliitis,
osteoid osteoma, tarsal coalition, osteomyelitis, intraarticular osteochondral fragments, and
advanced osteonecrosis.

Magnetic resonance imaging (MRI) has significantly advanced the ability to image
musculoskeletal structures. MRI can provide multiplanar images with fine anatomic detail and
contrast resolution. Other advantages are the absence of ionizing radiation and adverse effects
and the superior ability to visualize bone marrow and soft tissue periarticular structures.
However, the high cost and long procedural time of MRI limit its use in the evaluation of
musculoskeletal disorders. MRI should be used only when it will provide necessary information
that cannot be obtained by less expensive and noninvasive means.
MRI can image fascia, vessels, nerve, muscle, cartilage, ligaments, tendons, pannus, synovial
effusions, cortical bone, and bone marrow. Visualization of particular structures can be
enhanced by altering the pulse sequence to produce either T1-weighted or T2-weighted spin
echo, gradient echo, or inversion recovery [including short tau inversion recovery (STIR)
images. Because of its sensitivity to changes in marrow fat, MRI is a sensitive although
nonspecific means of detecting osteonecrosis and osteomyelitis. Because of its enhanced soft
tissue resolution, MRI is more sensitive than arthrography or CT for the diagnosis of soft tissue
injuries (e.g., meniscal and rotator cuff tears), intraarticular derangements, and spinal cord
damage following injury, subluxation, or synovitis of the vertebral facet joints.

OSTEOARTHRITIS is the commonest joint disease of humans. Among the elderly, knee OA is the
leading cause of chronic disability in developed countries. Under the age of 55 years the joint
distribution of OA in men and women is similar; in older individuals, hip OA is more common in
men, while OA of interphalangeal joints and the thumb base is more common in women.
Similarly, radiographic evidence of knee OA and, especially symptomatic knee OA, is more
common in women than in men.
Clinical Features
The joint pain of OA is often described as a deep ache and is localized to the involved joint.
Typically, the pain of OA is aggravated by joint use and relieved by rest, but, as the disease
progresses, it may become persistent. Nocturnal pain, interfering with sleep, is seen
particularly in advanced OA of the hip and may be enervating. Stiffness of the involved joint
upon arising in the morning or after a period of inactivity (e.g., an automobile ride) may be
prominent but usually lasts less than 20 min. Systemic manifestations are not a feature of
primary OA.
Because articular cartilage is aneural, the joint pain in OA must arise from other structures. In
some cases it may be due to stretching of nerve endings in the periosteum covering
osteophytes; in others, to microfractures in subchondral bone or from medullary hypertension
caused by distortion of blood flow by thickened subchondral trabeculae. Joint instability,
leading to stretching of the joint capsule, and muscle spasm may also be sources of pain.
In some patients with OA, joint pain may be due to synovitis. In advanced OA, histologic
evidence of synovial inflammation may be as marked as that in the synovium of a patient with
rheumatoid arthritis.
Physical examination of the OA joint may reveal localized tenderness and bony or soft tissue
swelling. Bony crepitus (the sensation of bone rubbing against bone, evoked by joint
movement) is characteristic. Synovial effusions, if present, are usually not large. Palpation may
reveal some warmth over the joint. Periarticular muscle atrophy may be due to disuse or to
reflex inhibition of muscle contraction. In the advanced stages of OA, there may be gross
deformity, bony hypertrophy, subluxation, and marked loss of joint motion. The notion that OA
is inexorably progressive, however, is incorrect. In many patients the disease stabilizes; in
some, regression of joint pain and even of radiographic changes occurs.
Although the diagnosis of OA is often straightforward because of the high prevalence of
radiographic changes of OA in asymptomatic individuals, it is important to ensure that joint
pain in a patient with radiographic evidence of OA is not due to some other cause, such as soft
tissue rheumatism (e.g., anserine bursitis at the knee, trochanteric bursitis at the hip),
radiculopathy, referral of pain from another joint (e.g., 25% of patients with hip disease have
pain referred to the knee), entrapment neuropathy, vascular disease (claudication), or some
other type of arthritis (e.g., crystal-induced synovitis, septic arthritis). These are all common
pitfalls in the diagnosis of OA. It is usually not difficult to differentiate OA from a systemic
rheumatic disease, such as rheumatoid arthritis, because, in the latter diseases, joint
involvement is usually symmetric and polyarticular, with arthritis in wrists and
metacarpophalangeal joints (which are generally not involved in OA), and there are also
constitutional features such as prolonged morning stiffness, fatigue, weight loss, or fever.
Laboratory And Radiographic Findings
The diagnosis of OA is usually based on clinical and radiographic features. In the early stages,
the radiograph may be normal, but joint space narrowing becomes evident as articular
cartilage is lost. Other characteristic radiographic findings include subchondral bone sclerosis,
subchondral cysts, and osteophytosis. A change in the contour of the joint, due to bony
remodeling, and subluxation may be seen. Although tibiofemoral joint space narrowing has
been considered to be a radiographic surrogate for articular cartilage thinning, in patients with
early OA who do not have radiographic evidence of bony changes (e.g., subchondral sclerosis
or cysts, osteophytes), joint space narrowing alone does not accurately indicate the status of
the articular cartilage. Similarly, osteophytosis alone, in the absence of other radiographic
features of OA, may be due to aging rather than to OA.

As indicated above, there is often great disparity between the severity of radiographic findings,
the severity of symptoms, and functional ability in OA. Thus, while more than 90% of persons
over the age of 40 have some radiographic changes of OA in weight-bearing joints, only 30% of
these persons are symptomatic.
No laboratory studies are diagnostic for OA. Because primary OA is not systemic, the
erythrocyte sedimentation rate, serum chemistry determinations, blood counts, and urinalysis
are normal. Analysis of synovial fluid reveals mild leukocytosis (<2000 white blood cells per
microliter), with a predominance of mononuclear cells. Synovial fluid analysis is of particular
value in excluding other conditions, such as calcium pyrophosphate dihydrate deposition
disease, gout, or septic arthritis.
Prior to the appearance of radiographic changes, the ability to diagnose OA clinically without
an invasive procedure (e.g., arthroscopy) is limited. Approaches such as magnetic resonance
imaging (MRI) and ultrasonography have not been sufficiently validated to justify their routine
clinical use for diagnosis of OA or monitoring of disease progression.

GOUT is a metabolic disease most often affecting middle-aged to elderly men. It is typically
associated with an increased uric acid pool, hyperuricemia, episodic acute and chronic arthritis,
and deposition of MSU crystals in connective tissue tophi and kidneys.
Acute and Chronic Arthritis Acute arthritis is the most frequent early clinical manifestation of
gout. Usually, only one joint is affected initially, but polyarticular acute gout is also seen in male
hypertensive patients with ethanol abuse as well as in postmenopausal women. The
metatarsophalangeal joint of the first toe is often involved, but tarsal joints, ankles, and knees
are also commonly affected. In elderly patients, finger joints may be inflamed. Inflamed
Heberden's or Bouchard's nodes may be a first manifestation of gouty arthritis. The first
episode of acute gouty arthritis frequently begins at night with dramatic joint pain and
swelling. Joints rapidly become warm, red, and tender, and the clinical appearance often
mimics a cellulitis. Early attacks tend to subside spontaneously within 3 to 10 days, and most of
the patients do not have residual symptoms until the next episode. Several events may
precipitate acute gouty arthritis: dietary excess, trauma, surgery, excessive ethanol ingestion,
adrenocorticotropic hormone (ACTH) and glucocorticoid withdrawal, hypouricemic therapy,
and serious medical illnesses such as myocardial infarction and stroke.
After many acute mono- or oligoarticular attacks, a proportion of gouty patients may present
with a chronic nonsymmetric synovitis, causing potential confusion with rheumatoid arthritis.
Less commonly, chronic gouty arthritis will be the only manifestation and, more rarely, the
disease will manifest as inflamed or noninflamed periarticular tophaceous deposits in the
absence of chronic synovitis.
Women represent only 5 to 17% of all patients with gout. Premenopausal gout is a rare
occurrence and accounts for only about 17% of all women with gout; it is seen mostly in
individuals with a strong family history of gout. A few kindreds of precocious gout in young
females caused by decreased renal urate clearance and renal insufficiency have been
described. Most women with gouty arthritis are postmenopausal and elderly, have arterial
hypertension causing mild renal insufficiency, and are usually receiving diuretics. Also, most of
these patients have underlying degenerative joint disease, and inflamed tophaceous deposits
may be seen on Heberden's and Bouchard's nodes.
Laboratory Diagnosis Even if the clinical appearance strongly suggests gout, the diagnosis
should be confirmed by needle aspiration of acutely or chronically inflamed joints or
tophaceous deposits. Acute septic arthritis, several of the other crystalline-associated
arthropathies, palindromic rheumatism, and psoriatic arthritis may present with similar clinical
features. During acute gouty attacks, strongly birefringent needle-shaped MSU crystals with
negative elongation are largely intracellular. Synovial fluid cell counts are elevated from 2000
to 60,000/uL. Effusions appear cloudy due to leukocytes, and large amounts crystals
occasionally produce a thick pasty or chalky joint fluid. Bacterial infection can coexist with urate
crystals in synovial fluid; if there is any suspicion of septic arthritis, joint fluid must also be
cultured. MSU crystals can often be demonstrated in the first metatarsophalangeal (MTP) joint
and in knees not acutely involved with gout. Arthrocentesis of these joints is a useful technique
to establish the diagnosis of gout between attacks.
Radiographic Features Cystic changes, well-defined erosions described as punched-out lytic
lesions with overhanging bony edges (Martel's sign), associated with soft tissue calcified
masses are characteristic radiographic features of chronic tophaceous gout. However, similar
radiographic signs can also be observed in erosive osteoarthritis, destructive apatite
arthropathies, and rheumatoid arthritis.

RHEUMATOID ARTHRITIS
Signs and Symptoms of Articular Disease Specific symptoms usually appear gradually as several
joints, especially those of the hands, wrists, knees, and feet, become affected in a symmetric
fashion. Pain, swelling, and tenderness may initially be poorly localized to the joints. Pain in
affected joints, aggravated by movement. Generalized stiffness is frequent and is usually
greatest after periods of inactivity. Morning stiffness of greater than 1-h duration is an almost
invariable feature of inflammatory arthritis and may serve to distinguish it from various
noninflammatory joint disorders. Notably, however, the presence of morning stiffness may not
reliably distinguish between chronic inflammatory and noninflammatory arthritides, as it is also
found frequently in the latter. The majority of patients will experience constitutional symptoms
such as weakness, easy fatigability, anorexia, and weight loss. Although fever to 40°C occurs on
occasion, temperature elevation in excess of 38°C is unusual and suggests the presence of an
intercurrent problem such as infection.
Clinically, synovial inflammation causes swelling, tenderness, and limitation of motion. Warmth
is usually evident on examination, especially of large joints such as the knee, but erythema is
infrequent. Pain originates predominantly from the joint capsule, which is abundantly supplied
with pain fibers and is markedly sensitive to stretching or distention. Joint swelling results from
accumulation of synovial fluid, hypertrophy of the synovium, and thickening of the joint
capsule. Initially, motion is limited by pain. The inflamed joint is usually held in flexion to
maximize joint volume and minimize distention of the capsule. Later, fibrous or bony ankylosis
or soft tissue contractures lead to fixed deformities.
Although inflammation can affect any diarthrodial joint, RA most often causes symmetric
arthritis with characteristic involvement of certain specific joints such as the proximal
interphalangeal and metacarpophalangeal joints. The distal interphalangeal joints are rarely
involved. Synovitis of the wrist joints is a nearly uniform feature of RA and may lead to
limitation of motion, deformity, and median nerve entrapment (carpal tunnel syndrome).
Synovitis of the elbow joint often leads to flexion contractures that may develop early in the
disease. The knee joint is commonly involved with synovial hypertrophy, chronic effusion, and
frequently ligamentous laxity. Pain and swelling behind the knee may be caused by extension
of inflamed synovium into the popliteal space (Baker's cyst). Arthritis in the forefoot, ankles,
and subtalar joints can produce severe pain with ambulation as well as a number of
deformities. Axial involvement is usually limited to the upper cervical spine. Involvement of the
lumbar spine is not seen, and lower back pain cannot be ascribed to rheumatoid inflammation.
On occasion, inflammation from the synovial joints and bursae of the upper cervical spine leads
to atlantoaxial subluxation. This usually presents as pain in the occiput but on rare occasions
may lead to compression of the spinal cord.
With persistent inflammation, a variety of characteristic joint changes develop. These can be
attributed to a number of pathologic events, including laxity of supporting soft tissue
structures; damage or weakening of ligaments, tendons, and the joint capsule; cartilage
degradation; muscle imbalance; and unopposed physical forces associated with the use of
affected joints. Characteristic changes of the hand include (1) radial deviation at the wrist with
ulnar deviation of the digits, often with palmar subluxation of the proximal phalanges ("Z"
deformity); (2) hyperextension of the proximal interphalangeal joints, with compensatory
flexion of the distal interphalangeal joints (swan-neck deformity); (3) flexion contracture of the
proximal interphalangeal joints and extension of the distal interphalangeal joints (boutonniere
deformity); and (4) hyperextension of the first interphalangeal joint and flexion of the first
metacarpophalangeal joint with a consequent loss of thumb mobility and pinch. Typical joint
changes may also develop in the feet, including eversion at the hindfoot (subtalar joint),
plantar subluxation of the metatarsal heads, widening of the forefoot, hallux valgus, and lateral
deviation and dorsal subluxation of the toes.
Rheumatoid nodules develop in 20 to 30% of persons with RA. They are usually found on
periarticular structures, extensor surfaces, or other areas subjected to mechanical pressure,
but they can develop elsewhere, including the pleura and meninges. Common locations include
the olecranon bursa, the proximal ulna, the Achilles tendon, and the occiput. Nodules vary in
size and consistency and are rarely symptomatic, but on occasion they break down as a result
of trauma or become infected. They are found almost invariably in individuals with circulating
rheumatoid factor.
Clinical weakness and atrophy of skeletal muscle are common. Muscle atrophy may be evident
within weeks of the onset of RA and is usually most apparent in musculature approximating
affected joints. Muscle biopsy may show type II fiber atrophy and muscle fiber necrosis with or
without a mononuclear cell infiltrate.
Laboratory Findings
No tests are specific for diagnosing RA. However, rheumatoid factors, which are autoantibodies
reactive with the Fc portion of IgG, are found in more than two-thirds of adults with the
disease. Widely utilized tests largely detect IgM rheumatoid factors. The presence of
rheumatoid factor is not specific for RA. Rheumatoid factor is found in 5% of healthy persons.
In addition, a number of conditions besides RA are associated with the presence of rheumatoid
factor. These include systemic lupus erythematosus, Sjogren's syndrome, chronic liver disease,
sarcoidosis, interstitial pulmonary fibrosis, infectious mononucleosis, hepatitis B, tuberculosis,
leprosy, syphilis, subacute bacterial endocarditis, visceral leishmaniasis, schistosomiasis, and
malaria. In addition, rheumatoid factor may appear transiently in normal individuals after
vaccination or transfusion and may also be found in relatives of individuals with RA.
Normochromic, normocytic anemia is frequently present in active RA. It is thought to reflect
ineffective erythropoiesis; large stores of iron are found in the bone marrow. In general,
anemia and thrombocytosis correlate with disease activity. The white blood cell count is usually
normal, but a mild leukocytosis may be present.
The erythrocyte sedimentation rate is increased in nearly all patients with active RA. The levels
of a variety of other acute-phase reactants including ceruloplasmin and C-reactive protein are
also elevate.
Synovial fluid analysis confirms the presence of inflammatory arthritis, although none of the
findings is specific. The fluid is usually turbid, with reduced viscosity, increased protein content,
and a slightly decreased or normal glucose concentration. The white cell count varies between
5 and 50,000/uL; polymorphonuclear leukocytes predominate. A synovial fluid white blood cell
count >2000/uL with more than 75% polymorphonuclear leukocytes is highly characteristic of
inflammatory arthritis, although not diagnostic of RA.
Radiographic Evaluation
Early in the disease, roentgenograms of the affected joints are usually not helpful in
establishing a diagnosis. They reveal only that which is apparent from physical examination,
namely, evidence of soft tissue swelling and joint effusion. As the disease progresses,
abnormalities become more pronounced, but none of the radiographic findings is diagnostic of
RA. The diagnosis, however, is supported by a characteristic pattern of abnormalities, including
the tendency toward symmetric involvement. Juxtaarticular osteopenia may become apparent
within weeks of onset. Loss of articular cartilage and bone erosions develop after months of
sustained activity. The primary value of radiography is to determine the extent of cartilage
destruction and bone erosion produced by the disease, particularly when one is monitoring the
impact of therapy with disease-modifying drugs or surgical intervention. Other means of
imaging bones and joints, including 99mTc bisphosphonate bone scanning and magnetic
resonance imaging, may be capable of detecting early inflammatory changes that are not
apparent from standard radiography but are rarely necessary in the routine evaluation of
patients with RA.

RHEUMATIC FEVER
A migratory polyarthritis is one of the five major criteria of the rheumatic fever like as: carditis,
Sydenham's chorea, subcutaneous nodules, and erythema marginatum.
The carditis of acute rheumatic fever is a pancarditis involving the pericardium, myocardium,
and endocardium, resulting in the most serious complication - valvular stenosis and/or
regurgitation. The mitral valve is involved most frequently, followed by the aortic valve.
A migratory polyarthritis is present in as many as 75% of cases, most often affecting the ankles,
wrists, knees, and elbows over a period of days. It usually does not affect the small joints of the
hands or feet and seldom involves the hip joints. Since salicylates and other anti-inflammatory
drugs usually cause prompt resolution of joint symptoms, it is important that the clinician not
prescribe these medications until it is determined whether the arthritis is migratory. The
arthritis of acute rheumatic fever is extremely painful. Pain can be controlled with codeine or
similar analgesics until the diagnosis is established. The difference between arthralgia
(subjective joint pain) and arthritis (joint pain and swelling) must be understood. Too often,
arthralgia is used (incorrectly) as a major criterion.
Sydenham's chorea occurs in fewer than 10% of patients with rheumatic fever. While differing
from the other manifestations, this central nervous system disorder is a part of the rheumatic
fever complex and should be managed as such. Many patients who appear to have only chorea
may present several decades later with evidence of typical rheumatic valvular disease.
Subcutaneous nodules and erythema marginatum are rare major manifestations, usually
present in fewer than 10% of cases. Subcutaneous nodules are found over extensor surfaces of
joints, are seen most often in patients with long-standing rheumatic heart disease, and are
extremely rare in patients experiencing an initial attack. Erythema marginatum is an
uncommon manifestation. It is an evanescent macular eruption with rounded bordersѕusually
concentrated on the trunk.
The minor criteria are nonspecific and may be present in many clinical conditions.
To fulfill the Jones criteria, either two major criteria, or one major criterion and two minor
criteria, plus evidence of an antecedent streptococcal infection are required. The latter may be
provided by recovery of the organism on culture or by evidence of an immune response to one
of the commonly measured group A streptococcal antibodies (e.g., anti-streptolysin O, anti-
deoxyribonuclease B, anti-hyaluronidase).
Both the clinical microbiology and the clinical immunology laboratories have important roles in
confirming the diagnosis of rheumatic fever. At least 80% of patients with acute rheumatic
fever have an elevated anti-streptolysin O titer at presentation. If one employs two additional
streptococcal antibody tests such as the anti-DNAse B or anti-hyaluronidase test, the
percentage of patients who show evidence of a preceding group A streptococcal infection will
rise to more than 95%.
Reference source
Harrison’s principles of internal medicine.-.16th ed.- McGraw-Hill, Medical Publishing Division,
2005. – p. 2029 – 2050.

Test for self-control

Control questions:
1. What types of origin can rheumatological and related diseases have?
2. Symptoms and signs of inflammatory origin of articular syndrome.
3. Laboratory investigation of patients with articular syndrome.
4. Symptoms, signs and laboratory tests of rheumatoid arthritis
5. Symptoms, signs and laboratory tests of rheumatic polyartritis
6. Symptoms, signs and laboratory tests of osteoarthritis
7. Symptoms, signs and laboratory tests of gout
Practical task
1. Revealing and assessment of symptoms and signs of rheumatoid arthritis, osteoarthritis
2. Revealing and assessment of symptoms and signs rheumatic polyartritis, gout
3. Revealing and assessment of laboratory test at patients with articular syndrome.
 TOPIC 44
Clinical, laboratory and instrumental examination of the patients with
allergic diseases. Clinical presentation and emergency care of acute
allergy and coma
Importance of the topic
Every year number of patients with allergic diseases is increasing. Clinical
presentations of the diseases sometimes specific and easy for recognizing but
sometimes they have unspecific signs and atypical course that does them difficult for
diagnostics and therapy. Allergy can produce serious problems with health due to
affecting most of the internal organs and systems that sometimes may be life-
threatening state. Ability to recognizing symptoms and signs of allergy is very
important for every doctor or student.

2. Concrete aims:
─ To study main symptoms of allergic diseases
─ To study main signs of allergic diseases
─ To study laboratory tests for confirming allergic diseases
3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the immunocompetent system
Pathologic physiology Principles of the allergic reactions
Pathologic anatomy Morphological changes in organs due to allergic reactions
4. Task for self-depending preparation to practical training
4.1. List of the main terms that should know student preparing practical training

Term Term
anaphylaxis angioedema
atopy stridor
urticarial eruptions specific IgE antibodies

4.2. Theoretical questions:

132. How must patient with allergy be investigated?
133. Definition and causes of anaphylaxis.
134. Symptoms and signs of anaphylaxis.
135. Definition and clinical presentation of the urticaria.
136. Definition and clinical presentation of the angioedema
137. Laboratory tests for revealing allergic diseases.
4.3. Practical task that should be performed during practical training
123. Revealing and assessment of allergic symptoms
124. Revealing and assessment of allergic signs
125. Revealing and assessment of laboratory test at patients with allergy.
Topic content
Clinical examination of patient with allergy
Inquiry: skin rush from local till diffuse and itch, dyspnea, stuffiness and itch in nose, sneezing,
rhinorrhea, lacrimation, photophobia, itch in mouth, nausea, vomiting, diarrhea, stomachache,
fever, headache, irritation, fatigue, oedema that sometimes can be flash-like at site contacted
with allergen.
Taking history: Congenital inclination to allergy, contact with harmful and allergenic products,
ask about allergens
Physical examination: change of patient behavior, it can be exited or depressed. Different types
of rush, fast skin oedema .
Blood analysis – eosinophilia, histamine test for differentiating pseudoallergic syndrome.
Sputum examination – eosinophilia.
Specific allergic tests – skin allergic tests, immunologic assays (IgE investigations: total, specific
antibodies and others)
Anaphylaxis
The life-threatening anaphylactic response of a sensitized human appears within minutes after
administration of specific antigen and is manifested by respiratory distress often followed by
vascular collapse or by shock without antecedent respiratory difficulty. Cutaneous
manifestations exemplified by pruritus and urticaria with or without angioedema are
characteristic of such systemic anaphylactic reactions. Gastrointestinal manifestations include
nausea, vomiting, crampy abdominal pain, and diarrhea.
Predisposing factors and etiology
There is no convincing evidence that age, sex, race, occupation, or geographic location
predisposes a human to anaphylaxis except through exposure to some immunogen. According
to most studies, atopy does not predispose individuals to anaphylaxis from penicillin therapy or
venom of a stinging insect but is a risk factor for allergens in food or latex.
The materials capable of eliciting the systemic anaphylactic reaction in humans include the
following: heterologous proteins in the form of hormones (insulin, vasopressin, parathormone),
enzymes (trypsin, chymotrypsin, penicillinase, streptokinase), pollen extracts (ragweed, grass,
trees), nonpollen extracts (dust mites, dander of cats, dogs, horses, and laboratory animals),
food (milk, eggs, seafood, nuts, grains, beans, gelatin in capsules), antiserum (antilymphocyte
gamma globulin), occupation-related proteins (latex rubber products), and Hymenoptera
venom (yellow jacket, yellow and baldfaced hornets, paper wasp, honey bee, imported fire
ants); polysaccharides such as dextran and thiomerosal as a vaccine preservative; and most
commonly drugs such as protamine and antibiotics (penicillins, cephalosporins, amphotericin B,
nitrofurantoin, quinolones), local anesthetics (procaine, lidocaine), muscle relaxants
(suxamethonium, gallamine, pancuronium), vitamins (thiamine, folic acid), diagnostic agents
(sodium dehydrocholate, sulfobromophthalein), and occupation-related chemicals (ethylene
oxide), which are considered to function as haptens that form immunogenic conjugates with
host proteins. The conjugating hapten may be the parent compound, a nonenzymatically
derived storage product, or a metabolite formed in the host.
Clinical manifestations
Individuals differ in the time of appearance of symptoms and signs, but the hallmark of the
anaphylactic reaction is the onset of some manifestation within seconds to minutes after
introduction of the antigen, generally by injection or less commonly by ingestion. There may be
upper or lower airway obstruction or both. Laryngeal edema may be experienced as a "lump"
in the throat, hoarseness, or stridor, while bronchial obstruction is associated with a feeling of
tightness in the chest and/or audible wheezing. Patients with bronchial asthma are predisposed
to severe involvement of the lower airways. A characteristic feature is the eruption of well-
circumscribed, discrete cutaneous wheals with erythematous, raised, serpiginous borders and
blanched centers. These urticarial eruptions are intensely pruritic and may be localized or
disseminated. They may coalesce to form giant hives, and they seldom persist beyond 48 h. A
localized, nonpitting, deeper edematous cutaneous process, angioedema, may also be present.
It may be asymptomatic or cause a burning or stinging sensation.
Patients dying of vascular collapse without antecedent hypoxia from respiratory insufficiency
have visceral congestion with a presumptive loss of intravascular blood volume. The associated
electrocardiographic abnormalities, with or without infarction, noted in some patients may
reflect a primary cardiac event or be secondary to a critical reduction in blood volume.
The angioedematous and urticarial manifestations of the anaphylactic syndrome have been
attributed to release of endogenous histamine.
Diagnosis
The diagnosis of an anaphylactic reaction depends largely on an accurate history revealing the
onset of the appropriate symptoms and signs within minutes after the responsible material is
encountered. When only a portion of the full syndrome is present, such as isolated urticaria,
sudden bronchospasm in a patient with asthma, or vascular collapse after intravenous
administration of an agent, it may be appropriate to consider a complement-mediated immune
complex reaction, an idiosyncratic response to any of the nonsteroidal anti-inflammatory
agents, or the direct effect of certain drugs or diagnostic agents on mast cells. Intravenous
administration of a chemical mast cell-degranulating agent, including opiate derivatives and
radiographic contrast media, may elicit generalized urticaria, angioedema, and a sensation of
retrosternal oppression with or without clinically detectable bronchoconstriction or
hypotension. Aspirin and other nonsteroidal anti-inflammatory agents such as indomethacin,
aminopyrine, and mefenamic acid may precipitate a life-threatening episode of obstruction of
upper or lower airways, especially in patients with asthma, that is clinically reminiscent of
anaphylaxis but is not associated with a detectable IgE response.
Radioimmunoassays have demonstrated specific IgE antibodies in patients with anaphylactic
reactions, but such approaches require purified antigens. Elevations of b-tryptase levels in
serum implicate mast cell activation in an adverse systemic reaction and are particularly
informative with episodes of hypotension during general anesthesia or when there has been a
fatal outcome.
Urticaria and angioedema
Definition
Urticaria and angioedema may appear separately or together as cutaneous manifestations of
localized nonpitting edema; a similar process may occur at mucosal surfaces of the upper
respiratory or gastrointestinal tract. Urticaria involves only the superficial portion of the
dermis, presenting as well-circumscribed wheals with erythematous raised serpiginous borders
with blanched centers that may coalesce to become giant wheals. Angioedema is a well-
demarcated localized edema involving the deeper layers of the skin, including the
subcutaneous tissue. Recurrent episodes of urticaria and/or angioedema of less than 6 weeks'
duration are considered acute, whereas attacks persisting beyond this period are designated
chronic.
Predisposing factors and etiology
The occurrence of urticaria and angioedema is probably more frequent than usually described
because of the evanescent, self-limited nature of such eruptions, which seldom require medical
attention when limited to the skin. Although persons in any age group may experience acute or
chronic urticaria and/or angioedema, these lesions increase in frequency after adolescence,
with the highest incidence occurring in persons in the third decade of life; indeed, one survey
of college students indicated that 15 to 20% had experienced a pruritic wheal reaction.
Urticaria and/or angioedema occurring during the appropriate season in patients with seasonal
respiratory allergy or as a result of exposure to animals or molds is attributed to inhalation or
physical contact with pollens, animal dander, and mold spores, respectively. However, urticaria
and angioedema secondary to inhalation are relatively uncommon compared to urticaria and
angioedema elicited by ingestion of fresh fruits, shellfish, fish, milk products, chocolate,
legumes including peanuts, and various drugs that may elicit not only the anaphylactic
syndrome with prominent gastrointestinal complaints but also chronic urticaria.
Additional etiologies include physical stimuli such as cold, heat, solar rays, exercise, and
mechanical irritation. The physical urticarias can be distinguished by the precipitating event
and other aspects of the clinical presentation. Dermographism, which occurs in 1 to 4% of the
population, is defined by the appearance of a linear wheal at the site of a brisk stroke with a
firm object or by any configuration appropriate to the eliciting event. Dermographism has a
prevalence that peaks in the second to third decades. It is not influenced by an atopic diathesis
and has a duration generally of less than 5 years. Pressure urticaria, which often accompanies
dermographism or chronic idiopathic urticaria, presents in response to a sustained stimulus
such as a shoulder strap or belt, running (feet), or manual labor (hands). Cholinergic urticaria is
distinctive in that the pruritic wheals are of small size (1 to 2 mm) and are surrounded by a
large area of erythema; attacks are precipitated by fever, a hot bath or shower, or exercise and
are presumptively attributed to a rise in core body temperature. Exercise-related anaphylaxis
can be limited to erythema and pruritic urticaria but may progress to angioedema of the face,
oropharynx, larynx, or intestine or to vascular collapse; it is distinguished from cholinergic
urticaria by presenting with wheals of conventional size and by not occurring with fever or a
hot bath. Cold urticaria, either acquired or hereditary, is local at body areas exposed to low
ambient temperature or cold objects (ice cube) but can progress to vascular collapse with
immersion in cold water (swimming). Solar urticaria is subdivided into three groups by the
response to specific portions of the light spectrum. Vibratory angioedema may occur after
years of occupational exposure or can be idiopathic; it may be accompanied by cholinergic
urticaria. Other rare forms of physical allergy, always defined by stimulus-specific elicitation,
include local heat urticaria, aquagenic urticaria from contact with water of any temperature
(sometimes associated with polycythemia vera), and contact urticaria from direct interaction
with some chemical substance.
Clinical manifestations
Urticarial eruptions are distinctly pruritic, involve any area of the body from the scalp to the
soles of the feet, and appear in crops of 24- to 72-h duration, with old lesions fading as new
ones appear. The most common sites for urticaria are the extremities and face, with
angioedema often being periorbital and in the lips. Although self-limited in duration,
angioedema of the upper respiratory tract may be life-threatening due to laryngeal
obstruction, while gastrointestinal involvement may present with abdominal colic, with or
without nausea and vomiting, and may precipitate unnecessary surgical intervention. No
residual discoloration occurs with either urticaria or angioedema unless there is an underlying
process leading to superimposed extravasation of erythrocytes.
Diagnosis
The rapid onset and self-limited nature of urticarial and angioedematous eruptions are
distinguishing features. Additional characteristics are the occurrence of the urticarial crops in
various stages of evolution and the asymmetric distribution of the angioedema. Urticaria
and/or angioedema involving IgE-dependent mechanisms are often appreciated by historic
considerations implicating specific allergens or physical stimuli, by seasonal incidence, and by
exposure to certain environments. Direct reproduction of the lesion with physical stimuli is
particularly valuable because it so often establishes the cause of the lesion. The diagnosis of an
environmental allergen based on the clinical history can be confirmed by skin testing or assay
for allergen-specific IgE in serum. IgE-mediated urticaria and/or angioedema may or may not
be associated with an elevation of total IgE or with peripheral eosinophilia. Fever, leukocytosis,
and an elevated sedimentation rate are absent.
Urticaria and angioedema must be differentiated from contact sensitivity, a vesicular eruption
that progresses to chronic thickening of the skin with continued allergenic exposure. They must
also be differentiated from atopic dermatitis, a condition that may present as erythema,
edema, papules, vesiculation, and oozing proceeding to a subacute and chronic stage in which
vesiculation is less marked or absent and scaling, fissuring, and lichenification predominate in a
distribution that characteristically involves the flexor surfaces. In cutaneous mastocytosis, the
reddish brown macules and papules, characteristic of urticaria pigmentosa, urticate with
pruritus upon trauma; and in systemic mastocytosis, without or with urticaria pigmentosa,
there is an episodic systemic flushing with or without urticaria but no angioedema.
Reference source
Harrison’s principles of internal medicine.-.16th ed.- McGraw-Hill, Medical Publishing Division,
2005. – p. 1947 – 1956.

Test for self-control

Control questions:
1. How must patient with allergy be investigated?
2. Definition and causes of anaphylaxis.
3. Symptoms and signs of anaphylaxis.
4. Definition and clinical presentation of the urticaria.
5. Definition and clinical presentation of the angioedema
6. Laboratory tests for revealing allergic diseases.
Practical task
1. Revealing and assessment of allergic symptoms
2. Revealing and assessment of allergic signs
3. Revealing and assessment of laboratory test at patients with allergy.
 TOPIC 45
Conclusion module control including test-control of the theoretical
training, control of the practical skills, assessment of the instrumental
investigation reports
10. Importance of the topic
Conclusion module control is very important for strengthening and checking knowledge
obtained during study at the department. It needs for repeating and systematization all learned
theoretical material and training practical skills.
2. Concrete aims:
─ To check students theoretical knowledge
─ To check students practical skills

3. Basic training level

Previous subject Obtained skill

Normal anatomy Anatomy of the gastrointestinal,
renal, hemopoetic,
endocrinology systems
Normal physiology Functions of the gastrointestinal, renal, hemopoetic,
endocrinology systems
Histology Ontogenesis of the gastrointestinal, renal, hemopoetic,
endocrinology systems.
Propedeutics to internal Subjective, objective and instrumental examinations of the
medicine patients with diseases of the gastrointestinal, renal,
hemopoetic, endocrinology systems.

LIST OF QUESTIONS FOR CONCLUSION CONTROL

1. Visual examination of the abdomen, revealing main symptoms.

2. Surface tentative palpation of the abdomen: methodological algorithm, analysis of results
and diagnostic significance.
3. Theoretical basis and principles of deep sliding palpation according to Obraztsov and
Strazhesko.
4. Deep sliding systematic palpation of the intestine: sigmoid and caecum, their characteristics
in normal and pathology.
5. Deep sliding systematic palpation of the intestine: ascending and descending colons, their
characteristics in normal and pathology.
6. The methods of the greater curvature of stomach evaluation.
7. Deep sliding systematic palpation of transverse colon: its characteristics in normal and
pathology.
8. The technique of liver palpation. The normal liver characteristics (liver lower edge,
consistency, surface, painfulness) and their possible changers on pathology.
9. The technique of spleen palpation and the main causes of its size enlargement.
10. The methods for free fluid in abdominal cavity determination.
11. Percussion of the liver by Obraztsov: the subsequent, rules, parameters in normal and
pathological conditions.
12. Percussion of the liver by Curlov: the subsequent, rules, parameters in normal and
pathological conditions.
13. Percussion of the spleen. The rules and the main causes of spleen enlargement.
14. The syndrome of dyspepsia: etiology, pathogenesis, clinical, laboratory and instrumental
methods of diagnosis.
15. The syndrome of dysphagia: etiology, pathogenesis, clinical, laboratory and instrumental
methods of diagnosis.
16. The types of bile tract dyskinesia: etiology, pathogenesis, clinical, laboratory and
instrumental methods of diagnosis.
17. The syndrome of portal hypertension: etiology, pathogenesis, clinical, laboratory and
instrumental methods of diagnosis.
18. The syndrome of jaundice: etiology, pathogenesis, clinical, laboratory and instrumental
methods of diagnosis.
19. The syndrome of gastro-intestinal bleeding: etiology, pathogenesis, clinical, laboratory and
instrumental methods of diagnosis.
20. Constipation syndrome: etiology, pathogenesis, clinical, laboratory and instrumental
methods of diagnosis.
21. Diarrhea syndrome: etiology, pathogenesis, clinical, laboratory and instrumental methods
of diagnosis.
22. Nephrotic syndrome: etiology, pathogenesis, clinical, laboratory and instrumental methods
of diagnosis.
23. The urinate syndrome: etiology, pathogenesis, clinical, laboratory and instrumental
methods of diagnosis.
24. The syndrome of acute renal failure: etiology, pathogenesis, clinical, laboratory and
instrumental methods of diagnosis.
25. The syndrome of chronic renal failure: etiology, pathogenesis, clinical, laboratory and
instrumental methods of diagnosis.
26. The syndrome of anemia: etiology, pathogenesis, clinical, laboratory and instrumental
methods of diagnosis.
27. Hyperplasic syndrome on blood system diseases: etiology, pathogenesis, clinical, laboratory
and instrumental methods of diagnosis.
28. Hemorrhagic syndromes: classification, pathogenesis, clinical, laboratory and instrumental
methods of diagnosis.
29. The syndrome of hyperthyroidism: etiology, pathogenesis, clinical features, laboratory and
instrumental methods of diagnosis.
30. The syndrome of hypothyroidism: etiology, pathogenesis, clinical features, laboratory and
instrumental methods of diagnosis.
31. Articular syndrome: main causes, clinical presentation, laboratory and instrumental
examinations.
32. Chronic gastritis: modern classification, etiology, chief clinical features and diagnosis.
33. Peptic ulcer disease: classification, etiology, chief clinical features and diagnosis.
34. Chronic cholecystites, cholangities: classification, etiology, chief clinical features and
diagnosis.
35. Gall-stone disease: etiology, the stage of development, chief clinical features and diagnosis.
36. Hepatitis: etiology, modern classification, chief clinical features and diagnosis.
37. Liver cirrhosis: etiology, modern classification, chief clinical features and diagnosis.
38. Acute and chronic glomerulonephritis: etiology, modern classification, chief clinical features
and diagnosis.
39. Acute and chronic pyelonephritis: etiology, modern classification, chief clinical features and
diagnosis.
40. Anemia: classification and chief syndromes.
41. Iron deficiency anemia: etiology, pathogenesis, chief clinical features and laboratory
 criteria.
42. B12- foliate deficiency anemia: etiology, pathogenesis, chief clinical features and laboratory
criteria.
43. Hemolytic anemia: classification, chief syndromes and laboratory criteria.
44. Chronic leukemia: main syndromes, laboratory criteria.
45. Hemophilia: etiology, classification, chief clinical features and diagnosis.
46. Thrombocytopenia: etiology, chief clinical features and diagnosis.
47. Hemorrhagic vasculitis (Shenlain-Haenocha disease): etiology, chief clinical features and
diagnosis.
48. Diabetes mellitus: classification, main symptoms and syndromes, laboratory diagnostic.
49. Allergy: clinical presentation, diagnostics.

THE LIST OF PRACTICAL SKILLS

1. To conduct inquiring of the patient with digestive system ’s damage. To define the chief
symptoms.
2. To carry out inspection of the abdomen. To define the clinical significance of obtained
symptoms.
3. To make palpation of the thyroid gland, to evaluate obtained results.
4. To carry out superficial palpation of the abdomen. To define the clinical significance of
obtained symptoms.
5. To make palpation of the sigmoid colon. To define the clinical significance of obtained
symptoms.
6. To make palpation of the caecum. To define the clinical significance of obtained
symptoms.
7. To conduct palpation of the ascending colon. To define the clinical significance of
obtained symptoms.
8. To make palpation of the descending colon. To define the clinical significance of
obtained symptoms.
9. To conduct palpation of the transverse colon. To define the clinical significance of
obtained symptoms.
10. To make palpation of the liver. To define the clinical significance of obtained symptoms.
11. To carry out palpation of the spleen. To define the clinical significance of obtained
symptoms.
12. To conduct palpation of the kidneys. To define the clinical significance of obtained
symptoms.
13. To determine the greater curvature of stomach, to analyze obtained results.
14. To determine the free fluid in abdominal cavity, to evaluate obtained results.
15. To conduct percussion of the liver, to define the clinical significance of obtained data.
16. To conduct percussion of the spleen, to define the clinical significance of obtained data.
17. To conduct inquiring, inspection and palpation of the abdomen at the patient with
gastritis. To recognize the major syndromes.
18. To analyze the results of stomach contents at the patient with chronic gastritis. To
define the state of gastric secretion.
19. To carry out inquiring, inspection and palpation of the abdomen at the patient with
peptic ulcer disease. To identify the chief syndromes and try to recognize the localization of
ulcer.
20. To conduct inquiring, inspection and palpation of the abdomen at the patient with
chronic cholecystitis. To check the prominent symptoms specific for biliary system damage. To
define the major syndromes.
21. To conduct inquiring, inspection and palpation of the abdomen at the patient with
chronic cholangities. To define the major syndromes.
22. To evaluate the results of duodenal intubation at the patient with biliary tract damage.
To identify the major symptoms and syndromes.
23. To carry out inquiring and objective examination in patient with chronic hepatitis or liver
cirrhosis. To define the major symptoms and syndromes.
24. To carry out inquiring and objective examination at the patient with chronic hepatitis or
liver cirrhosis. To define the major syndromes based on biochemical blood and urinary tests.
25. To conduct inquiring and objective examination at the patient with chronic renal disease
(glomerulonephritis or pyelonephritis). To classify the major syndromes.
26. To analyze the results of laboratory examination: general urine test, urine analysis by
Nechiporenko and Zemnitsky. To define the major symptoms and syndromes. To make
conclusion on the subject of the character of renal damage.
27. To conduct inquiring and objective examination at the patient with anemia. To identify
the chief symptoms and syndromes, with taking into consideration results of clinical blood test
determine the type of anemia.
28. To analyze the results of clinical blood test at the patient with leukemia. To determine
the chief laboratory symptoms and type of chronic leukemia.
29. To carry out inquiring and objective examination at the patient with diabetes mellitus.
To assess the pulse on the arteries of upper and low extremities and blood pressure. To define
the major symptoms and syndromes.
30. To carry out inquiring and objective examination at the patient with thyroid gland
disease. Palpation of the thyroid gland. To define the main symptoms and syndromes.
To carry out inquiring and visual inspection of the patient with allergy.