SYTEMIC PATHOLOGY

PREPARED BY:
HENRY MUROKI
DEPARTMAENT OF HEALTH SCIENCES
MAASAI MARA UNIVERSITY
 Pulmonary Diseases

MAASAI MARA UNIVERSITY NURSING 2.3

Revi
ew:
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Basi
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Review: Oxygen Transport Pathway
• Inspired Oxygen via ambient
air
• Airways
• Lungs and chest wall
• Diffusion
• Perfusion
• Myocardial function
• Tissue extraction and use of
O2
• Return of partially
desaturated blood & CO2 to
the lungs
Review: Oxygen Transport Pathway
Lung anatomy
• The lung consists of five lobes. The left lung has a superior
and inferior lobe, while the right lung has superior, middle,
and inferior lobes. Thin walls of tissue called fissures separate
the different lobes.
• Right bronchus is more vertical than the left one thus
aspiration is more common in the right than in the left
• Progressive branching of trachea, bronchi, bronchioles ( no
cartilage or sub mucosal glands), terminal bronchioles, acini
gas exchanging units, terminal respiratory unit.
• Below the vocal cords , there is pseudo stratified tall columnar
ciliated epithelium.
Review: Broncho-Pulmonary
Segments
 Mechanics of Breathing
• Inspiration
– Diaphragm pushes downwards, lowering
intrapulmonary pressure
• Expiration
– Diaphragm relaxes, raising intrapulmonary
pressure
• Resistance to airflow
– Largely determined by airway diameter
 The Mechanics of
Inspiration and Expiration

Fig 10.6
 Muscles of Respiration
• Inspiration
– Diaphragm contracts
downward, lowering
intrapulmonary
pressure
• Primary MMs:
– Diaphragm,
intercostals
• Accessory MMs:
– SCM, Scalenes,
Serratus Ant, Pecs,
trapezius, erector
spinae Fig 10.7
 Muscles of Respiration
• Expiration:
– Diaphragm relaxes, raising
intrapulmonary pressure
• Primary (during quiet
breathing):
– Relaxation of diaphragm &
intercostals
• Accessory Expiration
(during active breathing):
– Rectus Abdominis
– Obliquus externus
– Obliqueu internus
– Transverse abdominis
Review: Mechanical Factors in Breathing

• Flow of air into lungs is result of pressure

differences, there are several important
factors to consider with this process
– Resistance to breathing
• Lung compliance (how easily lungs inflate)
• Chest wall compliance (how easily chest wall expands
with inspiration)
– Airway resistance
 Review: Diffusion
• Action of air (o2
and CO2) crossing
the alveolar-
capillary
membrane
• Cross the
surfactant lining
• This process can be
significantly
affected in the
diseased lung
Review: Perfusion
• Blood flow of the
pulmonary
circulation
• Position significantly
affects perfusion
• Gravity-dependent
lung segments have
the greatest amount
of perfusion
 Vital Signs: Respiratory Rate

• Breaths inspired or expired per

minute, depth of breathing
also described
• Increase in RR
– pain, anxiety, medications, fever,
activity, pulmonary disease
• Decrease in RR
– sleeping, medications,
anesthesia
 RR: Clinical Application
• RR increases immediately with increased
workload and decreases immediately during
recovery
• Factors affecting RR
– age, body size, body position, patient awareness
• Chest wall and abdomen expansion occurs with
inspiration & should be symmetrical.
• Periodic deep breathing (sighs) should be less
than 5 per minute.
 Oxygen Saturation (SaO2)
• Clinical application
– < 90% is
• Percent saturation of contraindication to
oxygen bound to exercise, < 90%, O2
hemoglobin in the supplementation
arterial blood is termed needed
SaO2 – Exception in patients
• Normal range with chronic lung
– 95-100% disease who may
• Measured with a pulse chronically function
oximeter. with Sats at 50-60%
 Review of pathophysiology
hypoxemia signs & symptoms
Pa02 (mmHg) Signs & Symptoms
80-100 Normal
60-80 Moderate tachypnea & dyspnea
50-60 Malaise, nausea
Possible onset of respiratory distress
Poor judgment, motor incoordination, slowed reaction times

35-50 Respiratory distress & arrhythmias

Marked confusion, agitation
25-35 Marked respiratory distress
Lethargy, loss of consciousness
Lactic acidosis (Build up of lactate in the body <pH in blood)

<25 Hypoventilation, apnea

Bradycardia, myocardial depression, shock
Cardiac arrest
 Vital Signs Across the Lifespan –
Accepted Normal Values

AGE HR BP RR
Neonates 120 – 200 60-90/30-60 40 - 80

Infant< 100 – 160 70-95/45-65 20 – 40

1yr
1 – 6 years 70 - 140 80-110/60- 20 - 35
70
6 – 12 60 - 100 90-116/65- 15 - 25
years 75
Adolescen 60 - 100 100-120/60-80 12 - 20
t/
 Pathophysiology Pulmonary conditions
• Pneumonia
• Adult Respiratory Distress
Syndrome (ARDS) • Respiratory Failure
• Atelectasis • SCI
• Asthma • Surgical Procedures
• TB
• Bronchiectasis
• Cystic Fibrosis
• Fibrotic conditions
• Infectious diseases
• Neoplasm
• Orthopedic impairments
Pathophysiology Overview of Lung Disease

• As lung disease progresses in severity, the

pathophysiology progresses to involve the:
– Heart
– Arterial & venous systems
• Resulting in a plethora of systemic symptoms
– Right ventricular failure/cor pulmonale
– Increased systemic venous pressure
• LE edema
• Liver ascites
• Jugular venous distension
– Decreased cardiac output to arterial system
Two Main Categories of Lung Disease

• Obstructive Lung Disease

• Restrictive Lung Disease

*Some patients may have both

components.

Asbestos
 Obstructive Lung Disease
• Characterized by an:
– obstruction to airflow with inflamed and easily collapsible airways,
& problems exhaling (“like trying to breath through a staw”)
–Rate of expiration is reduced.
–Lungs are “fine,” but bronchi are obstructed.

• Ultimately affects mechanical function & gas exchange

• Characteristic physical symptoms:
– Chronic cough
– Mucus expectoration
– Wheezing
– Dyspnea on exertion
– Decreased expiratory flow rates
 Obstructive Lung Disease
Early Adult
• Cystic Fibrosis • Chronic Bronchitis
• Asthma • Emphysema
• Bronchiectasis • Chronic Obstructive
Pulmonary Disease-
mixed
 Chronic Bronchitis
• Morphology :
– Increased mucous
production from
bronchioles
– Structural changes to
bronchi
– Chronic swelling and • Impairments;
inflammation of – Hypertrophy of mucous
bronchi and secreting glands
bronchioles – Insufficient oxygenation of
the alveoli
– Ciliary action impaired
 Chronic Bronchitis
• Clinical Signs
– Thick sputum
– Increased use of accessory
• Clinical Diagnosis muscles
– Productive cough – Persistent cough
present for 3 months – Increased PAP (8-
during 2 consecutive 20mmhg)
years
– Wheeze
– Pulmonary function
– Dyspnea
tests
– Cyanosis
– X-ray
– V/Q abnormalities
 Long term treatment of chronic bronchitis with
PEP mask and chest physiotherapy
- Christensen, E. 2020

 The PEP group had significantly less cough and

mucous production and fewer exacerbations
compared with the control.

 No difference in FEV1 at one month however

by 12 months the control group had declined
and PEP group improved FEV1.
 Emphysema
• Primary Causes:
– Smoking and Pollutants
(ie. Jikos)
• Characterized by:
• Impairments:
– Abnormal & permanent
enlargement of terminal – Alveoli over-inflated &
airways expiration is difficult
– Destruction of alveolar – Loss of elastic recoil
walls – Collapse of airways
– Increased lung
– Airflow obstruction
compliance
– Chronic, nonreversible
 Restrictive Lung Dysfunction
• Not a disease, but
dysfunction caused by many
other diseases or conditions
• Abnormal reduction in
pulmonary ventilation due to:
– Decreased lung compliance
– Decreased chest wall
compliance
– Decreased lung volumes
– Increased work of breathing
Restrictive Lung Dysfunction

Pulmonary causes

Cardiovascular causes

Neuromuscular causes

Musculoskeletal causes

Other causes
 BREATHING
• During gaseous exchange in the lungs, the partial pressures of oxygen
(O₂) and carbon dioxide (CO₂) play a crucial role in the diffusion of these
gases between the alveoli and the blood in the pulmonary capillaries.
The typical partial pressures in the alveoli and blood are as follows:
•
• Oxygen (O₂) Pressure:
•
• In the alveoli: The partial pressure of oxygen (P_O₂) is approximately
100 mmHg.
• In the blood (pulmonary capillaries) entering the alveoli: The partial
pressure of oxygen is around 40 mmHg.
• This difference in partial pressure allows oxygen to diffuse from the
alveoli into the blood.
 BREATHING
• Carbon Dioxide (CO₂) Pressure:
•
• In the alveoli: The partial pressure of carbon dioxide
(P_CO₂) is about 40 mmHg.
• In the blood (pulmonary capillaries) entering the
alveoli: The partial pressure of carbon dioxide is
around 45 mmHg.
• This difference in partial pressure allows carbon
dioxide to diffuse from the blood into the alveoli,
where it can be exhaled.
 TYPES OF BREATHING
Eupnea (Normal Breathing):
• Description: Eupnea is the normal, quiet breathing that occurs
at rest.
• Characteristics: It involves regular, rhythmic breathing with
both inspiration and expiration occurring without conscious
effort. The diaphragm and intercostal muscles primarily
facilitate it.
Tachypnea:
• Description: Tachypnea is rapid, shallow breathing.
• Characteristics: The respiratory rate is increased, often due to
fever, anxiety, exercise, or respiratory conditions like
pneumonia. It can indicate a need for more oxygen or the
removal of excess carbon dioxide.
 TYPES OF BREATHING
• Bradypnea:
• Description: Bradypnea is abnormally slow
breathing.
• Characteristics: The respiratory rate is
decreased, which can be caused by drug
overdose (e.g., opioids), head injuries, or
metabolic disorders. It often indicates a
reduced demand for oxygen or impaired
respiratory control.
Dyspnea:
• Description: Dyspnea refers to difficult or labored breathing.
• Characteristics: It can occur with physical activity (exertional
dyspnea) or at rest (resting dyspnea). Causes include heart
failure, lung diseases (like asthma or COPD), or anxiety.
Hyperpnea:
• Description: Hyperpnea is an increase in the depth and rate
of breathing.
• Characteristics: It is often a normal response to exercise or
increased metabolic demand. In some pathological
conditions, it can be seen with fever or anemia.
Apnea:
• Description: Apnea is the absence of breathing.
• Characteristics: It can be temporary (as in sleep apnea) or
prolonged (as in respiratory arrest). Sleep apnea involves brief
pauses in breathing during sleep, while respiratory arrest is a
medical emergency requiring immediate intervention.
Hyperventilation:
• Description: Hyperventilation is increased ventilation beyond
the metabolic needs.
• Characteristics: It results in excessive loss of CO₂ (hypocapnia),
leading to symptoms like dizziness, tingling, and
lightheadedness. Causes include anxiety, panic attacks, or
metabolic acidosis.
Hypoventilation:
• Description: Hypoventilation is decreased ventilation that
does not meet the body’s metabolic needs.
• Characteristics: It leads to increased CO₂ levels (hypercapnia)
and can result from respiratory muscle weakness, obstructive
lung disease, or central respiratory depression.
Cheyne-Stokes Respiration:
• Description: Cheyne-Stokes respiration is a cyclical pattern of
breathing.
• Characteristics: It involves periods of deep, rapid breathing
followed by periods of apnea. This type of breathing can be
seen in heart failure, stroke, traumatic brain injuries, and
Kussmaul Breathing:
• Description: Kussmaul breathing is deep and labored
breathing.
• Characteristics: It is a compensatory mechanism for metabolic
acidosis, particularly diabetic ketoacidosis. It helps to expel
CO₂ and reduce acidity in the blood.
Biot’s Respiration:
• Description: Biot’s respiration is an irregular breathing pattern.
• Characteristics: It involves groups of quick, shallow breaths
followed by regular or irregular periods of apnea. This pattern
is often associated with damage to the medulla oblongata due
to stroke, trauma, or opioid use.
 Atelectasis

• Etiology
• Refers to incomplete expansion of lungs as in
neonatal atelectasis ( primary ) or to the
collapse of previously inflated lungs
( secondary or acquired)
• Its Restrictive
• Atelectasis predisposes to infections and is
reversible except the contraction atelectasis
type due to scarring of the aveoli.
 Three main categories:

Resorptive (Obstructive) Atelectasis:

• Caused by obstruction in the airway, such as a mucous
plug, foreign body, tumor, or external compression by
lymph nodes.
Compressive Atelectasis:
• Occurs when external pressure is exerted on the lung,
commonly due to pleural effusion, pneumothorax, or
hemothorax.
Contraction (Cicatrization) Atelectasis:
• Results from fibrosis or scarring of lung tissue, often
due to chronic inflammatory diseases, infections, or
radiation therapy.
 Pathogenesis

Resorptive (Obstructive) Atelectasis:

• Obstruction prevents air from reaching distal
airways. As trapped air is absorbed into the
bloodstream, the affected lung segment collapses
due to loss of volume.
Compressive Atelectasis:
• External forces compress the lung tissue, reducing
its volume and preventing adequate expansion.
Contraction Atelectasis:
• Fibrotic changes in the lung or pleura cause
retraction and shrinkage of lung tissue, limiting its
ability to expand.
 Gross Morphology:

• Affected lung areas appear collapsed,

shrunken, and often darker in color.
• Microscopic Morphology:
• Alveolar spaces are collapsed.
• May show evidence of inflammation or
fibrosis depending on the etiology.
• Long-standing atelectasis can lead to
irreversible scarring and fibrosis.
• Atelectasis is the loss of lung volume with the
absence of air in part or all of the lung
• Caused by hypoventilation secondary to pain during
ventilation, internal bronchial obstruction, external
bronchial compression, low tidal volumes,
neurologic insult
• Often seen post-operatively
• On X-ray, generally this is accompanied by increased
density and possibly elevation of the
hemidiaphragm, or mediastinal displacement
 Atelectasis

• Decreased breath sounds, dyspnea, tachycardia,

increased temp, CXR with plate-like streak
ARDS (Acute respiratory distress syndrome)
• Also called shock lung, diffuse alveolar damage, acute alveolar
injury
• It’s a clinical syndrome caused by diffuse alveolar capillary
damage leading to accumulation of fluid and hyaline membrane
lining the alveolar.
• Leads to respiratory insufficiency, cyanosis, then multi-organ
failure.
• Gross morphology
• Lungs are heavy, firm, red, and boggy vascular engorgement,
and the accumulation of alveolar fluid rich in infective organisms
Causes Has various etiologies.
• Infections, physical injuries, inhaled irritants, chemical injury,
multiple transfusions, DIC (disseminated intravascular
coagulation).
• Causes- aspiration of a foreign body, CABG, sepsis, multiple
blood transfusions, oxygen toxicity, trauma, pneumonia.Protein
and water enter into the alveoli.
• Reduced lung compliance is significant. Alveolar collapse.
Resolution is unusual and fibrosis occurs.
 ARDS
– Severe hypoxemia
– Increased permeability of the alveolar capillary membrane
with protein and water enter alveoli, alveolar collapse
– Non-cardiogenic pulmonary edema
A disease process that results in acute hypoxia secondary to
a rapid deterioration in respiratory status eg drowning, fluid
overload, aspiration.

– < 50% survive

– Some get full recovery, others end up with restrictive lung
disease
 Obstructive pulmonary disease

Emphysema
• It’s a lung condition with permanent enlargement of air
spaces distal to the terminal bronchioles with destruction of
their walls but with no fibrosis.
Gross
• Lungs are voluminous overlapping the heart
Histological appearance
• Large dilated alveoli separated by thin septa
• The bronchioles and vessels are compressed by the
emphysematous airspaces.
 Emphysema
• Primary Causes:
– Smoking and Pollutants
(eg. Jikos cigarettes )
• Characterized by:
• Impairments:
– Abnormal & permanent
enlargement of terminal – Alveoli over-inflated &
airways expiration is difficult
– Destruction of alveolar – Loss of elastic recoil
walls – Collapse of airways
– Increased lung
– Airflow obstruction
compliance
– Chronic, nonreversible
 Healthy Lung

Emphysema
 Emphysema
• Clinical Signs
– Orthopnea
– Scant sputum
production
• Clinical Diagnosis – Increased use of
– History accessory muscles
– Pulmonary function – Chronic cough
tests – Dyspnea
– X-ray (bullae present) –  chest AP diameter
– Distant breath sounds (barrel chested)
– Right sided heart failure
 Asthma

• Is a chronic inflammatory disorder of the airways

causes recurrent episodes of wheezing
breathlessness chest tightness and cough particularly
at night or early morning
Gross morphology of lungs
• Lungs are over distended with air
• Small areas of atelectasis may be seen.
• Thick mucus plugs occluding the bronchi and
bronchioles
 Asthma

• Obstructive lung disease

• Reversible
• Chronic inflammatory disease of the large airways
• Increased responsiveness of the trachea and
bronchi to stimuli (allergens, exercise, cold)
– inflammationoverproduction of mucousairway
narrowing
• Acute attacks can be mild or life threatening
 Asthma
• Factors precipitating an
attack
– Allergens (extrinsic
asthma)
• Pollen, animals, feathers,
molds
– Non-allergic (intrinsic
asthma)
• Respiratory infections
• Inhaled irritants
• Weather
• Medications
• Emotions
Histology
• Mucus plugs contain whorls of shed epithelium
giving rise to Curschmann spirals (Microscopic spiral
shaped mucus plugs).
• Numerous eosinophils and charcot-leyden crystals
are seen (eosinophil membrane protein crystals)
• Features of air way remodelling
– Thickening of basement membrane
– Hypertrophy of bronchial wall muscle
– Submucosal glands increase in size
– Edema and inflammatory infiltrate in bronchial wall
especially eosinophils and mast cells.
 Brochiectasis
• Is a chronic lung disease characterized by
permanent dilation of bronchi and bronchioles
caused by destruction of muscle and elastic
tissue.
• There is production of lots of sputum
• Etiology and pathogenesis
– Obstruction and infections
– Primary ciliary diskinesia -there is poor function of
cilia with retention of sputum
– Allergic brochopulmonary aspergilosis – a
hypersensitivity to fungus infection (Aspergilus
fumigatus).
 Bronchiectasis
• Localized, irreversible,
progressive dilation of bronchi
caused by destruction of the
muscle and elastic tissue.
• Bronchi are dilated, inflamed
and easily collapsible resulting
in obstruction and impaired
clearance of secretions
• Bronchiectasis is associated with
a wide range of disorders, but it
usually results from bacterial
infections.
 Bronchiectasis
Associated with:
• chronic infections such
as TB
Normal • Aspiration
• Cystic fibrosis
• Immune system
impairment

Bronchiectasis
 Signs & symptoms:
Bronchiectasis • Consistent productive
cough
• Sputum is copious, foul
smelling, bad breath
• Hemoptysis (bloody
cough)
• Weight loss
• Anemia
• Crackles & wheezes
• Loud breath sounds
• Cyanosis
• Clubbing
• Dyspnea
• Right sided heart failure
Gross morphology
• Airways are dilated
• Mucopulurent secretions fill the dilated bronchi.
Histology
• Intense acute and chronic inflammatory cells within
the walls
• Necrotizing ulceration of the walls
• Squamous metaplasia may be present
• In chronic cases fibrosis of bronchial walls appear.
Diseases of vascular origin
Pulmonary Embolism
•
Etiology:

Venous Thromboembolism (VTE): The most

common cause, typically originating from deep vein
thrombosis (DVT) in the legs.

• This is a blood clot (thrombi) within the pulmonary

arteries.
• It usually originates from the deep veins of the legs
in more than 95%

• Thrombus from the peripheral venous circulation

becomes embolic and lodges in pulmonary
circulation. Small emboli do not cause infarction.
• History:
– DVT, recent surgery, prolonged bed rest, recent air
Predisposing factors are
– Cardiac disease, immobility, hip fracture, hypercoagulable
states, indwelling central venous catheter.
• Large emboli impact in the main pulmonary artery or
lodge at the bifurcation as a saddle embolus.
• Smaller emboli travel far and cause infarction of the
peripheral parts of the lungs.
• Pathogenesis:
Virchow's Triad: Hypercoagulability (e.g., cancer,
genetic disorders), stasis (e.g., prolonged
immobility), and endothelial injury (e.g., surgery,
trauma).

Thrombus Formation: Blood clots form in the deep

veins, often of the lower extremities, travel to the
lungs, and obstruct pulmonary arteries, leading to
ventilation-perfusion mismatch, hypoxemia, and
increased pulmonary artery pressure.
• Morphology:
Gross: Emboli appear as firm, red-blue masses
in pulmonary arteries.
Microscopic: Lines of Zahn (alternating layers
of platelets/fibrin and RBCs) indicate pre-
mortem clotting. Pulmonary infarcts are
wedge-shaped, hemorrhagic, and located in
the periphery of the lung.
Chronic PE: Can lead to pulmonary
hypertension, right ventricular hypertrophy,
and chronic thromboembolic pulmonary
hypertension (CTEPH).
• Clinical Manifestations:
Acute PE: Sudden onset of dyspnea, chest pain
(pleuritic), tachypnea, tachycardia, cough,
hemoptysis, syncope, and signs of DVT (e.g.,
leg swelling, pain).

Massive PE: Can cause shock, hypotension,

and sudden death due to right ventricular
failure.
Chronic PE: Symptoms of pulmonary
hypertension, including dyspnea on exertion,
fatigue, and signs of right heart failure (e.g.,
edema, ascites).
 Pulmonary Embolism
• Symptoms:
– Sudden onset of dyspnea
– Tachycardia
– Hypoxemia
– Cyanosis
– Chest pain
– Hemoptysis
– If infarction: CXR shows decreased
vascular markings, high diaphragm,
infiltrate or effusion
• This is an emergency situation and
can be seen with our patients
acutely. Be aware of sx to report to
 Pulmonary hypertension

• Can either be primary( where the cause is not known) or

secondary where the causes could be:
– COAD (Chronic obstructive airway disease)
– Acquired or congenital heart disease like mitral stenosis
– Recurrent thromboemboli
– Autoimmune disorders especially systemic sclerosis causes
inflammation, intimal fibrosis, medial hypertrophy and finally PHTN.
 Review of pathophysiology:
pulmonary hypertension
• Pulmonary hypertension is the
narrowing of the pulmonary
arterioles within the lung.
• The narrowing of the
arterioles creates resistance
and an increased work load
for the heart.
• The heart becomes enlarged
from pumping blood against
the resistance.
 Review of pathophysiology:
pulmonary hypertension
• Etiology:
Primary (Idiopathic): Often with no
identifiable cause, may have
genetic predisposition
Secondary: Results from other
conditions, including:
Chronic obstructive pulmonary
disease (COPD)
Interstitial lung diseases, Chronic
thromboembolic disease, Left
heart disease (heart failure, mitral
valve disease), Connective tissue
diseases (e.g., scleroderma), HIV
infection
• Etiology:

Primary (Idiopathic): Often with no identifiable cause, may have genetic

predisposition ( gene mutations).

Secondary: Results from other conditions, including:

Chronic obstructive pulmonary disease (COPD)

Interstitial lung diseases

Chronic thromboembolic disease

Left heart disease (heart failure, mitral valve disease)

Connective tissue diseases (e.g., scleroderma)

HIV infection
• Pathogenesis:

Vascular Remodeling: Hypertrophy and hyperplasia of the

pulmonary artery smooth muscle.

Endothelial Dysfunction: Impaired production of

vasodilators (e.g., nitric oxide, prostacyclin) and increased
production of vasoconstrictors (e.g., endothelin-1).

Inflammation and Autoimmunity: Inflammatory cells

infiltrate pulmonary vessels.

Thrombosis in Situ: Small pulmonary arteries and arterioles

may have microthrombi.
• Morphology:

Pulmonary Arteries: Thickening of the arterial walls due to

smooth muscle hypertrophy and fibrosis.

Plexiform Lesions: Complex vascular formations often seen in

advanced stages.

Medial Hypertrophy: Increased thickness of the muscular

layer of the arteries.

Intimal Proliferation: The inner layer of the blood vessel wall

proliferates and narrows the vessel lumen.

Small Vessel Obliteration: Progressive narrowing and eventual

obliteration of small pulmonary arteries and arterioles.
• Clinical Manifestations:

Early Symptoms: Often nonspecific and include:

Dyspnea on exertion

Fatigue

Chest discomfort

Syncope (fainting)

Progressive Symptoms: As the disease advances:

Increasing shortness of breath, even at rest

Edema (swelling) in the ankles or legs

• Cyanosis (bluish skin coloration)

Palpitations

Symptoms of right heart failure (e.g., jugular

venous distension, hepatomegaly)
 Review : Cor pulmonale
• Pulmonary
hypertension present
• Change in structure &
function of the right
ventricle with dilation
and hypertrophy
• right sided heart
failure (without left
heart failure)
 Review : Cor pulmonale
• Symptoms in the progressive
disease are chronic cough, chest
pain, distal swelling bilaterally
because of back-up in circulation,
shortness of breath (SOB), fatigue
& weakness
• Acute cor pulmonale may occur 
medical emergency because it can
be due to a pulmonary embolus
• Cor Pulmonale is common in
multiple restrictive dysfunctions
Cystic Fibrosis
Etiology
Hereditary disease
characterized by
thickening of secretions
of all exocrine glands,
leading to obstruction
( eg. Pancreas, lungs,
GI).
The number 1 reason for
death from this disease
is respiratory
complications. Life
expectancy 20-40 years.
 Cystic Fibrosis
• Increased viscosity of mucus gland secretions
• Bacterial infections occur frequently
• Lung disease starts in small airways, progresses to larger
airways
• Repeated infection >> impaired pulmonary function
• V/Q abnormalities
• Later:
• pulmonary HTN
• cor pulmonale
• right ventricular failure
• respiratory failure
 Cystic Fibrosis (CF)
• Pulmonary symptoms: • Other symptoms:
– Early Childhood onset of – Pancreatic enzyme
symptoms deficiency
– Increased RR – Liver and GI obstruction
– Cough, Tenacious sputum – Low weight
– Chronic lung infections – Reproductive
deficiency/urinary
– Crackles/wheezes
incontinence
– Sinusitis – Digital clubbing
– Low expiratory flow – Osteoporosis/osteopenia
– Accessory mm use – Glucose intolerance CF
related diabetes
CYSTIC Fibrosis: Medical Diagnosis
• Genetic testing
• Sweat test
– increased chloride concentration in the sweat
• Chest X-ray:
– hyperinflation, peribronchial thickening,
atelectasis; upper lobes usually more involved
• Sputum culture:
– recurrent infections
– Staphlococcus & Pseudomonas common
Gross morphology
• Atherosclerosis (Atheromatous deposits) in the vessels
• Muscular thickness of the vascular wall.
Clinical course
• Primary ph affects mostly females 20-40 yrs.
• Present with dyspnea and fatigue and chest pain.
 Bacterial pneumonia
• Bacterial pneumonia has two gross patterns. Lobular
bronchopneumonia and lobar pneumonia
Bronchopneumonia (lobular)
• Characterized by patchy exudative lung parenchymal
consolidation. Frequently bilateral and basal since secretions
gravitate into the lower lobes.
Gross appearance
• Elevated, focal areas of palpable consolidation and
suppuration
Histological appearance
• Neutrophilic suppurative exudate in the air spaces and the
airways
 Lobar pneumonia
consolidation of a large portion of a lobe or an entire lobe
• Normal resolution can occur but when organization
occurs, fibrosis arises and then scars form.
• Aggressive infection produces abscess.
Lobar pneumonia
• There is a consolidation of a large portion of or entire
lobe of the lung.
• Mainly by pneumococci though others like
k.pneumonia, staphylococcal and streptococcal
bacteria may cause.
• It has four stages of inflammatory response in the following order:
congestion
• Predominates in the first 24hrs
• The lungs are heavy, boggy (too wet), and red
Red hepatization
• lungs are red, firm, and airless with liver-like consistency.
• Histologically, there is massive confluent (flowing) exudation with
red cells, neutrophils, and fibrin filling the air spaces.
Gray hepatization
• Grossly the lungs are gray-brown and dry.
• Histologically there is disintegration of RBC with persistence of
fibrinosuppurative exudate that gives them the gray-brown color.
Resolution stage
• Organisation occurs and normal lung structure is restored.
 Types of pneumonia
• Pneumonia is an infection that inflames the air
sacs in one or both lungs.
• Importance: Understanding different types
helps in diagnosis and treatment.
• Structure: Classification, etiology,
pathogenesis, morphology, and clinical
manifestations
 Classification of Pneumonia
• Causative Agent: Bacterial, viral, fungal, aspiration.
• Location: Lobar, lobular (bronchopneumonia),
interstitial.
• Setting: Community-acquired (CAP), hospital-
acquired (HAP), ventilator-associated (VAP),
healthcare-associated (HCAP).
• Specific Pathogens: Streptococcus pneumoniae,
Mycoplasma pneumoniae, Legionella pneumophila,
etc.
 .

Bacterial Pneumonia
• Etiology: Streptococcus pneumoniae,
Haemophilus influenzae, Klebsiella
pneumoniae, Staphylococcus aureus.
• Pathogenesis: Bacterial invasion, alveolar
inflammation, immune response.
• Morphology: Lobar consolidation, patchy
bronchopneumonia.
• Clinical Manifestations: High fever, productive
cough, chest pain, dyspnea.
Viral Pneumonia
• Etiology: Influenza, RSV, adenovirus, coronaviruses (SARS-CoV-2).
• Pathogenesis: Viral replication in respiratory epithelium, immune
response.
• Morphology: Interstitial inflammation.
• Clinical Manifestations: Fever, dry cough, headache, muscle pain.

Fungal Pneumonia
• Etiology: Histoplasma, Coccidioides, Pneumocystis jirovecii.
• Pathogenesis: Inhalation of spores, immune response.
• Morphology: Granulomas, interstitial inflammation.
• Clinical Manifestations: Chronic cough, weight loss, night sweats, fever.
Aspiration Pneumonia
• Content:
• Etiology: Inhalation of food, liquid, vomit.
• Pathogenesis: Chemical irritation, secondary
bacterial infection.
• Morphology: Patchy inflammation, necrosis.
• Clinical Manifestations: Cough, fever, foul-
smelling sputum, respiratory distress.
Lobar Pneumonia
• Etiology: Often bacterial, particularly Streptococcus
pneumoniae.
• Pathogenesis: Rapid spread through alveoli, lobar consolidation.
• Morphology: Consolidated lobe, intra-alveolar exudate.
• Clinical Manifestations: Sudden high fever, chills, productive
cough, pleuritic chest pain.
Bronchopneumonia (Lobular Pneumonia)
• Etiology: Various bacteria including Staphylococcus aureus,
Klebsiella pneumoniae.
• Pathogenesis: Infection centered around bronchioles, patchy
spread.
• Morphology: Patchy consolidation.
• Clinical Manifestations: Insidious onset, cough, low-grade fever,
scattered crackles.
Interstitial Pneumonia
• Etiology: Often viral or atypical bacteria (e.g., Mycoplasma
pneumoniae).
• Pathogenesis: Inflammation of interstitial tissues.
• Morphology: Diffuse interstitial infiltrates.
• Clinical Manifestations: Gradual onset, dry cough,
dyspnea, fatigue.
Community-Acquired Pneumonia (CAP)
• Etiology: Streptococcus pneumoniae, Haemophilus
influenzae, viruses.
• Pathogenesis: Acquisition outside hospital.
• Clinical Manifestations: Varied based on pathogen, typical
symptoms.
Hospital-Acquired Pneumonia (HAP)
• Etiology: Pseudomonas aeruginosa, Staphylococcus aureus.
• Pathogenesis: Infection after 48 hours of hospital admission.
• Clinical Manifestations: Severe symptoms, often in critically ill
patients.
Ventilator-Associated Pneumonia (VAP)
• Etiology: Similar to HAP, often multidrug-resistant organisms.
• Pathogenesis: Infections in mechanically ventilated patients.
• Clinical Manifestations: Fever, purulent sputum, lung infiltrates.
Healthcare-Associated Pneumonia (HCAP)
• Etiology: Similar to HAP.
• Pathogenesis: Infections in patients with recent healthcare
exposure.
• Clinical Manifestations: Similar to HAP, varied severity.
• Specific Pathogen-Related Pneumonias
• Pneumococcal Pneumonia: Streptococcus pneumoniae,
lobar consolidation, rust-colored sputum.
• Legionnaires' Disease: Legionella pneumophila,
contaminated water, severe form.
• Mycoplasma Pneumonia: Mycoplasma pneumoniae,
walking pneumonia, milder symptoms.
• Chlamydial Pneumonia: Chlamydia pneumoniae, mild
symptoms, interstitial involvement.
Diagnosis and Treatment
Diagnosis: Clinical evaluation, imaging (chest X-ray),
microbiological tests.
Treatment: Antibiotics (bacterial), antivirals (viral), antifungals
(fungal), supportive care.
Prevention
• Vaccination: Pneumococcal,
influenza vaccines.
• Infection Control: Hand hygiene,
personal protective equipment (PPE).
• Lifestyle: Smoking cessation, healthy
diet, regular exercise
Complications of pneumonia
• Abscess formation . Common with Klebsiella and
type 3 pneumococci infections.
• Empyema. This happens when the infection spreads
to the pleural cavity causing pus in the cavity.
• Organization of the exudate into fibrotic scar tissue.
• Bacteremia and sepsis to the heart valves,
pericardium, brain, kidneys, spleen or joints causing
meningitis, arthritis, endocarditis, abscesses.
Clinical presentation
• Abrupt onset of high fever,shaking chills, and
productive cough, pleuritic pain and
hemoptysis may also be present.
Community acquired atypical pneumonia
• By viral and mycoplasma pneumoniae.
• M. pneumoniae affects mainly the young and
the old
Gross appearance of lung
• Patchy or lobar areas of congestion are seen. Appear red-blue.
There is no consolidation hence the term atypical.
Histologically there is
• Interstitial pneumonitis (mononuclear Inflammatory cells
within the alveolar walls. These include lymphocytes,
histiocytes, and occasional plasma cells.)
• Widened edematous alveolar walls
• A pink hyaline membrane lining the alveolar walls reflecting
diffuse alveolar damage like in ARDS.
Lung abscess
• It is a local suppurative process within the lung
characterised by necrosis of lung tissue
• Causative organisims are introduced through the following
ways:
– Aspiration of the infective material as in alcoholism, coma,
anesthesia, sinusitis
– Primary bacterial infection especially with Staphylococus
aureus, K.pneumoniae, and type 3 pneumococcus.
– Septic emboli from septic thrombi or cardiac valve
vegetation.
– Neoplasia as in tumour obstruction of respiratory tree
leading to infections.
– Direct traumatic penetration of the lung
– Spread of infections from the adjacent organs such as
esophagus
Histological appearance. There is suppurative (neutrophils) and
destruction of the lung parenchyma with a central area of
cavitation.
 Tuberculosis
• Caused by bacterial
infection (Mycobacterium
tuberculosis)
• Transmitted by airborne
droplets via coughing once
person develops “active
TB”- can spread to 10-15
persons in year
• Lungs primary site (but can
have locations in spine)
• Lesions seen in lungs on X-
ray Tuberculosis
• Symptoms are fatigue,
weight loss, night sweats,
low grade fever, productive
cough, hemoptysis, SOB
• Disease can be latent for
numerous years, 10%
becomes “active”
• Disease is treatable and
preventable but highly
lethal immuno-
compromised pts, ie HIV, 6
months treatment
• Resistant strands of MDR
TB and XDR TB have
evolved
 Tuberculosis
• A chronic communicable disease caused by mycobacterium tuberculosis
• TB is defined as a disease caused by members of the M. tuberculosis complex,
which includes the tubercle bacillus (M. tuberculosis), M. bovis, M. africanum,
M. microti and M. canetti
• Can have either primary or secondary
PRIMARY
• Occurs in persons lacking previous contact with the bacilli
• Begins as a single granulomatous lesion ( Ghon focus) in
the distal air spaces of the lower part of the upper lobe or
the upper part of the lower lobe close to the pleura.
• From the Ghon focus the bacilli either free or within
phagocytes drain into the hilar nodes which also caseate
forming a lesion called Ghon complex( combination of the
parenchymal lung lesion and the nodal involvement).
• In most cases ( 95%) the infection is contained through
cell mediated immunity forming local fibrosis and
calcification (Ranke complex)
• In 5% there is hematogenous spread.
Transmission:
• Airborne spread of infectious droplets, usually indoors,
with poor ventilation
• Source: Person with TB of the lung, coughing
• One cough produces 3000 nuclei, survive better in dark
• Higher density of droplets, longer time of exposure
increase transmission
• Factors that enhance transmission: Individual behavior:
when coughing, spitting
• Immigration, overcrowding
• Occupation: Miners, nurses, lab, morgue
• Poverty- Overcrowding, poor preventive medicine,
malnutrition
Gross
• Gray white granulomas with
• Central areas of caseous necrosis
Histology
• Granulomatous inflammation composed of
central caseation surrounded by epithelioid
cells, giant cells of Langerhans, lymphocytes
and plasma cells.
• In immunocompromised persons, there may
be no granulomatous response and if it
occurs it may not have central areas of
caseous necrosis (formation of soft cheese
like material due extensive tissue
destruction).
SECONDARY PULMONARY TUBERCULOSIS
• Initial lesion is a small focus of consolidation less
than 2cm at the the apices of the lungs where
there is high oxygen concentration
• Its an active infection in a previously sensitized
individual
• Can either be reactivation of dormant bacilli from
the primary lesion or it may come from
exogenous sources.
• Localised apical secondary pulmonary Tb may
heal with fibrosis spontaneously or after therapy
or May progress into progressive pulmonary
tuberculosis especially in the old and the
immunocompromised
• tuberculous bronchopneumonia, cavitary
tuberculosis
MILIARY TUBERCULOSIS
• occurs when bacilli drain the rough lymphatics. The
lesions are small 2mm foci of yellow-white
consolidation throughout the lung
• Pleural effusions, tuberculosis empyema may develop
when the pleura is involved.
• Endotracheal, and laryngeal tuberculosis
• Systemic miliary TB Bacilli disseminated through
arterial system to any organ.
• Isolated organ tuberculosis eg meninges( tuberculous
meningitis), renal tuberculosis, adrenal tuberculosis,
bones, fallopian tubes, vertebrae (Potts disease),
• Lymphadenitis. Most frequent form of extrapulmonary
Tb. Mainly in the cervical region (Scrofula).
• Intestinal tuberculosis due to swallowing of infected
material or drinking contaminated milk.
• Gross
• Gray-white areas of caseation with or without
cavitation.
 Clinical manifestations

• Latent (Asymptomatic) Infection: The vast

majority of children with tuberculosis
infection develop no signs or symptoms at any
time.
• Occasionally, the initiation of infection is
marked by several days of low-grade fever and
mild cough.
• Rarely, the child experiences a clinically
significant disease with high fever, cough,
malaise, and flu-like symptoms that resolve
within a week.
• These children have a reactive tuberculin skin test
• Symptomatic: Nonproductive cough and mild
dyspnea or wheezing, especially at night, are the
most common symptoms
• Systemic complaints such as fever, night sweats,
anorexia, and decreased activity occur less often.
• Some infants have difficulty gaining weight or
develop a true failure-to-thrive presentation that
does not improve significantly until after several
months of treatment
• Signs
• Serous pleurisy, cold abscess, mottled nodes, gibbus,
CXR- diffuse or hilar shadows
 Respiratory Distress Syndrome (RSD)
• Etiology
• Alveolar collapse in
infants resulting from
lung immaturity,
inadequate level of
pulmonary surfactant
and constructure of
relatively tiny airways
secondary to
inflammation.
Morphology
• Lungs apper firm airless red-purple in colour
• Heavy and fail to float indicating lack of
aeration
• Fibrosis thickening of the alveola septa
 Respiratory Distress Syndrome (RSD)
• Physical Findings:
– Respiratory distress
– Crackles
– Tachypnea
– Hypoxemia
– Cyanosis
– Accessory mm use • increased work of
– Expiratory grunting, breathing secondary to
flaring nares handling should be
– CXR weighed against the
benefits
 Respiratory Failure
• Etiology:
Type I (Hypoxemic): Conditions that cause a
failure in oxygenation, such as pneumonia,
pulmonary edema, ARDS (acute respiratory
distress syndrome), interstitial lung diseases,
and pulmonary embolism.
• Type II (Hypercapnic): Conditions that result in
inadequate ventilation, such as COPD, asthma,
drug overdose, neuromuscular diseases, and
chest wall deformities.
• Most often caused by respiratory disease
– Decreased oxygen intake e.g. COPD, high altitude
– Impaired diffusion e.g. pneumonia
– Hypoventilation e.g. drug overdose
• Patient will present with tachypnea, cyanosis,
headache, confusion, seizures
•
Pathogenesis
• Hypoxemic Respiratory Failure: Results from
severe ventilation-perfusion (V/Q) mismatch,
shunting (blood bypasses the lungs), or
impaired diffusion.

Hypercapnic Respiratory Failure: Due to

alveolar hypoventilation, which leads to
elevated arterial CO2 levels (hypercapnia).
Causes include decreased respiratory drive,
increased airway resistance, and decreased
respiratory muscle function.
• Morphology:
Hypoxemic: Can show diffuse alveolar
damage in ARDS, interstitial
inflammation and fibrosis in interstitial
lung disease, or alveolar filling with fluid
or pus in pneumonia or pulmonary
edema.
Hypercapnic: May show signs of chronic
lung changes like emphysema in COPD,
muscle atrophy in neuromuscular
diseases, or structural abnormalities in
chest wall deformities.
 Respiratory Failure
• Can be caused by ventilatory insufficiency and
decreased minute ventilation
– CNS disorders e.g. drug overdose
– Neuromuscular disorders e.g. SCI
– Chest wall abnormality e.g. trauma
– Severe obstructive lung disease e.g. COPD
• Increased physiologic dead space
– Adequate ventilation, poor perfusion with lack of
CO2 removal
Pulmonary Embolism
• Thrombus from the peripheral
venous circulation becomes
embolic and lodges in
pulmonary circulation. Small
emboli do not cause
infarction.
• History:
– DVT, recent surgery, prolonged
bed rest, recent air travel
NEOPLASTIC CONDITIONS OF LUNGS.
• 90-95% are epithelial (carcinomas)
• 5% are bronchial carcinoids
• 2-5% are mesenchymal (sarcomas) and others.
Carcinomas
Etiologic factors
• Tobacco smoking is the main factor. Its dose
dependent and the risk is decreased after cessation.
It reaches the baseline after 10 yrs. Squamous cell
carcinoma and the small cell carcinoma show highest
association.
• Radiation exposure
• Asbestos. All histologic types are associated.
• Air polution especially with radon
• Viruses HPV
Classification of carcinomas
• Squamous cell carcinoma 25-40%
• Adenocarcinoma 25-40%
• Small cell carcinoma 20-25%
• Large cell carcinoma 10-15%
Squamous cell carcinoma
• More in males
• Closely associated with smoking
• Arise centrally in the large bronchi
Adenocarcinoma
• Most common histologic type
• Most encountered in females and in non smokers
• Peripherally located and grow more slowly than the
squamous cell carcinoma
• Of the adenocarcinomas only bronchioalveolar type
(BAC) has a distinct features
• Has cylindrical cells growing along preexisting
structures like the alveolar septa wall without
destroying them or invasion BAC doesn’t
metastasizes.
Small cell carcinoma
• Very aggressive with frequent widespread
metastasis thus it’s a high grade tumour.
• Regarded as a systemic disease since almost all
patients have metastasis to lymph nodes at the
time of presentation.
Large cell carcinoma
• Its an undifferentiated malignant epithelial
tumour lacking cytologic features of small cell
carcinoma and glandular or squamous
differentiation.
Patterns of spread of lung tumours
1. Direct spread to other organs
2. Lymphatic spread
3. Haematogenous spread
Adrenal glands are involved in more than 50% liver in 30-
50%, brain in 20%, and bone in 20%
4. Aerogenous spread
Spread within the lung itself. This is mainly with the
bronchioalveolar carcinoma.