1.Community-acquired pneumonia. Definition. Etiology. Risk factors. Clinic. Severity.

Clinical and
laboratory indicators of severe course. 2.Community-acquired pneumonia. Clinic. Clinical signs for emergency hospitalization of patients. 3.Nosocomial pneumonia. Definition. Risk factors for development. Features of the clinic. Diagnostics.
Ans: Community-Acquired Pneumonia (CAP): Community-acquired pneumonia (CAP) refers to an acute Antimicrobial Therapy Standards. :: ans::Community-Acquired Pneumonia (CAP):The clinical Empirical antimicrobial therapy. Ans: Nosocomial Pneumonia : Definition: Nosocomial pneumonia, also
infection of the lung parenchyma acquired outside of hospital or long-term care settings. It is a common presentation of CAP can vary widely, but common symptoms and signs include:- *Respiratory known as hospital-acquired pneumonia (HAP), is a lung infection that occurs 48 hours or more after
and potentially serious illness that affects the alveoli and the surrounding tissues, leading to symptoms Symptoms*: - Cough: May be productive (with sputum) or dry.- Dyspnea: Shortness of breath, difficulty hospital admission, which was not incubating at the time of admission. This category also includes
such as cough, fever, chest pain, and difficulty breathing. breathing.- Pleuritic chest pain: Sharp or stabbing pain that worsens with deep breathing or coughing.- ventilator-associated pneumonia (VAP), which arises more than 48-72 hours after endotracheal
Etiology: The etiological agents of CAP are diverse and can include:- Bacteria, - Streptococcus Sputum production: Can be clear, purulent, or blood-tinged.- *Systemic Symptoms*:- Fever and chills.- intubation. Risk Factors for Development: Several factors increase the risk of developing nosocomial
pneumoniae (most common), - Haemophilus influenza, - Mycoplasma pneumonia, - Legionella Fatigue and malaise.- Sweating.- Headache and myalgia (muscle pain).- *Physical Examination Findings*: pneumonia:- *Hospital Environment*: - Prolonged hospital stay, especially in the intensive care unit
pneumophila, - Chlamydia pneumonia,. - *Viruses*: Influenza virus, - Respiratory syncytial virus (RSV), - Tachypnea: Increased respiratory rate.- Tachycardia: Increased heart rate.- Hypotension: Low blood (ICU) - Use of mechanical ventilation (primary risk factor for VAP) - Invasive procedures (e.g., central
Adenovirus, - Coronaviruses (e.g., SARS-CoV-2). - *Fungi*: Less common in immunocompetent pressure, especially in severe cases.- Crackles (rales): Heard on lung auscultation, indicating alveolar venous catheters, endotracheal tubes) - Surgery, especially thoracic or abdominal surgery- *Patient-
individuals, more common in immunocompromised patients. involvement.- Dullness to percussion: Suggests consolidation or effusion. - Decreased breath sounds: Related*: - Advanced age - Pre-existing lung conditions (e.g., chronic obstructive pulmonary disease,
Risk Factors: Several factors can increase the risk of developing CAP:- *Age*: Very young children and Over areas of consolidation or effusion. Clinical Signs for Emergency Hospitalization: Patients with CAP cystic fibrosis) - Immunosuppression (e.g., HIV, chemotherapy, corticosteroids) - Comorbidities such as
older adults,. - *Chronic diseases*: Such as chronic obstructive pulmonary disease (COPD), asthma, should be evaluated for the need for emergency hospitalization based on clinical signs and severity. diabetes mellitus, heart failure, and renal failure - Altered mental status leading to aspiration risk-
diabetes, and heart disease,. - *Immunosuppression*: Including HIV infection, chemotherapy, and use of Indications for emergency hospitalization include:1. *Severe Respiratory Compromise*: - Respiratory *Other Factors*: - Prior antibiotic use - Poor oral hygiene and colonization of the oropharynx with
immunosuppressive drugs,. - *Lifestyle factors*: Smoking, alcohol abuse, and exposure to pollutants,. - rate >30 breaths per minute. - Severe hypoxemia: Oxygen saturation (SpO2) <90% on room air or PaO2 pathogenic organisms - Use of sedatives or paralytics,. Features of the Clinic : Nosocomial pneumonia
*Socioeconomic factors*: Low socioeconomic status, crowded living conditions,. - *Recent respiratory <60 mm Hg. - Use of accessory muscles for breathing, grunting, or flaring of nostrils. 2. *Hemodynamic presents with symptoms and signs similar to other types of pneumonia but can be more severe due to
infections*: Recent viral upper respiratory tract infections can predispose to bacterial pneumonia. Instability*: - Systolic blood pressure <90 mm Hg or mean arterial pressure <65 mm Hg. - Heart rate the often compromised health status of hospitalized patients:- *Respiratory Symptoms*:- New or
Clinical Presentation (Clinic): Symptoms of CAP can vary but typically include:- *Respiratory symptoms*: >125 beats per minute. - Signs of septic shock: Requiring vasopressors to maintain blood pressure.3. worsening cough - Increased sputum production, often purulent - Shortness of breath (dyspnea) -
Cough (productive or dry), shortness of breath, pleuritic chest pain, and sputum production,. - *Systemic *Altered Mental Status*: - Confusion, disorientation, or decreased level of consciousness.4. *Multilobar Pleuritic chest pain- *Systemic Symptoms*: - Fever or hypothermia - Chills and rigors- Tachycardia-
symptoms*: Fever, chills, fatigue, and malaise,. - *Physical examination findings*: Crackles (rales), Involvement or Rapid Radiographic Progression*: - Extensive or multilobar infiltrates on chest X-ray. - Malaise and fatigue. - *Physical Examination Findings*: - Rales or crackles heard on lung auscultation -
decreased breath sounds, and dullness to percussion over affected areas. Radiographic evidence of effusion or cavitation. 5. *Significant Comorbid Conditions*: - Presence of Decreased breath sounds or bronchial breath sounds - Dullness to percussion indicating consolidation
Severity: The severity of CAP can range from mild to life-threatening. Various scoring systems are used chronic obstructive pulmonary disease (COPD), heart failure, chronic kidney disease, liver cirrhosis, or or effusion Diagnostics:Diagnosis of nosocomial pneumonia involves a combination of clinical
to assess severity and guide treatment decisions, including: - *CURB-65*: Evaluates Confusion, Urea immunosuppression. 6. *Laboratory Abnormalities*: - Leukopenia (WBC <4,000/µL) or leukocytosis evaluation, imaging, and microbiological testing:- *Clinical Evaluation*: - Assessment of symptoms and
level, Respiratory rate, Blood pressure, and age ≥65 years,. - *PSI (Pneumonia Severity Index)*: More (WBC >15,000/µL). - Elevated blood urea nitrogen (BUN) >20 mg/dL.- Elevated serum creatinine physical signs - Evaluation of risk factors and history of recent hospital procedures or intubation-
complex, considers multiple factors to classify patients into risk categories, Clinical and Laboratory indicating renal impairment.- High levels of inflammatory markers: C-reactive protein (CRP), *Imaging*: - Chest X-ray: Look for new or progressive infiltrates, consolidation, or pleural effusion -
Indicators of Severe Course: Indicators of a severe course of CAP include:*Clinical indicators:*-High fever procalcitonin. Antimicrobial Therapy Standards: Antimicrobial therapy for CAP should be initiated Chest CT scan: Provides more detailed imaging, useful in complex cases- *Microbiological Testing*:-
or hypothermia,Tachypnea (respiratory rate >30 breaths/min),Hypotension (systolic BP <90 mm promptly, with the choice of antibiotics guided by the likely pathogens, patient risk factors, and severity Sputum culture: To identify causative organisms and their antibiotic susceptibility - Blood cultures: To
Hg),Altered mental status (confusion),Severe hypoxemia (low oxygen saturation), *Laboratory of the disease.1. *Outpatient Treatment*: - Previously Healthy Patients, No Recent Antibiotic Use:- detect bacteremia associated with pneumonia- Endotracheal aspirate or bronchoalveolar lavage (BAL) in
indicators:*- Elevated white blood cell count or leukopenia (WBC >15,000/µL or <4,000/µL),- High levels Macrolide (e.g., azithromycin or clarithromycin) or doxycycline.- *Patients with Comorbidities or Recent ventilated patients: To obtain lower respiratory tract samples- *Laboratory Tests*: - Complete blood
of C-reactive protein (CRP) and procalcitonin (markers of severe infection and inflammation),.- Blood Antibiotic Use*: - Respiratory fluoroquinolone (e.g., levofloxacin, moxifloxacin) or a beta-lactam (e.g., count (CBC): Elevated or low white blood cell count - Inflammatory markers: Elevated C-reactive protein
urea nitrogen (BUN) and serum creatinine levels indicating renal impairment,. - Evidence of bacteremia amoxicillin-clavulanate) plus a macrolide.2. *Inpatient Treatment (Non-ICU)* - Respiratory (CRP) or procalcitonin. Empirical Antimicrobial Therapy: Empirical therapy should cover a broad range of
or sepsis (positive blood cultures)*Radiographic indicators:*- Extensive involvement or multilobar fluoroquinolone (e.g., levofloxacin, moxifloxacin) alone.- Beta-lactam (e.g., ceftriaxone, cefotaxime, potential pathogens, including multi-drug resistant organisms, until specific pathogens and
infiltrates on chest X-ray,. - Presence of pleural effusion or cavitation,.: Management:-Management of ampicillin-sulbactam) plus a macrolide. 3. *Inpatient Treatment (ICU)*:- Beta-lactam (e.g., ceftriaxone, susceptibilities are identified: 1. *Empirical Therapy for Non-ICU Patients*:- Coverage typically includes
CAP involves supportive care, appropriate antimicrobial therapy, and hospitalization for severe cases. cefotaxime, ampicillin-sulbactam) plus either azithromycin or a respiratory fluoroquinolone.- For Gram-positive cocci (e.g., Staphylococcus aureus), Gram-negative bacilli (e.g., Escherichia coli, Klebsiella
Treatment choices are guided by the suspected pathogen, patient risk factors, and severity of illness. patients with penicillin allergy: Respiratory fluoroquinolone plus aztreonam.4. *Special spp., Pseudomonas aeruginosa), and atypical bacteria. - Common Regimens: - Piperacillin-tazobactam
Empirical antibiotic therapy is typically started while awaiting culture results, with adjustments made Considerations*:- *MRSA Coverage*: If MRSA is suspected, add vancomycin or linezolid.- *Pseudomonas or- Cefepime or- Levofloxacin or - Carbapenem (e.g., meropenem) if resistance is suspected 2.
based on specific pathogen identification and antibiotic susceptibility. Coverage*: If Pseudomonas is suspected, use piperacillin-tazobactam, cefepime, or meropenem, plus a *Empirical Therapy for ICU Patients or Suspected VAP*: - Broad-spectrum coverage is essential, often
second agent like ciprofloxacin or levofloxacin. Duration of Therapy:- The typical duration of including MRSA and Pseudomonas aeruginosa.- Common Regimens: - Anti-pseudomonal beta-lactam
antimicrobial therapy for CAP is 5-7 days for most patients, but it may be extended depending on clinical (e.g., piperacillin-tazobactam, cefepime, or meropenem) plus - MRSA coverage (e.g., vancomycin or
response, severity of illness, and presence of complications. Monitoring and Follow-Up:- Patients should linezolid) plus- Second anti-pseudomonal agent (e.g., levofloxacin or aminoglycoside)3. *Special
be monitored for clinical improvement within 48-72 hours after initiation of therapy.- Follow-up chest X- Considerations*:- Adjust therapy based on local antibiogram data and patient-specific factors.- De-
ray may be necessary to ensure resolution, particularly in patients with persistent symptoms or high-risk escalate therapy based on culture results and clinical response.
features.

9.Bronchial asthma. Clinic. Severity. Diagnosis. Step therapy. Criteria for controlling bronchial asthma.
4.Pleurisy dry. Definition. Etiology. Risk factors. Clinic, diagnostics. Treatment. Ans: Pleurisy Dry (Dry 7. COPD. Definition Etiology. Pathogenesis. Clinic. Diagnosis with the definition of the stage, group, Ans: Bronchial Asthma Clinic: - Symptoms: Wheezing, shortness of breath, chest tightness, and cough,
Pleuritis) Definition:- Dry pleurisy, or dry pleuritis, is an inflammation of the pleura (the lining of the taking into account the risk of exacerbation. Ans: chronic obstructive pulmonary disease often worse at night or early morning. - Triggers: Allergens, exercise, cold air, respiratory infections,
lungs and chest cavity) without the production of significant pleural fluid. This condition often results in (COPD):Definition:COPD is a common respiratory condition characterized by cough, dyspnea, and stress. Severity:- *Intermittent*: Symptoms <2 days/week, nighttime awakenings <2 times/month.-
sharp chest pain that worsens with breathing or coughing. Etiology: Dry pleurisy can be caused by airflow limitation. Prevalence varies by age and country, affecting approximately 10% of individuals aged *Mild Persistent*: Symptoms >2 days/week but not daily, nighttime awakenings 3-4 times/month.-
various conditions, including:- Infections: Viral (most common), bacterial, fungal, tuberculosis- 40 years or older. It ranks among the top causes of death in the United States and globally. Etiology: *Moderate Persistent*: Daily symptoms, nighttime awakenings >1 time/week but not nightly.- *Severe
Autoimmune diseases: Rheumatoid arthritis, lupus- Pulmonary embolism- Trauma to the chest- Smoking: Major risk factor; elicits abnormal inflammatory response damaging airways and alveoli. Other Persistent*: Symptoms throughout the day, nightly awakenings. Diagnosis: - *History and Physical
Malignancy: Lung cancer or metastases Risk Factors:- Respiratory infections- Chronic lung diseases Risk Factors: Chronic lung diseases, occupational exposures, radon exposure, family history. Examination*: Assess symptoms and triggers.- *Spirometry*: FEV1/FVC <0.70, reversibility with
(e.g., COPD, asthma)- Autoimmune disorders- Smoking- Recent chest trauma or surgery Clinic- Sharp, Pathogenesis: Smoking-induced inflammation damages airways and alveoli. Airflow limitation results bronchodilator (FEV1 increase >12% and 200 mL).- *Peak Flow Monitoring*: Variability in peak
stabbing chest pain, often localized and exacerbated by deep breathing, coughing, or sneezing - Pleural from chronic inflammation, bronchitis, and emphysema. Diagnosis and Staging: Spirometry: Key expiratory flow.- *Allergy Testing*: Identify potential triggers. Step Therapy (GINA Guidelines), *Step
friction rub heard on auscultation - Possible mild fever and malaise Diagnostics :- Clinical evaluation diagnostic test. Stages: Mild (Stage 1): FEV1 ≥ 80% predicted. Moderate (Stage 2): FEV1 50-79% 1*: Low-dose ICS-formoterol as needed, *Step 2*: Low-dose ICS daily or as-needed low-dose ICS-
based on symptoms and physical examination. - Imaging: Chest X-ray, ultrasound, or CT scan to rule out predicted. Severe (Stage 3): FEV1 30-49% predicted. Very severe (Stage 4): FEV1 < 30% predicted. formoterol. *Step 3*: Low-dose ICS-LABA. *Step 4*: Medium/high-dose ICS-LABA.*Step 5*: High-dose
other causes and assess pleural involvement. - Blood tests: Inflammatory markers, autoimmune Groups: Group A: Low symptoms, low risk. Group B: Low symptoms, high risk. Group C: High ICS-LABA, add-on treatment (e.g., biologics). Criteria for Controlling Asthma- *Controlled*: Symptoms
markers. - Sometimes, pleural fluid analysis if small amounts of fluid are presentTreatment:- Address symptoms, low risk. Group D: High symptoms, high risk. Risk of Exacerbation: Determines treatment ≤2 days/week, no nighttime awakenings, no interference with normal activity, normal lung function, and
underlying cause (e.g., antibiotics for bacterial infection, anticoagulation for pulmonary embolism)- Pain approach. infrequent use of rescue medication.
management: NSAIDs (e.g., ibuprofen) or acetaminophen- Rest and supportive care- Treat associated - *Partly Controlled*: Some symptoms and limitations.
conditions (e.g., corticosteroids for autoimmune diseases),. Conclusion:Dry pleurisy involves 8. COPD. The COPD phenotype with frequent exacerbations, definition. Diagnostic criteria. Treatment. - *Uncontrolled*: Frequent symptoms, nighttime awakenings, limitations, and low lung function.
inflammation of the pleura without significant fluid production, leading to sharp chest pain. Diagnosis is Ans: Chronic Obstructive Pulmonary Disease (COPD) with Frequent Exacerbations, Definition: COPD with
based on clinical assessment and imaging, with treatment focused on managing the underlying cause frequent exacerbations is a phenotype of COPD characterized by frequent worsening of symptoms 10.Bronhial asthma. Definition. Basic anti-inflammatory and bronchodilator therapy. Ans:
and relieving symptoms. beyond normal day-to-day variations, often requiring additional treatment. Frequent exacerbations are *Definition:Bronchial asthma is a chronic inflammatory disease of the airways characterized by variable
typically defined as two or more exacerbations per year. Diagnostic Criteria: The diagnosis of COPD with and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness, and underlying
frequent exacerbations involves: 1. *Clinical History*: - A history of at least two exacerbations per year. - inflammation. This condition results in episodes of wheezing, breathlessness, chest tightness, and
Symptoms of COPD: Chronic cough, sputum production, and dyspnea. 2.Spirometry*:Post- coughing, particularly at night or early in the morning. Basic Anti-Inflammatory Therapy: Anti-
5.Pleurisy exudative. Definition. Etiology. Risk factors. Clinic, diagnosis with differentiation of exudate bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation.- FEV1 value helps inflammatory therapy is crucial in the management of asthma as it targets the underlying inflammation
and transudate in the pleural cavity. Ans: Definition: Pleurisy, also known as pleuritis, is inflammation of determine the severity of airflow limitation (GOLD stages 1-4). 3. *Assessment Tools*: - COPD of the airways. The main classes of anti-inflammatory medications include:1. *Inhaled Corticosteroids
the pleura—the thin tissue lining the lungs and chest wall. It often causes severe chest pain that worsens Assessment Test (CAT) or Modified Medical Research Council (mMRC) Dyspnea Scale to evaluate (ICS):* - *Examples:* Beclomethasone, Budesonide, Fluticasone, Mometasone. - *Mechanism:*
during breathing 1.Etiology (Causes):Exudative Pleurisy: This type results from inflammation, infection, symptom burden. - Frequent exacerbations assessment: Defined as ≥2 exacerbations per year or ≥1 Reduce airway inflammation, decrease mucus production, and improve overall lung function. -
tumors, lung injury, or other underlying conditions. Common causes include:Infections (bacterial, viral, exacerbation requiring hospitalization. Treatment: Treatment for COPD with frequent exacerbations *Usage:* Typically used as a long-term control medication.2. *Leukotriene Modifiers:* - *Examples:*
or parasitic),. Collection of excess fluid, air, or blood between pleural layers,. Autoimmune diseases (e.g., focuses on reducing symptoms, preventing exacerbations, and improving quality of life. The treatment Montelukast, Zafirlukast. - *Mechanism:* Block the action of leukotrienes, which are inflammatory
lupus, rheumatoid arthritis),. Tumors or cancer of the lungs,. Pulmonary embolism (blood clot in lung plan typically includes: 1. *Pharmacological Therapy*: - *Bronchodilators*: - Long-acting beta-agonists chemicals the body releases after coming in contact with an allergen. - *Usage:* Can be used alone or
vessels),. Trauma or chest/rib injury,. Certain drugs (e.g., hydralazine),. Heart or abdominal organ (LABAs) (e.g., salmeterol, formoterol). - Long-acting muscarinic antagonists (LAMAs) (e.g., tiotropium, in conjunction with ICS.3. *Mast Cell Stabilizers:* - *Examples:* Cromolyn sodium, Nedocromil. -
problems. Risk Factors: Risk factors vary based on the underlying cause (e.g., infections, autoimmune umeclidinium). - Combination inhalers (LABA + LAMA) for better control. - *Inhaled Corticosteroids *Mechanism:* Prevent the release of inflammatory mediators from mast cells. - *Usage:* Less
diseases, cancer). Individuals with a history of lung disease, recent chest trauma, or exposure to toxic (ICS)*: - Often combined with LABA (e.g., fluticasone/salmeterol, budesonide/formoterol) for patients commonly used due to the availability of more effective medications.4. *Systemic Corticosteroids:* -
substances are at higher risk 1.Clinical Presentation:Symptoms: Severe chest pain (worsens with with a history of exacerbations and high eosinophil counts. -Phosphodiesterase-4 Inhibitors*:- *Examples:* Prednisone, Prednisolone. - *Mechanism:* Reduce severe inflammation and are used for
breathing), cough, shortness of breath, tenderness in the chest, fever, and chills (especially in Roflumilast for patients with severe COPD associated with chronic bronchitis and a history of acute exacerbations. - *Usage:* Used for short-term management of severe asthma or
infections).Physical Examination: Stethoscope examination reveals lung sounds and pleural rubbing. exacerbations. - *Antibiotics*: - Macrolides (e.g., azithromycin) for patients with recurrent exacerbations.Basic Bronchodilator Therapy: Bronchodilators are used to relax the muscles around the
Diagnostic Tests: Chest X-ray (detects inflammation),. CT scan (provides detailed images),. Ultrasound exacerbations, particularly with evidence of bacterial infections. 2.*Non-Pharmacological Therapy*: - airways, making it easier to breathe. They are categorized based on their duration of action:1. *Short-
(evaluates pleural effusion),. Thoracentesis (examines pleural fluid),. Thoracoscopy (visualizes the *Pulmonary Rehabilitation*: - Comprehensive programs including exercise training, education, and Acting Beta-Agonists (SABAs):* - *Examples:* Albuterol (Salbutamol), Levalbuterol. - *Mechanism:*
irritated area) 13.Differentiating Exudate vs. Transudate: - Exudate: High protein level (>35g/L); caused behavior change to improve physical and emotional condition. - *Smoking Cessation*: - Essential for Quickly relax bronchial smooth muscle and relieve acute symptoms. - *Usage:* Used for immediate
by inflammation, infection, or tumors. Transudate: Low protein level (<25g/L); due to all patients who smoke, using counseling and pharmacotherapy (e.g., nicotine replacement, varenicline, relief of asthma symptoms and before exercise to prevent exercise-induced bronchoconstriction.2.
hydrostatic/oncotic pressure imbalance. bupropion). - *Vaccinations*: - Influenza and pneumococcal vaccines to prevent respiratory *Long-Acting Beta-Agonists (LABAs):* - *Examples:* Salmeterol, Formoterol. - *Mechanism:* Provide
infections. - *Oxygen Therapy*: - For patients with severe resting hypoxemia (PaO2 ≤55 mm Hg or prolonged bronchodilation and are used for long-term control when combined with ICS. - *Usage:* Not
SaO2 ≤88%). 3. *Management of Exacerbations*: - *Short-acting Bronchodilators*: - Increase use used as monotherapy but in conjunction with ICS for persistent asthma.3. *Anticholinergics:* - *Short-
during exacerbations (e.g., albuterol, ipratropium). - *Systemic Corticosteroids*: - Oral prednisolone acting example:* Ipratropium. - *Long-acting example:* Tiotropium. - *Mechanism:* Block the action
for 5-7 days during exacerbations. - *Antibiotics*: - If bacterial infection is suspected, based on of acetylcholine on airways to reduce bronchoconstriction. - *Usage:* Often used in combination with
sputum purulence, increased volume, and dyspnea. 4. *Monitoring and Follow-Up*: - Regular follow- beta-agonists for additional bronchodilation.4. *Theophylline:* - *Examples:* Theophylline. -
up visits to assess symptom control, exacerbation history, and adherence to therapy. - Spirometry to *Mechanism:* Relaxes the smooth muscles of the airways and decreases the response of the airways to
monitor disease progression. irritants. - *Usage:* Less commonly used due to its narrow therapeutic range and potential side effects.

11.Bronchiectatic disease. Definition. Clinic. Diagnostics. Treatment. Features of antimicrobial therapy.

Ans: Bronchiectatic Disease (Bronchiectasis). Definition:- Bronchiectasis is a chronic condition
characterized by permanent dilation and destruction of the bronchial walls due to chronic inflammation
and infection. Clinical Features: -- Chronic cough with copious sputum production- Recurrent respiratory 13.Chronic pulmonary heart. Definition. Etiology. Pathogenesis. Clinic. Diagnosis of pulmonary 14.Respiratory failure. Definition. Etiology. Pathogenesis. Clinic. Severity classification . Diagnostics.
infections- Hemoptysis (coughing up blood)- Dyspnea (shortness of breath)- Wheezing and crackles on hypertension syndrome. Ans: Chronic Pulmonary Heart (Cor Pulmonale): Definition:-Chronic pulmonary Treatment. Ans: Respiratory Failure:- Definition:-Respiratory failure is a condition in which the
auscultation- Fatigue. Diagnostics :-- *High-Resolution CT (HRCT)*: Gold standard for visualizing heart disease (cor pulmonale) is the enlargement and failure of the right ventricle of the heart as a respiratory system fails to maintain adequate gas exchange, resulting in hypoxemia (low blood oxygen)
bronchial dilation and wall thickening.- *Sputum Culture*: To identify pathogens.- *Pulmonary Function response to increased resistance or high blood pressure in the lungs (pulmonary hypertension). Etiology: and/or hypercapnia (high blood carbon dioxide).Etiology:-- *Pulmonary Diseases*: COPD, pneumonia,
Tests (PFTs)*: Often show an obstructive pattern.- *Blood Tests*: To identify underlying conditions.- -- *Chronic Obstructive Pulmonary Disease (COPD)*- *Interstitial Lung Diseases*: Such as pulmonary acute respiratory distress syndrome (ARDS), pulmonary fibrosis.- *Neuromuscular Disorders*: Guillain-
*Chest X-Ray*: May show suggestive signs but less sensitive than HRCT. ,. Treatment: 1. *Airway fibrosis.- *Pulmonary Vascular Diseases*: Including pulmonary embolism and primary pulmonary Barré syndrome, myasthenia gravis, spinal cord injuries.- *Central Nervous System Disorders*: Stroke,
Clearance*: Chest physiotherapy and devices to clear mucus. 2. *Medications*: - Bronchodilators - hypertension.- *Sleep-Disordered Breathing*: Such as obstructive sleep apnea.- *Chest Wall Disorders*: drug overdose, traumatic brain injury.- *Chest Wall Disorders*: Kyphoscoliosis, severe obesity.
Inhaled corticosteroids - Mucolytics 3. *Antibiotic Therapy*: - Acute Exacerbations: Guided by sputum Such as kyphoscoliosis. Pathogenesis:-- *Pulmonary Hypertension*: Chronic lung diseases cause Pathogenesis:-- *Type 1 (Hypoxemic) Respiratory Failure*: Due to impaired oxygen exchange, often
culture. - Chronic Suppression: Long-term, low-dose antibiotics (e.g., macrolides). 4. *Vaccinations*: hypoxia, leading to pulmonary vasoconstriction and remodeling of pulmonary arteries, increasing caused by diseases affecting the lung parenchyma, leading to low oxygen levels (PaO2 < 60 mmHg).-
Influenza and pneumococcal vaccines. 5. *Surgery*: In severe or localized cases not responsive to pulmonary arterial pressure.- *Right Ventricular Overload*: The right ventricle must work harder to *Type 2 (Hypercapnic) Respiratory Failure*: Due to inadequate ventilation, leading to elevated carbon
medical treatment. Features of Antimicrobial Therapy- *Choice of Antibiotics*: Based on sputum pump blood through the constricted pulmonary arteries, leading to hypertrophy and eventual dilation dioxide levels (PaCO2 > 50 mmHg), commonly seen in conditions affecting the airway, muscles, or
culture and sensitivity.- *Duration*: Typically 10-14 days for acute exacerbations; long-term for chronic and failure of the right ventricle. Clinical Features:-- *Dyspnea*: Shortness of breath, initially on exertion central nervous system. Clinical Features:-- *Dyspnea*: Shortness of breath.- *Cyanosis*: Bluish
suppression.- *Routes*: Oral, intravenous, or inhaled depending on the severity and pathogen. and later at rest.- *Fatigue and Weakness*: Due to reduced cardiac output.- *Chest Discomfort*: May discoloration of skin and mucous membranes.- *Tachypnea*: Rapid breathing.- *Use of Accessory
be present.- *Peripheral Edema*: Swelling of legs and ankles.- *Cyanosis*: Bluish discoloration of the Muscles*: Neck and shoulder muscles to assist breathing.- *Altered Mental Status*: Confusion,
skin and mucous membranes.- *Jugular Venous Distension*: Visible swelling of the neck veins.- agitation, or lethargy.- *Fatigue*: Due to increased work of breathing. Severity Classification:-- *Mild*:
*Hepatomegaly*: Enlarged liver due to congestion. Diagnosis of Pulmonary Hypertension Syndrome :-1. PaO2 60-79 mmHg; PaCO2 46-59 mmHg.- *Moderate*: PaO2 40-59 mmHg; PaCO2 60-69 mmHg.-
*Clinical Examination*: Signs of right heart failure and pulmonary hypertension.2. *Imaging*: - *Chest *Severe*: PaO2 < 40 mmHg; PaCO2 > 70 mmHg. Diagnostics:-- *Arterial Blood Gas (ABG) Analysis*: To
12.Abscess of the lung. Definition. Etiology. Clinic. Diagnostics. Treatment. Ans: Lung Abscess Definition: X-Ray*: Enlargement of the right heart border. - *Echocardiography*: To assess right ventricular size measure PaO2, PaCO2, and pH levels.- *Pulse Oximetry*: To monitor oxygen saturation (SpO2).- *Chest
A lung abscess is a localized collection of pus within the lung tissue, resulting from the necrosis of lung and function and estimate pulmonary arterial pressure. - *CT Scan*: To evaluate lung parenchyma and X-Ray/CT Scan*: To identify underlying causes such as pneumonia or ARDS.- *Pulmonary Function Tests
parenchyma. Etiology: - *Bacterial Infection*: Often due to aspiration pneumonia caused by anaerobic pulmonary vasculature.3. *Electrocardiography (ECG)*: Signs of right ventricular hypertrophy and (PFTs)*: To evaluate the extent of lung dysfunction.- *Electrocardiography (ECG)*: To rule out cardiac
bacteria (e.g., Bacteroides, Fusobacterium), Staphylococcus aureus, or gram-negative bacilli.- strain.4. *Pulmonary Function Tests (PFTs)*: To evaluate underlying lung disease.5. *Right Heart causes of respiratory distress. Treatment:- *Oxygen Therapy*: To correct hypoxemia.- *Mechanical
*Aspiration*: Inhalation of oropharyngeal or gastric contents, especially in patients with altered Catheterization*: Gold standard for measuring pulmonary artery pressures.6. *Blood Tests*: To rule out Ventilation*: - *Non-Invasive Ventilation (NIV)*: For patients with moderate respiratory failure. -
consciousness.- *Other Causes*: Septic emboli, bronchial obstruction (e.g., tumor), or direct spread secondary causes and assess the severity of heart failure (e.g., BNP levels). *Invasive Ventilation*: For severe cases, using endotracheal intubation.- *Medications*: -
from nearby infections. Clinical Features: - *Fever and Chills*: Persistent or high-grade fever.- *Cough*: *Bronchodilators*: For airway obstruction. - *Antibiotics*: For infections. - *Corticosteroids*: For
Productive with foul-smelling or purulent sputum.- *Chest Pain*: Pleuritic chest pain.- *Dyspnea*: inflammation. - *Diuretics*: For pulmonary edema.- *Treat Underlying Causes*: Management of the
Shortness of breath.- *Night Sweats*: Common in chronic cases.- *Weight Loss and Fatigue*: specific condition causing respiratory failure.- *Supportive Care*: Hydration, nutrition, and monitoring in
Generalized symptoms of chronic infection. Diagnostics:- - *Chest X-Ray*: Reveals a cavitary lesion with an intensive care setting if needed.
an air-fluid level.- *CT Scan*: Provides detailed imaging of the abscess and surrounding lung tissue.-
*Sputum Culture and Sensitivity*: To identify causative organisms.- *Blood Tests*: Elevated white blood
cell count and inflammatory markers.- *Bronchoscopy*: Sometimes used to obtain samples or rule out
obstructive lesions. Treatment :-- *Antibiotic Therapy*: Broad-spectrum antibiotics, initially empirical
and then tailored based on culture results (e.g., clindamycin, beta-lactam/beta-lactamase inhibitors).-
*Percutaneous Drainage*: If the abscess is large or does not respond to antibiotics.- *Supportive Care*:
Oxygen therapy, hydration, and nutritional support.- *Surgery*: Rarely needed but considered for
refractory cases or complications like hemorrhage.
15. Acute rheumatic fever. Definition. Clinic for heart damage: symptomatology, physical signs.
Diagnostics with instrumental and laboratory research. Ans: Acute Rheumatic Fever (ARF):- Definition:-
Acute rheumatic fever is an inflammatory disease that can develop as a complication of untreated or 16.Acute rheumatic fever. Extracardiac lesions: chorea, abdominal pain syndrome, skin manifestations.
inadequately treated group A streptococcal pharyngitis, affecting the heart, joints, skin, and central Clinic, diagnostics. The principles of treatment and prevention . Ans:- Acute Rheumatic Fever (ARF):-
nervous system.Heart Damage (Rheumatic Carditis) :-*Symptomatology*:- *Carditis*: Inflammation of Extracardiac Lesions*1. Chorea (Sydenham's Chorea)*- *Clinic*: - Involuntary, rapid, jerky movements
the heart, particularly affecting the endocardium, myocardium, and pericardium.- *Symptoms*: - Chest affecting the face, hands, and feet.- Emotional lability, irritability, and poor coordination. - Muscle
pain or discomfort - Palpitations - Fatigue - Shortness of breath *Physical Signs*:-- *Murmurs*: weakness and hypotonia.- *Diagnostics*: - Clinical observation of characteristic movements. - History 17. Mitral heart disease: mitral valve insufficiency. Etiology. Description of the violation of intracardiac
Indicative of mitral or aortic regurgitation.- *Tachycardia*: Especially out of proportion to fever.- of recent streptococcal infection. - Exclusion of other causes of chorea.*2. Abdominal Pain Syndrome*- and extracardiac hemodynamics. Clinic. Ans: Mitral Valve Insufficiency (Mitral Regurgitation). Etiology:-
*Pericardial Friction Rub*: If pericarditis is present.- *Heart Failure Signs*: Such as edema and *Clinic*: - Diffuse, cramping abdominal pain. - Sometimes mimics acute abdomen, leading to *Rheumatic Heart Disease*: Leading cause globally.- *Degenerative Valve Disease*: Myxomatous
hepatomegaly in severe cases.Diagnostics:-*Laboratory Tests*:- *Throat Culture*: To detect group A unnecessary surgical interventions. - Associated with fever and other systemic symptoms.- degeneration, mitral valve prolapse.- *Ischemic Heart Disease*: Papillary muscle dysfunction or
streptococcus.- *Rapid Antigen Detection Test (RADT)*: For streptococcal infection.- *Elevated Acute *Diagnostics*: - Clinical evaluation and exclusion of other causes of abdominal pain. - Supporting rupture.- *Infective Endocarditis*: Destruction of valve leaflets.- *Congenital Malformations*: Such as
Phase Reactants*: Increased erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).- *Anti- evidence of recent streptococcal infection.*3. Skin Manifestations*- *Erythema Marginatum*: - cleft mitral valve.- *Trauma*: Blunt chest trauma causing chordae tendineae rupture. Intracardiac
Streptolysin O (ASO) Titer*: Elevated levels indicate a recent streptococcal infection.*Instrumental Painless, non-itchy rash with pink rings on the trunk and proximal limbs. - Rash may come and go and is Hemodynamics:-- *Regurgitant Flow*: During systole, blood flows back from the left ventricle (LV) into
Tests*:- *Echocardiography*: To assess the extent of valvular damage and carditis.- not affected by heat.- *Subcutaneous Nodules*: - Firm, painless nodules located over bony the left atrium (LA).- *Increased Left Atrial Pressure*: Due to the backflow of blood, leading to LA
*Electrocardiography (ECG)*: May show prolonged PR interval or other conduction abnormalities prominences or tendons. - Often associated with severe carditis.- *Diagnostics*: - Clinical examination dilation and pressure increase.- *Left Ventricular Volume Overload*: Increased volume load due to the
associated with myocarditis.- *Chest X-Ray*: Can reveal cardiomegaly if significant carditis is to identify characteristic rash and nodules. - Supporting evidence of recent streptococcal infection. combined volume of blood from the LA and pulmonary veins, leading to LV dilation and hypertrophy.-
present.Diagnosis of ARF is based on the Jones Criteria, which include major criteria (carditis, Principles of Treatment:- *Anti-Inflammatory Therapy*: - *Aspirin or NSAIDs*: To reduce inflammation *Elevated Pulmonary Venous Pressure*: Increased LA pressure transmits back to the pulmonary veins
polyarthritis, chorea, erythema marginatum, and subcutaneous nodules) and minor criteria (fever, and pain. - *Corticosteroids*: For severe carditis.- *Antibiotic Therapy*: - *Penicillin*: To eradicate and capillaries, potentially causing pulmonary hypertension. Extracardiac Hemodynamics:-- *Pulmonary
arthralgia, elevated acute phase reactants, and prolonged PR interval on ECG). A combination of these streptococcal infection (10-day course). - *Secondary Prophylaxis*: Long-term penicillin prophylaxis to Congestion*: Due to elevated pulmonary venous pressure, leading to pulmonary edema and shortness
criteria, along with evidence of preceding streptococcal infection, is required for diagnosis. prevent recurrence.- *Supportive Care*: - Bed rest during the acute phase. - Management of symptoms of breath.- *Reduced Cardiac Output*: Effective forward cardiac output decreases due to regurgitation,
such as heart failure if present. Prevention:-- *Primary Prevention*: - Prompt and adequate treatment leading to fatigue and exercise intolerance Clinical Features:-- *Symptoms*: - *Dyspnea*: Shortness of
of streptococcal pharyngitis with antibiotics.- *Secondary Prevention*: - Long-term antibiotic breath, initially with exertion and later at rest. - *Orthopnea and Paroxysmal Nocturnal Dyspnea*: Due
prophylaxis (e.g., monthly benzathine penicillin G injections) to prevent recurrence of ARF. - Duration of to pulmonary congestion. - *Fatigue and Weakness*: Due to decreased forward cardiac output. -
prophylaxis depends on the presence and severity of carditis, often extending for at least 5-10 years or *Palpitations*: From atrial fibrillation or increased sympathetic activity.- *Physical Signs*: -
until adulthood. *Holosystolic Murmur*: Heard best at the apex, radiating to the axilla. - *S3 Gallop*: Indicative of
increased LV filling pressures. - *Displaced Apical Impulse*: Due to LV enlargement. - *Signs of Heart
Failure*: Peripheral edema, ascites, and hepatomegaly in advanced cases.Understanding these elements
helps in diagnosing and managing mitral valve insufficiency effectively.

18.Mitral heart disease: stenosis. Etiology. Description of intracardiac and extracardiac hemodynamics. 19. Aortic heart disease: aortic valve insufficiency. Etiology. Description of intracardiac and extracardiac
Clinic. Ans: Mitral Valve Stenosis. Etiology:- *Rheumatic Heart Disease*: Most common cause, resulting hemodynamics. Clinic. Treatment. Ans: Aortic Valve Insufficiency: Short Answer:-*Etiology:*-
from post-inflammatory scarring and fusion of the valve leaflets.- *Congenital Malformations*: Rarely, *Rheumatic Fever*: Chronic rheumatic heart disease leading to valve damage.- *Congenital Bicuspid
individuals are born with a narrowed mitral valve.- *Other Causes*: Calcific degeneration, systemic Aortic Valve*: Leading to premature wear and tear.- *Degenerative Changes*: Age-related degeneration
diseases like systemic lupus erythematosus, and carcinoid syndrome (rare). Intracardiac Hemodynamics or calcification.- *Infective Endocarditis*: Infection leading to valve destruction.- *Aortic Root Dilation*: 20.Aortic heart disease: stenosis ostii aortae. Etiology. Description of intracardiac and extracardiac
:-- *Obstruction of Blood Flow*: Narrowing of the mitral valve impedes blood flow from the left atrium Due to conditions like Marfan syndrome, syphilis, or aortic dissection.*Intracardiac Hemodynamics:*- hemodynamics. Clinic. Treatment. Ans: Aortic Stenosis:- *Etiology:*- *Congenital Bicuspid Aortic Valve*:
(LA) to the left ventricle (LV) during diastole.- *Increased Left Atrial Pressure*: To overcome the *Volume Overload in the Left Ventricle*: Due to backflow of blood from the aorta during diastole.- *Left Most common cause in younger patients.- *Age-Related Calcific Degeneration*: Most common cause in
obstruction, the LA pressure rises, leading to LA dilation.- *Reduced Left Ventricular Filling*: Decreased Ventricular Dilatation and Hypertrophy*: As a compensatory mechanism to accommodate increased elderly patients.- *Rheumatic Heart Disease*: Leads to valve thickening and fusion, less common now in
blood flow to the LV, reducing end-diastolic volume and stroke volume.- *Elevated Pulmonary Venous volume.- *Increased Stroke Volume*: Initially to maintain cardiac output.*Extracardiac developed countries.*Intracardiac Hemodynamics:*- *Increased Left Ventricular Pressure*: Due to
Pressure*: Increased LA pressure transmits backward to the pulmonary veins and capillaries, causing Hemodynamics:*- *Increased Pulse Pressure*: Due to high systolic and low diastolic pressures.- obstruction of blood flow from the left ventricle to the aorta.- *Left Ventricular Hypertrophy*:
pulmonary congestion. Extracardiac Hemodynamics:-- *Pulmonary Hypertension*: Chronic elevation of *Decreased Coronary Perfusion*: Due to reduced diastolic pressure, potentially leading to myocardial Compensatory response to increased afterload.- *Reduced Stroke Volume*: Due to impaired ejection of
pulmonary venous pressure leads to increased pulmonary arterial pressure and eventually right ischemia.- *Pulmonary Congestion*: Secondary to left ventricular dysfunction in advanced blood from the left ventricle.*Extracardiac Hemodynamics:*- *Increased Afterload*: Leads to increased
ventricular hypertrophy and failure.- *Right-Sided Heart Failure*: Due to chronic pulmonary stages.*Clinical Presentation:*- *Dyspnea*: Initially on exertion, progressing to orthopnea and myocardial oxygen demand and potential ischemia.- *Decreased Coronary Perfusion*: Especially during
hypertension, resulting in systemic venous congestion. Clinical Features:-- *Symptoms*: - *Dyspnea*: paroxysmal nocturnal dyspnea.- *Angina*: Due to decreased coronary perfusion.- *Palpitations*: Often exertion, leading to angina.- *Pulmonary Hypertension*: Secondary to left ventricular failure, causing
Shortness of breath, initially on exertion and later at rest. - *Orthopnea and Paroxysmal Nocturnal due to increased stroke volume and left ventricular hypertrophy.- *Wide Pulse Pressure*: Notable on increased pressure in the pulmonary circulation.*Clinical Presentation:*- *Exertional Dyspnea*: Due to
Dyspnea*: Due to pulmonary congestion. - *Fatigue*: Resulting from decreased cardiac output. - physical examination.- *Auscultatory Findings*: Early diastolic murmur, best heard along the left sternal inability to increase cardiac output during activity.- *Angina*: Resulting from increased myocardial
*Hemoptysis*: Coughing up blood due to rupture of bronchial veins - *Palpitations*: Often from atrial border, often accompanied by a bounding pulse (Corrigan pulse).*Treatment:*- *Medical oxygen demand and decreased supply.- *Syncope*: Often exertional, due to fixed cardiac output and
fibrillation secondary to LA enlargement.- *Physical Signs*: - *Mitral Facies*: Malar flush due to Management*: Vasodilators like ACE inhibitors or nifedipine to reduce afterload, beta-blockers for rate inability to meet increased demands.- *Heart Failure Symptoms*: Such as orthopnea and paroxysmal
reduced cardiac output. - *Loud S1 and Opening Snap*: Characteristic sounds heard on auscultation. - control, and diuretics for symptom relief.- *Surgical Intervention*: Aortic valve replacement or repair, nocturnal dyspnea in advanced stages.- *Auscultatory Findings*: Systolic ejection murmur best heard at
*Diastolic Murmur*: Low-pitched, rumbling murmur best heard at the apex with the patient in the left indicated for symptomatic patients or those with significant left ventricular dysfunction.- *Regular the right second intercostal space, often radiating to the carotids.*Treatment:*- *Medical
lateral decubitus position. - *Signs of Right-Sided Heart Failure*: Jugular venous distention, Monitoring*: For asymptomatic patients with periodic echocardiograms to assess progression. Timely Management*: Limited efficacy, primarily for symptom relief. Includes beta-blockers and diuretics, but
hepatomegaly, peripheral edema, and ascites in advanced stages.Mitral stenosis diagnosis and diagnosis and management are crucial to prevent irreversible cardiac damage and improve prognosis. care must be taken not to reduce preload excessively.- *Surgical Intervention*: Aortic valve replacement
management require understanding these elements to provide effective treatment and improve patient (AVR) is the definitive treatment for symptomatic patients or those with severe stenosis. - *Surgical
outcomes AVR*: Open-heart surgery to replace the valve. - *Transcatheter Aortic Valve Replacement (TAVR)*:
Less invasive alternative for high-risk surgical patients.- *Balloon Aortic Valvuloplasty*: Temporary
6.Lung cancer. Risk factors. Clinical and anatomical classification. Central cancer. Diagnosis, the role of measure, usually for bridging to definitive surgery. => Early diagnosis and appropriate intervention are
radiation methods in the study of patients. Ans: Risk Factors for Lung Cancer:Active smoking is a major crucial to improve outcomes and prevent complications such as heart failure and sudden cardiac death.
risk factor. - Passive smoking (exposure to environmental tobacco smoke). -Chronic lung diseases (e.g., Regular monitoring with echocardiography is essential for asymptomatic patients with mild to moderate
chronic obstructive lung disease, idiopathic pulmonary fibrosis). -Occupational exposure (asbestos, stenosis.
arsenic, chromium, cadmium, nickel). Radon exposure, Family history of lung cancer, Organic dust
exposure. Clinical and Anatomical Classification:Non-Small Cell Lung Cancer (NSCLC): Most common
type. Subtypes: Adenocarcinoma, squamous cell carcinoma, large cell carcinoma.Small Cell Lung Cancer
(SCLC): Rapid growth, often metastasizes early. Central Cancer: Arises near the main bronchi or within
the lung hilum. -May cause obstruction, leading to symptoms like cough, hemoptysis, and wheezing.
Diagnosis: Chest radiography for high-risk patients with symptoms.Computed tomography (CT) and
positron emission tomography (PET) if needed.Role of Radiation Methods:Evaluate tumor extent
(staging).Assess functional status.Guide treatment planning and prognosis

22. Infectious endocarditis. Features of the clinic in the elderly and senile, drug addicts. Diagnostics. 23.Arterial hypertension . Definition. Etiology. Risk factors. Classification by degree, stage, stratification
21.Infectious endocarditis. Definition. Etiology. Pathogenesis. Indications for surgical treatment. Ans: Treatment. Ans: Infectious Endocarditis: Features, Diagnostics, and Treatment *Features of the Clinic in of the risk of cardiovascular complications. Ans: Arterial Hypertension: - *Definition:* :- Arterial
Infectious Endocarditis:-*Definition:*Infectious endocarditis (IE) is an infection of the inner lining of the Different Populations:* 1. *Elderly and Senile:* - *Atypical Presentation*: Symptoms may be less hypertension is a chronic condition characterized by persistently elevated blood pressure in the arteries,
heart (endocardium), typically involving the heart valves. It is characterized by the formation of specific, such as general malaise, weight loss, or fatigue, rather than classic fever and heart murmur. - typically defined as a systolic blood pressure (SBP) of ≥140 mmHg and/or a diastolic blood pressure
vegetations composed of fibrin, platelets, microorganisms, and inflammatory cells.*Etiology:*- *Higher Incidence of Comorbidities*: Conditions like diabetes, renal insufficiency, and degenerative (DBP) of ≥90 mmHg. *Etiology:*:- - *Primary (Essential) Hypertension*: No identifiable cause, accounts
*Bacterial Causes*: Most common, including: - Staphylococcus aureus: Particularly in intravenous drug valvular disease are more common, complicating the clinical picture. - *Increased Risk of Embolism*: for 90-95% of cases.- *Secondary Hypertension*: Identifiable causes such as renal disease, endocrine
users and patients with healthcare-associated infections. - Streptococcus viridans: Commonly More frequent embolic events to organs such as the brain and spleen. - *Higher Mortality*: Due to disorders, medication side effects, and sleep apnea. *Risk Factors:*:- - *Non-Modifiable*: Age, family
associated with dental procedures and native valve endocarditis. - Enterococci: Often from delayed diagnosis and the presence of multiple comorbid conditions. 2. *Drug Addicts:* - *Common history, ethnicity.- *Modifiable*: Obesity, physical inactivity, poor diet (high salt intake), excessive
gastrointestinal or genitourinary tract infections. - Coagulase-negative Staphylococci: Especially in Pathogens: *Staphylococcus aureus is the most frequent cause, often involving the tricuspid valve. - alcohol consumption, smoking, stress. *Classification by Degree:*:- 1. *Normal*: SBP < 120 mmHg and
prosthetic valve endocarditis.- *Fungal Causes*: Less common, often in immunocompromised patients.- *Right-Sided Endocarditis*: Tricuspid valve involvement leads to septic pulmonary emboli, presenting DBP < 80 mmHg , 2. *Elevated*: SBP 120-129 mmHg and DBP < 80 mmHg, 3. *Hypertension Stage 1*:
*Other Pathogens*: Including HACEK group organisms (Haemophilus, Aggregatibacter, Cardiobacterium, with symptoms such as cough, pleuritic chest pain, and hemoptysis. - *Systemic Symptoms*: Fever, SBP 130-139 mmHg or DBP 80-89 mmHg, 4. *Hypertension Stage 2*: SBP ≥ 140 mmHg or DBP ≥ 90
Eikenella, Kingella).*Pathogenesis:* :- 1. *Endothelial Damage*: Pre-existing valve disease, turbulent chills, and night sweats are common, with potential for skin lesions and track marks indicating mmHg, 5. *Hypertensive Crisis*: SBP ≥ 180 mmHg and/or DBP ≥ 120 mmHg,. *Classification by Stage:*1.
blood flow, or direct trauma can damage the endocardium. 2. *Platelet and Fibrin Deposition*: intravenous drug use. - *Rapid Onset and Progression*: Acute presentation with rapid clinical *Stage 1 Hypertension*: Mild, managed with lifestyle changes and possibly medication., .2. *Stage 2
Damaged endothelium leads to the formation of a sterile thrombus on the valve. 3. *Bacteremia*: Entry deterioration.*Diagnostics:* 1. *Clinical Assessment*: Thorough history and physical examination, Hypertension*: Moderate, often requires combination drug therapy., .3. *Stage 3 Hypertension*:
of microorganisms into the bloodstream, often through dental, surgical, or other invasive procedures. 4. including attention to risk factors (e.g., intravenous drug use, recent dental work, presence of prosthetic Severe, associated with high risk of complications, requires aggressive management. *Stratification of
*Adherence and Colonization*: Microorganisms adhere to the sterile thrombus, forming vegetations. 5. valves). 2. *Blood Cultures*: Multiple sets (usually three) taken from different sites before initiating Cardiovascular Risk:* - *Low Risk*: No risk factors, no target organ damage or cardiovascular disease.-
*Vegetation Formation*: Ongoing deposition of fibrin and platelets, along with bacterial proliferation, antibiotics to identify the causative organism. 3. *Echocardiography*: - *Transthoracic *Moderate Risk*: 1-2 risk factors, no target organ damage or cardiovascular disease.- *High Risk*: 3 or
leads to growth of vegetations. 6. *Systemic Embolization and Immune Response*: Fragments of Echocardiography (TTE)*: Initial imaging modality to detect vegetations, abscesses, or new valvular more risk factors, target organ damage, diabetes, or established cardiovascular or renal disease. => Risk
vegetations can embolize to distant sites, causing infarctions or abscesses; immune complexes can form, regurgitation. - *Transesophageal Echocardiography (TEE)*: More sensitive, especially for detecting stratification helps in tailoring treatment to prevent complications such as heart attack, stroke, and
causing glomerulonephritis and other immune-mediated damage. *Indications for Surgical Treatment:* small vegetations, prosthetic valve involvement, and complications like abscesses. 4. *Laboratory kidney disease.
1. *Heart Failure*: Caused by severe valve dysfunction, particularly acute heart failure unresponsive to Tests*: Elevated inflammatory markers (ESR, CRP), anemia, and positive rheumatoid factor. Urinalysis
medical therapy. 2. *Uncontrolled Infection*: Persistent bacteremia or fungemia despite appropriate may show proteinuria or hematuria due to glomerulonephritis. 5. *Imaging*: Additional imaging (e.g.,
antibiotic therapy, or the presence of difficult-to-treat organisms like fungi or multidrug-resistant CT, MRI) to identify embolic events or abscesses in other organs. *Treatment: 1. *Antibiotic Therapy*: -
bacteria. 3. *Prevention of Embolization*: Large vegetations (especially >10 mm) with high risk of *Empiric Therapy*: Broad-spectrum antibiotics started after blood cultures are drawn, tailored based on
embolization, or recurrent embolic events despite antibiotic therapy. 4. *Perivalvular Infection*: patient’s history and local microbial patterns (e.g., vancomycin with ceftriaxone or gentamicin). -
Evidence of abscess formation, fistula, or dehiscence of a prosthetic valve. 5. *Prosthetic Valve *Targeted Therapy*: Adjusted based on culture results and sensitivity testing, often requiring prolonged
Endocarditis*: Particularly when associated with significant prosthetic dysfunction or complications like intravenous antibiotic treatment (4-6 weeks). 2. *Surgical Intervention*: - Indicated for severe valve
abscesses. => Surgical intervention aims to remove infected tissue, repair or replace affected valves, and dysfunction causing heart failure, uncontrolled infection, prevention of embolization, or presence of
address complications such as abscesses, thereby improving patient outcomes and preventing further complications such as abscesses. 3. *Supportive Care*: Management of complications like heart failure,
complications. renal insufficiency, and embolic events.4. *Monitoring*: Regular follow-up with blood cultures,
echocardiography, and clinical assessment to ensure resolution of infection and monitor for
complications.5. *Prevention*: In high-risk patients, prophylactic antibiotics before dental or surgical
procedures. => Early diagnosis and appropriate management are crucial to improve outcomes in
patients with infectious endocarditis, especially in high-risk populations such as the elderly and
intravenous drug users.
24.Arterial hypertension. Diagnosis of target organ damage: heart, blood vessels, kidneys. Clinical signs.
Research Methods. Treatment. Ans: ( Arterial Hypertension: Diagnosis of Target Organ Damage, Clinical 25.Arterial hypertension. Definition. Risk factors. The principles of non-drug and drug treatment.
Signs, Research Methods, and Treatment) *Diagnosis of Target Organ Damage:*:- *1. Heart:* - *Clinical Prevention . Ans: *Arterial Hypertension: Definition, Risk Factors, Treatment Principles, and
Signs*: Left ventricular hypertrophy (LVH), angina, heart failure, arrhythmias. - *Research Methods*: Prevention*,. *Definition:*:- Arterial hypertension (high blood pressure) is a chronic medical condition
- *Echocardiography*: Detects LVH and cardiac function. - *Electrocardiography (ECG)*: Identifies LVH in which the blood pressure in the arteries is elevated. Blood pressure is measured in millimeters of
and ischemic changes. - *Chest X-ray*: Can show cardiomegaly and pulmonary congestion.*2. Blood mercury (mmHg) and is expressed as two numbers: systolic pressure (when the heart beats) over 26.Hypertensive crisis, uncomplicated and complicated. Clinic of uncomplicated hypertensive crisis.
Vessels:* - *Clinical Signs*: Peripheral artery disease, aortic aneurysm, carotid artery stenosis. - diastolic pressure (when the heart is at rest). Hypertension is generally defined as having a blood Emergency care algorithm. Ans: Hypertensive Crisis: - *Hypertensive crisis* refers to a severe increase in
*Research Methods*: - *Doppler Ultrasound*: Assesses blood flow in peripheral arteries. - *Ankle- pressure of 140/90 mmHg or higher. *Risk Factors:* - *Modifiable:* Obesity, sedentary lifestyle, high blood pressure that can lead to significant health complications. It is categorized into two types: 1.
Brachial Index (ABI)*: Evaluates peripheral artery disease. - *Carotid Ultrasound*: Detects carotid salt diet, excessive alcohol intake, smoking, stress, and poor dietary habits. - *Non-modifiable:* Age, *Uncomplicated Hypertensive Crisis (Hypertensive Urgency)* 2. *Complicated Hypertensive Crisis
artery stenosis.*3. Kidneys:* - *Clinical Signs*: Proteinuria, chronic kidney disease (CKD), reduced family history, genetics, and ethnicity (higher prevalence in African-Americans). *Principles of Non-Drug (Hypertensive Emergency)* Uncomplicated Hypertensive Crisis (Hypertensive Urgency) ,. *Definition:*-
glomerular filtration rate (GFR). - *Research Methods*: - *Serum Creatinine and GFR Calculation*: Treatment:* ,. 1. *Lifestyle Modifications:* - Weight loss if overweight or obese. - Regular physical A severe elevation in blood pressure (typically >180/120 mm Hg) without acute target organ damage.
Assesses kidney function. - *Urinalysis*: Detects proteinuria and microalbuminuria. - *Renal activity (e.g., 30 minutes of moderate exercise most days of the week). - Dietary changes (DASH diet: *Clinical Features:* - Severe headache - Shortness of breath- Nosebleeds- Severe anxiety,. *Emergency
Ultrasound*: Evaluates kidney size and structure.*Treatment:*- *Lifestyle Modifications*: - Weight loss rich in fruits, vegetables, whole grains, and low in saturated fats). - Reducing salt intake (less than 2,300 Care Algorithm:* 1. *Assessment:* - Measure blood pressure accurately. - Assess for symptoms and
- Regular physical activity - Dietary changes (DASH diet, reduced sodium intake) - Limited alcohol mg/day). - Limiting alcohol consumption (no more than two drinks per day for men and one drink per signs of end-organ damage - Evaluate patient's medical history and current medications.,. 2.
consumption - Smoking cessation- *Pharmacotherapy*: - *First-Line Agents*: ACE inhibitors or ARBs, day for women). - Smoking cessation. - Stress management techniques (e.g., mindfulness, meditation, *Intervention:*- Gradual reduction of blood pressure over 24-48 hours. - Oral antihypertensive
calcium channel blockers, diuretics. - *Additional Agents*: Beta-blockers, aldosterone antagonists, as relaxation exercises). *Principles of Drug Treatment:*:- 1. *Medication Classes:* - *Diuretics:* Help medications such as: - Labetalol - Clonidine - Captopril ,. 3. *Monitoring:* - Regular monitoring of
needed. - *Combination Therapy*: Often required for stage 2 hypertension or higher.- *Regular kidneys remove excess sodium and water, reducing blood volume. - *ACE Inhibitors:* Prevent the blood pressure. - Follow-up appointments to ensure blood pressure control. ,. Complicated
Monitoring and Follow-up*: To ensure effective blood pressure control and monitor for complications. formation of a hormone that narrows blood vessels. - *Angiotensin II Receptor Blockers (ARBs):* Block Hypertensive Crisis (Hypertensive Emergency) ,. *Definition:*- A severe elevation in blood pressure
the action of a hormone that narrows blood vessels. - *Calcium Channel Blockers:* Prevent calcium (typically >180/120 mm Hg) with evidence of acute target organ damage (e.g., encephalopathy,
from entering heart and blood vessel muscle cells, leading to relaxed vessels. - *Beta-Blockers:* Reduce myocardial infarction, pulmonary edema, stroke, aortic dissection, acute renal failure). *Clinical
the heart rate and the heart's output of blood. - *Others:* Such as alpha-blockers, centrally acting Features:* - Neurological deficits (e.g., confusion, stroke symptoms) - Chest pain (myocardial ischemia
agents, and vasodilators.*Prevention:* ,. - Maintaining a healthy diet with low salt and balanced or infarction) - Severe dyspnea (pulmonary edema) - Acute kidney injury signs (reduced urine output)
nutrients. - Regular physical activity. - Maintaining a healthy weight.- Avoiding tobacco use.- Limiting *Emergency Care Algorithm:* ,.1. *Assessment:* - Immediate evaluation of blood pressure and
alcohol consumption.- Regular monitoring of blood pressure.- Managing stress effectively.=> Early symptoms. - Rapid assessment for signs of end-organ damage. - Diagnostic tests as needed (e.g., ECG,
detection and consistent management of hypertension are crucial to prevent complications such as CT scan, blood tests). ,. 2. *Intervention:* - Immediate hospitalization in an intensive care unit (ICU). -
heart disease, stroke, and kidney damage. Intravenous antihypertensive agents for rapid blood pressure reduction, such as: - Sodium
nitroprusside - Nicardipine - Labetalol ,. 3. *Monitoring:* - Continuous blood pressure monitoring.
- Frequent reassessment of target organ function. - Adjust treatment based on response and
underlying cause. ,. 4. *Follow-Up:* - Gradual transition to oral antihypertensive medications. - Long-
term management of hypertension to prevent recurrence.=> In both types of hypertensive crises, timely
and appropriate intervention is crucial to prevent serious complications and improve patient outcomes.

29.IHD: angina pectoris (stable). Definition. Clinic, functional classes. Antianginal groups of drugs.
Prevention. Ans: *Ischemic Heart Disease (IHD): Stable Angina Pectoris* ,. *Definition:*:- Stable angina
pectoris is chest pain or discomfort that occurs predictably with exertion or stress and is relieved by rest
or nitroglycerin, caused by transient myocardial ischemia without permanent damage.,. *Clinical
27.Hypertensive crisis. Classification. Hypertensive crisis complicated by heart damage. Emergency care 28.IHD: angina pectoris (stable). Definition. Pathogenesis. Clinic, functional classes. Diagnostics. Self-help Presentation:* :- - *Chest Pain:* Typically retrosternal, described as pressure, squeezing, or heaviness.-
algorithm. Ans: *Hypertensive Crisis:* *Classification:* 1. *Hypertensive Urgency:* Severe hypertension with an attack of angina pectoris. Ans: *Ischemic Heart Disease (IHD): Stable Angina Pectoris*: *Radiation:* Pain may radiate to the arms, neck, jaw, or back.- *Duration:* Usually lasts 1-5 minutes,
(typically >180/120 mmHg) without acute target organ damage.,. 2. *Hypertensive Emergency:* Severe *Definition:*: Stable angina pectoris is chest pain or discomfort that occurs predictably with exertion or relieved by rest or nitroglycerin.- *Triggers:* Brought on by physical exertion, emotional stress, cold
hypertension with evidence of acute target organ damage (e.g., encephalopathy, myocardial infarction, stress and is relieved by rest or nitroglycerin. It is due to transient myocardial ischemia without causing weather, or heavy meals. :- *Functional Classes (Canadian Cardiovascular Society Classification):*
stroke, heart failure, aortic dissection, acute renal failure).*Hypertensive Crisis Complicated by Heart permanent damage. *Pathogenesis:*: Stable angina is primarily caused by atherosclerosis of the 1. *Class I:* Angina only with strenuous or prolonged physical activity. ,. 2. *Class II:* Slight limitation of
Damage:*:- This refers to a hypertensive emergency where the elevated blood pressure causes acute coronary arteries, leading to a fixed narrowing that limits blood flow. During increased demand (e.g., ordinary activity; angina with walking or climbing stairs rapidly, walking uphill, or in cold/windy
cardiac complications, such as:- Myocardial infarction (heart attack)- Acute heart failure- Acute exercise), the restricted blood flow results in ischemia and chest pain. *Clinical Presentation:*- *Chest conditions.,. 3. *Class III:* Marked limitation of ordinary physical activity; angina with walking 1-2 blocks
pulmonary edema *Emergency Care Algorithm:* 1. *Immediate Assessment:* - Confirm blood Pain:* Typically retrosternal, described as pressure, squeezing, or heaviness.- *Radiation:* Pain may on level ground or climbing one flight of stairs. ,. 4. *Class IV:* Inability to carry out any physical activity
pressure readings. - Assess for symptoms and signs of acute target organ damage (e.g., chest pain, radiate to the arms, neck, jaw, or back.- *Duration:* Usually lasts 1-5 minutes, relieved by rest or without discomfort; angina may occur at rest.,. *Antianginal Groups of Drugs:*:- 1. *Nitrates:* -
shortness of breath, neurological deficits). 2. *Initial Stabilization:* - Place the patient in a nitroglycerin.- *Triggers:* Brought on by physical exertion, emotional stress, cold weather, or heavy Nitroglycerin (short-acting) - Isosorbide mononitrate (long-acting) - Mechanism: Vasodilation, reducing
comfortable position. - Ensure airway, breathing, and circulation (ABCs). 3. *Intravenous Access:* - meals. *Functional Classes (Canadian Cardiovascular Society Classification):* 1. *Class I:* Angina only myocardial oxygen demand.,. 2. *Beta-blockers:*:- - Metoprolol, Atenolol - Mechanism: Reduce heart
Establish IV access for administration of medications. 4. *Medications:* - Administer IV with strenuous or prolonged physical activity. 2. *Class II:* Slight limitation of ordinary activity; angina rate and contractility, decreasing oxygen demand.,,. 3. *Calcium Channel Blockers:*:- - Amlodipine,
antihypertensives. Common options include: - Sodium nitroprusside - Labetalol - Nicardipine - with walking or climbing stairs rapidly, walking uphill, or in cold/windy conditions. 3. *Class III:* Marked Diltiazem, Verapamil - Mechanism: Vasodilation and reduced myocardial contractility.,. 4. *Antiplatelet
Adjust medications based on response and clinical condition. 5. *Monitor and Reassess:* - Continuous limitation of ordinary physical activity; angina with walking 1-2 blocks on level ground or climbing one Agents:* - Aspirin, Clopidogrel - Mechanism: Prevent platelet aggregation, reducing the risk of
cardiac monitoring and frequent blood pressure measurements. - Monitor for signs of end-organ flight of stairs. 4. *Class IV:* Inability to carry out any physical activity without discomfort; angina may thrombosis.,. 5. *Statins:* - Atorvastatin, Rosuvastatin - Mechanism: Lower LDL cholesterol, reducing
damage. 6. *Specialized Care:* - Depending on the specific complication (e.g., myocardial infarction, occur at rest. *Diagnostics:* - *History and Physical Exam:* Assessment of symptom characteristics and plaque formation. ,. 6. *Ranolazine:* - Mechanism: Improves myocardial metabolism, reducing anginal
heart failure), initiate appropriate therapies such as oxygen, diuretics, nitrates, antiplatelets, or risk factors.- *Electrocardiogram (ECG):* May show ischemic changes during an episode.- *Stress symptoms.,. *Prevention:*: 1. *Lifestyle Modifications:* - Regular exercise - Healthy diet (low in
anticoagulants. - Prepare for potential advanced interventions (e.g., cardiac catheterization for Testing:* Exercise ECG or imaging (e.g., nuclear, echocardiography) to provoke and identify ischemia.- saturated fats, high in fruits and vegetables) - Smoking cessation - Weight management,. 2. *Control
myocardial infarction). 7. *Transfer:* - Transfer the patient to a critical care unit for further monitoring *Coronary Angiography:* Definitive test to visualize coronary artery blockages. - *Blood Tests:* Lipid of Risk Factors:* - Blood pressure management - Diabetes control - Lipid management,. 3. *Regular
and management. - Consider transfer to a facility with specialized care if necessary.=> Early profile, glucose, and markers of cardiac damage if acute coronary syndrome is suspected. *Self-help Medical Follow-up:* - Routine check-ups - Adherence to prescribed medications,. 4. *Stress
recognition and prompt treatment are crucial to minimize the risk of irreversible damage and improve with an Attack of Angina Pectoris:* 1. *Stop Activity:* Sit or lie down to rest immediately. 2. Management:* - Techniques such as yoga, meditation, or counseling => Implementing these measures
outcomes. *Medications:* Take sublingual nitroglycerin (0.3-0.6 mg) and repeat every 5 minutes up to 3 doses if can significantly reduce the risk and severity of stable angina and improve overall cardiovascular health
needed. 3. *Relaxation Techniques:* Practice deep breathing or other stress-reduction techniques. 4.
*Seek Help:* If pain persists after 3 doses of nitroglycerin or lasts more than 20 minutes, seek 30. IHD: in vasospastic (variant, Prinzmetal) angina pectoris. On the particular pathogenesis and clinic.
emergency medical assistance, as this may indicate unstable angina or myocardial infarction. => Ans: *Ischemic Heart Disease (IHD): Vasospastic (Variant, Prinzmetal) Angina Pectoris*,.
Understanding and adhering to these guidelines can help manage stable angina effectively and prevent *Pathogenesis:*:- Vasospastic angina, also known as Prinzmetal's angina, is caused by a transient spasm
complications. of a coronary artery, leading to a temporary reduction in blood flow and myocardial ischemia. Unlike
stable angina, it is not primarily due to atherosclerotic plaques but to hyperreactivity of the coronary
arteries. Triggers for the spasm can include cold exposure, stress, smoking, or certain medications.
*Clinical Presentation:* ,. - *Chest Pain:* Severe, often occurring at rest, typically in the early morning
hours.- *Duration:* Pain episodes can last from a few minutes to 30 minutes.- *Associated Symptoms:*
May include palpitations, syncope, and diaphoresis.- *Relief:* Pain is relieved by nitrates and calcium
channel blockers.- *ECG Changes:* Transient ST-segment elevation during pain episodes, which
normalizes when the pain subsides. => Understanding the distinct mechanisms and clinical features of
vasospastic angina is crucial for appropriate diagnosis and treatment, differentiating it from other forms
of angina

31.Acute coronary syndrome. Definition. Pathogenesis. The standard of emergency care for acute
coronary syndrome with ST segment elevation. Ans: *Acute Coronary Syndrome (ACS):**Definition:*- 33. 32. IHD: myocardial infarction. Definition. Etiology. Pathogenesis. Classification. Diagnostics. Ans: 34.IHD: myocardial infarction. Definition. ECG signs. Clinical options. Clinic, diagnosis, treat
Acute Coronary Syndrome encompasses a range of urgent heart conditions including unstable angina, *Ischemic Heart Disease (IHD): Myocardial Infarction (MI)**Definition:*- Myocardial infarction (MI), *Ischemic Heart Disease (IHD): Myocardial Infarction (MI)**Definition:*- Myocardial infarction (MI),
NSTEMI (non-ST-elevation myocardial infarction), and STEMI (ST-elevation myocardial infarction). It is commonly known as a heart attack, is the irreversible death of myocardial tissue due to prolonged commonly known as a heart attack, is the irreversible death of myocardial tissue due to prolonged
characterized by sudden, reduced blood flow to the heart. *Pathogenesis:*- ACS is primarily caused by ischemia.*Etiology:*- *Atherosclerosis:* The primary cause, leading to plaque rupture and thrombus ischemia. *ECG Signs:*- *ST-Elevation MI (STEMI):* - ST-segment elevation in two or more contiguous
the rupture of an atherosclerotic plaque in a coronary artery, leading to thrombus (blood clot) formation formation.- *Coronary artery spasm:* Severe, transient narrowing of a coronary artery.- *Emboli:* leads. - Pathological Q waves may develop later. - T-wave inversion after a few hours.- *Non-ST-
and subsequent partial or complete occlusion of the artery. This results in myocardial ischemia and, if Obstruction by embolic material.- *Vasculitis:* Inflammation of coronary vessels.- *Cocaine use:* Elevation MI (NSTEMI):* - ST-segment depression. - T-wave inversion. - No persistent ST-segment
untreated, myocardial infarction.- *Standard of Emergency Care for ACS with ST Segment Elevation Induces coronary artery spasm or thrombosis. *Pathogenesis:*1. *Plaque Rupture:* An atherosclerotic elevation.*Clinical Options:*- *STEMI:* Complete occlusion of a coronary artery, leading to full-
(STEMI):* 1. *Immediate Assessment:* - Rapid clinical evaluation and 12-lead ECG within 10 minutes of plaque in a coronary artery ruptures.2. *Thrombus Formation:* A blood clot forms at the site of rupture, thickness myocardial infarction.- *NSTEMI:* Partial occlusion of a coronary artery, leading to
presentation. 2. *Medications:* - *Aspirin:* Chewed (162-325 mg) to inhibit platelet aggregation. - partially or completely occluding the artery.3. *Ischemia:* Reduced blood flow causes oxygen subendocardial myocardial infarction.*Clinic:*- *Symptoms:* - Severe chest pain (pressure, squeezing,
*P2Y12 Inhibitor:* Clopidogrel, ticagrelor, or prasugrel. - *Nitroglycerin:* Sublingual or IV for pain relief, deprivation in the myocardial tissue.4. *Myocyte Death:* Prolonged ischemia results in the death of or heaviness), typically lasting more than 20 minutes. - Pain may radiate to the arms, neck, jaw, or back -
unless contraindicated. - *Morphine:* For pain control if nitrates are insufficient. - *Oxygen:* If myocardial cells, leading to infarction.*Classification:*1. *ST-Elevation Myocardial Infarction (STEMI):* Associated symptoms: Shortness of breath, nausea, vomiting, diaphoresis (sweating), and anxiety.-
hypoxemia (oxygen saturation <90%). 3. *Reperfusion Therapy:* - *Primary Percutaneous Coronary Full-thickness necrosis of the myocardium, characterized by ST-segment elevation on ECG.2. *Non-ST- *Signs:* - Tachycardia or bradycardia. - Hypotension or hypertension. - Signs of heart failure (e.g.,
Intervention (PCI):* Preferred if available within 90 minutes of first medical contact. - *Thrombolytic Elevation Myocardial Infarction (NSTEMI):* Partial-thickness necrosis, without ST-segment elevation but jugular venous distension, crackles on lung auscultation).*Diagnosis:*1. *Clinical History and Physical
Therapy:* If PCI is unavailable within the recommended timeframe, administer thrombolytics within 30 with elevated cardiac biomarkers.3. *Type 1 MI:* Spontaneous MI due to primary coronary event (e.g., Examination:* - Evaluation of chest pain characteristics and associated symptoms. - Assessment of risk
minutes of hospital arrival. 4. *Anticoagulation:* - Unfractionated heparin or low molecular weight plaque rupture).4. *Type 2 MI:* MI secondary to ischemic imbalance (e.g., increased oxygen demand, factors (e.g., age, hypertension, diabetes, smoking).2. *Electrocardiogram (ECG):* - Identifying ST-
heparin to prevent further thrombus formation. 5. *Beta-blockers:* - Administered unless reduced supply).*Diagnostics:*1. *Clinical History and Physical Exam:* - Symptoms: Chest pain, radiating segment changes (elevation or depression), T-wave inversion, and Q waves.3. *Cardiac Biomarkers:* -
contraindications exist (e.g., heart failure, bradycardia, hypotension). 6. *Statins:* - High-intensity statin pain, shortness of breath, nausea, diaphoresis. - Risk factors: Age, sex, family history, hypertension, Elevated troponin levels (most specific and sensitive marker). - Elevated creatine kinase-MB (CK-MB).4.
therapy initiated early. 7. *Monitoring and Supportive Care:* - Continuous ECG monitoring. - diabetes, smoking, hyperlipidemia.2. *Electrocardiogram (ECG):* - STEMI: ST-segment elevation. - *Imaging:* - Echocardiography to assess wall motion abnormalities. - Coronary angiography to identify
Management of complications (e.g., arrhythmias, heart failure). 8. *Transfer to a Specialized Center:* - If NSTEMI: ST-segment depression or T-wave inversion.3. *Cardiac Biomarkers:* - Elevated troponin levels and treat occluded arteries.*Treatment:*1. *Immediate Management:* - *Aspirin:* To inhibit platelet
initial hospital is not equipped for PCI, transfer to a facility that can perform the procedure promptly. => (most specific and sensitive). - Creatine kinase-MB (CK-MB).4. *Imaging:* - Echocardiography: To assess aggregation. - *P2Y12 Inhibitor:* Clopidogrel, ticagrelor, or prasugrel. - *Nitroglycerin:* For chest pain
These steps are critical to restoring blood flow, minimizing heart damage, and improving survival wall motion abnormalities. - Coronary angiography: To identify and treat the occluded artery.5. relief. - *Morphine:* For pain control if necessary. - *Oxygen:* If hypoxemia is present.2. *Reperfusion
outcomes in patients with STEMI. *Additional Tests:* - Chest X-ray: To rule out other causes of chest pain and assess heart size. - Blood Therapy:*
tests: Complete blood count, lipid profile, and renal function tests. => Accurate diagnosis and prompt - *Primary Percutaneous Coronary Intervention (PCI):* Preferred method for STEMI, performed within
treatment are critical for improving outcomes in patients with myocardial infarction. 90 minutes of first medical contact.
- *Thrombolytic Therapy:* If PCI is not available within the recommended timeframe for STEMI.
3. *Anticoagulation:*
- Unfractionated heparin or low molecular weight heparin.
4. *Beta-blockers:*
- Administered unless contraindicated to reduce myocardial oxygen demand.
5. *Statins:*
- High-intensity statin therapy initiated early.
6. *Long-term Management:*
- Lifestyle modifications (e.g., diet, exercise, smoking cessation).
- Medications for secondary prevention (e.g., antiplatelets, ACE inhibitors, beta-blockers, statins).

Prompt diagnosis and treatment are essential to minimize myocardial damage and improve patient
outcomes in myocardial infarction.
 37. Chronic heart failure. Definition. Diagnostics. Non-drug treatment . Therapy that improves the
35. Chronic heart failure. Definition. Etiology. Clinic. Classification by stage and functional classes. 36. Chronic heart failure. Definition. Etiology. Clinic of left ventricular and right ventricular heart prognosis of chronic heart failure.
*Chronic Heart Failure (CHF)* failure.(Short answer) ### Chronic Heart Failure
### Chronic Heart Failure
*Definition:* *Definition:*
Chronic heart failure is a clinical syndrome characterized by the inability of the heart to pump sufficient *Definition:* Chronic heart failure (CHF) is a long-term condition where the heart is unable to pump blood effectively
blood to meet the body's metabolic demands or to do so only at elevated filling pressures. Chronic heart failure (CHF) is a long-term condition where the heart is unable to pump blood effectively to meet the body's needs, leading to symptoms like fatigue, dyspnea, and fluid retention.
to meet the body's needs. This results in insufficient blood flow to organs and tissues, leading to
*Etiology:* symptoms and various functional impairments. *Diagnostics:*
- *Coronary artery disease (CAD)*: The most common cause, leading to myocardial infarction and 1. *Clinical Evaluation:* History and physical examination.
subsequent heart failure. *Etiology:* 2. *Electrocardiogram (ECG):* Identifies arrhythmias, ischemia, and other heart conditions.
- *Hypertension*: Chronic high blood pressure causing left ventricular hypertrophy and heart failure. - *Coronary Artery Disease (CAD):* Narrowing or blockage of coronary arteries reducing blood supply to 3. *Echocardiogram:* Assesses heart structure and function, including ejection fraction.
- *Cardiomyopathies*: Conditions affecting the heart muscle's structure and function. the heart. 4. *Chest X-ray:* Detects pulmonary congestion and cardiomegaly.
- *Valvular heart disease*: Malfunctioning heart valves impairing cardiac function. - *Hypertension:* High blood pressure increases the heart's workload. 5. *Blood Tests:* Includes BNP or NT-proBNP levels, kidney function, electrolytes, and thyroid function.
- *Other causes*: Including congenital heart defects, myocarditis, and certain medications or toxins. - *Cardiomyopathy:* Disease of the heart muscle, including dilated, hypertrophic, and restrictive types. 6. *Stress Test:* Evaluates exercise tolerance and identifies ischemia.
- *Valvular Heart Disease:* Dysfunction of heart valves affecting blood flow within the heart. 7. *Cardiac MRI/CT:* Provides detailed images of heart anatomy and function.
*Clinical Presentation:* - *Congenital Heart Disease:* Structural heart defects present from birth. 8. *Coronary Angiography:* Identifies coronary artery disease.
- *Symptoms*: Fatigue, dyspnea (especially on exertion), orthopnea (difficulty breathing lying down), - *Myocarditis:* Inflammation of the heart muscle, often due to infection.
paroxysmal nocturnal dyspnea (sudden awakening with shortness of breath), edema (swelling in legs, - *Arrhythmias:* Abnormal heart rhythms affecting heart function. *Non-Drug Treatment:*
ankles), and weight gain. - *Chronic Diseases:* Conditions like diabetes, obesity, and chronic kidney disease. 1. *Lifestyle Modifications:*
- *Signs*: Elevated jugular venous pressure, peripheral edema, pulmonary crackles, and possibly signs of - *Diet:* Low-sodium diet to reduce fluid retention.
systemic congestion or low cardiac output. *Clinic of Left Ventricular Heart Failure:* - *Exercise:* Regular physical activity tailored to patient capability.
- *Dyspnea:* Shortness of breath, especially during exertion or lying down (orthopnea). - *Weight Management:* Maintaining a healthy weight.
*Classification by Stage (American College of Cardiology/American Heart Association):* - *Paroxysmal Nocturnal Dyspnea:* Sudden shortness of breath at night. - *Fluid Restriction:* Limiting daily fluid intake in some patients.
1. *Stage A*: At high risk for heart failure, but without structural heart disease or symptoms. - *Fatigue and Weakness:* Due to reduced cardiac output. 2. *Patient Education:* Understanding disease, self-monitoring, and symptom recognition.
2. *Stage B*: Structural heart disease but without signs or symptoms of heart failure. - *Pulmonary Congestion:* Cough, wheezing, and crackles in lungs due to fluid accumulation. 3. *Device Therapy:*
3. *Stage C*: Structural heart disease with prior or current symptoms of heart failure. - *Tachycardia:* Increased heart rate as the body attempts to compensate for poor blood flow. - *Implantable Cardioverter Defibrillator (ICD):* Prevents sudden cardiac death.
4. *Stage D*: Refractory heart failure requiring specialized interventions. - *Cardiac Resynchronization Therapy (CRT):* Improves heart function in select patients.
*Clinic of Right Ventricular Heart Failure:*
*Functional Classification (New York Heart Association - NYHA):* - *Peripheral Edema:* Swelling in the legs, ankles, and feet. *Therapy That Improves Prognosis:*
1. *Class I*: No limitation of physical activity; ordinary physical activity does not cause symptoms. - *Ascites:* Accumulation of fluid in the abdomen. 1. *Angiotensin-Converting Enzyme Inhibitors (ACEIs) or Angiotensin II Receptor Blockers (ARBs):*
2. *Class II*: Slight limitation of physical activity; comfortable at rest, but ordinary physical activity - *Hepatomegaly:* Enlarged liver with possible tenderness. Reduce mortality and hospitalization.
results in symptoms. - *Jugular Venous Distension:* Visible neck veins due to increased venous pressure. 2. *Beta-Blockers:* Improve survival and reduce symptoms.
3. *Class III*: Marked limitation of physical activity; comfortable at rest, but less than ordinary activity - *Fatigue and Weakness:* Similar to left ventricular failure, from inadequate blood supply to tissues. 3. *Mineralocorticoid Receptor Antagonists (MRAs):* Decrease morbidity and mortality.
causes symptoms. 4. *SGLT2 Inhibitors:* Recently shown to improve outcomes in heart failure.
4. *Class IV*: Unable to carry on any physical activity without discomfort; symptoms of heart failure at Understanding the distinctions between left and right ventricular heart failure helps in diagnosing and 5. *Sacubitril/Valsartan (ARNI):* Combination therapy that improves survival and reduces
rest. managing the specific symptoms and underlying causes of heart failure. hospitalization.
6. *Hydralazine and Isosorbide Dinitrate:* Beneficial for specific patient groups, especially African
Understanding these stages and classes helps guide treatment and management strategies for patients Americans.
with chronic heart failure.
These therapies, along with lifestyle modifications and patient education, form a comprehensive
approach to managing chronic heart failure and improving patient outcomes.

40. Chronic kidney disease. Classification. The principles of non-drug and drug therapy. Prevention.
38. Acute glomerulonephritis. Definition. Clinical options for the course. Complications Treatment, 39: Chronic glomerulonephritis. Definition. Clinical options. Diagnostics. Treatment. ### Chronic Kidney Disease (CKD)
regimen, diet, drug therapy. *Classification:*: CKD is classified based on the glomerular filtration rate (GFR) and albuminuria levels:
### Acute Glomerulonephritis ### Chronic Glomerulonephritis - *Stages Based on GFR:*
*Definition:* - *Stage 1:* GFR ≥ 90 mL/min/1.73 m² (normal or high with kidney damage)
*Definition:* Chronic glomerulonephritis (CGN) is a long-term, progressive disease characterized by inflammation and - *Stage 2:* GFR 60-89 mL/min/1.73 m² (mild decrease with kidney damage)
Acute glomerulonephritis (AGN) is an inflammatory condition affecting the glomeruli in the kidneys, gradual scarring of the glomeruli, leading to chronic kidney disease and potentially end-stage renal - *Stage 3a:* GFR 45-59 mL/min/1.73 m² (mild to moderate decrease)
leading to hematuria, proteinuria, hypertension, and renal insufficiency. disease. - *Stage 3b:* GFR 30-44 mL/min/1.73 m² (moderate to severe decrease)
- *Stage 4:* GFR 15-29 mL/min/1.73 m² (severe decrease)
*Clinical Options for the Course:* *Clinical Options:* - *Stage 5:* GFR < 15 mL/min/1.73 m² (kidney failure)
1. *Post-Infectious Glomerulonephritis:* Often follows infections like streptococcal throat or skin 1. *Asymptomatic Hematuria/Proteinuria:* Patients may present with blood and/or protein in the urine - *Albuminuria Categories:*
infections. without other symptoms. - *A1:* <30 mg/g (normal to mildly increased) - *A2:* 30-300 mg/g (moderately increased) - *A3:*
2. *Rapidly Progressive Glomerulonephritis (RPGN):* A severe form that progresses rapidly to kidney 2. *Nephrotic Syndrome:* Characterized by heavy proteinuria, hypoalbuminemia, edema, and >300 mg/g (severely increased)
failure. hyperlipidemia. *Principles of Non-Drug Therapy:*
3. *Primary Glomerulonephritis:* Includes diseases primarily affecting the kidneys (e.g., IgA 3. *Nephritic Syndrome:* Features include hematuria, hypertension, and mild to moderate proteinuria. 1. *Dietary Management:* - *Low Sodium:* Reduce dietary sodium to manage hypertension. -
nephropathy). 4. *Progressive Renal Insufficiency:* Gradual decline in kidney function over time. *Protein Restriction:* Tailored to reduce kidney workload. - *Potassium and Phosphorus Control:*
4. *Secondary Glomerulonephritis:* Associated with systemic diseases (e.g., lupus nephritis, vasculitis). Limit intake to prevent hyperkalemia and hyperphosphatemia.
*Diagnostics:* 2. *Lifestyle Modifications:* - *Regular Physical Activity:* Maintain cardiovascular health. - *Smoking
*Complications:* 1. *History and Physical Examination:* Includes assessment of blood pressure, edema, and systemic Cessation:* Reduce progression risk. - *Weight Management:* Maintain healthy body weight.
1. *Acute Kidney Injury (AKI):* Sudden loss of kidney function. symptoms. 3. *Education and Self-Management:* - *Patient Education:* Understanding disease, diet, and lifestyle
2. *Chronic Kidney Disease (CKD):* Long-term deterioration of kidney function. 2. *Urinalysis:* Detects hematuria, proteinuria, and casts. changes. - *Regular Monitoring:* Track blood pressure, blood sugar, and kidney function.
3. *Hypertensive Encephalopathy:* Severe hypertension affecting the brain. 3. *Blood Tests:* Measures kidney function (creatinine, BUN), electrolytes, albumin, and lipid profile. *Principles of Drug Therapy:*
4. *Heart Failure:* Due to volume overload and hypertension. 4. *Serological Tests:* Identify underlying causes (e.g., ANA for lupus, ANCA for vasculitis). 1. *Blood Pressure Control:* - *ACE Inhibitors/ARBs:* First-line to control hypertension and reduce
5. *Electrolyte Imbalances:* Including hyperkalemia and metabolic acidosis. 5. *Kidney Biopsy:* Provides definitive diagnosis and helps determine the type and severity of proteinuria.
glomerulonephritis. 2. *Glycemic Control:* - *Antidiabetic Medications:* Maintain target HbA1c levels in diabetic patients.
*Treatment:* 6. *Imaging:* Ultrasound to assess kidney size and rule out other conditions. 3. *Management of Anemia:* - *Erythropoiesis-Stimulating Agents (ESAs):* Treat anemia of CKD. -
- *Regimen:* *Iron Supplements:* If iron deficiency is present.
- *Rest:* Bed rest during the acute phase to reduce renal workload. *Treatment:* 4. *Bone Mineral Metabolism:* - *Phosphate Binders:* Manage hyperphosphatemia. - *Vitamin D
- *Monitoring:* Regular monitoring of blood pressure, kidney function, and electrolytes. 1. *General Measures:* Supplements:* Maintain bone health.
- *Blood Pressure Control:* Target BP < 130/80 mmHg using ACE inhibitors or ARBs. 5. *Lipid Management:* - *Statins:* Reduce cardiovascular risk.
- *Diet:* - *Proteinuria Reduction:* ACE inhibitors or ARBs to reduce protein excretion. 6. *Diuretics:* Manage fluid overload and hypertension.
- *Low-Sodium Diet:* To manage hypertension and fluid retention. - *Lifestyle Modifications:* Low-sodium diet, smoking cessation, weight management. *Prevention:*
- *Protein Restriction:* Depending on the level of kidney function. - *Monitoring:* Regular follow-up to monitor kidney function and proteinuria. 1. *Control of Risk Factors:*
- *Fluid Restriction:* In cases of significant fluid overload. 2. *Specific Therapies:* - *Hypertension Management:* Maintain optimal blood pressure.
- *Immunosuppressive Therapy:* For immune-mediated CGN (e.g., corticosteroids, cyclophosphamide, - *Diabetes Control:* Maintain blood glucose levels within target range.
- *Drug Therapy:* mycophenolate mofetil). 2. *Regular Screening:*
- *Antihypertensives:* To control blood pressure (e.g., ACE inhibitors, ARBs). - *Plasmapheresis:* In severe cases to remove harmful antibodies. - *High-Risk Populations:* Regular check-ups for those with diabetes, hypertension, or family history
- *Diuretics:* To manage fluid overload and hypertension. - *Treatment of Underlying Conditions:* Managing conditions like diabetes or infections that of CKD.
- *Immunosuppressive Agents:* In cases of RPGN or secondary glomerulonephritis (e.g., contribute to CGN. 3. *Healthy Lifestyle:* - *Balanced Diet:* Low in sodium, rich in fruits and vegetables.
corticosteroids, cyclophosphamide). 3. *Supportive Care:* - *Physical Activity:* Regular exercise. - *Avoidance of Nephrotoxins:* Limit use of NSAIDs and other
- *Antibiotics:* If post-infectious glomerulonephritis is confirmed, to treat underlying infection. - *Management of Edema:* Diuretics. kidney-damaging drugs.
- *Plasmapheresis:* In severe cases like RPGN, to remove harmful antibodies. - *Control of Hyperlipidemia:* Statins. 4. *Public Health Measures:*
- *Management of Anemia:* Erythropoiesis-stimulating agents if needed. - *Awareness Programs:* Educate about CKD risks and prevention.
A comprehensive approach involving rest, diet modification, and appropriate medications can effectively
manage acute glomerulonephritis and its complications. Early detection and targeted therapy can slow the progression of chronic glomerulonephritis and Implementing these principles can slow CKD progression, improve patient quality of life, and reduce the
improve patient outcomes. risk of complications.

41. Gastroesophageal reflux disease. Definition. Etiology. Pathogenesis. Clinic. Diagnostic Methods. 43. Chronic non-atrophic gastritis . Etiology. Clinic. Diagnostics. Treatment.
Treatment. 42. Chronic atrophic gastritis. Clinical features. Laboratory and instrumental diagnostic methods. ### Chronic Non-Atrophic Gastritis
### Gastroesophageal Reflux Disease (GERD) Features of the diet, drug treatment.
*Definition:* ### Chronic Atrophic Gastritis *Etiology:*
Gastroesophageal reflux disease (GERD) is a chronic condition where stomach acid or bile flows back - *Helicobacter pylori Infection:* Most common cause.
into the esophagus, leading to symptoms such as heartburn and regurgitation, and potentially causing *Clinical Features:* - *Chronic Use of NSAIDs:* Long-term use of nonsteroidal anti-inflammatory drugs.
damage to the esophageal lining. - *Dyspepsia:* Indigestion, bloating, and discomfort in the upper abdomen. - *Alcohol Consumption:* Irritates and inflames the stomach lining.
*Etiology:* - *Nausea and Vomiting:* Common in more severe cases. - *Smoking:* Contributes to mucosal damage.
1. *Lower Esophageal Sphincter (LES) Dysfunction:* Weak or relaxed LES allowing acid reflux. - *Loss of Appetite:* Leading to weight loss. - *Diet:* Spicy and acidic foods can exacerbate the condition.
2. *Hiatal Hernia:* Part of the stomach pushes up through the diaphragm. - *Anemia Symptoms:* Fatigue, weakness, and pallor due to vitamin B12 deficiency. - *Stress:* Can worsen symptoms and contribute to gastritis.
3. *Obesity:* Increased abdominal pressure promotes reflux. - *Gastrointestinal Bleeding:* Occasional, causing dark stools or anemia.
4. *Pregnancy:* Hormonal changes and increased abdominal pressure. - *Epigastric Pain:* Dull, aching pain in the upper stomach area. *Clinic:*
5. *Lifestyle Factors:* Diet (e.g., fatty foods, caffeine, alcohol), smoking, and large meals. - *Malabsorption:* Resulting in deficiencies of various nutrients, particularly iron and vitamin B12. - *Dyspepsia:* Persistent upper abdominal discomfort or pain.
6. *Medications:* Certain drugs like NSAIDs, calcium channel blockers, and anticholinergics. - *Nausea and Vomiting:* Common symptoms.
*Pathogenesis:* *Laboratory and Instrumental Diagnostic Methods:* - *Bloating and Belching:* Due to impaired digestion.
- *LES Dysfunction:* Allows gastric contents to reflux into the esophagus. 1. *Blood Tests:* - *Loss of Appetite:* Sometimes leading to weight loss.
- *Delayed Gastric Emptying:* Leads to increased gastric volume and pressure. - *Complete Blood Count (CBC):* To detect anemia. - *Epigastric Pain:* Pain or discomfort in the upper abdomen.
- *Esophageal Motility Disorders:* Impaired clearance of refluxed material. - *Serum Vitamin B12 Levels:* Low levels indicate malabsorption.
- *Increased Intra-abdominal Pressure:* Factors like obesity and pregnancy. - *Gastrin Levels:* Elevated in some cases of atrophic gastritis. *Diagnostics:*
- *Acid and Pepsin:* Cause mucosal damage and inflammation in the esophagus. - *Antibodies:* Presence of anti-parietal cell antibodies and intrinsic factor antibodies for autoimmune 1. *Endoscopy:* Visualizes inflammation of the stomach lining and allows for biopsy.
*Clinic:* gastritis. 2. *Histology:* Biopsy confirms inflammation without atrophy.
- *Heartburn:* Burning sensation in the chest, often after eating or at night. 2. *Endoscopy:* 3. *Urea Breath Test or Stool Antigen Test:* Detects H. pylori infection.
- *Regurgitation:* Sour or bitter-tasting acid backing up into the throat or mouth. - *Direct Visualization:* Assesses mucosal atrophy and collects biopsy samples. 4. *Blood Tests:*
- *Dysphagia:* Difficulty swallowing. 3. *Histology:* - Complete blood count (CBC) to detect anemia.
- *Chest Pain:* Can mimic heart disease. - *Biopsy Analysis:* Confirms atrophy, intestinal metaplasia, and chronic inflammation. - H. pylori serology to identify infection.
- *Chronic Cough, Laryngitis, and Asthma:* Due to irritation of the airways. 4. *Urea Breath Test or Stool Antigen Test:* ### treatment : antibiotics , amoxicillin , clerothmrothrycine , PPI : pentapresole
- *Hoarseness and Sore Throat:* From acid affecting the vocal cords. - *Helicobacter pylori Detection:* To identify H. pylori infection, a common cause.
*Diagnostic Methods:* 5. *Serum Pepsinogen Levels:*
1. *Clinical Evaluation:* Based on symptoms and medical history. - *Pepsinogen I and II:* Low levels of pepsinogen I and a low pepsinogen I/II ratio suggest atrophic
2. *Endoscopy:* Visualizes the esophagus and can detect inflammation, erosions, or strictures. gastritis.
3. *24-Hour pH Monitoring:* Measures acid levels in the esophagus.
4. *Esophageal Manometry:* Assesses esophageal motility and LES function. *Features of the Diet:*
5. *Barium Swallow Radiograph:* Detects structural abnormalities like hiatal hernia. 1. *Small, Frequent Meals:* Easier on the stomach.
*Treatment:* 2. *Avoid Irritants:* Such as spicy, acidic, fried foods, alcohol, and caffeine.
1. *Lifestyle Modifications:* 3. *Nutrient-Rich Foods:* Emphasize foods rich in vitamins, especially B12, iron, and folate.
- *Dietary Changes:* Avoid trigger foods (e.g., spicy, fatty foods, caffeine, alcohol). 4. *Bland Diet:* Focus on easily digestible foods.
- *Weight Loss:* Reduces abdominal pressure.
- *Elevate Head of Bed:* Prevents nighttime reflux. *Drug Treatment:*
- *Avoid Eating Before Bed:* Reduce reflux risk. 1. *Vitamin B12 Supplements:* For deficiency, administered orally or via injections.
2. *Medications:* 2. *Iron Supplements:* For anemia due to iron deficiency.
- *Antacids:* Neutralize stomach acid. 3. *Antacids:* To neutralize stomach acid and relieve symptoms.
- *H2 Receptor Blockers:* Reduce acid production (e.g., ranitidine, famotidine). 4. *Proton Pump Inhibitors (PPIs) or H2 Blockers:* Reduce acid production if indicated.
- *Proton Pump Inhibitors (PPIs):* Strongly reduce acid production (e.g., omeprazole, esomeprazole). 5. *Antibiotics:* To eradicate H. pylori infection if present (e.g., clarithromycin, amoxicillin,
- *Prokinetics:* Enhance esophageal motility and gastric emptying (e.g., metoclopramide). metronidazole).
3. *Surgical Treatment:* - *Fundoplication:* Strengthens the LES by wrapping the top of the stomach 6. *Prokinetics:* Enhance gastric motility if dyspepsia is significant (e.g., metoclopramide).
around it. - *LINX Device:* Magnetic ring implanted around the LES to prevent reflux.
Proper management through diet, supplementation, and appropriate medications can help alleviate
symptoms and prevent complications of chronic atrophic gastritis.
44. Peptic ulcer of the stomach and duodenum. Definition Etiology. Clinic. Diagnostics. Treatment.
### Peptic Ulcer of the Stomach and Duodenum (Short Answer) 45. Irritable bowel syndrome. Definition. Etiology. Pathogenesis. Clinic. Diagnostics. Treatment. 46.Chronic hepatitis Definition Etiology. Pathogenesis, features of viral hepatitis (B, D, C). Clinic.
### Irritable Bowel Syndrome (IBS) (Short Answer) Diagnostics.
#### Definition: ### Chronic Hepatitis (Short Answer)
A peptic ulcer is a sore on the lining of the stomach (gastric ulcer) or the first part of the small intestine #### Definition:
(duodenal ulcer). Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by chronic #### Definition:
abdominal pain and altered bowel habits in the absence of any organic disease. Chronic hepatitis is a condition characterized by ongoing inflammation of the liver that persists for at
#### Etiology: least six months, potentially leading to liver damage, fibrosis, and cirrhosis.
1. *Helicobacter pylori infection* #### Etiology:
2. *Nonsteroidal anti-inflammatory drugs (NSAIDs)* - *Multifactorial*: Includes genetic predisposition, gastrointestinal infections, food intolerances, and #### Etiology:
3. *Hypersecretory conditions (e.g., Zollinger-Ellison syndrome)* psychosocial factors such as stress and anxiety. 1. *Viral Infections*: Hepatitis B (HBV), Hepatitis C (HCV), and Hepatitis D (HDV).
4. *Lifestyle factors (smoking, alcohol, stress)* 2. *Autoimmune Hepatitis*: Immune system attacks liver cells.
5. *Other factors (genetic predisposition, certain medications)* #### Pathogenesis: 3. *Alcoholic Hepatitis*: Long-term excessive alcohol consumption.
- *Gut-Brain Axis Dysfunction*: Abnormal communication between the central nervous system and the 4. *Nonalcoholic Steatohepatitis (NASH)*: Fat accumulation in the liver, often associated with obesity
#### Clinic: enteric nervous system. and metabolic syndrome.
- *Epigastric pain*: Burning or gnawing, varying with meals. - *Motility Disorders*: Irregular bowel muscle contractions. 5. *Drug-induced Hepatitis*: Certain medications and toxins.
- *Bloating, belching, nausea, vomiting* - *Visceral Hypersensitivity*: Increased sensitivity to pain in the gastrointestinal tract.
- *Loss of appetite, weight loss* - *Intestinal Inflammation*: Low-grade inflammation in the gut. #### Pathogenesis:
- *Bleeding*: Hematemesis, melena - *Altered Gut Microbiota*: Imbalance in gut bacteria. - *Immune Response*: Chronic inflammation due to the immune system's response to persistent
- *Complications*: Perforation, penetration, obstruction infection or autoimmune triggers.
#### Clinic: - *Viral Replication*: Continuous replication of viruses like HBV, HCV, and HDV causes ongoing liver cell
#### Diagnostics: - *Abdominal Pain*: Often relieved by defecation. injury.
1. *Endoscopy (EGD)* - *Altered Bowel Habits*: Diarrhea, constipation, or alternating between both. - *Fibrosis and Cirrhosis*: Chronic inflammation leads to scar tissue formation, which can progress to
2. *H. pylori testing* (breath test, stool antigen test, biopsy) - *Bloating and Gas* cirrhosis and liver failure.
3. *Barium swallow radiography* - *Mucus in Stool*
4. *Laboratory tests* (for anemia, H. pylori) - *Symptoms Often Worsen with Stress* #### Features of Viral Hepatitis:
5. *Histology* (biopsy during endoscopy) - *Hepatitis B (HBV)*: Can cause both acute and chronic hepatitis. Chronic infection may lead to
#### Diagnostics: cirrhosis, liver failure, and hepatocellular carcinoma (HCC). Spread through blood, sexual contact, and
#### Treatment: - *Clinical Diagnosis*: Based on Rome IV criteria (recurrent abdominal pain, on average, at least one day perinatally.
1. *Eradication of H. pylori*: Antibiotics (clarithromycin, amoxicillin) + PPI (omeprazole) per week in the last three months, associated with two or more of the following: related to defecation, - *Hepatitis D (HDV)*: Requires co-infection with HBV for replication. More severe course and faster
2. *Reducing acid production*: PPIs, H2 receptor antagonists (ranitidine) change in stool frequency, change in stool form). progression to cirrhosis and HCC.
3. *Protecting the mucosa*: Sucralfate, misoprostol - *Exclusion of Other Conditions*: Through blood tests, stool tests, colonoscopy, and imaging as needed. - *Hepatitis C (HCV)*: Primarily causes chronic infection, leading to liver cirrhosis and HCC over decades.
4. *Lifestyle modifications*: Avoid NSAIDs, smoking cessation, reduce alcohol, manage stress - *Symptom Diaries*: Tracking food intake and symptoms. Spread through blood-to-blood contact.
5. *Surgery*: For complications like perforation or obstruction
#### Treatment: #### Clinic:
1. *Dietary Changes*: Low FODMAP diet, avoiding trigger foods. - *Symptoms*: Often asymptomatic initially. When present, symptoms include fatigue, jaundice,
2. *Medications*: abdominal pain, nausea, and joint pain.
- *Antispasmodics*: For pain relief. - *Chronic Symptoms*: Signs of liver dysfunction such as jaundice, spider angiomas, palmar erythema,
- *Laxatives or Antidiarrheals*: Depending on symptoms. and ascites may develop in advanced stages.
- *Antidepressants*: Low doses for pain relief and regulating bowel function.
3. *Probiotics*: To improve gut flora balance. #### Diagnostics:
4. *Psychological Therapies*: Cognitive-behavioral therapy, stress management. 1. *Liver Function Tests (LFTs)*: Elevated liver enzymes (ALT, AST).
5. *Regular Exercise*: Helps improve bowel function and reduce stress. 2. *Viral Serologies*: Detection of viral antigens, antibodies (HBsAg, anti-HCV), and viral load (HBV DNA,
HCV RNA).
3. *Liver Biopsy*: To assess the extent of liver inflammation and fibrosis.
4. *Imaging*: Ultrasound, elastography (FibroScan) to evaluate liver fibrosis.
5. *Autoimmune Markers*: For autoimmune hepatitis, such as ANA, ASMA, and anti-LKM1.

47.Cirrhosis of the liver. Definition. Etiology. Pathogenesis. Syndrome of portal hypertension, ascites.
Diagnostics. Treatment. 48. Cirrhosis of the liver. Definition Etiology. Diagnosis of chronic liver failure syndrome. Treatment. 49. Iron-deficiency anemia. Definition. Etiology. Pathogenesis. Clinic, syndromes. Diagnostics.
### Cirrhosis of the Liver (Short Answer) ### Cirrhosis of the Liver (Short Answer) Treatment.
#### Definition: ### Iron-Deficiency Anemia (Short Answer)
Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by various liver diseases and conditions, #### Definition:
such as hepatitis and chronic alcoholism. Cirrhosis is chronic liver disease characterized by irreversible scarring (fibrosis) and impaired liver #### Definition:
#### Etiology: function. Iron-deficiency anemia is a condition where there is a lack of adequate healthy red blood cells due to
1. *Chronic Alcoholism*: Prolonged excessive alcohol consumption. insufficient iron, leading to reduced oxygen transport in the body.
2. *Chronic Viral Hepatitis*: Hepatitis B and C. #### Etiology:
3. *Nonalcoholic Steatohepatitis (NASH)*: Fat accumulation in the liver. 1. *Chronic Alcoholism* #### Etiology:
4. *Autoimmune Hepatitis* 2. *Chronic Viral Hepatitis (HBV, HCV)* 1. *Inadequate Dietary Intake*: Low iron consumption.
5. *Biliary Diseases*: Primary biliary cholangitis, primary sclerosing cholangitis. 3. *Nonalcoholic Steatohepatitis (NASH)* 2. *Increased Iron Demand*: Pregnancy, growth spurts.
6. *Genetic Disorders*: Hemochromatosis, Wilson’s disease. 4. *Autoimmune Hepatitis* 3. *Chronic Blood Loss*: Gastrointestinal bleeding, heavy menstrual periods.
7. *Drug-induced Liver Disease*: Certain medications and toxins. 5. *Biliary Diseases (e.g., primary biliary cholangitis)* 4. *Malabsorption*: Conditions like celiac disease, gastric bypass surgery.
#### Pathogenesis: 6. *Genetic Disorders (e.g., hemochromatosis, Wilson’s disease)* 5. *Chronic Diseases*: Chronic kidney disease, chronic infections.
- *Chronic Liver Injury*: Persistent liver damage from various causes. 7. *Drug-induced Liver Disease*
- *Inflammation and Fibrosis*: Continuous inflammation leads to scar tissue formation. #### Pathogenesis:
- *Nodular Regeneration*: The liver tries to repair itself by forming regenerative nodules. #### Diagnosis of Chronic Liver Failure Syndrome: - *Iron Deficiency*: Leads to decreased hemoglobin synthesis.
- *Liver Dysfunction*: Progressive replacement of healthy liver tissue with scar tissue impairs liver 1. *Clinical Features*: - *Reduced Red Blood Cell Production*: Results in microcytic, hypochromic anemia (small, pale red
function. - Jaundice, ascites, hepatic encephalopathy, spider angiomas, palmar erythema, muscle wasting. blood cells).
#### Syndrome of Portal Hypertension and Ascites: 2. *Laboratory Tests*:
- *Portal Hypertension*: Increased blood pressure in the portal vein due to obstructed blood flow - Elevated liver enzymes (ALT, AST), bilirubin, decreased albumin, prolonged PT/INR, elevated serum #### Clinic and Syndromes:
through the liver. ammonia. - *General Symptoms*: Fatigue, weakness, pallor, shortness of breath, dizziness.
- *Causes*: Cirrhotic liver impedes normal blood flow. 3. *Imaging*: - *Specific Symptoms*: Pica (craving for non-nutritive substances), glossitis (inflamed tongue),
- *Complications*: Varices (enlarged veins, especially in the esophagus), splenomegaly (enlarged - Ultrasound, CT, MRI, elastography (FibroScan). koilonychia (spoon-shaped nails), angular cheilitis (cracks at the corners of the mouth).
spleen), and ascites. 4. *Liver Biopsy*:
- *Ascites*: Accumulation of fluid in the abdominal cavity due to increased pressure in the portal vein - Confirms extent of fibrosis and cirrhosis. #### Diagnostics:
and decreased albumin production by the liver. 5. *Endoscopy*: 1. *Complete Blood Count (CBC)*: Low hemoglobin, hematocrit, and mean corpuscular volume (MCV).
- *Symptoms*: Abdominal swelling, discomfort, and weight gain. - To detect esophageal varices. 2. *Serum Ferritin*: Low levels indicate depleted iron stores.
#### Diagnostics: 3. *Serum Iron and Total Iron-Binding Capacity (TIBC)*: Low serum iron, high TIBC, low transferrin
1. *Liver Function Tests (LFTs)*: Elevated liver enzymes, bilirubin, and decreased albumin. #### Treatment: saturation.
2. *Coagulation Tests*: Prolonged prothrombin time (PT) due to reduced synthesis of clotting factors. 1. *Lifestyle Modifications*: 4. *Peripheral Blood Smear*: Microcytic, hypochromic red blood cells.
3. *Imaging*: Ultrasound, CT scan, MRI to visualize liver structure and detect complications. - Abstinence from alcohol, dietary management (high-calorie, high-protein, low-sodium diet). 5. *Additional Tests*: To identify the underlying cause, such as stool tests for occult blood, endoscopy,
4. *Liver Biopsy*: Confirms diagnosis by showing the extent of fibrosis and cirrhosis. 2. *Medications*: and colonoscopy.
5. *Endoscopy*: To detect esophageal varices. - Diuretics (spironolactone, furosemide), beta-blockers (propranolol), lactulose and rifaximin (for
6. *Paracentesis*: Analysis of ascitic fluid to determine the cause of ascites. hepatic encephalopathy), antivirals for hepatitis, vitamin and mineral supplements. #### Treatment:
#### Treatment: 3. *Procedures*: 1. *Iron Supplementation*:
1. *Lifestyle Changes*: Abstaining from alcohol, maintaining a healthy diet. - Endoscopic variceal ligation, paracentesis, Transjugular Intrahepatic Portosystemic Shunt (TIPS). - *Oral Iron*: Ferrous sulfate, ferrous gluconate.
2. *Medications*: 4. *Liver Transplantation*: - *Parenteral Iron*: For those who cannot tolerate oral iron or have malabsorption.
- *Diuretics*: For ascites management (e.g., spironolactone, furosemide). - For end-stage liver disease or unmanageable complications. 2. *Dietary Changes*:
- *Beta-blockers*: To reduce portal hypertension (e.g., propranolol). 5. *Management of Complications*: - Increase intake of iron-rich foods (red meat, beans, fortified cereals).
- *Antiviral Therapy*: For viral hepatitis. - Hepatic encephalopathy, infections, bleeding varices. - Vitamin C to enhance iron absorption.
3. *Endoscopic Procedures*: Banding or sclerotherapy for variceal bleeding. 3. *Treat Underlying Causes*:
4. *Paracentesis*: To remove ascitic fluid. - Address sources of chronic blood loss, improve diet, treat malabsorption syndromes.
5. *Liver Transplantation*: For end-stage liver disease. 4. *Monitoring*:
6. *Management of Complications*: Treating hepatic encephalopathy, infections, and other related - Regular follow-up with CBC and iron studies to assess response to treatment.
issues.

51. Risk factors for chronic non – communicable diseases. The pyramid of food. Preventive
50. Risk factors for chronic non – communicable diseases. The formula of a healthy person. counseling algorithm for overweight and obesity. 52. Risk factors for chronic non – communicable diseases. Algorithm for preventive counseling while
Algorithm for brief prophylactic counseling for dyslipidemia. Risk Factors for Chronic Non-Communicable Diseases: smoking.
### Risk Factors for Chronic Non-Communicable Diseases Risk Factors for Chronic Non-Communicable Diseases:
#### Risk Factors: * Lifestyle: Smoking, unhealthy diet, lack of physical activity, excessive alcohol consumption.
1. *Lifestyle Factors*: - Poor diet (high in saturated fats, sugars, and low in fruits and vegetables) - * Genetics: Family history of these diseases can increase risk. * Smoking: A leading risk factor for heart disease, stroke, cancer, and lung disease.
Physical inactivity - Tobacco use - Excessive alcohol consumption * Age: Risk increases with age. * Unhealthy Diet: High intake of saturated fats, trans fats, added sugars, and sodium.
2. *Metabolic Factors*: - Obesity - Hypertension - Dyslipidemia - Diabetes * Environmental factors: Exposure to certain toxins or pollutants. * Physical Inactivity: Lack of regular exercise increases the risk of several NCDs.
3. *Environmental Factors*: - Exposure to pollution - Occupational hazards * Socioeconomic factors: Poverty, lack of access to healthcare, and education can contribute to poor * Excessive Alcohol Consumption: Can damage the liver, heart, and increase cancer risk.
4. *Genetic Predisposition*: Family history of chronic diseases. health choices. * Genetics: Family history of NCDs can increase an individual's risk.
### The Formula of a Healthy Person: * Age: The risk of NCDs generally increases with age.
1. *Balanced Diet*: High in fruits, vegetables, whole grains, lean proteins, and low in saturated fats, The Pyramid of Food: * Environmental Factors: Exposure to certain toxins or pollutants can contribute to NCDs.
sugars, and processed foods. * Socioeconomic Factors: Poverty, lack of access to healthcare, and education can lead to unhealthy
2. *Regular Physical Activity*: At least 150 minutes of moderate-intensity or 75 minutes of high-intensity The food pyramid is a visual representation of a healthy diet. It emphasizes: choices.
exercise per week.
3. *Avoidance of Tobacco*: No smoking or use of tobacco products. * Base: Fruits and vegetables (should be consumed most frequently) Algorithm for Preventive Counseling While Smoking:
4. *Moderate Alcohol Consumption*: If consumed, limit to moderate amounts (up to one drink per day * Middle: Grains (whole grains preferred)
for women and two for men). * Top: Proteins and fats (consumed in smaller amounts) 1. Assessment: Discuss the individual's smoking history, current smoking habits, and willingness to quit.
5. *Regular Health Check-ups*: Monitor blood pressure, cholesterol, blood sugar, and body weight. 2. Motivation & Education:
6. *Stress Management*: Techniques such as mindfulness, meditation, or yoga. Preventive Counseling Algorithm for Overweight and Obesity: * Highlight Risks: Explain the specific health risks associated with smoking, including NCDs.
7. *Adequate Sleep*: 7-9 hours of sleep per night. * Benefits of Quitting: Emphasize the immediate and long-term health benefits of quitting.
### Algorithm for Brief Prophylactic Counseling for Dyslipidemia: This algorithm is a step-by-step approach to helping individuals manage weight: 3. Develop a Quit Plan:
1. *Assess Risk Factors*: * Set a Quit Date: Encourage the individual to choose a specific date to stop smoking.
- Family history of cardiovascular disease. 1. Assessment: Measure weight, BMI, waist circumference, and assess lifestyle factors. * Identify Triggers: Work together to identify situations that trigger cravings and develop coping
- Personal history of hypertension, diabetes, obesity. 2. Goal Setting: Develop realistic weight loss goals (1-2 pounds per week). strategies.
- Lifestyle factors (diet, exercise, smoking, alcohol). 3. Behavioral Change: Focus on diet and physical activity changes, incorporating them gradually. * Choose Support Resources: Explore options like nicotine replacement therapy, counseling, support
2. *Measure Lipid Profile*: 4. Support: Provide encouragement, resources, and strategies for overcoming challenges. groups, or apps.
- Total cholesterol, LDL, HDL, triglycerides. 5. Monitoring: Regularly track progress and make adjustments as needed. 4. Provide Support:
3. *Evaluate Results*: * Regular Follow-up: Schedule regular check-ins to monitor progress and provide encouragement.
- Compare lipid levels to standard guidelines. Additional Information: * Address Challenges: Help the individual address any challenges they face during the quitting
4. *Provide Lifestyle Counseling*: process.
- *Diet*: Recommend a heart-healthy diet rich in fruits, vegetables, whole grains, lean protein, and low Chronic non-communicable diseases (NCDs) are a major global health issue. They are often preventable * Celebrate Success: Recognize and celebrate their achievements as they work towards quitting.
in saturated fats, trans fats, and cholesterol. with lifestyle modifications. * Encourage Prevention: Once the individual quits smoking, focus on preventing relapse and
- *Physical Activity*: Encourage at least 150 minutes of moderate-intensity exercise per week. maintaining a healthy lifestyle.
- *Weight Management*: Promote weight loss if overweight or obese.
- *Smoking Cessation*: Advise to quit smoking. Remember: Providing accurate information, personalized support, and ongoing encouragement are
- *Alcohol Moderation*: Limit alcohol intake. crucial components of successful smoking cessation counseling.
5. *Discuss Medication if Needed*:
- For patients with high cardiovascular risk or very high lipid levels, discuss statins or other lipid-
lowering medications.
6. *Follow-up and Monitoring*:
- Schedule regular follow-up appointments to monitor lipid levels and adherence to lifestyle changes
and medication.
By implementing these measures, the risk of chronic non-communicable diseases such as cardiovascular
diseases can be significantly reduced.
 55.Silicosis: etiology, pathogenesis, stage of disease, clinical and radiological characteristics, diagnostics,
53. Risk factors. Modified and non-modifiable. Target lipid levels depending on the level of total 54.Vibration disease: definition, classification, diagnostics, treatment, prevention. treatment.
coronary risk (SCORE scale). Definition: Etiology:
Risk Factors for Cardiovascular Disease: * Silicosis is a chronic lung disease caused by inhaling crystalline silica dust, a common component in
Vibration disease (also known as hand-arm vibration syndrome or HAVS) is a collection of disorders sand, rock, and soil.
* Modifiable: These are factors you can change to reduce your risk: caused by prolonged exposure to vibrations, typically through tools or machinery used in various * Occupations at risk: Mining, quarrying, construction, sandblasting, pottery, and glass manufacturing.
* Smoking occupations. Pathogenesis:
* High Blood Pressure * Silica dust particles irritate the lungs, leading to an inflammatory response.
* High Cholesterol Classification: * The body attempts to wall off the silica particles, forming nodules (small, hard lumps).
* Diabetes * These nodules impair lung function, leading to scarring and fibrosis (thickening and hardening of the
* Obesity * Vascular: Affects blood vessels, leading to numbness, tingling, and pain (e.g., Raynaud's lung tissue).
* Physical Inactivity phenomenon). Stages of Disease:
* Unhealthy Diet * Neuropathic: Affects nerves, causing numbness, tingling, and weakness in the hands. * Simple Silicosis: Early stage with minimal scarring. Usually asymptomatic.
* Non-Modifiable: These are factors you can't change: * Osteoarthritic: Affects joints, causing pain, stiffness, and joint degeneration. * Complicated Silicosis: More extensive scarring, leading to shortness of breath, coughing, and chest
* Age (risk increases with age) pain.
* Family History Diagnostics: * Accelerated Silicosis: Rapid progression of the disease, often seen in individuals with high exposure.
* Gender (men generally have a higher risk) * Acute Silicosis: Rare, rapid onset with severe inflammation and fluid buildup in the lungs.
* Ethnicity * Medical History: Detailed review of work history and exposure to vibrations. Clinical and Radiological Characteristics:
* Physical Exam: Assessing neurological and vascular function in the hands. * Clinical: Cough, shortness of breath, chest pain, wheezing, fatigue, weight loss.
Target Lipid Levels (Based on Total Coronary Risk - SCORE Scale) * Diagnostic Tests: * Radiological: Nodules and fibrosis visible on chest X-rays, CT scans can provide more detailed
* Doppler ultrasound to evaluate blood flow. information.
The SCORE scale estimates your 10-year risk of a fatal heart attack. It uses factors like age, gender, total * Nerve conduction studies to assess nerve function. Diagnostics:
cholesterol, smoking status, and blood pressure. * X-rays to examine joint damage. * Medical History: Detailed occupational history and exposure to silica dust.
* Physical Exam: Auscultation of the lungs for abnormal sounds.
| SCORE Risk Level | Target LDL Cholesterol (mg/dL) | Notes | Treatment: * Imaging: Chest X-ray, CT scan.
|---|---|---| * Pulmonary Function Tests: Measure lung capacity and airflow.
| Low Risk (≤ 1%) | <100 | | * Minimize Exposure: Reduce or eliminate exposure to vibrations as much as possible. * Biopsy: In some cases, a lung biopsy may be needed for confirmation.
| Moderate Risk (1-5%) | <100 | May require more intensive lifestyle modifications | * Medications: May be used to manage symptoms like pain and numbness. Treatment:
| High Risk (≥ 5%) | <70 | Consider statin therapy | * Physical Therapy: Can help improve circulation and muscle function. * No Cure: There's no cure for silicosis, but treatment focuses on managing symptoms and slowing
| Very High Risk (≥ 10%) | <55 | Aggressive lipid lowering recommended | * Surgery: In severe cases, surgery may be necessary to repair damaged nerves or blood vessels. disease progression.
* Oxygen Therapy: May be needed for severe shortness of breath.
Important Notes: Prevention: * Corticosteroids: Can help reduce inflammation and improve lung function.
* Bronchodilators: Can open airways and ease breathing.
* Individualized Targets: Target lipid levels may vary depending on individual factors like existing * Engineering Controls: Design tools and equipment that minimize vibration transmission. * Lung Transplantation: In advanced cases, lung transplantation may be an option.
cardiovascular disease and other health conditions. * Administrative Controls: Limit exposure duration, provide breaks, and rotate tasks. Prevention:
* Lifestyle Modifications: Lifestyle changes, including a healthy diet, regular exercise, and smoking * Personal Protective Equipment (PPE): Gloves and other protective equipment can help reduce
cessation, are essential for managing lipid levels and reducing cardiovascular risk. vibration transmission. * Engineering Controls: Ventilation systems, dust suppression, and use of silica-free alternatives.
* Medical Management: In some cases, medications like statins may be prescribed to lower cholesterol * Education & Training: Train workers on the risks of vibration exposure and preventive measures. * Personal Protective Equipment: Respirators, gloves, and protective clothing.
levels, especially in individuals with high or very high risk. * Regular Monitoring: Periodic medical checkups to detect early signs of vibration disease. * Regular Monitoring: Chest X-rays, pulmonary function tests, and medical examinations.

Remember: Always consult with your healthcare provider for personalized recommendations based on Key Points: Key Points:
your individual health status and risk factors.
* Vibration disease is a serious condition that can lead to long-term disability. * Silicosis is a preventable disease.
* Early detection and prevention are crucial to avoid permanent damage. * Early detection and intervention are crucial to improve outcomes.
* A multidisciplinary approach involving healthcare professionals, occupational health specialists, and * Workers exposed to silica dust should undergo regular health monitoring and be educated on safety
employers is necessary for effective management. measures.

58.Occupational mercury poisoning: hazardous industries, clinic, diagnosis, treatment, prevention.

56.Occupational bronchial asthma: etiology, pathogenesis, clinical features, diagnosis, treatment. 57. Acute and chronic poisoning by organophosphorus pesticides. Clinic, treatment, prevention. Hazardous Industries:
Etiology: Organophosphate Pesticides: A Class of Chemicals
* Mining (gold, mercury)
* Occupational bronchial asthma (OBA) is a type of asthma triggered by exposure to substances in the * Organophosphates are widely used as insecticides and herbicides. * Manufacturing (chlor-alkali, dental amalgams, thermometers, fluorescent lamps)
workplace. * They inhibit the enzyme acetylcholinesterase, which is essential for the breakdown of acetylcholine, a * Healthcare (medical instruments, dental fillings)
* Common triggers: Dusts (wood, flour, grain), chemicals (isocyanates, formaldehyde), fumes (welding neurotransmitter. * Research (laboratories, chemical processing)
smoke, paint), and animal allergens.
Acute Poisoning Clinical Presentation:
Pathogenesis:
* Clinical Presentation: * Acute (Inhalation): Respiratory distress, chest pain, cough, fever, metallic taste, nausea, vomiting.
* Repeated exposure to triggers sensitizes the airways. * SLUDGE: Salivation, Lacrimation, Urination, Defecation, Gastrointestinal upset, Emesis (vomiting) * Chronic (Long-term Exposure):
* Subsequent exposures lead to inflammation, bronchospasm (narrowing of airways), and airway * Miosis (constricted pupils) * Neurological: Tremors, ataxia (loss of coordination), peripheral neuropathy, memory problems,
hyperresponsiveness (increased sensitivity to stimuli). * Muscle weakness, tremors, fasciculations (muscle twitching) mood changes.
* Respiratory distress, bronchospasm, paralysis * Gastrointestinal: Nausea, vomiting, diarrhea, abdominal pain.
Clinical Features: * Confusion, seizures, coma * Renal: Proteinuria (protein in the urine), renal failure.
* Treatment: * Skin: Rash, discoloration.
* Symptoms typically develop after exposure at work, often within minutes to hours. * Decontamination: Remove contaminated clothing and wash affected skin.
* Wheezing, coughing, shortness of breath, chest tightness, and sometimes chest pain. * Antidote: Atropine, a drug that blocks the action of acetylcholine at the receptors. Diagnosis:
* Symptoms may worsen over time and can become persistent even outside of work. * Pralidoxime: A reactivator of acetylcholinesterase.
* Supportive Care: Oxygen, mechanical ventilation, and management of seizures. * Medical History: Detailed work history, exposure details.
Diagnosis: * Physical Examination: Neurological assessments, signs of organ damage.
Chronic Poisoning * Laboratory Tests: Blood and urine mercury levels, liver and kidney function tests.
* Thorough medical history, including work history and exposure details. * Imaging: Brain MRI to assess neurological damage.
* Physical exam: Auscultation of the lungs for wheezing. * Clinical Presentation: Long-term exposure can lead to:
* Pulmonary function tests: Demonstrate airway obstruction that improves after bronchodilator use. * Neuromuscular weakness Treatment:
* Challenge testing: Controlled exposure to suspected triggers can confirm diagnosis. * Peripheral neuropathy
* Exclusion of other causes: Rule out other forms of asthma and other lung diseases. * Cognitive impairments * Decontamination: Remove contaminated clothing and wash affected skin.
* Mood disorders * Chelating Agents: Drugs like dimercaprol (BAL) and penicillamine bind to mercury and facilitate its
Treatment: * Treatment: Similar to acute poisoning but may require longer-term management. excretion.
* Supportive Care: Management of symptoms, such as respiratory support and fluid replacement.
* Avoidance of triggers: The cornerstone of treatment. Prevention
* Medications: Prevention:
* Bronchodilators: Relieve bronchospasm. * Safe Handling Practices: Wear protective clothing, use proper ventilation, and follow manufacturer
* Inhaled corticosteroids: Reduce airway inflammation. instructions. * Engineering Controls: Ventilation systems, enclosed processes, replacement of mercury-containing
* Other medications: Leukotriene modifiers, anticholinergics. * Storage and Disposal: Store pesticides securely and dispose of them properly. materials.
* Education: About the condition, triggers, and management strategies. * Awareness and Education: Train workers on the risks and proper handling of organophosphates. * Personal Protective Equipment: Gloves, respirators, protective clothing.
* Workplace modifications: Engineering controls, ventilation systems, and personal protective * Regulation and Monitoring: Enforcement of pesticide regulations and monitoring of exposure levels. * Regular Monitoring: Periodic blood and urine mercury testing for workers.
equipment. * Worker Education: Training on safe handling practices, risk awareness, and emergency procedures.
Key Points:
Key Points: Key Points:
* Organophosphate poisoning is a serious medical emergency that requires prompt treatment.
* OBA is a serious condition that can significantly affect quality of life and work productivity. * Early intervention is crucial to prevent severe complications and long-term effects. * Mercury poisoning can have serious and long-lasting consequences.
* Early diagnosis and treatment are essential to prevent long-term lung damage and disability. * Prevention through safe handling and use of these chemicals is essential. * Early diagnosis and intervention are crucial to minimize damage and improve outcomes.
* Workplaces should implement preventive measures to minimize worker exposure to triggers. Remember: Always seek immediate medical attention if you suspect organophosphate poisoning. * Prevention is essential through strict adherence to safety protocols, engineering controls, and regular
monitoring.
Remember: Always consult with a healthcare professional for personalized recommendations based on
your individual symptoms, exposure history, and medical condition. Remember: Always seek medical attention if you suspect mercury poisoning.

59.Chronic lead poisoning: ways for lead to enter the body, major clinical syndromes (lead anemia, 60. Chronic pancreatitis: etiology, pathogenesis, clinical signs, diagnosis, treatment 61. Diseases of the biliary tract: etiology, pathogenesis, clinical signs, diagnosis, treatment
changes from the nervous system, gastrointestinal syndrome). Etiology: Etiology:
Ways Lead Enters the Body:
* Alcohol Abuse: The most common cause, leading to inflammation and fibrosis of the pancreas. - Gallstones (cholelithiasis)
* Inhalation: Lead dust from contaminated soil, paint, or industrial processes. * Genetic Predisposition: Mutations in genes like PRSS1, CTRC, SPINK1, and CFTR increase risk. - Inflammation (cholecystitis)
* Ingestion: Contaminated food, water, or soil, lead-based paint chips, toys. * Cystic Fibrosis: A genetic disorder affecting the pancreas and other organs. - Infection (cholangitis)
* Absorption: Through skin contact with lead-containing products. * Other Factors: Gallstones, autoimmune disorders, trauma, high triglyceride levels. - Tumors (benign or malignant)
- Congenital abnormalities
Major Clinical Syndromes: Pathogenesis:
Pathogenesis:
* Lead Anemia: * Inflammation and Fibrosis: Repeated attacks of pancreatitis damage the pancreas, leading to scar
* Impaired heme synthesis (production of hemoglobin) in red blood cells. tissue and loss of function. - Obstruction of bile flow
* Microcytic hypochromic anemia (small, pale red blood cells). * Exocrine Insufficiency: Reduced production of digestive enzymes, causing maldigestion and - Inflammation and damage to bile ducts and surrounding tissues
* Basophilic stippling (abnormal blue granules in red blood cells) visible on blood smear. malabsorption.
* Endocrine Insufficiency: Reduced production of insulin and glucagon, potentially leading to diabetes. Clinical signs:
* Neurological Changes:
* Peripheral neuropathy: Weakness, numbness, tingling in extremities. Clinical Signs: - Abdominal pain (right upper quadrant or epigastric)
* Encephalopathy (brain damage): Headache, seizures, coma, behavioral changes, cognitive - Jaundice (yellowing of skin and eyes)
impairment. * Pain: Severe, persistent abdominal pain, often radiating to the back, worse after meals, and - Fever
* Lead lines: Dark lines on the gums caused by lead deposition. associated with nausea and vomiting. - Nausea and vomiting
* Maldigestion and Malabsorption: Weight loss, diarrhea, steatorrhea (fatty stools). - Diarrhea or constipation
* Gastrointestinal Syndrome: * Diabetes: High blood sugar levels, increased thirst and urination. - Fatigue
* Abdominal pain, constipation, anorexia (loss of appetite), nausea, vomiting. * Other Symptoms: Jaundice (yellowing of the skin and eyes), fatigue, bloating, and abdominal
distension. Diagnosis:
Other Manifestations:
Diagnosis: - Laboratory tests (bilirubin, liver enzymes, etc.)
* Kidney damage: Proteinuria, renal failure. - Imaging studies (ultrasound, CT, MRI, etc.)
* Reproductive problems: Miscarriage, infertility. * Medical History: Detailed information about pain, symptoms, and risk factors. - Endoscopy and biopsy (if necessary)
* Cardiovascular disease: Increased risk of hypertension, atherosclerosis. * Physical Examination: Abdominal tenderness, signs of malabsorption.
* Bone changes: Lead deposition in bones can lead to weakness and fractures. * Laboratory Tests: Elevated amylase and lipase levels in blood, stool fat analysis. Treatment:
* Imaging Studies: Ultrasound, CT scan, or MRI to assess pancreas structure and function.
Key Points: * Endoscopy: Endoscopic retrograde cholangiopancreatography (ERCP) to visualize the pancreatic duct - Medications (antibiotics, pain management, etc.)
and take biopsies. - Endoscopic procedures (e.g., ERCP)
* Chronic lead poisoning is a serious and preventable condition. - Surgery (cholecystectomy, bile duct repair, etc.)
* Symptoms can be subtle and may develop gradually over time. Treatment: - Lifestyle changes (diet, weight management, etc.)
* Early diagnosis and intervention are essential to prevent long-term health consequences. * Pain Management: Analgesics, such as opioids, may be required.
* Enzyme Replacement Therapy: Pancreatic enzyme supplements to aid digestion. Note: This is a concise summary, and specific details may vary depending on the specific disease and
Remember: Regular blood lead level testing is recommended for individuals at risk of exposure, * Diabetes Management: Insulin or oral medications as needed. individual case.
particularly children. * Lifestyle Modifications: Alcohol abstinence, smoking cessation, a balanced diet, and weight
management.
* Surgery: In severe cases, procedures may be necessary to relieve pain or manage complications.
Key Points:
* Chronic pancreatitis is a progressive disease that can have significant impact on quality of life.
* Early diagnosis and treatment are crucial to slow progression and manage complications.
* Lifestyle modifications and adherence to medical recommendations are essential for long-term
management.