End Semester Cat: Respiratory Pathology: OmpathStudy

--- SECTION A: Respiratory Pathology SAQ CAT (Semester II, 2026) Q1. A 62-year-old smoker presents with progressive dyspnea and chronic productive cough. Tabulate emphysema and chronic bronchitis under: Definition, Aetiology, Pathogenesis, Morphology, Clinical presentation. (5 marks) Emphysema Chronic Bronchitis --- --- --- Definition Permanent enlargement of airspaces distal to the terminal bronchiole, with destruction of alveolar walls, without significant fibrosis Persistent productive cough for at least 3 months in each of 2 consecutive years, in the absence of another identifiable cause Aetiology Cigarette smoking (main cause); α1-antitrypsin deficiency; occupational dust exposure Cigarette smoking (main cause); air pollution; occupational irritant exposure; recurrent infections Pathogenesis Protease-antiprotease imbalance — smoke-activated neutrophils/macrophages release elastase, overwhelming α1-antitrypsin, leading to destruction of elastic tissue in alveolar walls; oxidative stress also inactivates antiproteases Chronic irritation → hypertrophy/hyperplasia of mucus-secreting glands in bronchi (↑Reid index) and goblet cell hyperplasia in bronchioles → mucus hypersecretion and airway obstruction Morphology Enlarged airspaces, loss of alveolar septa, "pink puffer" appearance grossly; classified as centriacinar, panacinar, paraseptal, or irregular Hypertrophied bronchial submucosal glands, increased Reid index ( 0.4), goblet cell hyperplasia, mucus plugging, chronic inflammatory infiltrate Clinical presentation Progressive dyspnea, minimal cough, pursed-lip breathing, weight loss, barrel chest, prolonged expiration ("pink puffer") Chronic productive cough, recurrent infections, cyanosis, overweight/oedematous ("blue bloater"), wheeze --- Q2. Compare and contrast acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). (5 marks) Similarities: Both represent a spectrum of acute diffuse alveolar damage from direct (pneumonia, aspiration) or indirect (sepsis, trauma) lung insults; both feature increased capillary permeability, non-cardiogenic pulmonary oedema, hypoxemia, and hyaline membrane formation on histology. Key contrast (severity-based): ALI is the milder/earlier end of the spectrum, with moderate hypoxemia (PaO2/FiO2 ratio 200–300 mmHg); ARDS represents the more severe form, with a PaO2/FiO2 ratio ≤200 mmHg (under the older AECC classification) and bilateral infiltrates on chest imaging. Under the current Berlin definition, "ALI" is no longer used as a separate term — instead ARDS is graded as mild (200–300), moderate (100–200), or severe (≤100) based on the PaO2/FiO2 ratio, with the old "ALI" category corresponding to what is now called mild ARDS. --- Q3. List five causes of non-cardiogenic pulmonary oedema. (5 marks) 1. Sepsis/septic shock 2. Acute pancreatitis 3. Aspiration pneumonitis 4. Inhalational injury (smoke, toxic gases) 5. Trauma with shock/fat embolism (Others acceptable: high altitude, near-drowning, drug overdose/reaction, transfusion-related acute lung injury (TRALI), radiation injury) --- Q4. A coal miner develops progressive dyspnoea. Tabulate simple coal workers' pneumoconiosis (CWP) and complicated pneumoconiosis (progressive massive fibrosis). (5 marks) Simple CWP Complicated CWP (PMF) --- --- --- Morphology Coal macules (accumulations of coal-laden macrophages) and coal nodules, mainly in upper lobes Coalescent fibrotic scars typically 2cm, often bilateral, in upper zones Symptoms Usually asymptomatic, minimal impairment of lung function Progressive dyspnoea, significant impairment of pulmonary function, cor pulmonale can develop Progression Generally non-progressive if further dust exposure ceases Progresses even after exposure ceases; may continue to enlarge Radiology Small nodular opacities Large, coalesced opacities, often with cavitation --- Q5. Compare and contrast centriacinar and panacinar emphysema. (5 marks) Centriacinar (centrilobular) Panacinar (panlobular) --- --- --- Distribution Central/proximal part of the acinus (respiratory bronchioles); distal alveoli spared Uniform destruction of the entire acinus, from respiratory bronchiole to terminal alveoli Lobe predilection Upper lobes, particularly upper zones Lower lobes predominantly Association Strongly associated with cigarette smoking Classically associated with α1-antitrypsin deficiency Severity pattern More severe/frequent in upper zones More uniform throughout affected lobe --- Q6. List five risk factors for chronic obstructive pulmonary disease. (5 marks) 1. Cigarette smoking (the major risk factor) 2. α1-antitrypsin deficiency 3. Occupational dust/chemical exposure 4. Air pollution (indoor biomass fuel smoke, outdoor pollution) 5. Recurrent childhood respiratory infections (Others acceptable: genetic factors/family history, low socioeconomic status, advancing age) --- SECTION B: Respiratory Pathology MCQ CAT 1 (23rd March 2026) Q1. 62-year-old, 45-pack-year smoker, chronic cough, haemoptysis