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Q1: Definition and diagnosis (2 min)
Examiner: Define COPD. How do you confirm the diagnosis and grade severity?
COPD is a common, preventable and treatable disease with persistent, progressive, not-fully-reversible airflow limitation caused by chronic inflammation from inhaled noxious particles, chiefly cigarette smoke. I confirm it with post-bronchodilator spirometry showing FEV1/FVC below 0.70 (after 400 mcg salbutamol), performed when the patient is clinically stable. Severity is graded by FEV1 percent predicted: GOLD 1 (at least 80), 2 (50 to 79), 3 (30 to 49), 4 (below 30, or below 50 with chronic respiratory failure). Two overlapping phenotypes — chronic bronchitis (productive cough for at least 3 months in 2 successive years) and emphysema (parenchymal destruction).
Q2: Pathophysiology — why is he breathless, and why does oxygen sometimes make him worse? (3 min)
Examiner: Explain the mechanism of airflow limitation and the danger of high-flow oxygen.
Inhaled particles activate macrophages and epithelium, which recruit neutrophils and CD8+ T-cells via TNF-alpha, IL-8 and LT-B4; neutrophil elastase and MMPs digest alveolar walls. Two lesions result: chronic bronchiolitis (small-airway inflammation, mucus and fibrosis — the major site of obstruction) and emphysema (loss of alveolar attachments and elastic recoil). Together these cause premature airway closure, air trapping and dynamic hyperinflation, flattening the diaphragm and increasing the work of breathing — the chief mechanism of exertional dyspnoea. Ventilation-perfusion mismatch causes hypoxaemia; advanced disease adds hypercapnia and type-2 respiratory failure.
High-flow oxygen precipitates CO2 narcosis by two dominant mechanisms: first, abolition of hypoxic pulmonary vasoconstriction worsens V/Q matching and increases dead space, lowering CO2 clearance; and second, the Haldane effect — oxygenated haemoglobin carries less CO2 as carbamino compounds, so more CO2 stays dissolved and raises PaCO2. The old "loss of hypoxic drive" is a minor contributor. Hence controlled oxygen, target SpO2 88 to 92 percent, and an early ABG.
Q3: Management of an acute exacerbation (3 min)
Examiner: Your COPD patient arrives drowsy, SpO2 84 percent, pH 7.29, PaCO2 75 mmHg. Walk me through your bundle.
ABCDE: sit upright, secure the airway. Controlled oxygen to SpO2 88 to 92 percent (Venturi 24 to 28 percent or nasal cannulae 1 to 2 L/min). Nebulised salbutamol 5 mg + ipratropium 500 mcg, driven with air, every 4 to 6 hours. Prednisolone 40 mg orally once daily for 5 days (REDUCE trial showed 5 days non-inferior to 14). Antibiotics if Anthonisen criteria (increased dyspnoea, sputum volume, sputum purulence) — amoxicillin-clavulanate 500/125 mg three times daily. Because pH is below 7.35 with PaCO2 at least 45 mmHg, start NIV (BiPAP) within 60 minutes — IPAP 10 to 15, EPAP 4 to 5 — and repeat the ABG at 1 hour looking for a rising pH and falling PaCO2. Look for and treat a trigger: pneumonia, pneumothorax (ruptured bulla), pulmonary embolism, heart failure. Escalate to invasive ventilation if NIV fails, consciousness falls, or the patient arrests.
Q4: Stable-disease therapy and prognosis (2 min)
Examiner: After discharge, how do you escalate his inhaled therapy, and what improves survival?
I group him by GOLD ABE: he is a frequent exacerbator (Group E) with high symptoms, so first-line is LABA + LAMA (e.g. tiotropium 18 mcg OD plus salmeterol or a fixed-dose LABA/LAMA). I add ICS only if his blood eosinophils are at least 300/microL — otherwise ICS adds pneumonia risk without benefit. If exacerbations persist I consider roflumilast 500 mcg OD (chronic bronchitis phenotype) and azithromycin 250 mg OD after an ECG. For every patient: smoking cessation (the only disease-modifier — varenicline, NRT, bupropion), vaccination (influenza, pneumococcal, COVID-19), pulmonary rehabilitation, and long-term oxygen therapy at least 15 h/day if PaO2 is at most 55 mmHg (or at most 59 with cor pulmonale) — the only other survival intervention. The BODE index predicts mortality better than FEV1 alone.