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Definition: post-bronchodilator FEV1/FVC below 0.70 with symptoms. Causes: cigarette smoke (main), occupational exposure, air pollution, alpha-1 antitrypsin deficiency. Pathology: chronic bronchitis (mucus hypersecretion) and emphysema (alveolar destruction). Symptoms: chronic cough, sputum, exertional dyspnoea. Signs: hyperinflation, prolonged expiration, wheeze, reduced breath sounds. Severity by spirometry and symptoms (GOLD groups) and exacerbation history. Management: smoking cessation (the most effective measure), vaccination, bronchodilators (long-acting beta-agonists and long-acting muscarinic antagonists), inhaled corticosteroids in frequent exacerbators, pulmonary rehabilitation, long-term oxygen therapy for chronic hypoxaemia, and treatment of exacerbations (short-acting bronchodilators, systemic steroids, antibiotics if purulent sputum).

Features: episodic wheeze, cough, chest tightness and dyspnoea, often nocturnal or triggered by allergens, exercise, cold air or infection. Diagnosis: variable symptoms plus spirometry showing reversibility (increase of FEV1 of 12 percent and 200 mL after bronchodilator), peak flow variability or bronchial challenge. Treatment follows a stepwise approach: as-needed inhaled corticosteroid-formoterol or short-acting beta-agonist, regular low-dose inhaled corticosteroid, add long-acting beta-agonist, higher doses, biologic agents (anti-IgE, anti-IL-5) in severe eosinophilic or allergic disease. Acute severe asthma: oxygen, nebulised salbutamol and ipratropium, systemic steroids, magnesium.

Community-acquired pneumonia: commonest cause Streptococcus pneumoniae; atypical organisms (Mycoplasma, Legionella, Chlamydophila), viruses and Haemophilus. Symptoms: fever, cough, purulent sputum, pleuritic pain, dyspnoea; signs: crackles, bronchial breathing, dullness to percussion. Chest X-ray shows consolidation. Severity: CURB-65 score (confusion, urea, respiratory rate, blood pressure, age 65 or more) guides admission. Treatment: amoxicillin (with a macrolide in more severe cases). Hospital-acquired and aspiration pneumonia involve Gram-negative organisms and anaerobes.

ILD: a group of diseases with inflammation and fibrosis of the interstitium: idiopathic pulmonary fibrosis (older smokers, bibasal crackles, honeycombing on HRCT; antifibrotic drugs nintedanib and pirfenidone), sarcoidosis, hypersensitivity pneumonitis, connective tissue disease. Symptoms: dry cough and progressive dyspnoea; finger clubbing; restrictive spirometry and low DLCO. Pulmonary hypertension: mean pulmonary artery pressure above 20 mmHg. Groups: pulmonary arterial hypertension, left heart disease, lung disease and hypoxia, chronic thromboembolic disease, and multifactorial. Signs: loud P2, right ventricular heave, raised jugular pressure, oedema; echocardiography and right heart catheterisation.

Transudate (heart failure, cirrhosis, nephrotic syndrome): low protein. Exudate (pneumonia, malignancy, tuberculosis, pulmonary embolism): Light criteria (pleural to serum protein above 0.5, LDH ratio above 0.6, pleural LDH above two thirds of the upper serum limit). Examination: stony dull percussion, absent breath sounds. Thoracentesis for diagnosis. Empyema requires drainage; pneumothorax is air in the pleural space (drain if large or symptomatic).

1. Give the spirometric definition of COPD. 2. What is the first-line management of stable asthma? 3. What does CURB-65 measure? 4. Which signs suggest idiopathic pulmonary fibrosis? 5. State Light's criteria.

1. Post-bronchodilator FEV1/FVC below 0.70. 2. Inhaled corticosteroid-containing therapy with as-needed reliever (stepwise approach). 3. Severity of community-acquired pneumonia to guide admission. 4. Dry cough, dyspnoea, bibasal crackles, clubbing, restrictive spirometry and honeycombing on HRCT. 5. An exudate if pleural/serum protein above 0.5, pleural/serum LDH above 0.6 or pleural LDH above two thirds of the upper serum limit.

Virchow triad: stasis, hypercoagulability, endothelial injury. Risk factors: surgery, immobility, cancer, pregnancy, oestrogens, thrombophilia, age. DVT: unilateral leg swelling, pain, warmth; PE: sudden dyspnoea, pleuritic pain, tachycardia, haemoptysis, syncope. Diagnosis: pre-test probability (Wells score), D-dimer if low probability, then compression ultrasound (DVT) or CT pulmonary angiography (PE). Treatment: anticoagulation (LMWH then direct oral anticoagulant or warfarin) for at least 3 months; thrombolysis for high-risk (massive) PE with shock. Prophylaxis in hospital: heparin and compression.

Kidney functions: filtration, tubular reabsorption and secretion, hormone production (erythropoietin, renin, calcitriol). Assessment: creatinine and eGFR, urinalysis (protein, blood, casts) and albumin-creatinine ratio, ultrasound. Syndromes: acute kidney injury, nephrotic and nephritic syndromes, chronic kidney disease. Common disturbances: hyperkalaemia (peaked T waves; treat with calcium, insulin-glucose, salbutamol, resonium, dialysis), hyponatraemia, metabolic acidosis.

Symptoms: breathlessness, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, oedema. Signs: raised jugular venous pressure, third heart sound, crackles, displaced apex beat, peripheral oedema. Investigations: BNP or NT-proBNP, ECG, chest X-ray (cardiomegaly, upper lobe diversion, effusions), echocardiography (ejection fraction). Classification: NYHA functional class I-IV. Treatment: as for reduced ejection fraction with ACE inhibitor/ARNI, beta-blocker, MRA and SGLT2 inhibitor, diuretics for symptoms, device therapy (ICD, cardiac resynchronisation) in selected patients.

1. State the Virchow triad. 2. How is suspected PE investigated? 3. Which investigations are used to diagnose heart failure? 4. How is hyperkalaemia treated acutely?

1. Stasis, hypercoagulability, endothelial injury. 2. Pre-test probability (Wells), D-dimer if low risk, CT pulmonary angiography. 3. Clinical assessment, BNP or NT-proBNP, ECG, chest X-ray and echocardiography. 4. Intravenous calcium to protect the heart, insulin with glucose, salbutamol, potassium binders and dialysis if needed.

Diagnosis: fasting glucose at least 126 mg/dL, HbA1c at least 6.5 percent, 2-hour OGTT at least 200 mg/dL, or random glucose at least 200 mg/dL with symptoms. Type 1 needs insulin; type 2 is treated with lifestyle and drugs: metformin first, then SGLT2 inhibitors or GLP-1 receptor agonists (particularly with cardiovascular or renal disease), DPP-4 inhibitors, sulfonylureas, and insulin. Targets: HbA1c about 7 percent (individualised), blood pressure below 130/80, LDL according to risk. Monitoring: retinal screening, urine albumin, foot examination. Emergencies: diabetic ketoacidosis (insulin infusion, fluids, potassium) and hypoglycaemia (glucose, glucagon).

Anaemia: haemoglobin below 13 g/dL in men and 12 g/dL in women. Symptoms: fatigue, pallor, dyspnoea, tachycardia. - Microcytic (MCV below 80): iron deficiency (low ferritin; look for bleeding), thalassaemia trait, anaemia of chronic disease. - Normocytic: chronic disease, acute blood loss, renal failure, haemolysis (raised reticulocytes, bilirubin and LDH, low haptoglobin). - Macrocytic (MCV above 100): vitamin B12 and folate deficiency (megaloblastic), alcohol, hypothyroidism, myelodysplasia. Investigations: blood count, reticulocytes, ferritin and iron studies, B12, folate, renal and thyroid function, blood film. Treatment addresses the cause: oral or intravenous iron, B12 injections, transfusion when severe.

1. Which drugs are preferred in type 2 diabetes with cardiovascular disease? 2. What is the typical HbA1c target? 3. Give the classification of anaemia by MCV with an example of each. 4. Which findings suggest haemolysis?

1. GLP-1 receptor agonists or SGLT2 inhibitors (after metformin). 2. About 7 percent, individualised. 3. Microcytic: iron deficiency; normocytic: chronic disease; macrocytic: B12 deficiency. 4. Raised reticulocytes, bilirubin and LDH with low haptoglobin.