Q1. Which receptor mediates beta-blocker-induced bronchospasm? A. Beta-1 B. Beta-2 C. Beta-3 D. Alpha-1 ANSWER: B — Beta-2. Why: beta-2 receptors on bronchial smooth muscle mediate relaxation. Blocking them permits bronchoconstriction. A: beta-1 is cardiac and renal; blockade causes bradycardia. C: beta-3 acts on adipose tissue and detrusor muscle. D: alpha-1 blockade causes vasodilation and postural hypotension. LEARNING POINT: adverse effects of this class are the mirror of normal beta-2 function.

Q2. Which agent is LEAST appropriate for a patient with asthma who requires rate control? A. Bisoprolol B. Metoprolol C. Propranolol D. Atenolol ANSWER: C — Propranolol. Why: propranolol is non-selective and blocks bronchial beta-2. The other three are cardioselective and relatively safer, though selectivity is dose-dependent and none is truly "safe". LEARNING POINT: cardioselectivity is relative, never absolute.

Q3. Renin release from juxtaglomerular cells is mediated by: A. Beta-1 B. Beta-2 C. Alpha-1 D. Muscarinic ANSWER: A — Beta-1. Why: renal juxtaglomerular beta-1 receptors trigger renin release; blocking them reduces angiotensin II and aldosterone, which is a major part of the antihypertensive effect. LEARNING POINT: beta-1 is not only cardiac — "one heart, one pair of kidneys" is the version worth remembering.

Q4. A 62-year-old on chronic atenolol stops it abruptly. Two days later he has severe angina and a heart rate of 130. The mechanism is: A. Direct myocardial toxicity B. Beta-receptor upregulation causing catecholamine supersensitivity C. Accumulated drug metabolites D. Reflex vagal withdrawal ANSWER: B — receptor upregulation. Why: chronic blockade upregulates beta receptors. On sudden withdrawal, normal circulating catecholamines act on an increased receptor population, producing rebound tachycardia, hypertension and ischaemia. A: beta-blockers are not directly cardiotoxic. C: atenolol is renally excreted largely unchanged. D: does not explain the delayed, sustained rebound. LEARNING POINT: always taper over 1–2 weeks.

Q5. A patient with beta-blocker overdose remains bradycardic and hypotensive despite fluids and atropine. The most appropriate specific therapy is: A. Adrenaline infusion B. Glucagon C. Calcium gluconate D. Sodium bicarbonate ANSWER: B — Glucagon. Why: glucagon raises cardiac cAMP through its own Gs-coupled receptor, bypassing the blocked beta receptor entirely, so competitive blockade cannot antagonise it. A: adrenaline acts AT the blocked receptor and may be out-competed by the blockade. C: calcium is the specific measure in calcium channel blocker toxicity. D: bicarbonate is used for sodium-channel-blocking drugs such as tricyclic antidepressants. LEARNING POINT: the antidote is chosen for the pathway it uses, not because it is a stimulant.

Q6. A 25-year-old with cocaine-induced chest pain, BP 200/115 and pulse 138. Which is CONTRAINDICATED as initial therapy? A. Diazepam B. Propranolol C. Nitroglycerin D. Aspirin ANSWER: B — Propranolol. Why: blocking beta leaves alpha-mediated vasoconstriction unopposed, worsening coronary spasm and blood pressure. A: benzodiazepines reduce central sympathetic drive and are first-line. C: nitrates relieve coronary vasoconstriction. D: appropriate if ischaemia is suspected. LEARNING POINT: alpha before beta — the same rule governs phaeochromocytoma.

Q7. A 70-year-old on atenolol 50 mg daily for years is admitted with gastroenteritis. eGFR falls from 60 to 25. On day two her pulse is 36. The dose was never changed. The best explanation is: A. Tachyphylaxis B. Reduced renal clearance causing drug accumulation C. A new conduction system disease D. Drug interaction with oral rehydration salts ANSWER: B — reduced renal clearance. Why: atenolol is hydrophilic and renally excreted. Acute kidney injury reduces clearance, so an unchanged dose becomes a functional overdose. A: tachyphylaxis would reduce, not increase, the effect. C: possible but far less likely given the clear temporal link to the AKI. D: no such interaction. LEARNING POINT: hydrophilic agents accumulate when kidneys fail. This is the clinical value of the solubility split.

Q8. Which combination carries the highest risk of complete heart block? A. Metoprolol + amlodipine B. Metoprolol + verapamil C. Atenolol + ramipril D. Bisoprolol + furosemide ANSWER: B — Metoprolol + verapamil. Why: verapamil is a non-dihydropyridine CCB that slows the AV node, as does the beta-blocker. Together they can produce severe bradycardia, complete block or asystole. A: amlodipine is a dihydropyridine and acts on vessels, not the AV node — this combination is safe. C, D: no AV nodal interaction. LEARNING POINT: the dihydropyridine / non-dihydropyridine distinction is what makes this question answerable.

Q9. A diabetic on propranolol becomes hypoglycaemic. Which sign is PRESERVED? A. Tremor B. Palpitations C. Sweating D. Anxiety ANSWER: C — Sweating. Why: sweating in hypoglycaemia is mediated by sympathetic CHOLINERGIC fibres, not adrenergic ones, so beta blockade does not suppress it. Tremor, palpitations and anxiety are all adrenergic and are masked. LEARNING POINT: "beta-blockers mask ALL warning signs" is the classic distractor. Sweating survives.

Q10. Which beta-blocker carries a distinctive risk of torsades de pointes? A. Atenolol B. Sotalol C. Bisoprolol D. Nebivolol ANSWER: B — Sotalol. Why: sotalol has additional class III (potassium channel blocking) activity, prolonging the QT interval. The others have no significant class III effect. LEARNING POINT: sotalol is the exception in almost every beta-blocker generalisation — treat it as its own case.

Q11. A patient with severe decompensated heart failure, cold peripheries and pulmonary oedema is on no cardiac drugs. Regarding beta-blockade, the correct action is: A. Start carvedilol immediately for mortality benefit B. Start high-dose metoprolol tartrate C. Stabilise first; introduce a beta-blocker only once euvolaemic and stable D. Beta-blockers are contraindicated in heart failure permanently ANSWER: C — stabilise first, introduce later. Why: in decompensation, output depends on sympathetic drive, and removing it acutely worsens the patient. Once stable and euvolaemic, a beta-blocker with mortality evidence is started low and titrated slowly. A, B: correct drug class, dangerously wrong timing. D: false — this is a cornerstone of chronic HFrEF therapy. LEARNING POINT: acute and chronic heart failure are different pharmacological situations. Timing is the whole answer.

Q12. Which is the agent of choice for hypertension in pregnancy among the following? A. Atenolol B. Labetalol C. Propranolol D. Sotalol ANSWER: B — Labetalol. Why: labetalol combines beta and alpha-1 blockade and has the best-established safety record in pregnancy of these options. A: atenolol has been associated with fetal growth restriction and is generally avoided. C, D: not the agents of choice; sotalol carries QT risk. LEARNING POINT: pregnancy is one of the comorbidities that overrides the usual selectivity reasoning.