Cardiovascular pharmacology: anti-ischemic and antiarrhythmic drugs MCQs With Answer

Introduction

This blog provides targeted multiple-choice questions on cardiovascular pharmacology, focusing on anti-ischemic and antiarrhythmic drugs tailored for M.Pharm students. The set emphasizes mechanisms of action, pharmacokinetics, clinical indications, adverse effects, drug interactions and monitoring requirements commonly tested at an advanced level. Each MCQ aims to deepen conceptual understanding rather than rote memorization, connecting electrophysiology and hemodynamic principles to pharmacologic effects. Explanatory focus includes nitrate tolerance, beta-blocker selectivity, CCB subclasses, Vaughan–Williams classification nuances, proarrhythmia risks (QT prolongation/torsades), and management of drug-specific toxicities. Use these MCQs to self-assess and refine clinical pharmacology reasoning for examinations and postgraduate practice.

Q1. Which of the following best describes the primary mechanism by which organic nitrates relieve exertional angina?

• Direct myocardial calcium channel blockade to reduce contractility
• Selective coronary artery dilation increasing coronary perfusion pressure
• Biotransformation to nitric oxide which increases cGMP causing venodilation and decreased preload
• Inhibition of late sodium current reducing diastolic wall tension

Correct Answer: Biotransformation to nitric oxide which increases cGMP causing venodilation and decreased preload

Q2. The most accepted mechanism for development of tolerance to organic nitrates during continuous therapy is:

• Upregulation of soluble guanylate cyclase
• Depletion of vascular thiol (sulfhydryl) groups and oxidative inactivation of biotransformation pathways
• Increased hepatic clearance due to enzyme induction
• Enhanced sympathetic activity exclusively

Correct Answer: Depletion of vascular thiol (sulfhydryl) groups and oxidative inactivation of biotransformation pathways

Q3. Why is coadministration of phosphodiesterase‑5 (PDE5) inhibitors with nitrates contraindicated?

• Increased risk of coronary vasospasm
• Severe hypotension because both increase cGMP leading to excessive vasodilation
• Enhanced platelet aggregation and thrombosis
• Mutual inhibition of hepatic metabolism causing toxicity

Correct Answer: Severe hypotension because both increase cGMP leading to excessive vasodilation

Q4. Ivabradine reduces anginal symptoms primarily by which electrophysiologic action?

• Blocking L‑type calcium channels in ventricular myocytes
• Inhibiting the funny current (If) in the sinoatrial node to reduce heart rate without altering contractility
• Increasing vagal tone by muscarinic receptor agonism
• Blocking beta‑1 receptors to decrease heart rate and contractility

Correct Answer: Inhibiting the funny current (If) in the sinoatrial node to reduce heart rate without altering contractility

Q5. Ranolazine relieves ischemia mainly through which cellular mechanism?

• Inhibition of HMG‑CoA reductase reducing cholesterol synthesis
• Late sodium current (INaL) inhibition reducing intracellular sodium and calcium overload
• Direct arterial vasodilation via NO release
• Beta‑2 receptor agonism improving coronary flow

Correct Answer: Late sodium current (INaL) inhibition reducing intracellular sodium and calcium overload

Q6. Beta‑blockers decrease myocardial oxygen demand predominantly by which of the following effects?

• Increasing preload through venoconstriction
• Decreasing heart rate and myocardial contractility via antagonism of beta‑1 receptors
• Selective dilation of coronary microvessels
• Blocking fast sodium channels in ventricles

Correct Answer: Decreasing heart rate and myocardial contractility via antagonism of beta‑1 receptors

Q7. Which antianginal drug primarily slows AV nodal conduction and can increase PR interval, making it useful for rate control in supraventricular tachycardia?

• Amlodipine
• Verapamil
• Nitroglycerin
• Ranolazine

Correct Answer: Verapamil

Q8. In the Vaughan–Williams classification, which subclass of Class I antiarrhythmics produces the most marked slowing of conduction velocity with minimal change in action potential duration?

• Class Ia (e.g., procainamide)
• Class Ib (e.g., lidocaine)
• Class Ic (e.g., flecainide, propafenone)
• Class II (beta‑blockers)

Correct Answer: Class Ic (e.g., flecainide, propafenone)

Q9. Which property best characterizes lidocaine as an antiarrhythmic agent?

• Oral class Ic drug with prolonged half‑life used for supraventricular tachycardia
• IV class Ib agent with rapid kinetics preferentially acting on ischemic ventricular tissue to shorten action potential duration
• Class III oral agent that prolongs QT interval
• Nonselective beta blocker used for atrial fibrillation rate control

Correct Answer: IV class Ib agent with rapid kinetics preferentially acting on ischemic ventricular tissue to shorten action potential duration

Q10. Which statement about amiodarone is most accurate?

• It is a pure class III agent with no effects on other channels or receptors
• It has multiple channel and receptor effects (class I–IV), a long half‑life, and requires thyroid and liver monitoring
• It is rapidly eliminated and safe in pregnancy without monitoring
• It commonly causes nephrotoxicity as its principal toxicity

Correct Answer: It has multiple channel and receptor effects (class I–IV), a long half‑life, and requires thyroid and liver monitoring

Q11. Which antiarrhythmic drug combines beta‑blocking activity with potassium channel blockade and is associated with QT prolongation and torsades de pointes?

• Propranolol
• Sotalol
• Mexiletine
• Verapamil

Correct Answer: Sotalol

Q12. Which antiarrhythmic is well known to cause a reversible lupus‑like syndrome with positive anti‑histone antibodies when used chronically?

• Procainamide
• Flecainide
• Amiodarone
• Digoxin

Correct Answer: Procainamide

Q13. Which adverse effect is classically associated with quinidine therapy?

• Cinchonism (tinnitus, headache, visual disturbances)
• Renal tubular acidosis
• Hyperthyroidism
• Pulmonary fibrosis

Correct Answer: Cinchonism (tinnitus, headache, visual disturbances)

Q14. The recommended specific antidote for severe life‑threatening digoxin toxicity is:

• Intravenous calcium gluconate
• Activated charcoal
• Digoxin‑specific Fab antibody fragments
• Intravenous potassium chloride

Correct Answer: Digoxin‑specific Fab antibody fragments

Q15. Adenosine terminates certain paroxysmal supraventricular tachycardias primarily by which mechanism?

• Beta‑1 receptor antagonism slowing AV nodal conduction
• Activation of A1 receptors causing transient AV nodal hyperpolarization via increased K+ efflux and reduced cAMP
• Direct blockade of fast sodium channels in ventricles
• Inhibition of L‑type calcium channels in ventricular myocardium

Correct Answer: Activation of A1 receptors causing transient AV nodal hyperpolarization via increased K+ efflux and reduced cAMP

Q16. Which antiarrhythmic is most characteristically associated with pulmonary fibrosis and both hypo‑ and hyperthyroidism due to its iodine content?

• Flecainide
• Amiodarone
• Mexiletine
• Procainamide

Correct Answer: Amiodarone

Q17. Class III antiarrhythmic drugs exert their primary antiarrhythmic effect by:

• Blocking fast sodium channels to reduce conduction velocity
• Antagonizing beta receptors to reduce automaticity
• Blocking potassium channels to prolong repolarization and increase effective refractory period
• Enhancing acetylcholine release to slow AV nodal conduction

Correct Answer: Blocking potassium channels to prolong repolarization and increase effective refractory period

Q18. The pharmacologic concept of ‘use‑dependence’ with sodium channel blockers means which of the following?

• Drug effect is greater at slower heart rates
• Drug effect is independent of heart rate
• Drug produces increased sodium channel blockade at higher heart rates because it preferentially binds open or inactivated channels
• Drug only works in resting tissue and not during tachycardia

Correct Answer: Drug produces increased sodium channel blockade at higher heart rates because it preferentially binds open or inactivated channels

Q19. Which antiarrhythmic is generally preferred when treating serious ventricular arrhythmias in patients with significant structural heart disease or left ventricular dysfunction?

• Flecainide
• Amiodarone
• Propafenone
• Disopyramide

Correct Answer: Amiodarone

Q20. Intravenous magnesium sulfate is the treatment of choice for torsades de pointes because it:

• Directly antagonizes sodium channels to shorten QRS
• Blocks beta receptors reducing ectopy
• Stabilizes myocardial membranes, suppresses early afterdepolarizations and terminates polymorphic ventricular tachycardia
• Is a potassium channel opener that shortens QT interval

Correct Answer: Stabilizes myocardial membranes, suppresses early afterdepolarizations and terminates polymorphic ventricular tachycardia

Download