Calcium channel blockers – Verapamil MCQs With Answer

Calcium channel blockers – Verapamil MCQs With Answer
Verapamil is a phenylalkylamine calcium channel blocker widely taught in B.Pharm pharmacology for its distinctive cardiovascular effects. This concise review covers verapamil’s mechanism (L‑type calcium channel blockade), pharmacokinetics (extensive hepatic metabolism, CYP3A4, high protein binding, low oral bioavailability), therapeutic uses (supraventricular tachycardia, angina, hypertension, hypertrophic cardiomyopathy), major adverse effects (bradycardia, AV block, constipation, negative inotropy), clinically important interactions (digoxin, beta‑blockers, CYP3A4 inhibitors, grapefruit juice), dosing forms (IV and oral immediate/extended‑release), and overdose management. This summary emphasizes mechanism of action, indications, adverse effects, drug interactions, therapeutic monitoring, dosing adjustments in hepatic impairment, and clinical pharmacology essentials prioritized for B.Pharm students. Now let’s test your knowledge with 30 MCQs on this topic.

Q1. Which pharmacological class does verapamil belong to?

• Dihydropyridine calcium channel blocker
• Phenylalkylamine calcium channel blocker
• Benzothiazepine calcium channel blocker
• Cardioselective beta blocker

Correct Answer: Phenylalkylamine calcium channel blocker

Q2. What is the primary mechanism of action of verapamil?

• Blockade of N‑type calcium channels in neurons
• Blockade of L‑type calcium channels in cardiac and smooth muscle
• Activation of beta‑adrenergic receptors
• Inhibition of ACE enzyme

Correct Answer: Blockade of L‑type calcium channels in cardiac and smooth muscle

Q3. Compared with dihydropyridine CCBs, verapamil has a greater effect on:

• Peripheral arterial vasodilation causing reflex tachycardia
• Renal vasodilation and natriuresis
• Cardiac contractility and AV nodal conduction
• Platelet aggregation inhibition

Correct Answer: Cardiac contractility and AV nodal conduction

Q4. Which of the following is a primary clinical indication for verapamil?

• Paroxysmal supraventricular tachycardia (PSVT)
• Acute deep vein thrombosis
• Type 1 diabetes mellitus
• Asthma exacerbation

Correct Answer: Paroxysmal supraventricular tachycardia (PSVT)

Q5. Which adverse effect is classically associated with verapamil?

• Constipation
• Hyperglycemia
• Ototoxicity
• Thrombocytopenia

Correct Answer: Constipation

Q6. Verapamil interacts with digoxin primarily by:

• Decreasing digoxin absorption from the gut
• Inducing renal clearance of digoxin
• Increasing digoxin plasma levels via P‑glycoprotein inhibition
• Directly displacing digoxin from myocardial receptors

Correct Answer: Increasing digoxin plasma levels via P‑glycoprotein inhibition

Q7. The effect of verapamil on AV nodal conduction is to:

• Speed AV nodal conduction and shorten PR interval
• No effect on AV nodal conduction
• Slow AV nodal conduction and prolong PR interval
• Cause bundle branch block without PR change

Correct Answer: Slow AV nodal conduction and prolong PR interval

Q8. Typical oral bioavailability of verapamil is best described as:

• High (around 80–90%)
• Moderate (around 50–70%)
• Low (about 20–35% due to first‑pass metabolism)
• Negligible (less than 5%)

Correct Answer: Low (about 20–35% due to first‑pass metabolism)

Q9. Which hepatic enzyme is primarily responsible for verapamil metabolism?

• CYP2D6
• CYP1A2
• CYP3A4
• Monoamine oxidase

Correct Answer: CYP3A4

Q10. Co‑administration of verapamil with a beta‑blocker increases the risk of:

• Hypokalemia with muscle cramps
• Severe bradycardia and high‑degree AV block
• Rebound hypertension on withdrawal
• Renal stone formation

Correct Answer: Severe bradycardia and high‑degree AV block

Q11. Which clinical property differentiates verapamil from nifedipine (a dihydropyridine)?

• Verapamil causes more reflex tachycardia than nifedipine
• Verapamil has stronger negative inotropic and AV nodal suppressive effects
• Verapamil is primarily an arteriolar vasodilator with minimal cardiac effects
• Verapamil is a potassium channel opener

Correct Answer: Verapamil has stronger negative inotropic and AV nodal suppressive effects

Q12. In verapamil overdose, an appropriate first‑line emergency treatment is:

• Intravenous calcium (e.g., calcium gluconate)
• Activated charcoal only
• Naloxone administration
• Immediate hemodialysis as sole therapy

Correct Answer: Intravenous calcium (e.g., calcium gluconate)

Q13. The major hemodynamic effect of verapamil that reduces myocardial oxygen demand is:

• Marked systemic vasoconstriction raising afterload
• Decrease in heart rate and contractility reducing cardiac output
• Increase in preload via venoconstriction
• Selective increase in left ventricular ejection fraction

Correct Answer: Decrease in heart rate and contractility reducing cardiac output

Q14. For acute termination of PSVT in the hospital, verapamil is commonly administered by which route?

• Intravenous bolus
• Topical patch
• Intramuscular injection
• Inhalation

Correct Answer: Intravenous bolus

Q15. Verapamil is approximately what degree of plasma protein bound?

• Less than 10%
• About 30–40%
• Approximately 90% or greater
• Not protein bound

Correct Answer: Approximately 90% or greater

Q16. The typical elimination half‑life of immediate‑release verapamil is closest to:

• 1–2 hours
• 3–7 hours
• 12–24 hours
• 48–72 hours

Correct Answer: 3–7 hours

Q17. Verapamil relieves angina primarily by which mechanism?

• Increasing myocardial oxygen demand
• Decreasing myocardial oxygen demand via reduced heart rate and contractility
• Blocking thromboxane A2 synthesis
• Directly dissolving coronary plaques

Correct Answer: Decreasing myocardial oxygen demand via reduced heart rate and contractility

Q18. On ECG, verapamil most commonly causes which change?

• Shortened QT interval
• Prolonged PR interval
• ST‑segment elevation in V1–V3
• U‑wave prominence

Correct Answer: Prolonged PR interval

Q19. Verapamil is generally contraindicated in which cardiac condition?

• Asymptomatic bradycardia with normal AV conduction
• Decompensated systolic heart failure with low ejection fraction
• Mild, well‑controlled hypertension
• Stable angina with normal LV function

Correct Answer: Decompensated systolic heart failure with low ejection fraction

Q20. Grapefruit juice increases verapamil plasma concentrations by:

• Inducing renal transporters that excrete verapamil
• Inhibiting intestinal and hepatic CYP3A4, reducing first‑pass metabolism
• Increasing gastric pH and enhancing absorption
• Binding verapamil in the gut to form insoluble complexes

Correct Answer: Inhibiting intestinal and hepatic CYP3A4, reducing first‑pass metabolism

Q21. Verapamil affects which membrane transporter contributing to drug interactions?

• Organic anion transporting polypeptide (OATP)
• P‑glycoprotein (P‑gp)
• Monoamine transporter (SERT)
• Glucose transporter GLUT4

Correct Answer: P‑glycoprotein (P‑gp)

Q22. The major active metabolite of verapamil is:

• Nifedipine
• Norverapamil
• Dehydro‑felodipine
• Verapamil glucuronide (inactive)

Correct Answer: Norverapamil

Q23. Verapamil is contraindicated in atrial fibrillation when coexisting with:

• Left bundle branch block only
• Wolf‑Parkinson‑White (WPW) syndrome with accessory pathway conduction
• Mild mitral valve prolapse
• Controlled hypothyroidism

Correct Answer: Wolf‑Parkinson‑White (WPW) syndrome with accessory pathway conduction

Q24. Which oral adverse effect can occur with long‑term verapamil therapy?

• Gingival hyperplasia
• Severe xerostomia leading to ulcers
• Oral fungal infection as primary effect
• Loss of taste (ageusia)

Correct Answer: Gingival hyperplasia

Q25. Constipation from verapamil is due to:

• Anticholinergic blockade in enteric neurons
• Inhibition of smooth muscle calcium channels in the gastrointestinal tract reducing motility
• Direct opioid receptor activation in the gut
• Malabsorption from pancreatic exocrine suppression

Correct Answer: Inhibition of smooth muscle calcium channels in the gastrointestinal tract reducing motility

Q26. How should verapamil dosing be approached in significant hepatic impairment?

• No dose adjustment is required
• Increase dose due to reduced protein binding
• Reduce dose or extend dosing interval because of impaired metabolism
• Switch to verapamil IV bolus daily

Correct Answer: Reduce dose or extend dosing interval because of impaired metabolism

Q27. An advantage of extended‑release verapamil formulations is:

• Higher peak‑to‑trough variability compared with immediate release
• Less frequent dosing with reduced peak side effects and more stable plasma levels
• Complete avoidance of first‑pass metabolism
• Immediate termination of PSVT when taken orally once

Correct Answer: Less frequent dosing with reduced peak side effects and more stable plasma levels

Q28. Verapamil is considered first‑line therapy for pulmonary arterial hypertension (PAH):

• True — it is standard therapy for PAH
• False — it is not a primary treatment for PAH
• True — but only in combination with bosentan
• False — it worsens systemic hypertension only

Correct Answer: False — it is not a primary treatment for PAH

Q29. Verapamil may be beneficial in hypertrophic obstructive cardiomyopathy because it:

• Increases contractility to overcome obstruction
• Decreases contractility and heart rate, reducing outflow gradient
• Acts as a vasopressor to raise blood pressure
• Directly reduces myocardial fibrosis within hours

Correct Answer: Decreases contractility and heart rate, reducing outflow gradient

Q30. Which monitoring is most important when initiating verapamil therapy?

• Serial measurements of serum verapamil concentration
• ECG monitoring for PR prolongation and blood pressure monitoring for hypotension
• Daily 24‑hour urine collection for verapamil metabolites
• No monitoring is required for cardiac or hemodynamic effects

Correct Answer: ECG monitoring for PR prolongation and blood pressure monitoring for hypotension

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

Mail- Sachin@pharmacyfreak.com