Digoxin is a prototype cardiac glycoside used in the pharmacotherapy of congestive heart failure and rate control in atrial fibrillation. This introduction emphasizes digoxin’s mechanism (inhibition of Na+/K+-ATPase), positive inotropic and vagotonic effects, pharmacokinetics (oral bioavailability, renal elimination, long half‑life) and its narrow therapeutic index. B.Pharm students should master adverse effects, classic toxicity signs, ECG changes, important drug interactions (quinidine, amiodarone, verapamil, diuretics), monitoring (serum digoxin level, electrolytes, renal function), dosing principles, and antidotal therapy with digoxin immune Fab. Understanding these aspects is essential for safe dispensing and clinical decision‑making. Now let’s test your knowledge with 30 MCQs on this topic.
Q1. What is the primary molecular target of digoxin in cardiac myocytes?
- Voltage‑gated calcium channels
- Sodium channels in the sinoatrial node
- Inhibition of Na+/K+-ATPase in cardiac myocytes
- Beta‑1 adrenergic receptors
Correct Answer: Inhibition of Na+/K+-ATPase in cardiac myocytes
Q2. Which of the following best describes digoxin’s predominant pharmacodynamic effect?
- Negative inotropy and positive chronotropy
- Positive inotropy and increased vagal tone leading to decreased AV conduction
- Pure vasodilation with decreased preload
- Direct beta‑adrenergic agonism
Correct Answer: Positive inotropy and increased vagal tone leading to decreased AV conduction
Q3. A classic ECG change seen with therapeutic digoxin is:
- Prolonged QT interval
- Marked PR interval shortening
- Increased PR interval and “scooped” ST depression
- Delta waves and widened QRS
Correct Answer: Increased PR interval and “scooped” ST depression
Q4. The widely quoted therapeutic serum concentration range for digoxin in many references is approximately:
- 0.05–0.2 ng/mL
- 0.5–2.0 ng/mL
- 5–10 ng/mL
- 10–20 ng/mL
Correct Answer: 0.5–2.0 ng/mL
Q5. The primary route of elimination for digoxin is:
- Hepatic metabolism by CYP450 enzymes
- Biliary excretion after glucuronidation
- Renal excretion of unchanged drug
- Pulmonary elimination
Correct Answer: Renal excretion of unchanged drug
Q6. The purpose of digitalization (loading dose) when initiating digoxin therapy is to:
- Prevent gastrointestinal side effects
- Rapidly achieve therapeutic plasma concentrations
- Reduce renal clearance of the drug
- Eliminate the need for serum monitoring
Correct Answer: Rapidly achieve therapeutic plasma concentrations
Q7. Which clinical symptom is classically associated with digoxin toxicity?
- Hearing loss
- Yellow‑green visual halos
- Night sweats
- Profuse lacrimation
Correct Answer: Yellow‑green visual halos
Q8. In acute severe digoxin overdose, which electrolyte abnormality is commonly present and indicates a poor prognosis?
- Hypokalemia
- Hypernatremia
- Hyperkalemia
- Hypomagnesemia
Correct Answer: Hyperkalemia
Q9. Which antiarrhythmic drug is known to increase serum digoxin concentration by inhibiting P‑glycoprotein and reducing clearance?
- Lidocaine
- Amiodarone
- Propranolol
- Atropine
Correct Answer: Amiodarone
Q10. Concomitant use of which diuretic most increases the risk of digoxin toxicity by causing hypokalemia?
- Spironolactone
- Furosemide (loop diuretic)
- Amiloride
- Acetazolamide
Correct Answer: Furosemide (loop diuretic)
Q11. The specific antidote for life‑threatening digoxin toxicity is:
- Intravenous calcium gluconate
- High‑dose insulin with glucose
- Digoxin immune Fab (antibody fragments)
- Activated charcoal only
Correct Answer: Digoxin immune Fab (antibody fragments)
Q12. The elimination half‑life of digoxin in patients with normal renal function is approximately:
- 2–4 hours
- 12–16 hours
- 36–48 hours
- 7–10 days
Correct Answer: 36–48 hours
Q13. For which cardiac condition is digoxin most appropriately indicated?
- First‑line therapy for hypertrophic obstructive cardiomyopathy
- Symptomatic heart failure with reduced ejection fraction to improve symptoms and control rate in AF
- To acutely lower blood pressure in hypertensive crisis
- Primary prevention of myocardial infarction
Correct Answer: Symptomatic heart failure with reduced ejection fraction to improve symptoms and control rate in AF
Q14. Digoxin slows ventricular rate in atrial fibrillation primarily by:
- Direct blockade of atrial sodium channels
- Increasing sympathetic tone to the AV node
- Enhancing vagal (parasympathetic) tone and decreasing AV nodal conduction
- Increasing conduction through the accessory pathway
Correct Answer: Enhancing vagal (parasympathetic) tone and decreasing AV nodal conduction
Q15. Digoxin is contraindicated in which of the following arrhythmias?
- Atrial fibrillation with slow ventricular response
- Sinus bradycardia
- Ventricular fibrillation
- Supraventricular tachycardia due to AV nodal reentry
Correct Answer: Ventricular fibrillation
Q16. When is it most appropriate to measure a serum digoxin concentration for accurate interpretation?
- 30 minutes after an oral dose
- Immediately after intravenous bolus
- At least 6–8 hours after dosing or at steady state to allow distribution
- Only during symptomatic toxicity
Correct Answer: At least 6–8 hours after dosing or at steady state to allow distribution
Q17. How does inhibition of Na+/K+-ATPase by digoxin lead to increased cardiac contractility?
- Direct activation of ryanodine receptors
- Reduced Na+ gradient decreases Na+/Ca2+ exchange, increasing intracellular Ca2+
- Inhibition of L‑type calcium channels
- Stimulation of beta‑1 receptors to increase cAMP
Correct Answer: Reduced Na+ gradient decreases Na+/Ca2+ exchange, increasing intracellular Ca2+
Q18. Which effect of digoxin contributes to its ability to control ventricular rate in atrial fibrillation?
- Shortening of AV nodal refractory period
- Prolongation of AV nodal refractory period
- Increased conduction through the His‑Purkinje system
- Potent vasodilation of coronary arteries
Correct Answer: Prolongation of AV nodal refractory period
Q19. Chronic digoxin toxicity commonly presents with which symptom cluster?
- Polyuria, polydipsia, weight gain
- Nausea, vomiting, visual disturbances, and assorted arrhythmias
- Headache, hematuria, tinnitus
- Rash, arthralgia, eosinophilia
Correct Answer: Nausea, vomiting, visual disturbances, and assorted arrhythmias
Q20. Which macrolide antibiotic can increase digoxin levels by altering gut flora or P‑glycoprotein interactions?
- Azithromycin
- Erythromycin
- Penicillin V
- Ceftriaxone
Correct Answer: Erythromycin
Q21. What is the typical effect of digoxin on the QT interval?
- Marked prolongation of QT interval
- Shortening of QT interval
- No change in QT interval
- Alternating long and short QT intervals
Correct Answer: Shortening of QT interval
Q22. Which antiarrhythmic is well known to displace digoxin from tissue binding sites and increase serum levels?
- Quinidine
- Mexiletine
- Sotalol
- Dofetilide
Correct Answer: Quinidine
Q23. Which electrolyte imbalance most commonly predisposes a patient to digoxin toxicity?
- Hypernatremia
- Hypokalemia
- Hypercalcemia
- Hyponatremia
Correct Answer: Hypokalemia
Q24. In a patient with reduced renal function, digoxin dosing should be:
- Increased because of decreased tissue binding
- Unchanged since drug is hepatically cleared
- Reduced dose or longer dosing interval due to renal clearance
- Switched to continuous infusion without dose change
Correct Answer: Reduced dose or longer dosing interval due to renal clearance
Q25. Which route of administration provides 100% bioavailability of digoxin?
- Oral tablet
- Oral elixir
- Intravenous injection
- Transdermal patch
Correct Answer: Intravenous injection
Q26. The mechanism of action of digoxin immune Fab is:
- Enzymatic degradation of digoxin in plasma
- Antibody fragments bind free digoxin to form inactive complexes excreted renally
- Induction of hepatic enzymes to accelerate clearance
- Competitive antagonism at Na+/K+-ATPase
Correct Answer: Antibody fragments bind free digoxin to form inactive complexes excreted renally
Q27. A characteristic ST‑segment change described with digoxin is:
- Elevation with tombstone appearance
- Downsloping, “scooped” ST depression
- Marked ST flattening without depression
- ST segment elevation in leads V1–V3
Correct Answer: Downsloping, “scooped” ST depression
Q28. Which serum electrolytes should be monitored routinely in patients on chronic digoxin therapy?
- Sodium and chloride
- Potassium and magnesium
- Calcium and phosphate only
- Bicarbonate and lactate
Correct Answer: Potassium and magnesium
Q29. Regarding long‑term outcomes in heart failure, digoxin therapy is best described as:
- Consistently reducing all‑cause mortality
- Increasing mortality in most trials
- Reducing hospitalizations but not significantly lowering overall mortality
- Causing complete reversal of ventricular remodeling
Correct Answer: Reducing hospitalizations but not significantly lowering overall mortality
Q30. Digoxin should be avoided or used with extreme caution in which clinical situation?
- Atrial fibrillation with rapid ventricular response without accessory pathway
- Atrial fibrillation associated with Wolff‑Parkinson‑White syndrome
- Chronic stable angina with normal AV conduction
- Asymptomatic sinus bradycardia
Correct Answer: Atrial fibrillation associated with Wolff‑Parkinson‑White syndrome
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.
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