A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 58-year-old African-American man with a history of congestive heart failure presents to the emergency room with headache, frequent vomiting, diarrhea, anorexia, and heart palpitations. He is taking a drug that binds the sodium-potassium pump in myocytes. EKG reveals ventricular dysrhythmia. Which of the following is likely also present in the patient?
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A
BronchoconstrictionIncorrect. Bronchoconstriction is associated with beta-blockers or muscarinic agonists — not digoxin.
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B
Changes in color visionCorrect. xanthopsia (yellow-green vision) and altered color perception are classic findings of digoxin toxicity.
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C
Decreased PR intervalIncorrect. Digoxin actually prolongs the PR interval (it slows AV nodal conduction via increased vagal tone) — it does not shorten it.
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D
CoughIncorrect. Dry cough is the classic adverse effect of ACE inhibitors (bradykinin accumulation) — not digoxin.
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E
HyperkalemiaIncorrect. Hyperkalemia is a feature of digoxin toxicity in acute overdose (Na/K-ATPase inhibition raises extracellular K), but the classic visual disturbance (xanthopsia) is the more specific and commonly tested toxicity finding here.
↑ Tap an answer to reveal the reasoning
Answer: B. A patient with heart failure taking a drug that binds the Na+/K+ ATPase and developing GI symptoms (nausea, vomiting, diarrhea, anorexia), neurologic symptoms (headache), arrhythmias, and changes in color vision is showing classic digoxin (digitalis) toxicity. Digoxin inhibits Na+/K+ ATPase in cardiac myocytes, increasing intracellular Na+, which reduces Na+/Ca2+ exchanger activity, raising intracellular Ca2+ and enhancing contractility.
Digoxin toxicity is a high-yield exam topic for its unique visual symptoms: yellow-green halos around lights, blurred vision, scotomas, and altered color perception ("xanthopsia"). These reflect digoxin's effect on Na+/K+ ATPase in photoreceptors and the visual cortex.
Other classic findings: GI upset, fatigue, AV nodal block, atrial tachycardia with AV block, and ventricular dysrhythmias. Risk factors include hypokalemia (potentiates toxicity because K+ and digoxin compete at the pump), renal failure (digoxin is renally cleared), and old age. Treatment of severe toxicity: digoxin-specific antibody fragments (Digibind/DigiFab).
**Why each option:**
**A.** Bronchoconstriction is associated with beta-blockers or muscarinic agonists — not digoxin.
**B.** Correct: xanthopsia (yellow-green vision) and altered color perception are classic findings of digoxin toxicity.
**C.** Digoxin actually prolongs the PR interval (it slows AV nodal conduction via increased vagal tone) — it does not shorten it.
**D.** Dry cough is the classic adverse effect of ACE inhibitors (bradykinin accumulation) — not digoxin.