Cardiovascular Drugs USMLE Step 1 Practice Question
A 68-year-old woman with heart failure with reduced ejection fraction and stage 3 chronic kidney disease presents with a 2-day history of nausea, vomiting, and yellow-green visual disturbances. She has been taking digoxin 0.25 mg daily for 8 months. Vital signs: temperature 37.1°C, blood pressure 108/72 mmHg, heart rate 42 bpm with regular rhythm. Laboratory results: serum creatinine 2.1 mg/dL, potassium 3.2 mEq/L, serum digoxin level 3.2 ng/mL (therapeutic range 0.5–2.0 ng/mL). ECG shows sinus bradycardia without atrioventricular block. Which of the following best explains the mechanism by which digoxin toxicity is producing this patient's bradycardia?
Answer choices
- ACompetitive inhibition of beta-1 adrenergic receptors on nodal tissue, reducing cAMP-dependent pacemaker activity
- BIncreased intracellular calcium in sinoatrial node cells, which directly hyperpolarizes the membrane potential
- CInhibition of the Na+/K+-ATPase pump, leading to increased vagal acetylcholine sensitivity and enhanced parasympathetic effects at the sinoatrial nodeCorrect answer
- DDirect blockade of L-type calcium channels in pacemaker cells of the sinoatrial node, decreasing spontaneous depolarization
- EInhibition of adenosine deaminase, increasing extracellular adenosine which activates inhibitory A1 receptors on nodal tissue
- FIncreased intracellular potassium concentration causing membrane hyperpolarization and reduced automaticity in pacemaker cells
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