Cardiovascular Drugs USMLE Step 1 Practice Question
A 65-year-old woman with heart failure and reduced ejection fraction (HFrEF, EF 35%) presents to clinic for follow-up. Current medications include lisinopril 10 mg daily, metoprolol succinate 47.5 mg daily, and furosemide 40 mg daily. Her symptoms have been stable on this regimen for 6 months. To further optimize her therapy, sacubitril/valsartan is initiated at a standard starting dose. Two days later, she reports a persistent dry cough and mild dyspnea on exertion. Vital signs: BP 108/62 mmHg, HR 78 bpm, RR 20/min, SpO2 98% on room air. Labs: K+ 5.4 mEq/L (previously 4.8), Cr 1.1 mg/dL (baseline 1.0). Physical exam shows no orthopnea, jugular venous pressure normal, and clear lung fields. Which of the following best explains her clinical deterioration?
Answer choices
- ASacubitril competitively inhibits neprilysin at the glomerulus, reducing urinary potassium excretion and causing hyperkalemia-induced cough reflex
- BValsartan's angiotensin II receptor blockade causes direct airway smooth muscle contraction, independent of ACE inhibitor effects
- CConcurrent use of lisinopril and sacubitril/valsartan results in excessive RAAS inhibition; the cough is attributable to lisinopril-induced accumulation of bradykinin and substance P in the respiratory tractCorrect answer
- DMetoprolol enhances the bioavailability of sacubitril, causing toxic accumulation and direct lung parenchymal inflammation
- EFurosemide-induced hypokalemia has been masked by initiation of dual RAAS inhibitors, and the cough is a compensatory response to intracellular potassium shifts
- FSacubitril/valsartan monotherapy causes direct mast cell degranulation in the airways, triggering a non-ACE inhibitor cough mechanism unrelated to baseline lisinopril use
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