Cardiovascular Drugs USMLE Step 1 Practice Question
A 41-year-old man with hyperlipidemia and hypertension presents to the emergency department with severe diffuse myalgias, dark urine, and tea-colored urine for 3 days. He started atorvastatin 80 mg daily 8 weeks ago. Two weeks ago, he was prescribed clarithromycin for community-acquired pneumonia. Vital signs are stable. Physical examination reveals diffuse muscle tenderness. Laboratory studies show: creatine kinase 7,200 U/L (normal <200), myoglobin 380 ng/mL (normal <110), serum creatinine 1.8 mg/dL (baseline 1.0), urinalysis with brown granular casts and dipstick positive for blood without RBCs on microscopy. Which of the following best explains the mechanism of this patient's current clinical presentation?
Answer choices
- AClarithromycin inhibits CYP3A4, reducing atorvastatin metabolism and increasing intramuscular statin accumulationCorrect answer
- BAtorvastatin directly inhibits myofibrillar ATPase, causing dose-dependent myotoxicity independent of drug interactions
- CClarithromycin competitively binds to HMG-CoA reductase, potentiating statin effects on muscle cholesterol depletion
- DClarithromycin induces CYP2D6, accelerating atorvastatin metabolism and promoting formation of toxic metabolites
- ECombined atorvastatin and clarithromycin therapy causes myositis through direct immune-mediated muscle inflammation unrelated to drug metabolism
- FAtorvastatin causes acute kidney injury, which then leads to reduced clarithromycin excretion and systemic toxicity affecting muscles
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