Lipid Biochemistry USMLE Step 1 Practice Question
A 50-year-old woman on bile acid sequestrant therapy for hypercholesterolemia presents with fatigue and dyspnea. Vital signs: BP 142/88 mmHg, HR 92/min, RR 18/min, temp 37°C, SpO2 98% on room air. Labs reveal LDL cholesterol 400 mg/dL, triglycerides 380 mg/dL, and homozygous APOE2/E2 genotype. Liver function tests are normal. Which mechanism best explains her paradoxical lipid profile deterioration despite sequestrant therapy?
Answer choices
- AAPOE2 increases apolipoprotein C-III expression, reducing lipoprotein lipase activity
- BIncreased hepatic cholesterol synthesis with impaired LDL receptor expression due to APOE2 isoformCorrect answer
- CBile acid sequestrants increase VLDL secretion from enterocytes
- DAPOE2 prevents hepatic cholesterol uptake independent of the LDL receptor
- EBile acid sequestrants directly inhibit HMG-CoA reductase
- FBile acid sequestrants competitively inhibit APOE-mediated cholesterol uptake in hepatocytes, causing compensatory upregulation of de novo cholesterol synthesis
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