Lipid Biochemistry USMLE Step 1 Practice Question
A 28-year-old man presents with recurrent pancreatitis and is found to have fasting triglycerides of 800 mg/dL and total cholesterol of 350 mg/dL. Vital signs show BP 128/82 mmHg, HR 88 bpm, RR 16, and temperature 37°C. Genetic testing reveals an apoC-II gene mutation. Despite 12-hour fasting, triglyceride levels remain markedly elevated. Lipid electrophoresis shows increased chylomicrons. Which mechanism best explains his persistent hypertriglyceridemia?
Answer choices
- AApoC-II mutations prevent cholesterol esterification
- BApoC-II inhibits hepatic triglyceride synthesis
- CApoC-II is required for VLDL assembly in the liver
- DApoC-II is a required cofactor for lipoprotein lipase activityCorrect answer
- EApoC-II deficiency increases apoB-100 production
- FApoC-II mutations impair the uptake of chylomicron remnants by hepatic LDL receptors
See the full explanation
Get the correct-answer rationale, why each distractor is wrong, the underlying mechanism, and high-yield associations — plus adaptive practice that targets your weak areas — with a free MedBoardPRO account.