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Lipid Metabolism & Physiology Flashcards

7 cards from real CLS practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.

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  1. Which lipoprotein is the major carrier of triglycerides in the fasting state?

    Answer: VLDL

    In the fasting state, VLDL produced by the liver is the predominant triglyceride-carrying lipoprotein, as intestinal chylomicron production ceases after an overnight fast.

  2. ApoC-III inhibits lipid clearance by which mechanisms?

    Answer: Inhibiting LPL activity and blocking hepatic remnant receptor uptake

    ApoC-III inhibits lipoprotein lipase activity and interferes with receptor-mediated hepatic uptake of triglyceride-rich lipoprotein remnants, raising triglyceride levels; its reduction is a therapeutic target.

  3. Niemann-Pick C1-Like 1 (NPC1L1) protein is the target of which lipid-lowering medication?

    Answer: Ezetimibe

    Ezetimibe inhibits NPC1L1, the intestinal transporter responsible for absorbing dietary and biliary cholesterol, reducing cholesterol delivery to the liver and lowering LDL-C by 15-20%.

  4. In the context of metabolic syndrome, which pattern of lipoprotein abnormality is most characteristic?

    Answer: Low HDL-C, elevated triglycerides, and small dense LDL particles

    Metabolic syndrome is associated with an atherogenic dyslipidemia triad: elevated triglycerides, low HDL-C, and increased small dense LDL particles, driven by insulin resistance and excess hepatic VLDL production.

  5. What is the primary mechanism by which niacin (nicotinic acid) raises HDL-C levels?

    Answer: Inhibiting hepatic ApoA-I catabolism and reducing CETP activity

    Niacin raises HDL-C primarily by inhibiting hepatic uptake and catabolism of ApoA-I, slowing HDL turnover; it also reduces hepatic VLDL secretion, which decreases CETP-mediated cholesteryl ester transfer from HDL.

  6. Which enzyme converts arachidonic acid to thromboxane A2, which promotes platelet aggregation?

    Answer: Cyclooxygenase (COX)

    Cyclooxygenase (COX-1 and COX-2) converts arachidonic acid to prostaglandin H2, which is then converted to thromboxane A2 by thromboxane synthase in platelets, promoting platelet aggregation and vasoconstriction.

  7. Familial combined hyperlipidemia (FCHL) is characterized by overproduction of which apolipoprotein?

    Answer: ApoB-100

    FCHL is caused by hepatic overproduction of ApoB-100-containing VLDL particles, leading to variable phenotypes of elevated LDL-C, elevated triglycerides, or both, often within the same family.

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