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Diagnosis & Classification of Dyslipidemia 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. A patient has triglycerides of 950 mg/dL. According to the Endocrine Society classification, this level is best described as:

    Answer: Severe hypertriglyceridemia

    Triglycerides ≥500 mg/dL are classified as very high (severe hypertriglyceridemia), which carries risk of pancreatitis.

  2. Which lipoprotein pattern is characterized by elevated VLDL and chylomicrons, causing a creamy supernatant and turbid infranatant on refrigerated plasma?

    Answer: Fredrickson Type V

    Fredrickson Type V involves elevations of both VLDL and chylomicrons, producing the classic creamy top layer and turbid bottom on standing plasma.

  3. A patient on a standard fasting lipid panel shows total cholesterol 240 mg/dL, triglycerides 130 mg/dL, HDL 45 mg/dL. The Friedewald-estimated LDL-C would be approximately:

    Answer: 169 mg/dL

    Friedewald formula: LDL = TC − HDL − (TG/5) = 240 − 45 − 26 = 169 mg/dL.

  4. Which of the following conditions most commonly causes secondary hypercholesterolemia?

    Answer: Hypothyroidism

    Hypothyroidism decreases LDL receptor activity and lipoprotein lipase activity, leading to elevated LDL-C and sometimes TG.

  5. In the classification of dyslipidemias, 'dysbetalipoproteinemia' is synonymous with which Fredrickson phenotype?

    Answer: Type III

    Type III hyperlipoproteinemia (dysbetalipoproteinemia) is characterized by accumulation of IDL/remnant particles and is associated with apoE2/E2 homozygosity.

  6. A non-HDL cholesterol level of 190 mg/dL in a patient with TG of 300 mg/dL would classify as:

    Answer: High

    Non-HDL-C of 160–189 mg/dL is borderline high; ≥190 mg/dL is classified as high per ATP III/ACC-AHA thresholds.

  7. Which genetic mutation is the most frequent cause of familial hypercholesterolemia in the general population?

    Answer: LDLR mutations

    Mutations in the LDL receptor gene (LDLR) account for approximately 85–90% of molecularly confirmed familial hypercholesterolemia cases.

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