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.
Read the first 7 Diagnosis & Classification of Dyslipidemia flashcards as text
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.
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.
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.
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.
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.
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.
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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