Lipid Panel Interpretation 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 Lipid Panel Interpretation flashcards as text
A patient on a high-intensity statin has a follow-up LDL-C of 58 mg/dL (down from 142 mg/dL at baseline). How should this response be interpreted?
Answer: Adequate response; high-intensity statin should achieve ≥50% LDL-C reduction
High-intensity statin therapy is expected to lower LDL-C by ≥50%; this patient achieved a 59% reduction, which is a satisfactory pharmacologic response.
Which secondary cause of dyslipidemia classically produces elevated triglycerides and decreased HDL-C (type IV pattern)?
Answer: Poorly controlled type 2 diabetes mellitus
Poorly controlled type 2 diabetes causes insulin resistance that increases VLDL production and reduces lipoprotein lipase activity, leading to elevated TG, low HDL-C, and small dense LDL—a classic type IV pattern.
What does a coronary artery calcium (CAC) score of zero add to lipid panel interpretation for an intermediate-risk patient?
Answer: Identifies a low-risk group that may safely defer statin therapy and intensify lifestyle modification
A CAC score of zero in an intermediate-risk patient indicates very low near-term ASCVD event risk and supports deferral of statin therapy with aggressive lifestyle modification and reassessment.
A 45-year-old man has LDL-C 195 mg/dL, normal TG, normal HDL-C, no secondary causes, and a family history of premature ASCVD. According to the Dutch Lipid Clinic Network criteria, what diagnosis is most likely?
Answer: Heterozygous familial hypercholesterolemia
The combination of LDL-C ≥190 mg/dL, absence of secondary causes, and family history of premature ASCVD meets diagnostic criteria for heterozygous familial hypercholesterolemia using the Dutch Lipid Clinic Network scoring system.
After initiating fenofibrate therapy, which lipid panel change would you most expect at 3 months?
Answer: 20–50% reduction in TG and 10–20% increase in HDL-C
Fibrates primarily activate PPARα, increasing lipoprotein lipase activity and reducing VLDL synthesis, resulting in 20–50% TG reduction and 10–20% HDL-C increase with modest and variable effects on LDL-C.
A postmenopausal woman starts oral estrogen-based hormone therapy. Which lipid panel change is most expected?
Answer: LDL-C decreases and TG increases
Oral estrogen decreases LDL-C by upregulating hepatic LDL receptors but increases triglycerides by stimulating hepatic VLDL synthesis, a pattern that can exacerbate pre-existing hypertriglyceridemia.
In interpreting a lipid panel for cardiovascular risk, which metric has been shown to be the best predictor of ASCVD events when LDL-C and apoB are discordant?
Answer: Apolipoprotein B
When LDL-C and apoB are discordant, apoB is the superior predictor of ASCVD events because it directly quantifies the total burden of atherogenic lipoprotein particles rather than their cholesterol content.
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