Secondary Causes of Dyslipidemia Flashcards

A clinician suspects secondary dyslipidemia in a patient with new-onset elevated TG and LDL-C. Which initial laboratory workup is MOST appropriate?

Answer: TSH, fasting glucose/HbA1c, urinalysis with spot urine protein/creatinine ratio, and LFTs

A systematic workup for secondary causes includes thyroid function, diabetes screening, renal function with proteinuria assessment, and liver function tests.

Growth hormone deficiency in adults is associated with which lipid pattern?

Answer: Elevated LDL-C, elevated triglycerides, and low HDL-C

Adult GH deficiency promotes visceral adiposity and insulin resistance, causing a pro-atherogenic lipid profile with elevated LDL-C, elevated TG, and low HDL-C.

Which antiretroviral drug class is associated with LEAST metabolic disturbance in HIV patients?

Answer: Integrase strand transfer inhibitors

Integrase inhibitors (e.g., dolutegravir, raltegravir) have minimal direct effect on lipid metabolism, though they may still promote weight gain.

A patient with psoriasis on systemic retinoid therapy (acitretin) has TG of 420 mg/dL. The BEST initial management step is:

Answer: Assess cardiovascular risk, counsel on alcohol/diet, and consider fibrate if TG remains elevated

Retinoid-induced hypertriglyceridemia warrants dietary counseling (reduce alcohol, simple carbs, fat) and, if TG remains high, fibrate therapy while collaborating with the prescribing provider.

Which lipid abnormality pattern is characteristic of hypothyroidism-induced dyslipidemia as opposed to primary hypercholesterolemia?

Answer: Hypothyroidism more often also elevates triglycerides and CK, with TSH providing the diagnostic clue

Hypothyroidism may elevate both LDL-C and TG, and is accompanied by elevated CK and TSH, distinguishing it from primary hypercholesterolemia.

Tamoxifen, used in breast cancer treatment, can cause which lipid effect?

Answer: Severe hypertriglyceridemia, particularly in women with pre-existing hypertriglyceridemia

Tamoxifen's estrogenic activity in the liver stimulates VLDL production, and in susceptible women (baseline elevated TG), it can precipitate severe hypertriglyceridemia.

In a patient with chronic inflammatory disease (e.g., rheumatoid arthritis) who starts effective anti-inflammatory therapy, which lipid change is PARADOXICALLY observed?

Answer: LDL-C and total cholesterol may rise as inflammation subsides (lipid paradox)

The 'lipid paradox' in inflammatory diseases means active inflammation suppresses LDL-C, so effective treatment normalizes LDL upward — yet cardiovascular risk still falls overall.