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Statin Therapy & Pharmacology 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. Statin-associated muscle symptoms (SAMS) are most accurately defined as which of the following?

    Answer: A spectrum from myalgia without CK elevation to rhabdomyolysis with CK >10× ULN

    SAMS encompasses the full spectrum from mild myalgia (normal CK) through myositis (CK elevation) to life-threatening rhabdomyolysis (CK >10× ULN with renal injury).

  2. The PREDICTION score or similar tools for statin myopathy risk account for which of the following as the strongest pharmacogenomic predictor of statin-induced myopathy?

    Answer: SLCO1B1 521T>C variant (rs4149056)

    The SLCO1B1 521T>C variant reduces OATP1B1 transporter activity, impairing hepatic statin uptake and raising plasma concentrations, which significantly increases myopathy risk especially with simvastatin.

  3. A patient on atorvastatin 40 mg develops CK of 6× ULN without renal impairment or weakness. What is the recommended management?

    Answer: Hold atorvastatin, recheck CK weekly, and rechallenge with a lower dose once CK normalizes

    For asymptomatic CK elevation between 3–10× ULN without weakness, guidelines recommend withholding the statin, monitoring CK until normalization, and rechallenging at a lower dose or different statin.

  4. Which concomitant condition most dramatically increases the risk of statin-induced rhabdomyolysis independent of drug interactions?

    Answer: Hypothyroidism

    Untreated or undertreated hypothyroidism predisposes patients to myopathy and rhabdomyolysis, and statin therapy in this setting substantially amplifies that risk.

  5. Statin-associated autoimmune myopathy (SAAM) differs from typical SAMS because it is characterized by which finding?

    Answer: Persistent myopathy with anti-HMGCR antibodies after statin cessation

    SAAM is an immune-mediated necrotizing myopathy driven by anti-HMGCR autoantibodies that persists and may worsen even after statin discontinuation, requiring immunosuppressive treatment.

  6. Which laboratory abnormality beyond CK elevation should prompt monitoring in patients on statin therapy, particularly those on higher intensity regimens?

    Answer: Alanine aminotransferase and aspartate aminotransferase (hepatotoxicity screening)

    Although clinically significant statin hepatotoxicity is rare, baseline and periodic liver enzyme monitoring is recommended, especially when symptoms of hepatic dysfunction occur.

  7. Coenzyme Q10 (ubiquinone) supplementation has been proposed for statin-induced myalgia based on which pharmacologic rationale?

    Answer: Statins inhibit the mevalonate pathway, reducing CoQ10 biosynthesis alongside cholesterol

    Because CoQ10 is synthesized downstream of mevalonate via the same pathway statins block, statin use can reduce CoQ10 levels, potentially contributing to mitochondrial dysfunction in muscle.

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