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Lipid disorders flashcards

7 high-yield MRCP Part 1 cards from the Intellect Medicos Endocrinology & Diabetes course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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  1. Under the Simon Broome criteria, what lipid levels plus which other finding make familial hypercholesterolaemia DEFINITE in an adult?

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    Total cholesterol >7.5 or LDL >4.9 mmol/L, plus tendon xanthomas (patient or relative) or DNA evidence of an FH mutation.

    Why? The same cholesterol levels with a family history of premature MI or of high cholesterol make FH "possible".

  2. What is the inheritance and the commonest molecular defect in familial hypercholesterolaemia?

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    Autosomal dominant; LDL-receptor gene defect.

    Why? Heterozygous FH is common and milder; homozygous FH is rare and very severe and may need LDL apheresis.

  3. What is the first-line drug treatment for familial hypercholesterolaemia?

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    A high-intensity statin (atorvastatin or rosuvastatin).

    Why? Aim for at least a 50% fall in LDL cholesterol from baseline. Add ezetimibe if the target is not reached, and a PCSK9 inhibitor in severe cases.

  4. What is the mechanism of action of evolocumab?

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    PCSK9 inhibitor (monoclonal antibody) — it prevents LDL-receptor degradation.

    Why? More LDL receptors stay on the liver surface, so more LDL is cleared from the blood.

  5. What is the mechanism of action of fibrates?

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    PPAR-alpha agonists, which increase lipoprotein lipase expression.

    Why? They mainly lower triglycerides. Ezetimibe reduces intestinal cholesterol absorption; statins inhibit HMG-CoA reductase.

  6. For primary prevention of CVD (QRISK3 ≥10%, most type 1 diabetes, or CKD), which statin and dose does NICE offer?

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    Atorvastatin 20 mg once daily.

    Why? Aim for a ≥40% reduction in non-HDL cholesterol; titrate up to 80 mg if not achieved. Secondary prevention uses atorvastatin 80 mg.

  7. Palmar xanthomas are diagnostic of which Fredrickson hyperlipidaemia?

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    Type III (remnant hyperlipidaemia / dysbetalipoproteinaemia), due to abnormal ApoE.

    Why? IDL accumulates; fibrates are first-line treatment.

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