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Lipids & statins flashcards

7 high-yield MRCP Part 1 cards from the Intellect Medicos Cardiology 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. What is the mechanism of action of statins?

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   Competitive inhibition of HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis.

   Why? Less cholesterol in hepatocytes up-regulates LDL receptors, so more LDL is cleared from the blood.

2. For primary prevention, at what QRISK3 score does NICE offer a statin, and which drug and dose?

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   A 10-year risk of 10% or more: atorvastatin 20 mg daily.

   Why? NICE also says not to rule out atorvastatin 20 mg below 10% if the person prefers a statin or risk may be underestimated. Aim for a reduction in non-HDL cholesterol of more than 40%.

3. Which statin and dose does NICE offer for secondary prevention of cardiovascular disease?

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   Atorvastatin 80 mg daily (a lower dose if there are interactions, a high risk of side effects, or patient preference).

   Why? NICE aims for LDL cholesterol of 2.0 mmol/L or less (or non-HDL 2.6 mmol/L or less). Ezetimibe can be added if the target is not met, and NICE (2023) says it can be considered even when the target is met.

4. When should liver transaminases be checked in someone starting a statin?

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   At baseline, again 2–3 months after starting (or changing) treatment, and at 12 months — then only if clinically indicated.

   Why? The full lipid profile is also rechecked at 2–3 months. A transaminase rise of less than 3 times the upper limit of normal is not a reason to withhold a statin.

5. Why should simvastatin be withheld while a patient takes clarithromycin?

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   Clarithromycin inhibits CYP3A4, raising simvastatin levels and the risk of myopathy and rhabdomyolysis.

   Why? Simvastatin and atorvastatin are CYP3A4 substrates. Pravastatin and rosuvastatin are less affected.

6. What is the mechanism of action of ezetimibe?

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   It blocks the NPC1L1 sterol transporter, reducing intestinal absorption of cholesterol.

   Why? It is added to a statin when LDL targets are not met, or used alone if statins are not tolerated.

7. Familial hypercholesterolaemia: what is the inheritance and the commonest gene affected?

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   Autosomal dominant; the LDL receptor gene (LDLR).

   Why? Other genes are APOB and PCSK9 (gain of function). Clues are very high LDL, tendon xanthomata and premature coronary disease; diagnosis uses the Simon Broome or Dutch Lipid Clinic Network criteria.