Lipoproteins: familial hypercholesterolaemia: practice question

A Biochemistry question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Biochemistry · Lipoproteins: familial hypercholesterolaemia

Sample item

Tendon xanthomas and premature coronary disease with markedly raised LDL most commonly result from defective uptake through which receptor?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

A. LDL receptor

Classical familial hypercholesterolaemia is usually due to an LDL-receptor defect, reducing hepatic clearance of LDL. PCSK9 gain-of-function mutations can produce a similar phenotype.

Option by option

  • A. LDL receptor (correct)

    Correct. LDL receptors clear circulating LDL from plasma.

  • B. Scavenger receptor class B type I

    SR-BI mediates selective HDL cholesteryl-ester uptake.

  • C. VLDL receptor

    VLDL receptor is not the classic defect in familial hypercholesterolaemia.

  • D. Insulin receptor

    Insulin receptor defects cause severe insulin resistance, not isolated high LDL.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Biochemistry question

What is the answer to this Biochemistry question?

The best answer is A, LDL receptor. Classical familial hypercholesterolaemia is usually due to an LDL-receptor defect, reducing hepatic clearance of LDL.

Why is "Scavenger receptor class B type I" not the answer?

SR-BI mediates selective HDL cholesteryl-ester uptake.

Why is "VLDL receptor" not the answer?

VLDL receptor is not the classic defect in familial hypercholesterolaemia.

Why is "Insulin receptor" not the answer?

Insulin receptor defects cause severe insulin resistance, not isolated high LDL.

What concept does this question test?

It tests Lipoproteins: familial hypercholesterolaemia in Biochemistry. PCSK9 gain-of-function mutations can produce a similar phenotype.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Lipoproteins: familial hypercholesterolaemia?

Build one table of enzyme deficiency, disease, inheritance and key finding, then revise it by spaced recall. Then use the flashcards and the other Biochemistry questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.