Haemodynamics: homocystinuria and thrombosis: practice question

A Pathology 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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Pathology · Haemodynamics: homocystinuria and thrombosis

Sample item

A tall 19-year-old with long limbs, downward lens subluxation and learning difficulty presents with a deep vein thrombosis. Urine cyanide-nitroprusside test is positive. Which mechanism most directly promotes his thrombosis?

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

The answer and the reasoning

B. Endothelial injury from raised homocysteine

In classic homocystinuria (cystathionine beta-synthase deficiency) high homocysteine damages endothelium and promotes platelet and coagulation activation, causing arterial and venous thrombosis. Lens subluxation is typically downward, unlike Marfan syndrome where it is upward.

Option by option

  • A. Platelet activation by heparin-PF4 complexes

    Heparin-PF4 antibodies cause HIT, which needs heparin exposure.

  • B. Endothelial injury from raised homocysteine (correct)

    Correct. Homocysteine injures the endothelium and tips Virchow's triad towards thrombosis.

  • C. Resistance to inactivation of factor V

    Factor V resistance is the mechanism of factor V Leiden, not homocystinuria.

  • D. Release of tissue factor by tumour cells

    Tumour tissue factor drives thrombosis in cancer, and this patient has no tumour.

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 Pathology question

What is the answer to this Pathology question?

The best answer is B, Endothelial injury from raised homocysteine. In classic homocystinuria (cystathionine beta-synthase deficiency) high homocysteine damages endothelium and promotes platelet and coagulation activation, causing arterial and venous thrombosis.

Why is "Platelet activation by heparin-PF4 complexes" not the answer?

Heparin-PF4 antibodies cause HIT, which needs heparin exposure.

Why is "Resistance to inactivation of factor V" not the answer?

Factor V resistance is the mechanism of factor V Leiden, not homocystinuria.

Why is "Release of tissue factor by tumour cells" not the answer?

Tumour tissue factor drives thrombosis in cancer, and this patient has no tumour.

What concept does this question test?

It tests Haemodynamics: homocystinuria and thrombosis in Pathology. Lens subluxation is typically downward, unlike Marfan syndrome where it is upward.

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 Haemodynamics: homocystinuria and thrombosis?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology 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.