Haematology: von Willebrand disease: 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 · Haematology: von Willebrand disease

Sample item

A 20-year-old woman has menorrhagia and recurrent epistaxis, and her mother has similar problems. Platelet count is normal, bleeding time is prolonged, PT is normal and aPTT is mildly prolonged. Ristocetin-induced aggregation is reduced. Why is the aPTT prolonged in this disorder of platelet adhesion?

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

The answer and the reasoning

C. Von Willebrand factor stabilises factor VIII, so its lack lowers factor VIII levels

Von Willebrand factor mediates platelet adhesion to subendothelium through GPIb, and also binds and protects factor VIII in plasma. In its absence the factor VIII half-life shortens, so aPTT is prolonged while PT is normal. Ristocetin-induced aggregation, which depends on von Willebrand factor, is reduced.

Option by option

  • A. Von Willebrand factor directly activates factor XII

    Von Willebrand factor does not activate factor XII, which initiates the contact pathway.

  • B. Von Willebrand factor converts fibrinogen to fibrin

    Conversion of fibrinogen to fibrin is performed by thrombin.

  • C. Von Willebrand factor stabilises factor VIII, so its lack lowers factor VIII levels (correct)

    Correct. Deficient carrier protein leads to secondary factor VIII deficiency and a raised aPTT.

  • D. Von Willebrand factor is a cofactor for vitamin K dependent carboxylation

    Carboxylation of clotting factors depends on vitamin K, not on von Willebrand factor.

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 C, Von Willebrand factor stabilises factor VIII, so its lack lowers factor VIII levels. Von Willebrand factor mediates platelet adhesion to subendothelium through GPIb, and also binds and protects factor VIII in plasma.

Why is "Von Willebrand factor directly activates factor XII" not the answer?

Von Willebrand factor does not activate factor XII, which initiates the contact pathway.

Why is "Von Willebrand factor converts fibrinogen to fibrin" not the answer?

Conversion of fibrinogen to fibrin is performed by thrombin.

Why is "Von Willebrand factor is a cofactor for vitamin K dependent carboxyla…" not the answer?

Carboxylation of clotting factors depends on vitamin K, not on von Willebrand factor.

What concept does this question test?

It tests Haematology: von Willebrand disease in Pathology. In its absence the factor VIII half-life shortens, so aPTT is prolonged while PT is normal. Ristocetin-induced aggregation, which depends on von Willebrand factor, is reduced.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. 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 Haematology: von Willebrand disease?

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.