Blood and immunity: heparin-induced thrombocytopenia: practice question

A Physiology 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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Physiology · Blood and immunity: heparin-induced thrombocytopenia

Sample item

On day 7 of unfractionated heparin after cardiac surgery, a man's platelet count falls from 250,000 to 80,000 per microlitre and he develops a new deep vein thrombosis. Which mechanism is responsible?

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

The answer and the reasoning

D. IgG antibodies to heparin-platelet factor 4 complexes activate platelets through Fc receptors

In heparin-induced thrombocytopenia, antibodies bind heparin-PF4 complexes and activate platelets through FcgammaRIIa. Platelets are consumed and thrombin generation rises, so the patient is at risk of thrombosis despite a low count. Heparin must be stopped and a non-heparin anticoagulant used.

Option by option

  • A. Direct heparin toxicity to megakaryocytes causing marrow suppression

    Marrow suppression is not the mechanism, and it would not explain thrombosis.

  • B. Excess antithrombin activity causing a bleeding tendency

    Heparin acts through antithrombin, but this does not explain thrombocytopenia with thrombosis.

  • C. Antibodies against glycoprotein IIb/IIIa clearing platelets in the spleen

    Anti-IIb/IIIa antibodies are not the cause; the antigen is the heparin-PF4 complex.

  • D. IgG antibodies to heparin-platelet factor 4 complexes activate platelets through Fc receptors (correct)

    Correct. Antibody-mediated platelet activation causes both the fall in count and the thrombosis.

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 Physiology question

What is the answer to this Physiology question?

The best answer is D, IgG antibodies to heparin-platelet factor 4 complexes activate platelets through Fc receptors. In heparin-induced thrombocytopenia, antibodies bind heparin-PF4 complexes and activate platelets through FcgammaRIIa.

Why is "Direct heparin toxicity to megakaryocytes causing marrow suppression" not the answer?

Marrow suppression is not the mechanism, and it would not explain thrombosis.

Why is "Excess antithrombin activity causing a bleeding tendency" not the answer?

Heparin acts through antithrombin, but this does not explain thrombocytopenia with thrombosis.

Why is "Antibodies against glycoprotein IIb/IIIa clearing platelets in the sp…" not the answer?

Anti-IIb/IIIa antibodies are not the cause; the antigen is the heparin-PF4 complex.

What concept does this question test?

It tests Blood and immunity: heparin-induced thrombocytopenia in Physiology. Platelets are consumed and thrombin generation rises, so the patient is at risk of thrombosis despite a low count. Heparin must be stopped and a non-heparin anticoagulant used.

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 Blood and immunity: heparin-induced thrombocytopenia?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology 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.