Blood and immunity: platelet aggregation: 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: platelet aggregation

Sample item

A 6-year-old has had recurrent epistaxis and gum bleeding since infancy. Platelet count and morphology are normal and bleeding time is prolonged. Platelets fail to aggregate with ADP, collagen and thrombin, but ristocetin causes normal agglutination. Which platelet component is defective?

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

The answer and the reasoning

A. Glycoprotein IIb/IIIa, the fibrinogen receptor

Aggregation requires activated GPIIb/IIIa to bind fibrinogen and cross-link platelets. In Glanzmann thrombasthenia this receptor is deficient, so aggregation fails with all agonists while ristocetin-induced agglutination, which depends on GPIb and vWF, is normal.

Option by option

  • A. Glycoprotein IIb/IIIa, the fibrinogen receptor (correct)

    Correct. Absent GPIIb/IIIa prevents fibrinogen bridging, so aggregation fails with every agonist but ristocetin response is preserved.

  • B. Thromboxane A2 synthesis

    Defective thromboxane synthesis impairs arachidonate-dependent aggregation and is the target of aspirin, but does not abolish response to all agonists.

  • C. Dense granule ADP storage

    A storage pool defect gives poor secondary aggregation but not absent aggregation to all agonists.

  • D. Glycoprotein Ib, the von Willebrand factor receptor

    A GPIb defect would impair ristocetin agglutination, which is normal here.

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 A, Glycoprotein IIb/IIIa, the fibrinogen receptor. Aggregation requires activated GPIIb/IIIa to bind fibrinogen and cross-link platelets.

Why is "Thromboxane A2 synthesis" not the answer?

Defective thromboxane synthesis impairs arachidonate-dependent aggregation and is the target of aspirin, but does not abolish response to all agonists.

Why is "Dense granule ADP storage" not the answer?

A storage pool defect gives poor secondary aggregation but not absent aggregation to all agonists.

Why is "Glycoprotein Ib, the von Willebrand factor receptor" not the answer?

A GPIb defect would impair ristocetin agglutination, which is normal here.

What concept does this question test?

It tests Blood and immunity: platelet aggregation in Physiology. In Glanzmann thrombasthenia this receptor is deficient, so aggregation fails with all agonists while ristocetin-induced agglutination, which depends on GPIb and vWF, is normal.

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: platelet aggregation?

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.