Blood and immunity: Glanzmann thrombasthenia: 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: Glanzmann thrombasthenia

Sample item

A child has easy mucosal bleeding, a normal platelet count and a prolonged bleeding time. Platelets fail to aggregate with ADP, collagen and thrombin but agglutinate normally with ristocetin. Which platelet defect fits best?

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

The answer and the reasoning

A. Deficient glycoprotein IIb/IIIa

In Glanzmann thrombasthenia GPIIb/IIIa, the fibrinogen receptor, is deficient, so platelets cannot aggregate whatever the agonist. Ristocetin agglutination depends on GPIb and von Willebrand factor, which are intact, so it is normal.

Option by option

  • A. Deficient glycoprotein IIb/IIIa (correct)

    Correct. Absent GPIIb/IIIa abolishes aggregation but leaves ristocetin agglutination intact.

  • B. Deficient dense granule ADP storage

    Storage pool defect impairs the second wave of aggregation but not primary aggregation to all agonists.

  • C. Deficient von Willebrand factor

    Von Willebrand deficiency would also show abnormal ristocetin response and a prolonged aPTT.

  • D. Deficient glycoprotein Ib-IX

    Absent GPIb-IX (Bernard-Soulier) would give abnormal ristocetin agglutination and large platelets.

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, Deficient glycoprotein IIb/IIIa. In Glanzmann thrombasthenia GPIIb/IIIa, the fibrinogen receptor, is deficient, so platelets cannot aggregate whatever the agonist.

Why is "Deficient dense granule ADP storage" not the answer?

Storage pool defect impairs the second wave of aggregation but not primary aggregation to all agonists.

Why is "Deficient von Willebrand factor" not the answer?

Von Willebrand deficiency would also show abnormal ristocetin response and a prolonged aPTT.

Why is "Deficient glycoprotein Ib-IX" not the answer?

Absent GPIb-IX (Bernard-Soulier) would give abnormal ristocetin agglutination and large platelets.

What concept does this question test?

It tests Blood and immunity: Glanzmann thrombasthenia in Physiology. Ristocetin agglutination depends on GPIb and von Willebrand factor, which are intact, so it 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: Glanzmann thrombasthenia?

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.