The platelet aggregation tracing shown in the figure represents:

The platelet aggregation tracing shown in the figure represents:

• A. Von Willebrand disease
• B. Storage pool disease
• C. Glanzmann thrombasthenia
• D. Aspirin

Answer: (C)

When platelets fail to aggregate with most stimuli but still respond normally to ristocetin, it points to a defect in the platelet fibrinogen receptor, GPIIb/IIIa. This receptor is required for platelets to cross-link and form aggregates in response to most agonists such as ADP, collagen, epinephrine, and arachidonic acid. In Glanzmann thrombasthenia, GPIIb/IIIa is deficient or dysfunctional, so the aggregation traces for those agonists remain flat. Ristocetin-induced aggregation, however, relies on the vWF-GPIb interaction and does not require GPIIb/IIIa, so it stays normal. Therefore the tracing pattern—absent aggregation with the usual agonists but preserved response to ristocetin—best fits Glanzmann thrombasthenia.

When platelets fail to aggregate with most stimuli but still respond normally to ristocetin, it points to a defect in the platelet fibrinogen receptor, GPIIb/IIIa. This receptor is required for platelets to cross-link and form aggregates in response to most agonists such as ADP, collagen, epinephrine, and arachidonic acid. In Glanzmann thrombasthenia, GPIIb/IIIa is deficient or dysfunctional, so the aggregation traces for those agonists remain flat. Ristocetin-induced aggregation, however, relies on the vWF-GPIb interaction and does not require GPIIb/IIIa, so it stays normal. Therefore the tracing pattern—absent aggregation with the usual agonists but preserved response to ristocetin—best fits Glanzmann thrombasthenia.