Which set of platelet responses would be most likely associated with Glanzmann's thrombasthenia?

In Glanzmann's thrombasthenia, there is a deficiency or dysfunction of glycoprotein IIb/IIIa on the platelet surface, which is critical for platelet aggregation. The defect specifically affects the ability of platelets to bind to fibrinogen, which is essential for platelet aggregation. In this condition, the aggregation response to certain agonists provides important diagnostic information.

The correct choice indicates that platelet aggregation is normal in response to ristocetin but shows decreased aggregation to collagen, ADP, and epinephrine. Ristocetin induces platelet aggregation through a mechanism that does not require glycoprotein IIb/IIIa, as it works by promoting the interaction between von Willebrand factor and glycoprotein Ib on the platelet surface. Therefore, in Glanzmann's thrombasthenia, aggregation to ristocetin remains intact due to the functioning of glycoprotein Ib.

Conversely, aggregation to collagen, ADP, and epinephrine is decreased due to the lack of functional glycoprotein IIb/IIIa, which prevents the proper binding to fibrinogen and thus inhibits effective platelet aggregation in response to these stimuli. This profile of responses is indicative of Glanzmann's throm