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In addition to vasoconstriction, the primary hemostatic response to vascular injury is platelet plug formation. This consists of platelet adhesion to the vascular endothelium and simultaneous formation of platelet aggregates.
Quantitative and qualitative disorders of platelets result in defective primary hemostasis and predominantly mucocutaneous bleeding symptoms.
In vitro platelet function studies provide an assessment of platelet aggregation in response to agonists such as epinephrine, collagen, arachidonic acid, adenosine diphosphonate, and ristocetin.
Abnormalities in platelet aggregation responses to agonists could reflect medication effect (eg, aspirin or nonsteroidal anti-inflammatory use), or, less commonly, the presence of acquired conditions (eg, myeloproliferative diseases, renal failure), or congenital conditions (eg, Glanzmann thrombasthenia, Bernard-Soulier syndrome, Hermansky-Pudlak syndrome, storage pool disease, Wiskott-Aldrich syndrome).