The following animation overviews the physiology of coagulation by identifying key molecules involved -von Willebrand factor, collagen and fibronectin- as well as summarizing important steps: platelet activation, degranulation and aggregation.
Finally, it compares normal platelet aggregation with the mechanism of action of Gp IIa/IIIb inhibitors.
Some excerpts on the pharmacology of GP IIb/IIIa blockers, including their mechanism of action. From: Lippincott Illustrated Reviews: Pharmacology, 4 ed.
Eptifibatide and tirofiban
These two antiplatelet drugs act similarly to abciximab—namely, blocking the GP IIb/IIIa receptor . Eptifibatide [ep-ti-FIB-ih-tide] is a cyclic peptide that binds to GP IIb/IIIa at the site that interacts with the arginine-glycine-aspartic acid sequence of fibrinogen. Tirofiban [tye-roe-FYE-ban] is not a peptide, but it blocks the same site as eptifibatide. These compounds, like abciximab, can decrease the incidence of thrombotic complications associated with acute coronary syndromes. When intravenous infusion is stopped, these agents are rapidly cleared from the plasma, but their effect can persist for as long as 4 hours. [Note: Only intravenous formulations are available, because oral preparations of GP IIb/IIIa blockers are too toxic.] Eptifibatide and its metabolites are excreted by the kidney. Tirofiban is excreted unchanged by the kidney. The major adverse effect of both drugs is bleeding
In this image you can see an integration of the mechanism of action of antiplatelet agents and the role of IIb/IIIa antagonists. Source: Australian Prescriber.
Antiplatelet therapy after coronary occlusion. Aust Prescr 2007;30:92-6.