Adherence Initiated damage to endothelial cells which exposes adhesive

Adherence initiated damage to endothelial cells which

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Adherence Initiated damage to endothelial cells which exposes adhesive glycoproteins such as collagen and von Willebrand Factor in the subendothelium. VWF and other adhesive glycoproteins in the plasma deposit on the damaged area. Platelets adhere to the subendothelium through receptors that bind to the adhesive glycoproteins (GPIb, GPIa/IIa, GPIIb/IIa). N/A N/A Aggregation -induced by release of TXA2 and ADP by platelets, which induce functional fibrinogen receptors on the platelet. -adhesive glycoproteins bind simultaneously to GPIIb/IIIa on two different platelets -GPIIb/IIIa is the most abundant aggregator receptor on the platelet. -stabilization of the platelet plug (primary hemostatic plug or blood clot) occurs by activation of coagulation factors, thrombin, and fibrin. It is facilitated by fibrinogen bridges between receptors on the platelets. -heparin neutralizing factor enhances clot formation Glycoprotein IIb/IIIa inhibitors Aspirin Since the GPIIb-GIIIa-fibrinogen pathway is essential for the formation of a thrombus, it is an important target for blockage by antiplatelet drugs - Agents that block this final common pathway by blocking the binding of adhesive proteins to GP IIb- IIIa, termed GP IIb/IIIa antagonists, are currently considered the most powerful specific inhibitors of platelet participation in acute thrombosis: Abciximab (Reopro) Tirofiban (Aggrastat) Eptifibatide (Integrilin) Bivalirudin (Angiomax)
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N/A N/A Four Phases of Platelet Plug Formation Function Platelet Disorders Impairment of Normal Function Activation Immune Thrombocytopenic Purpura Most common cause of thrombocytopenia. Acute ITP: more common in children; usually secondary to infections that lead to large amounts of antigen in the blood, such as drug allergies or lupus.
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