Adherence initiated damage to endothelial cells which

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)

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.