Following the rupture of cells along the cell wall, several platelet aggregation factors are released and will interact with each other.
Following vascular injury, the circulating von Willebrand factor (VWF) binds to the collagen matrix at the site of exposed subendothelium. This leads to a conformational change in VWF allowing the binding of platelets through their membrane receptor glycoprotein Ib (GPIb). Platelets also bind directly to the collagen matrix via their GPIa receptor. This adhesion of the platelet initiates activation of the platelet and exposure of the GPIIb/IIIa receptor. Then the aggregation is promoted
by the binding of fibrinogen to the platelet GPIIb/IIIa complex. The activated platelets secrete factors that stimulate further aggregation and coagulation: serotonin (5-HT), thromboxane A2 (TxA2) and adenosine diphosphate (ADP). TxA2 is formed through conversion of arachidonic acid by cyclo-oxygenase (COX1) into the prostaglandin PgG2, which is then converted into TxA2. Serotonin and TxA2 induce vasoconstriction. At the same time the coagulation system is activated and the negatively charged surface of phospholipids (flip-flop mechanism) stimulates the formation of thrombin (factor IIa), which creates a network of fibrin.
Platelet adherence to the damaged site of a vessel wall occurs through
What is NOT true about platelets?
Extra info: A platelet life span is about 7 days.
Bleeding time is NOT increased in:
Extra info: The bleeding time depends on the number and function of the platelets as well as the interaction between the capillary wall and the platelets. Therefore, the whole blood clotting system is not involved. In massive blood transfusion, the platelet count is reduced. In von Willebrand's disease, the function of the platelets is abnormal. Clopidogrel inhibits platelet function.