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jkkjkkjkj - receptor GPIb on the endothelium Bleeding...

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Thrombosis - A thrombus is not the same as a clot. Thrombosis includes platelet activation and clotting. Thrombosis can be the result of changes in blood flow pattern or speed. If you have a hemostasis event that includes platelets and proteins from the coagulation cascade you’d have a thrombus. Clotting (hemostasis) is the activation of a protein cascade within the blood leading to formation of thrombin, which converts fibrinogen to fibrin. - Platelets contribute to hemostasis by adhereing to the underlying vessel wall, releasing pharmacologically active compounds, aggregating other platelets to form plugs, and provide co-factors for clotting (hemostasis). o Adhesion; Platelets bind to damaged endothelial cells or exposed sub- endothelium through glycoprotein receptors. Exposed collagen bind glycoprotein receptors GPIa on the platelet. vWF binds to the glycoprotein
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Unformatted text preview: receptor GPIb on the endothelium. Bleeding defects occur if no GPIa or GPIb. Platelet adherence leads to shape change, it spreads out. o Release; pre-formed and de-novo compounds that affect hemostasis and the metabolism of the vessel wall. Platelets releases PDGF, thrombospondin, platelet factor 4, fibrinogen, fibronectin and vWF from alpha granules. Platelets also release ATP, ADP, GDP, GTP, serotonin, and calcium from dense bodies. Can lead to the initiation of a clotting cascade. They also release arachidonate to make prostalandins that promote and prevent aggregation. o Aggregation; Platelets bind to each other using fibrinogen, which use GPIIb and IIIa integrins. The receptor may also bind vWF. The stimk...
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