PSL301H1 Lecture Notes - Lecture 5: Vasospasm, Endothelium, Hemostasis
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Document Summary
Thrombopoietin stimulates production of megakaryocytes increase platelet. 3 phases of hemostasis (hemo- = blood -stasis= stop ): vascular phases. Vasoconstriction promotes by serotonin, endothelin-1, and thromboxane a2: platelet phase. Platelets in the blood ready to act. In extracellular matrix, but when there"s an injury blood exposed to collagen activates platelets platelets release factors that attract more platelets platelets build up forming a clot. vonwillebrand factors: Binds to collagen then platelets, causing to aggregate. Platelets are not activated if no injury. When no injury: prostacyclin and nitric oxide (no) released by endothelial cells inhibits platelets adhesion, also a vasodilator. [adp, paf, serotonin, thromboxane a2] platelet aggregation vasoconstriction: coagulation phase. Enzyme breaks off fibrinogen = leaving an active component. Protease cascade protein cleaved and expose binding site for fibrinogen. Prothrombin inactive active x thrombin active cleaves fibrinogen to fibrin (now active); and cleave xiii to have active xiii (13) active xiii will cross link fibrin.
