CHAPTER-37.pdf - 37 NORMAL HEMOSTASIS AND COAGULATION...

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37 NORMAL HEMOSTASIS AND COAGULATION of 1 13 HEMOSTASIS Overview complex physiologic process that keeps circulating blood in a fluid state and then, when an injury occurs, produces a clot to stop bleeding, confines the clot to the site of injury, and finally dissolves the clot as the wound heals vasoconstriction + platelet aggregation + platelet adhesion + coagulation enzyme activation HEMOSTASIS Key cellular elements of hemostasis: cells of the vascular intima extravascular tissue factor (TF)-bearing cells platelets Plasma components: coagulation proteins and their inhibitors fibrinolytic proteins and their inhibitors Primary Hemostasis activated by desquamation and small injuries to blood vessels involves platelets and vascular intima Vasoconstriction and Platelet plug formation - reinforced by fibrin to control major bleeding in the long term initial, rapid, short-lived response to vessel damage procoagulant substances exposed or released by damaged or activated endothelial cells Defects in primary hemostasis that can cause debilitating, sometimes fatal, chronic hemorrhage: - collagen abnormalities - thrombocytopenia - qualitative platelet disorders - von Willebrand disease Secondary Hemostasis activated by large injuries to blood vessels and surrounding tissues involves platelets and coagulation systems delayed, long-term response the activator, tissue factor, is exposed on cell membranes fibrinolysis - the gradual digestion and removal of the fibrin clot as healing occurs - final event of hemostasis Vascular Intima in Hemostasis the interface between circulating blood and the body tissue Endothelial cells (EC) - monolayer of metabolically active cells in the innermost lining of blood vessels - form a smooth, unbroken surface that eases the fluid passage of bloods - supported by an elastin-rich internal elastic lamina (basement membrane), and its surrounding layer of connective tissues (elastin and collagen) Subendothelial cells connective tissue - Collagen and fibroblasts in veins - Collagen, fibroblasts, and smooth muscle cells in arteries *Smooth muscle cells in arteries and arterioles, but NOT in the walls of veins, venules, or capillaries, contract during primary hemostasis. Normally, intact vascular endothelium prevents thrombosis by inhibiting: - platelet aggregation - preventing coagulation activation and and propagation - enhancing fibrinolysis rochi
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37 NORMAL HEMOSTASIS AND COAGULATION of 2 13 Anticoagulant Properties of Intact Vascular Intima Procoagulant Properties of Damaged Vascular Intima Fibrinolytic Properties of Vascular Intima How ECs support/regulate fibrinolysis: secretion of tissue plasminogen activator (TPA) - binds to polymerized fibrin (together with plasminogen) during thrombus formation - activates fibrinolysis by converting plasminogen to plasmin, which gradually digests fibrin and restores blood flow providing inhibitors to prevent excessive plasmin generation, such as: -
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  • Fall '14
  • Plasmin, Factor XII, Normal Hemostasis

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