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Unformatted text preview: et Plug Platelets adhere to collagen in damaged blood vessel wall Platelets release chemicals that function in vasoconstriction or platelet aggregation Vasoconstriction: Serotonin Thromboxane A2 (conversion from phospholipids in platelet membrane) Platelet aggregation: ADP PAF (platelet-activating factor) platelet aggregation Figure 16-9c Figure 16-11 - Overview Table 16-4 Coagulation Inactive plasma proteins are activated in order to contribute to the clotting process Intrinsic and extrinsic pathways Intrinsic triggered by damage to lining of blood vessel (exposure to collagen in blood vessel wall) SLOWER (minutes) Extrinsic triggered by tissue damage which releases thromboplastin FASTER (seconds) Figure 16-12 Basic Process: Activation of Thrombin Thrombin: Fibrinogen Fibrin (stringy protein that forms clot) Calcium required for activation of various clotting factors Vitamin K required for production of prothrombin + other clotting factors Table 16-5 Prostacyclin and NO (nitrous oxide) - from healthy endothelial cells of blood vessel wall Prevents platelet aggregation from advancing past area of damage Plasmin enzyme that breaks up fibrin clot (fibrinolysis) Plasminogen Plasmin (activation via thrombin and tissue plasminogen activator) Heparin, antithrombin III, protein C Other endogenous anticoagulants Figure 16-13 Table 16-6 Heparin inhibits thrombin formation Aspirin keeps platelets from "sticking" together + prevents their release of clotting substances Citrate added to blood when donated or for tests; binds to calcium unavailable for clotting Warfarin (Coumadin) disrupts Vit. K activity Hemophilia One or more clotting factors are deficient or absent Most common form: Hemophilia A Factor VIII deficiency Figure 16-12...
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This note was uploaded on 04/29/2009 for the course BIOL 425 taught by Professor Tondi during the Fall '08 term at George Mason.
- Fall '08