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31 Cards in this Set
- Front
- Back
Steps of Hemostasis
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1. Vasoconstriction
2. Formation of platelet plug 3. formation of fibrin mesh 4. Dissolution of platelet clot |
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When broken blood vessel, what happens?
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-Endothelial cells release endothelin
-Platelets release serotonin |
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Formation of platelet plug?
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-endothelial cells release adhesion factors: Von Willebrand factor
-Platelets release thrombin & thromboxene Both make platelets sticky and cause them to aggregate |
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Formation of fibrin mesh
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Platelets release growth factors for repair
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Dissolution of platelet clot
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Plasmin
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Intrinsic pathway
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-In response to abnormal blood vessel wall.
-Activated by proteolysis of peptide bonds in inactive zymogen to active protease -Amplification |
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Extrinsic pathway
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-Substances released from injured tissues
-Trauma-->thromboplastin |
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Both intrinsic and extrinsic pathways converge at?
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Factor X
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Prothrombin--->thrombin
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Factor X
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Fibrinogen--->Fibrin
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Thrombin
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Fibrin cross-linked
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Factor XIIIa
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Serine Protease
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Has a critical Ser residue at active site
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Which are not serine proteases but are all activated by thrombin?
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tissue factor
fibrinogenfibrin factors VIIIa, Va, XIIIa |
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characteristics of fibrinogen
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highly negative charge, does not aggregate
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How does fibrinogen lose its central negative charge
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Upon activation by thrombin
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How does fibrin become cross-linked fibrin clot?
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An isopeptide bond formation between Gln and Lys side chains
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Deficiency in factor XIII causes?
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Bleeding
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Hemophilia A
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Factor VIII missing
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Hemophilia B
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Deficiency of factor IX
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Plasminogen--->Plasmin
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TPA=Tissue Plasminogen Activator
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Fibrin clot--->Free peptides (clot dissolved)
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Plasmin
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Regulation of clotting via endothelial cells
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Produce thrombomodulin
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Regulation via control of active thrombin
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1. regulation of prothrombin--->thrombin
2. inactivation of thrombin by anti-thrombin III |
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Regulation of the clotting cascade
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Amplification of cascade allows you to accumulate huge # of inhibitors for the early party of the pathway.
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In prothrombin, Glu---> GLA
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Vitamin K
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The affect of GLA
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Binds to Ca+2 ions-->anchors prothrombin to CM-->brings prothrombin close to factors Xa, Va which activate it-->thrombin
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what happenes to regulation when there is no vitamin K
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GLU cannot --> GLA -->no GLA-->no Ca+2 binding-->no anchoring to CM-->slow activation & poor clotting
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Antagonists of vitamin K
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Dicoumarol, Warfain-structural analogs of Vitamin K
-Can be used as anti-coagulants to prevent thromboses |
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Antithrombin belongs to SERPINS
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inactivates thrombin
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Heparin
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Negatively charged glycosaminoglycans that binds to antithrombin III-->promotes antithrombin III binding to thrombin-->irreversibly inactivates it
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Does antithrombin III inhibit only thrombin?
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No, it inhibits other serine proteases too.
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