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28 Cards in this Set
- Front
- Back
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primary hemostasis
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platelet plug formation
damaged endothelial cells interact w/ platelets via von Willebrand's factor (vWF) |
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von willebrand factor
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mediates platelet adhesion to exposed extracellular matrix
by binding to platelet membrane and collagen fibers in tissue thrombin and thromboxane increase Ca concentration of platelets |
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secondary hemostasis
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formation of crosslinked fibrin clot through activated clotting factors
takes place on plateles surface |
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forming a clot
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tightly controlled-abnormal clotting produces thrombus which causes vascular inclusion/infarction
1. endothelial cells 2. subendothelial tissue 3. platelets 4. clotting factors |
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inhibit blood clotting
form prostacyclin (inhibitor of platelet adhesion/aggregation) |
endothelial cells
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not normally exposed to blood
bound by platelets and clotting factors |
subendothelial tissue
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release proteins/vasoactive amines after binding to subendothelial tissue
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platelets
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plasma proteins that create proteolytic cascase that produces insoluble fibrin from soluble fibrinogen
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clotting factors
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platelet aggregation
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caused by fibrinogen binding to platelet receptors
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fibrin
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the postcursor of fibrinogen
form a soft gel transglutaminase triggers crosslinking |
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thrombin
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converts fibrinogen into fibrin
cleaves 2 bonds b/t Aa and BB chains, releasing fibrinopeptides A and B remaining peptide is fibrin monomer |
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thrombin formation
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limited to site of injury
produced from prothrombin by factor Xa inactive fragment also produced, contains 10 residues of g-carboxyglutamate (produced by hepatocytes in vit. K mediated reaction) |
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can be activated by extrnsic and intrinsic pathways
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factor X
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extrinsic pathway
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stab wound, GSW
factor VIIa-protease active only in presence of tissue factor |
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intrinsic pathway
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endothelial lining still intact or microdamaged
requires negatively charged surface to activate (i.e. glass) |
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contact phase activation
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iniating reactions of intrinsic pathway
requires kallikrein and factor XIIa (proteases) and kininogen (HMWK-activator protein) |
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contact activation steps
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factor XIIa activates factor XI
XI activates factor IX IX activates factor X factor VIII needed for last step |
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inhibition of clotting
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Antithrombin III (protease inhibitors) is activated by heparin (both intrinsic and extrinsic pathways)
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plasmin
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degrades fibrin clot
formed from plasminogen which bind fibrin clot used w/in 1 hour of acute MI |
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plasmin activation
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tissue type plasminogen activator (tPA)-serine protease that also binds to fibrin (needs both plasmin and fibrin to activate)
urokinase streptokinase (allosterically) |
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anticoagulants
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1. heparin
2. coumadin remove Ca ions all g-carboxyglutamate factors (prothrombin, VII, IX, X) depend on Ca |
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assessing blood clotting
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1. bleeding time
2. activated partial (aPTT) thromboplastin time 3. prothrombin time |
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prolong in platelet disorders
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bleeding time (most important assessment)
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measures efficacy of heparin
tests intrinsic and final common pathways |
aPTT
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prolonged in extrinsic and final common pathways
measures coumadin therapy |
PT
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intrinsic pathway summary
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initiated by KKK (kaolin, prekallikrein, high molecular wt kininogen)
measured by aPTT longer pathway and activation time order-TENET (XII, XI, IX, VIII, X) amplification phase of coagulation (big thrombin amounts) |
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extrinsic pathway summary
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VIIa activates X
measured by PT shorter pathway and activation time activation phase of coagulation (little thrombin amounts) |
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common pathway summary
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convergence of intrinsic and extrinsic pathways
Va cofactor for Xa VIIIa cofactor for IXa (8 follows 9) |
