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14 Cards in this Set
- Front
- Back
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Tissue factor
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Trigger
Transmembrane protein Found everywhere -Except in the bloodstream -Deletion is lethal Cofactor for Factor VIIa activity -Factor X activation – static system -Factor IX activation – flowing system TF-VIIa is inhibited by TFPI |
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Fibrin Clot Formation
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Requires thrombin
-major coagulation effector enzyme -converts finrinogen to fibrin -activates factor XIII --FXIIIa crosslinks fibrin -activates plts |
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Fibrin and Fibrinogen
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Fibrinogen
-Soluble, digested by plasmin Fibrin -Weak clot, easily digested by plasmin early in hemostasis if there is too much plasmin then you destroy the clot Gamma crosslinked Fibrin -Strong clot, can be digested by plasmin Alpha crosslinked Fibrin -Strong clot, resists plasmin digestion |
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Fibrinolysis
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Triggered by aPC
Plasmin is the effector enzyme Relatively non-specific serine protease Fibrin specificity is conferred by activation mechanism |
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Defective Hemostasis
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Decreased thrombin/plasmin ratio
Severe deficiency of a single factor Hemophilia Immune inhibitors Combined deficiency of many factors Vitamin K deficiency Liver disease Anticoagulation Warfarin Heparin Argatroban, Refludan, Angiomax Excess Fibrinolysis Liver disease Thrombolytic therapy |
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Hydraulic Forces
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Pressure difference across the vascular defect
Pressure gradient Assumes external pressure is 0. Ignores the effect of gravity |
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Shear Forces
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Flow velocity
Laminar versus turbulent Vessel diameter Blood viscosity Shear forces increase as -Linear velocity increases ---Activated coagulation factors are washed away -Viscosity increases -Vessel radius decreases -Flow changes from laminar to turbulent ---High flow rates ---Vessel irregularities |
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Tamponade
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In a closed space, as bleeding continues, external pressure rises to match internal pressure
Effectiveness depends on pressure difference If external pressure rises above a critical value all blood flow ceases and other structures are compromised giving a “compartment syndrome” |
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Activated Plts
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Platelets are activated by thrombin
Activated platelets -Promote coagulation -Stick to Fibrin -Stick to each other -Stick to subendothelial VWF ---Stickiness increases with shear rate |
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Venous Thrombosis and Virchow's triad
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Alteration in the vessel
-Damaged endothelium ---Exposes tissue factor ---Exposes collagen/VWF Alteration in the blood -Increased thrombin generation -Decreased plasmin response Stasis -Valve pockets -Area of hypoxia |
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Arterial Thrombosis
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Atherosclerotic plaques as focus
-Tissue factor exposure by smooth muscle cells Platelets are central -High shear setting -VWF involved Coagulation involved in thrombus growth |
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Inherited thrombophiic factors
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Protein C, Protein S, AT3 deficiencies
FV Leiden, G20210A mutations |
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Congenital Thrombophilic factors
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Factors II, VII, VIII, IX, XI, VWF, homocysteine
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acquired thrombophilic factors
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Age
Lupus anticoagulant, DIC Obesity, sedentary lifestyle, smoking Malignancy, surgery, pregnancy HIT/HITT |
