Coagulation factors

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Hemostasis requires four distinct and interrelated processes

  1. vascular constriction – caused by circulating catecholamines and arachidonic acid
  2. development of a platelet plug – requires presence of von Willibrand’s factor; plug forms thromboxane A2 (from arachidonic acid) which is a potent vasocontrictor and stimulant of platelet aggregation
  3. fibrin formation
    1. all clotting factors except calcium and factor VIII are produced in the liver (II, VII, IX and X as well as protein C and S require vitamin K)
      1. in liver disease, all factors except VIII are diminished
      2. biologic half life of factor VII is the shortest
    2. intrinsic pathway is initiated by activation of factor XII which activates factor XI which activates factor IX, factor IX activates factor X (activation of factor X is enhanced by the presence of factor VIII)
    3. in the extrinsic pathway, factor VII is the key; factor VII is activated by tissue thromboplastin which is a membrane lipoprotein, activated factor VII can activate factor X
    4. after activation of factor X by either pathway, factor X will convert prothrombin to thrombin with factor V enhancing the conversion of prothrombin to thrombin by factor X; thrombin converts fibrinogen to fibrin which is insoluble; fibrin monomers are then polymerized into chains by noncovalent forces and factor XIII is activated by thrombin to catalyze the cross linking of fibrin polymers
  4. fibrinolysis
    1. inhibitor plasma proteins such as thrombomodulin, antithrombin III, and protein C with its cofactor protein S control and modulate hemostasis; plasminogen activators from endothelial cells convert plasminogen to plasmin, plasmin will degrade fibrin and inactivate fators V and VIII
  5. coagulation factors: I-fibrinogen; II-prothrombin; III-thromboplastin; IV-calcium; V-proaccelerin; VI-proaccelerin; VII-proconvertin; VIII-antihemophilic factor A; IX-plasma thromboplasin component; X-Stuart-Prower factor; XI-antihemophilic factor C; XII-Hageman factor; XIII-fibrin stabilizing factor
  6. hypercoagulable states: immobility, malignancy, protein C and S deficiency, antithrombin III deficiency, prothrombin mutation, factor V Leiden mutation, lupus (even thought the PT and PTT are prolonged), heparin induced thrombocytopenia (also a paradox in that the platelet count is low however the platelets aggregate causing uncontrolled thrombosis)
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