1. APC
    • -cleave surface gp of Va and VIIIa
    • -stimulates the release of tPA
    • -inactivates inhibitors of t-PA
  2. alpha2-antiplasmin
    • -can not bind clot bound plasmin
    • -allows the destruction of a fibrin clot without the destruction of fibrinogen in circulation
  3. strptokinase
    not an enzyme but an allosteric modifier of human plasminogen that allows plasminogen to autocatylitically activate itself
  4. Plasminotigen activator release
    after stress
  5. Hemophilia A
    • -x linked
    • - bleeding into soft tissues (hematomas)
  6. Vitamin K
    • cofactor in the gamma carboxilation of factors 2,7,9,10
    • the carboxilation is of the glutamate side chain
    • carboxilated side chains bin to calcium and then to activates platelets
  7. AT3
    mostly thrombin but has some activity on 8,9,10,11
  8. High molecular wieght heparin
    Will bind to other plasma protein then AT3, this can cause the active amount in the blood to be reduced and spontaneous thrombi can be generated
  9. HITs
    • heparin binds to platelet factor four
    • induces a conformational change in PF4 causing the immune system to not recognize it
    • antibodies are made against heparin PF4 complex
    • when antibodies bind the platelets become activated
  10. Warfarin mechanism
    • bines vit K reductase enzyme needes to regenerate vit K
    • reduced gamma carboxilation, factors can not bind calcium or form complexes after coagulation is initiated
    • also blocks protein S and C
  11. Fondaparinux
    • pentasaccharide that enhances AT3 interaction with Xa
    • HIT is not a complication since fondaparinux does not bind for PF4
  12. Direct thrombin inhibitors?
    • Hirudin- discovered in leeches
    • irreversible reaction
    • bivalrudin, high binding aftinity for thrombin with a transient affect
Card Set
Biochem 45