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APC
- -cleave surface gp of Va and VIIIa
- -stimulates the release of tPA
- -inactivates inhibitors of t-PA
-
alpha2-antiplasmin
- -can not bind clot bound plasmin
- -allows the destruction of a fibrin clot without the destruction of fibrinogen in circulation
-
strptokinase
not an enzyme but an allosteric modifier of human plasminogen that allows plasminogen to autocatylitically activate itself
-
Plasminotigen activator release
after stress
-
Hemophilia A
- -x linked
- - bleeding into soft tissues (hematomas)
-
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
-
AT3
mostly thrombin but has some activity on 8,9,10,11
-
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
-
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
-
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
-
Fondaparinux
- pentasaccharide that enhances AT3 interaction with Xa
- HIT is not a complication since fondaparinux does not bind for PF4
-
Direct thrombin inhibitors?
- Hirudin- discovered in leeches
- irreversible reaction
- bivalrudin, high binding aftinity for thrombin with a transient affect
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