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31 Cards in this Set

  • Front
  • Back
Steps of Hemostasis
1. Vasoconstriction
2. Formation of platelet plug
3. formation of fibrin mesh
4. Dissolution of platelet clot
When broken blood vessel, what happens?
-Endothelial cells release endothelin
-Platelets release serotonin
Formation of platelet plug?
-endothelial cells release adhesion factors: Von Willebrand factor
-Platelets release thrombin & thromboxene
Both make platelets sticky and cause them to aggregate
Formation of fibrin mesh
Platelets release growth factors for repair
Dissolution of platelet clot
Intrinsic pathway
-In response to abnormal blood vessel wall.
-Activated by proteolysis of peptide bonds in inactive zymogen to active protease
Extrinsic pathway
-Substances released from injured tissues
Both intrinsic and extrinsic pathways converge at?
Factor X
Factor X
Fibrin cross-linked
Factor XIIIa
Serine Protease
Has a critical Ser residue at active site
Which are not serine proteases but are all activated by thrombin?
tissue factor
factors VIIIa, Va, XIIIa
characteristics of fibrinogen
highly negative charge, does not aggregate
How does fibrinogen lose its central negative charge
Upon activation by thrombin
How does fibrin become cross-linked fibrin clot?
An isopeptide bond formation between Gln and Lys side chains
Deficiency in factor XIII causes?
Hemophilia A
Factor VIII missing
Hemophilia B
Deficiency of factor IX
TPA=Tissue Plasminogen Activator
Fibrin clot--->Free peptides (clot dissolved)
Regulation of clotting via endothelial cells
Produce thrombomodulin
Regulation via control of active thrombin
1. regulation of prothrombin--->thrombin
2. inactivation of thrombin by anti-thrombin III
Regulation of the clotting cascade
Amplification of cascade allows you to accumulate huge # of inhibitors for the early party of the pathway.
In prothrombin, Glu---> GLA
Vitamin K
The affect of GLA
Binds to Ca+2 ions-->anchors prothrombin to CM-->brings prothrombin close to factors Xa, Va which activate it-->thrombin
what happenes to regulation when there is no vitamin K
GLU cannot --> GLA -->no GLA-->no Ca+2 binding-->no anchoring to CM-->slow activation & poor clotting
Antagonists of vitamin K
Dicoumarol, Warfain-structural analogs of Vitamin K
-Can be used as anti-coagulants to prevent thromboses
Antithrombin belongs to SERPINS
inactivates thrombin
Negatively charged glycosaminoglycans that binds to antithrombin III-->promotes antithrombin III binding to thrombin-->irreversibly inactivates it
Does antithrombin III inhibit only thrombin?
No, it inhibits other serine proteases too.