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23 Cards in this Set
- Front
- Back
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Platelets
General characteristics |
Anucleate discs of megakaryocyte origin
Normal 150-400K Life span 7-10 days (~1wk) Alpha granules are most abundant with procoagulants and anticoagulants Reactive surface |
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Alpha granules consist of
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von Willebrand factor - platelet adhesion
Fibrinogen - platelet aggregation Factor V – catalyst for coagulation Protein S - anticoagulation Platelet Factor 4 - neutralizes heparan |
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Summarize arachidonic acid pathway
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Collagen and thrombin stimulate the arachidonic acid pathway
PG-G2 and TXA2 are made and increase platelet activation, vasoconstriction and platelet aggregation |
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Platelets-describe functions
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Circulate in inactive state
activated by exposure to collagen/matrix proteins Activation results: ADHESION (GPIb and vWf) AGGREGATION (GPIIb/IIIa and fibrinogen) Conformational change w/ pseudopods (increase surface area) |
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How is platelet plug made?
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collagen induces platelet degranulation
vWf bridges platelets to collagen Fibrinogen binds Plt to plt via GPIIb/IIIa |
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What is the function of platelet plug?
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Limits bleeding temporarily but can not sustain it
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How is the platelet plug stabilized?
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Coagulation cascades solidify the platelet plug.
This process ultimately produces fibrin that stabilize platelet plug. |
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Name coagulation factors that are vitamin K-dependent.
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II, VII, IX, and X
Protein C and Protein S |
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Extrinsic pathway
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Major pathway for IN VIVO activation
Requires Tissue Factor (TF) for activation (extrinsic to vascular system) Tissue Factor acts as Cofactor/Receptor for FVII TF and Calcium bind to FVII to activate FVII |
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Intrinsic pathway
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Starts with collagen activation of FXII
FXlla activates HMWK and PK and FXI HMWK and PK are responsible for concentration and amplification of the cascade Importance of FXll, HMWK and PK in coagulation? |
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Which of the coagulation factor start the common coagulation pathway?
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Factor IX activation by Factor XI of the intrinsic pathway or Factor VII complex of the extrinsic pathway start the common pathway on the platelet surface.
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What does IX activate?
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Factor IX activate Factor X on the platelet surface when Ca2+ and Factor VIII are present. Ca2+ and FVIII are required to activate Factor X.
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Factor VIII
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Similar structure to Factor V – domains A,B, and C
cleaved and activated by thrombin FVIII carried intravascularly by vWf. The vWF acts to: stabilize FVIII prolongs T1/2 of Factor VIII transports to site of injury concentrates it at site of injury |
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Factor V
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Manufactured in platelets and liver (EXCEPTION)
Activated by thrombin which cleaves B domain Serves as anchor on platelet to attach FXa and II (prothrombin) |
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Final common pathway
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Prothrombinase Complex
Factor Xa with Ca, Phospholipid, and FV Converts prothombin (II) to thrombin (IIa) Thrombin converts fibrinogen to fibrin Fibrin formation |
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Control of coagulation
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Hemodilution
Hepatic and RES clearance Proteolytic effects of thrombin deactivates V, VIII, XI Inhibitors Fibrinolysis |
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Inhibitors
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Inhibitors bind to receptor site, e.g.
Antithrombin III (AT III) Protein C and S (require vitamin K) Tissue Factor Inhibitor: key inhibitor of coagulation pathway |
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Anti-thrombin III
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ATIII inactivated thromin (IIa) and Xa but very slowly
ATIII binds to heparin/heparan which catalyzes this reaction and inactivates the factors more permanently Heparin/Heparan dissociates and binds again to another Thrombin |
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Proteins C and S
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Vitamin K dependent
Protein S is cofactor Activated Protein C (APC) can inhibit free FV only APC + Protein S can inactivate free and bound FV |
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Tissue Factor Inhibitor
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TFI binds to factor Xa and inhibits factor Vlla and factor Xa
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Two types of fibrinolysis
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Cellular fibrinolysis
Plasma fibrinolysis |
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Plasma fibrinolysis
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Plasminogen to plasmin
Intrinsic Activation (more key to the fibrinolysis than in vivo coagulation)- FXII, FXI, PK, HK, and Kallikrein Extrinsic Activation tPA (tissue plasminogen activator) 4 minute half life Circulates bound to Plasminogen Activator Inhibitor High affinity for fibrin |
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Plasmin
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Main function is to degrade fibrin
Also degrades multiple coagulation factors Breaks fibrin into split products Rapidly inactivated in fluid phase but protected when bound to clot |
