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29 Cards in this Set
- Front
- Back
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prostacyclin
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-secreted by endothelial cells
-platelet aggregation inhibitor |
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nitrous oxide
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-secreted by endothelial cells
-platelet inhibitor and relaxes vasculature |
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CD39
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-found on the surface of endothelial cells
-ecto-ADPase: breaks down ADP released from platelets |
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heparin sulfate
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-secreted by endothelial cells
-inhibits thrombin |
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Tissue Factor Pathway Inhibitor (TFPI)
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-secreted by endothelial cells
-inhibits activation of the coagulation mechanism |
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Thrombomodulin
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-found on surface of endothelial cells
-activates Protein C which inactivates Factor Va and VIIIa, inhibiting fibrin formation |
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Tissue Plasminogen Activator (TPA)
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-secreted by endothelial cells
-initiates fibrinolysis |
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Plasminogen Activator Inhibitor (PAI-1)
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-secreted by endothelial cells
-Anti-fibrinolytic |
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von Willebrand's factor
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-synthesized in the endothelial cells and megakaryocytes
Functions: - Mediate platelet adhesion to the collagen in the subendothelium -Bind Factor VIII to protect it from proteolysis in the plasma. - Note: Plasma vWF is unable to bind to non-activated platelets in circulation. |
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ADAMTS13
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cleaves the ultralarge multimers into smaller vWF multimers as they are secreted by the endothelial cells. congenital or acquired decrease in the activity of this enzyme may lead to thrombotic thrombocytopenic purpura (TTP).
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Platelet adhesion requires the following
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# Collagen in exposed subendothelium
# Platelet GP Ib-IX (found on resting platelets) # von Willebrand Factor (vWF) |
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Thromboxane A2 (TxA2)
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-released by activated platelets
-promotes release of substances from the platelet granules -promotes activation and aggregation of other platelets -TxA2 has a very short half-life in the plasma |
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Thrombospondin
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enhances platelet adherence and aggregation by attaching to platelet receptors
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Aspirin
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-inactivates cyclooxygenase by acetylating it
-result is the decreased ability of platelets to synthesize thromboxane A2(a pro-aggregation agent) -inhibits the endothelial cells from synthesizing prostacyclin or PGI2 (an anti-aggregation agent). |
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Primary vs Secondary Aggregation
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Primary Aggregation is reversible
* Adherent platelets release ADP * Fibrinogen binds to calcium-GP IIb-IIIa complexes on the activated platelet Secondary Aggregation is irreversible * Mediated by release of substances from platelet granules * Involves the formation of Thromboxane A2 |
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Platelet aggregation requires the following
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-Platelet GP IIb-IIIa
-Fibrinogen -Calcium |
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I
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Fibrinogen
72-120 hr plasma half-life Acute Phase Reactant (Levels increase in inflammation, pregnancy, oral contraceptives) Highest Plasma Concentration Not Present in Serum |
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II
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Prothrombin
72 hr plasma half-life Not Present in Serum |
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III
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Tissue Factor (found on surface of extravascular cells)
no plasma half-life |
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V
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Labile Factor
12 hr plasma half-life Storage Labile Unstable in EDTA Not Present in Serum |
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VII
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Stable Factor
3-6 hr plasma half-life Shortest Plasma Half-Life Activated at Cold Temperatures |
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VIII
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-anti-Hemoplilic factor
-8-12 hr plasma half-life -Storage Labile -Acute Phase Reactant (Levels increase in inflammation, pregnancy, oral contraceptives) -Not Present in Serum -bound to von Willebrand Factor in plasma |
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IX
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Christmas factor
24 hr plasma half-life |
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X
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Stuart-Prower Factor
36 hr plasma half-life |
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XI
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Plasma Thromboplastin antecedent
72 hr plasma half-life |
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XII
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Hageman Factor
48 hr plasma half-life |
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PK
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Prekalikrein (Fletcher Factor)
35 hr plasma half-life |
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HMWK
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high molecular weight kininogen
150 hr plasma half-life |
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XIII
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Fibrin-stabilizing factor
240 hr plasma half-life Not Present in Serum |
