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19 Cards in this Set
- Front
- Back
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Overall goal of hemostasis |
Creation of platelet plug but with significant injury requires formation of a stable fibrin clot. |
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Steps to primary hemostasis |
injury to the vessel vasoconstriction platelet adhesion platelet activation platelet aggregation. |
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blood vessel layers |
Intima - inner most layer- separating blood from the sub endothelial surface. media - sub endothelial space - extremely thrombogenic and very active - contains collagen and fibronectin Adventitia -controls blood flow by influencing the vessels degree of contraction based on release of mediators from the endothelial layer. |
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Vasoconstrictors/Vasodilators |
Both regulators are releasers from intima and effect the adventitia Constrictors - thromboxane A2, endothelin, ADP (adenosine diphosphate) Dilation - Nitric Oxide, Prostacyclin. Dilation dominates in non-injured vessels to ensure adequate blood flow |
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Platelets |
Life span 8-12 days normal 150-300 formed in bone marrow from megakaryocytes no nucleus, DNA, or RNA= don't reproduce Platelets are blood inactive 33% sequestered in spleen |
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Activated platelets |
Activated by the presence of Tissue Factor Receptor sites - GP Ib= binds platelets to vWF GP IIb/IIIa binds platelet to platelet Granules released alpha and dense |
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Mechanism of Injury |
Low shear= platelets attach to collagen via integrin receptors on their surface high shear= causes release of NO which prevents platelet adhesion and binding of fibrinogen. -- Requires vWF |
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Vasoconstriction |
ANS mediated immediate vasoconstriction, lasts 20-30 minutes Serotonin, Thromboxane A2 and ADP are released (constrict and limit blood loss) Decreased NO and increased endothelin |
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Adhesion |
Collagen and vWF exposed to blood at site of injury decrease NO allows platelets to get closer to injured area of vessel |
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Von Willibrand Factor |
floating around in blood secreted from endothelial cells at site of injury binds to subendothelial collagen binds GpIb receptor of platelets |
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Activation |
Binding of GpIb receptor activates phospholipase C (PLC) which changes shape of platelet |
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Degranulation |
IP3 causes degranulation Alpha grannule= fibrinogen and vWF Dense = serotonin (smooth muscle cells), ADP (activates platelets and promotes aggregation), calcium (needed for 2nd hemostasis), histamine, epi Thromboxane A2 - opposite of prostacycline = cause amore platelet to activate and helps with aggregation |
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Aggregation |
Mediated primarily through GpIIbIIa binds to fibrinogen allowing platelets to bind to other platelets creates clump of a plug of platelets at site of injury |
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Aspirin |
Impairs platelet aggregation for the lifespan of the platelet 8-12 days |
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Nsaids |
inhibits platelet aggregation for 24-48 hours |
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integrilin/aggrastat |
reversibly binds to platelet receptor= prevent binding of fibrinogen |
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plavix |
inhinit binding adp to the platelet... inhibits platelet aggregation |
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first responders |
platelet first responder to the bleeding... key to activation of the coagulation cascade. |
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Primary hemostasis is controlled by what |
thromboxane and prostacyclin balance |
