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31 Cards in this Set
- Front
- Back
hemostasis
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1. Series of tightly regulated processes that maintain blood in a fluid state in normal vessels
2. Permit the rapid formation of a hemostatic clot at the site of a vascular injury. -Term includes aspects of normal physiology (i.e., processes promoting normal blood flow) as well as pathophysiology (i.e., processes that respond to vascular damage). |
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thrombosis
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1. Hemostasis at the wrong time in the wrong place.
2. Thrombosis refers to blood clot (thrombus) formation within intact vessels that should not contain thrombus. |
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thrombus (plural: thrombi)/Blood Clot
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1. final product of the blood coagulation step in hemostasis.
2. It is achieved via the aggregation of platelets that form a platelet plug, and the activation of the coagulation cascade. |
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Thrombus vs. Thrombosis
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A thrombus is normal in cases of vascular injury but pathologic in instances of thrombosis
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arteriolar vasoconstriction:
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1. reflex neurogenic mechanism in arterioles that decreases the flow of blood, in this context to the site of vascular injury.
2. The reduction in blood flow to the site of vascular injury is the first step of hemostasis |
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endothelin
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a potent endothelium-derived vasoconstrictor that mediates arteriolar vasoconstriction
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platelet adherence
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1. platelets adhere to subendothelial extracellular matrix (ECM), which is exposed only when the endothelium is injured.
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Platelet Activation
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Activation of platelets results in a dramatic shape change (from small rounded discs to flat plates with markedly increased surface area), as well as the release of secretory granules. Within minutes the secreted products recruit additional platelets (aggregation) to form a hemostatic plug. Platelet adherence and activation is the second step of hemostasis and is called primary hemostasis
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Platelet Aggregation and Hemostatic Plug
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Within minutes the secreted products recruit additional platelets (aggregation) to form a hemostatic plug. Platelet adherence and activation is the second step of hemostasis and is called primary hemostasis
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Primary Hemostasis
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Platelet adherence and activation is the second step of hemostasis and is called primary hemostasis
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Name the 4 steps that occur after platelet adherence
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1. activation
2. aggregation 3. hemostati plug 4. primary hemostatis |
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Tissue factor
from where is it produced? what does it act in conjuctation with? what is activated? what is produced? |
1. is a gateway substance (along with factor VII) to the extrinsic pathway of coagulation.
2. It is a membrane-bound procoagulant glycoprotein synthesized by endothelial cells 3. It acts in conjunction with factor VII as the major in vivo initiator of the coagulation cascade 4. eventually culminating in thrombin generation |
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Thrombin
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cleaves circulating fibrinogen into insoluble fibrin, creating a fibrin meshwork, and also induces additional platelet recruitment and activation
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Secondary Hemostatis
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Tissue factor + factor VII -> extrinsic pathway of coagulation cascade -> thrombin -> soluble fibrin (from fibrinogen) -> fibrin meshwork -> consolidation of initial platelet plug
*also induces additional platelet recruitment and activation |
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soluble fibrin
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formed via thrombin cleavage of fibrinogen
forms a meshwork to consolidate initial platelet plug |
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3rd step of hemostatis
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activation of coagulation cascade
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tissue plasminogen activation (t-PA)
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1. One of several components of the counter-regulatory mechanism that reverses the outcome of secondary hemostasis.
2. This reversal of secondary hemostasis is the fourth and final step of hemostasis. |
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4th/final step of hemostatis
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reversal of secondary hemostatis via tissue plasminogen activation
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prostacyclin (PGI2) and nitric oxide (NO)
1. produced by what cells? 2. effects? |
1. produced by the endothelial cells
-stimulated by several factors produced during coagulation (e.g., thrombin and cytokines). 2. Potent vasodilators and inhibitors of platelet aggregation |
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adenosine diphosphatase
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produced by endothelial cells
impede platelet adhesion |
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adenosine diphosphatase
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1. produced by endothelial cells
2. degrades adenosine diphosphate (ADP) and further inhibits platelet aggregation |
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what 4 molecules contribute to anticoagulation?
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1. heparin-like molecules
2. thrombomodulin 3. tissue factor pathway inhibitor (TFPI) 4. antithrombin III |
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Heparin-like molecules
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greatly enhances the inactivation of thrombin and several other coagulation factors through the plasma protein antithrombin III
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Thrombomodulin
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1. binds to thrombin and converts it from a procoagulant into an anticoagulant via its ability to activate protein C, which inhibits clotting by inactivating factors Va and VIIIa
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Protein C
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1. Inhibits clotting via inactivation of factors Va and VIIIA
2. activated by thrombomodulin binding to thrombin |
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protein S
produced by what? |
1. produced by endothelium
2. a co-factor for protein C, and tissue factor pathway inhibitor (TFPI), a cell surface protein that directly inhibits tissue factor-factor VIIa and factor Xa activities |
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and tissue factor pathway inhibitor (TFPI)
found where? |
a cell surface protein that directly inhibits tissue factor-factor VIIa and factor Xa activities
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tissue-type plasminogen activator (t-PA):
what process does it reverse? |
1. a protease that cleaves plasminogen to form plasmin; plasmin, in turn, cleaves fibrin to degrade thrombi.
2. This process reverses steps 1, 2, and 3 of hemostasis. |
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von Willebrand factor (vWF)
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1. a product of normal endothelial cells and an essential cofactor for platelet binding to extracellular matrix in the second step of hemostasis to form the hemostatic plug of primary hemostasis.
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tissue factor: prothrombitic effects of endothelium
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the major activator of the extrinsic clotting cascade. In response to cytokines (e.g., tumor necrosis factor [TNF] or interleukin-1 [IL-1]) or bacterial endotoxin, endothelial cells synthesize tissue factor.
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plasminogen activator inhibitor (PAI):
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1. a protein (a serine protease inhibitor) produced by endothelium that limits fibrinolysis and tends to favor thrombosis.
2. Humans have several PAI genes. |