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45 Cards in this Set
- Front
- Back
Endothelial products
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1.) collagen
2.) endothelin-1 3.) Tissue Thromboplastin |
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Collagen
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plts. intrinsic, and extrinsic pathways
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endothelin-1
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vasoconstriction
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tissue thromboplastin
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tissue phospholipoprotein, activates F 7 (extrinsic), capable of converting prothrombin to thrombin
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Prothrombotic
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1.) Plt.-activating factor
2.) Tissue factor 3.) von Willebrand factor 4.) plasminogen activator 5.) Factor V |
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Plt activating factor
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in endothelium
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tissue factor
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extrinsic pathway
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vWf
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coagulation factor produced in endothelial cells
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plasminogen activator
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clot removal, stops and break clots
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factor V
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coagulation factor produced in endothelial cells, also in
megakaryocytes |
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Antithrombotic
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1.) Prostacyclin
2.) Thrombomodulin 3.) Tissue plasminogen activator (tPA) 4.) Urokinase 5.) Heparin-like molecules |
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prostacyclin
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prevents plt. adhesion and aggregation
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thrombomodulin
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starts sequence, binds protein C, S and thrombin
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tissue plasminogen activator (tPA)
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fibrinolysis
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Urokinase
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fibrinolysis
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Disrupted Endothelium
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- activates factor 12 (intrinsic)
- exposes collagen - vasoconstriction by endothelin-1 and angiotensin 2 - fibrinolysis starts at the same time as coagulation to balance |
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Glycocalyx
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– surface coat, unique coating, protein coat mediates adhesion and allows adherence of coagulation proteins
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Membrane
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- 2 proteins exposed for adhesion and aggregation
* glycoprotein Ib * glycoprotein IIb/IIIa - open canalicular system |
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glycoprotein Ib
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binds vWF
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glycoprotein IIb/IIIa
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binds fibrinogen
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Open canalicular system
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canals run through plt, delivers contents to
surface |
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Granules
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- Alpha granules
- Dense granules - Lysosomes - Factor 5, plt factor 3, and glycogen |
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Alpha granules
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1.) plt factor 4
2.) plt growth factor 3.) beta thromboglobulin 4.) vWF 5.) thrombospondin |
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Dense granules
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1.) ADP and ATP
2.) calcium 3.) serotonin |
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lysosomes
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hydrolase enzymes
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Adhesion
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- plts adhere to collagen mediated by vWF
1.) filament contract, turns disk to sphere, pseudopods form 2.) contraction and release epinephrine and serotonin promotes vasoconstriction - alpha granules go out and in - release – dense ADP/ATP accelerates plt aggregation, irreversible, adhesion is reversible 3.) glycoproteins IIb/IIIa and Ib appears on the membrane, binds fibrinogen and vWF, increases adhesiveness and helps initiate aggregation |
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Bernard-Soulier Syndrome
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- hereditary
- cell membrane disorder - glycoprotein Ib is absent, Ib is the primary receptor for vWF - have difficulty ADHERING, vWF is necessary for adhesion to subendothelial tissue - aggregation studies normal except for ristocetin |
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Glanzmann’s thrombasthenia
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- cell membrane disorder
- lacking IIb/IIIa - decreased fibrinogen binding - AGGREAGATION affected, aggregation studies abnormal |
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Aggregation
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requires the release reaction to happen first
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Which of the following factors is found in the endothelial cells?
A.) Factor V B.) Factor XII C.) Factor I D.) Factor XIII |
A.) Factor V
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What helps prevent platelets from adhering to normal endothelial cells?
A.) collagen B.) glycoprotein Ib C.) glycoprotein IIb/IIIa D.) vWF E.) prostacyclin |
E.) prostacyclin
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Plt factor 4, beta thromboglobulin, thrombospondin, and plt growth factor are all contained in the:
A.) alpha granules B.) dense granules C.) lysosomes D.) cytoplasm |
A.) alpha granules
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In Bernard Soulier Syndrome, this glycoprotein is decreased or absent:
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Ib
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The primary receptor for fibrin/fibrinogen
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IIb/IIIa
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The primary platelet receptor responsible for platelet adhesion
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Ib
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The cellular ultrastructural component(s) unique to platelets is/are:
A.) cytoplasmic membrane B.) glycocalyx C.) mitochondria D.) lysossomes |
B.) glycocalyx
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Platelet aggregation studies can help identify vW disease using which of the following reagents?
A.) ADP B.) Epinephrine C.) Collagen D.) Ristocetin |
D.) ristocetin
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Aspirin blocks the cyclooxygenase pathway by:
A.) attaching an -COOH to thrombomodulin B.) by deacytlyating antinomysin C.) by acetlyating prostaglandin synthetase D.) blocking the synthesis of kallekrein from prekallekrein |
C.) by acetlyating prostaglandin synthetase
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COX-2 inhibitors may put users at risk of a cardiac event because:
A.) it inhibits production of prostacyclin B.) it inhibits the production of thromboxane a2 C.) it does NOT inhibit the inflammatory response D.) it protects the stomach lining |
A.) it inhibits production of prostacyclin
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Glycoprotein Ib in the platelet membrane primarily binds to:
A.) fibrinogen B.) plt factor 3 C.) beta thromboglobulin D.) vWf |
D.) vWf
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Prostaglandin forms what?
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thromboxane A2 and prostacyclin
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Thromboxane A2
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required for platelet aggregation
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Prostacyclin
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inhibits platelet aggregation and adhesion
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COX-1
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protects the stomach lining and is responsible for the production of thromboxane A2
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COX-2
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- produces prostacyclin
- triggers the pain and inflammatory response - COX-2 inhibitor contributes to pain relief and reduction of inflammation, also decrease in prostacyclin |