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45 Cards in this Set

  • Front
  • Back
Endothelial products
1.) collagen
2.) endothelin-1
3.) Tissue Thromboplastin
Collagen
plts. intrinsic, and extrinsic pathways
endothelin-1
vasoconstriction
tissue thromboplastin
tissue phospholipoprotein, activates F 7 (extrinsic), capable of converting prothrombin to thrombin
Prothrombotic
1.) Plt.-activating factor
2.) Tissue factor
3.) von Willebrand factor
4.) plasminogen activator
5.) Factor V
Plt activating factor
in endothelium
tissue factor
extrinsic pathway
vWf
coagulation factor produced in endothelial cells
plasminogen activator
clot removal, stops and break clots
factor V
coagulation factor produced in endothelial cells, also in
megakaryocytes
Antithrombotic
1.) Prostacyclin
2.) Thrombomodulin
3.) Tissue plasminogen activator (tPA)
4.) Urokinase
5.) Heparin-like molecules
prostacyclin
prevents plt. adhesion and aggregation
thrombomodulin
starts sequence, binds protein C, S and thrombin
tissue plasminogen activator (tPA)
fibrinolysis
Urokinase
fibrinolysis
Disrupted Endothelium
- activates factor 12 (intrinsic)
- exposes collagen
- vasoconstriction by endothelin-1 and angiotensin 2
- fibrinolysis starts at the same time as coagulation to balance
Glycocalyx
– surface coat, unique coating, protein coat mediates adhesion and allows adherence of coagulation proteins
Membrane
- 2 proteins exposed for adhesion and aggregation
* glycoprotein Ib
* glycoprotein IIb/IIIa
- open canalicular system
glycoprotein Ib
binds vWF
glycoprotein IIb/IIIa
binds fibrinogen
Open canalicular system
canals run through plt, delivers contents to
surface
Granules
- Alpha granules
- Dense granules
- Lysosomes
- Factor 5, plt factor 3, and glycogen
Alpha granules
1.) plt factor 4
2.) plt growth factor
3.) beta thromboglobulin
4.) vWF
5.) thrombospondin
Dense granules
1.) ADP and ATP
2.) calcium
3.) serotonin
lysosomes
hydrolase enzymes
Adhesion
- 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
Bernard-Soulier Syndrome
- 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
Glanzmann’s thrombasthenia
- cell membrane disorder
- lacking IIb/IIIa
- decreased fibrinogen binding
- AGGREAGATION affected, aggregation studies abnormal
Aggregation
requires the release reaction to happen first
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
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
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
In Bernard Soulier Syndrome, this glycoprotein is decreased or absent:
Ib
The primary receptor for fibrin/fibrinogen
IIb/IIIa
The primary platelet receptor responsible for platelet adhesion
Ib
The cellular ultrastructural component(s) unique to platelets is/are:
A.) cytoplasmic membrane
B.) glycocalyx
C.) mitochondria
D.) lysossomes
B.) glycocalyx
Platelet aggregation studies can help identify vW disease using which of the following reagents?
A.) ADP
B.) Epinephrine
C.) Collagen
D.) Ristocetin
D.) ristocetin
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
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
Glycoprotein Ib in the platelet membrane primarily binds to:
A.) fibrinogen
B.) plt factor 3
C.) beta thromboglobulin
D.) vWf
D.) vWf
Prostaglandin forms what?
thromboxane A2 and prostacyclin
Thromboxane A2
required for platelet aggregation
Prostacyclin
inhibits platelet aggregation and adhesion
COX-1
protects the stomach lining and is responsible for the production of thromboxane A2
COX-2
- produces prostacyclin
- triggers the pain and inflammatory response
- COX-2 inhibitor contributes to pain relief and reduction of inflammation, also decrease in prostacyclin