Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
26 Cards in this Set
- Front
- Back
What factors are involved in the extrinsic coagulation pathway?
|
Tissue factor converts VII to active form. Coverts X to active form.
|
|
What factors are involved in the intrinsic coagulation pathway?
|
Exposed collagen converts XII to active form, converts XI to active form, coverts IX to active form. Thrombin converts VIII to active form. VIII and IX convert X to active form.
|
|
What factors are involved in the common coagulation pathway?
|
X converted to active form. With V, converts II, converts fibrinogen to fibrin, which aggregates into a mesh with XIII.
|
|
What is the vessel's response to injury?
|
Vasoconstriction
Primary hemostasis (platelet plug) Secondary hemostasis (fibrin clot) Fibrinolysis |
|
What are the actions of thrombin? What are the modulators?
|
Cleaves fibrinogen
Platelet aggregation Activates XIII, VIII, and V Activates contact factor Activates protein C Modulated by antithrombin III and thrombomodulin. |
|
How is the platelet plug formed upon tissue injury?
|
vWF binds to exposed collagen, which then binds to GpI on platelets. Platelets release calcium and ADP. ADP induces GpIIb/IIIa expression, which binds to fibronigen on other platelets.
|
|
What are the three deficiencies associated with platelet binding? What are the mutations?
|
von Willebrand disease- deficiency in vWF
Bernard-Soulier syndrome- deficiency in GpIb Glanzmann thrombasthenia- GpIIb-IIIa |
|
How are factor VIII and vWF related?
|
Factor VIII is carried on vWF. When vWF binds to exposed collagen, VIII is released to join the coagulation cascade.
|
|
How is the extrinsic pathway initiated?
|
When blood is exposed to non-vascular tissue factor in the sub-endothelial space. TF binds to VII.
|
|
How is the intrinsic pathway initiated?
|
Intravascular contact activation with thrombogenic surface.
|
|
What are regulators of the coagulation pathway?
|
Antithrombin III blocks thrombin
Protein C and S block factor VIII and V Tissue factor pathway inhibitor blocks factor VII Fibrinolysis |
|
What molecules are anticoagulants?
|
antithrombin III
thrombomodulin Protein C, S Tissue factor pathway inhibitor Fibrinolysis PGI2 and NO Intact endothelium |
|
What molecules are procoagulant?
|
Tissue factor
Thrombin APC resistance vWF |
|
How does the endothelial cell inhibit coagulation?
|
Heparan sulfate
Prostacyclin and NO Thrombomoculin TFPI tPA |
|
What are facilitators of fibrinolysis?
|
Tissue plasminogen activator (tPA)
|
|
What are inhibitors of fibrinolysis?
|
Plasminogen activator inhibitor (blocks tPA degradation of plasminogen to plasmin)
alpha2 plasmin inhibitor (blocks plasmin degradation of fibrin) |
|
What is the process of fibrinolysis?
|
Plasminogen converted to plasmin by tPA.
Plasmin breaks down fibrin to monomers, then degraded into D-dimers. |
|
What is tested by prothrombin time?
|
Extrinsic pathway- factor VII deficiency; liver function; Warfarin function, Vitamin K deficiency
|
|
What is tested by partial thromboplastin time?
|
Intrinsic pathway- factors VIII, IX, XI; von Willebrand disease, Heparin function
|
|
How is the INR developed? What is it used for?
|
Aids in the monitoring of patients taking anticoagulants.
INR= (PT patient/ mean PT normals) ^ ISI (ISI- international sensitivity index) |
|
What diseases could be causing abnormal PT and aPTT?
|
Anticoagulant
Liver disease Vitamin K deficiency Factors II, V, X deficiency DIC Fibrinolysis Hypofibrinogenemia |
|
What are mixing studies? What do they detect?
|
Used to distinguish deficiency from inhibitor.
Patient's serum is mixed with normal plasma. In a deficiency, the abnormal test should be corrected with the mixing. In an inhibitor, the abnormal test will not be corrected with mixing test. |
|
What special tests are done for Von Willebrand disease?
|
VIII clotting activity
VIII antigen quantitative measure vWF antigen measurement vWF ristocetin cofactor activity Molecular testing |
|
What would be the causes of abnormal bleeding time?
|
vWF
Thrombocytopenia DIC Fibrinolysis Aspirin |
|
What are the results of DIC?
|
Consumption of platelets, fibrinogen, factors II, V, VIII, and depletion of antithrombin II.
Results in secondary fibrinolysis and anticoagulation |
|
Which factors are dependent on vitamin K? Where does the processing occur?
|
Factors II, VII, IX and X; protein C and S.
Carboxylation of the factors in the liver depend on vitamin K. |