Thrombosis Flashcards

1
Q

1) Diagram the intrinsic, extrinsic and “new” coagulation pathways.

A

intrinsic (in blood): Kalkrein + Factor 12 > Factor 11> Factor 9 +Factor 8 > Factor 10 + 5 > Factor II (prothrombin) > factor 13
extrinsic (in tissue): Factor 7 > Factor 7a (Tissue Factor) > Factor 10 (everything else same). especially effected by Vitamin K deficiency (Factors 2,7,9,10, are K dependent)
New:

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2
Q

2) Explain how PT and PTT tests are performed.

A

blood in lab. If PTT does not correct after mixing with fresh normal blood, anticlotting factors present. If deficiency in something will correct.

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3
Q

3) Name the four stages of hemostasis and explain what is occurring in each.

A

contraction of vessel - platelet aggregation - activation of coagulation cascade, thrombus and anti-thrombolis events ( endothelium release of RBCs, t-PA, thrombomodulin, etc)

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4
Q

4) Explain the “3 A’s” associated with the role of platelets in hemostasis.

A

adhesion due to Von Willebrands factor
activation - change in surface protein GPIIa
aggregation of fibrinogen due to cross-linking with GPIIb/IIIa on platelets

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5
Q

5) Name three functions of von Willebrands factor.

A

adhesion - conformational change leads to binding to GP1a
aggregation: binds platelet GPIIB/IIa
Factor 8 binding to site of hemorrhage

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6
Q

6) Explain the roll of factor XIII in coagulation.

A

cross-links lysine and glutamine chains to stabilize fibrin clot

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7
Q

7) Name the three inherent anticoagulant systems/mechanisms in the blood.

A

antithrombin: binds heparin, thrombin to neutralize Factors 9/10/11/12
thrombomodulin release from endothelial cells that binds Protein C and thrombin to inactive Factor 5 & 8,
fibrinoyltic systems: plasminogen from liver

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8
Q

8) Identify four types of hemophilia and the factors that are deficient in each.

A

Von Willebrands disease: most common. deficiency in VW
Hemophilia A: deficinency in factor 8
Hemophilia B: factor 9 deficiency
Hemophilia C: factor 11 deficiency. rare.

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9
Q

9) Name the three components of “Virchow’s triad” active in thrombosis.

A

endothelial injury, abnormal blood flow, hyper-coagulation

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10
Q

10) Explain the abnormality present in factor V Leiden hypercoagulability.

A

activated protein C resistance due to cleavage of receptor on Factor 5

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11
Q

11) Discuss the etiological, clinical, and laboratory findings associated with DIC.

A

inappropriate coagulation in vessels leads to consumption of pro-coagulants leading to bleeding.
elevated D-dimer (fibrinogen degradation), thrombocytopenia, prolonged coagulation time, fragmented red blood cells.
associated with: obstetrics (rare), sepsis, leukemias, viremia

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12
Q

12) Calculate an INR from a patient’s PT value and the normalized PT value.

A

(PT/mean PT)^INS (standardization of thromboplastin factors in that particular lab)

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13
Q

13) Explain the mechanism behind three forms of antiplatelet.

A

Coumadin: Vitamin K antagonist decreases 2, 7,9, 10
Heparins: inhibit thrombin action (factor 2)
t-PA, streptokinase: lyse clot

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