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31 Cards in this Set
- Front
- Back
What is a thrombus? |
Pathologic formation of an intravascular blood clot.
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Where can a thrombus be formed?
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In arteries or veins.
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What is the MC location of a venous thrombus?
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Deep veins of the lower limb below the knee.
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A thrombus is characterized by what?
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(1) Lines of Zahn
(2) Attachment to vessel wall R: RBC, F: PLT, fibrin |
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On autopsy, you observe a blood clot in the left anterior descending coronary artery. How could you determine if this clot was formed after he died (postmorten clot) or was the cause of his death?
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Lines of zahn and attachment to vessel wall is not seen in a postmorten clot.
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What are the major risk factors for thrombosis?
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Virchow's triad
(1) Disruption in blood flow (2) Endothelial cell damage (3) Hypercoagulable state |
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What is the normal healthy blood flow pattern called? What is the significance of this pattern of blood flow?
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Laminar pattern (layered).
It helps keep clotting factors dispersed and inactivated. |
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Provide three examples that abnormal blood flow (of Virchow's triad) can produce thrombosis.
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(1) Stasis for example. Immobilization increases the risk via stasis of blood.
(2) Cardiac wall dysfunction. A-fib. Atrium is not moving properly and blood is gonna become more static. (3) Aneurysm. (Balloon-like dilatation of a portion of the blood vessel). The pocket is going to disrupt laminar flow, causing irregular flow and increase the risk of thrombus formation. |
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Why does endothelial damage increase the risk for thrombosis?
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Because the endothelium is highly protective against the formation of a thrombus.
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What does the endothelium do to protect against the formation of thrombosis?
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(1) It's a barrier, hiding away subendothelial collagen and tissue factor.
(2) PGI2 (prostacyclin) synthesis. Blocks PLT aggregation. (3) NO causes vasodilation. (4) Heparin-like molecules. Activate antithrombin III, inactivates thrombin. (5) tPA, converts plasminogen to plasmin. (6) Thrombomodulin, takes thrombin and modulates its activity to activate protein C, which inactivates V and VIII. |
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Plasmin cleaves what?
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(1) Fibrin, fibrinogen
(2) Clotting factors (3) Blocks platelet aggregation |
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How is PGI2 and plasmin similar in their effect?
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Plasmin has many roles, but one of them is to block PLT aggregation, which is the role of PGI2.
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What are some examples of endothelial damage?
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(1) Atherosclerosis.
(2) Vasculitis (3) High levels of homocysteine |
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What inherited enzyme defect can cause an increase in the risk of thrombosis? What are its inheritance pattern?
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Homocystinuria (Cystathionine beta synthase deficiency; CBS). AR. Deficiency of cystathionine synthase which combines homocysteine with serine to create cystathionine.
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What are the ways by which we can have elevated homocysteine?
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(1) Vitamin B12 or folate deficiency.
- Can no longer convert homocysteine to methionine |
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Draw a simplified scheme of the role of B12 in the body (one of its roles).
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What is the life expectancy for patients with CBS?
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They usually die at a young age
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CBS deficiency is characterized clinically by [...]
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(1) Mental retardation
(2) Vessel thrombosis (3) Lens dislocation (4) Long slender fingers |
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How can you achieve a hypercoagulable state?
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Due to excessive procoagulant or defective anticoagulant proteins.
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What is the classic presentation of a person with a hypercoagulable state?
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They tend to have recurrent DVTs and DVTs at a young age.
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In a person with a hypercoagulable state, what other sites than the deep veins of the legs would clots occur?
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Hepatic and cerebral veins
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Lack of what natural endogenous anticoagulants can create a hypercoagulable state? Elaborate.
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Protein C and S deficiency.
(1) They normally inactivate V & VIII. (2) Decreased negative feedback on coagulation cascade. (3) Patients become hypercoagulable. |
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In protein C and protein S deficiencies, there is an increased risk for what?
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Warfarin skin necrosis.
- The transient initial window of hypercoagulation is more severe in these patients when they already have low levels of C and S and warfarin transiently makes it worse. |
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In warfarin therapy, what are the first factors to be degraded due to their shorter half life? What is the consequence?
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Protein C and protein S. A transient hypercoagulable state.
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What is factor V leiden?
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Patients have a mutated form of factor V. This makes it resistant to cleavage by protein C and protein S.
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What is the MC inherited cause of hypercoagulable state?
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Factor V leiden
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This disease is caused by a point mutation in prothrombin. What is it?
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Prothrombin 20210A. Results in increased gene expression. Promotes thrombus formation.
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This disorder induces a hypercoagulable state. It is caused by a deficiency in an anticoagulant that is normally enhanced by heparin-like molecules from endothelial cells. What is it?
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Antithrombin III deficiency. Decreases the protective effects of heparin-like molecules produced by endothelium, increasing the risk for thrombosis.
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A patient has a hypercoagulable state. You administer heparin at standard dosing. Later you note that his PTT has not increased. What is going on?
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Antithrombin III deficiency.
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In ATIII deficiency you have to give ____________ (low/high) doses of heparin to increase PTT.
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high
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What drug used by sexually active women can cause a hypercoagulable state? Why does this happen?
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Oral contraceptives.
Estrogen induces increased production of coagulation factors and increases the risk for thrombosis. |