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31 Cards in this Set

  • Front
  • Back

What is a thrombus?

Pathologic formation of an intravascular blood clot.
Where can a thrombus be formed?
In arteries or veins.
What is the MC location of a venous thrombus?
Deep veins of the lower limb below the knee.
A thrombus is characterized by what?
(1) Lines of Zahn
(2) Attachment to vessel wall

R: RBC, F: PLT, fibrin
(1) Lines of Zahn
(2) Attachment to vessel wall

R: RBC, F: PLT, fibrin
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?
Lines of zahn and attachment to vessel wall is not seen in a postmorten clot.
What are the major risk factors for thrombosis?
Virchow's triad

(1) Disruption in blood flow
(2) Endothelial cell damage
(3) Hypercoagulable state
Virchow's triad

(1) Disruption in blood flow
(2) Endothelial cell damage
(3) Hypercoagulable state
What is the normal healthy blood flow pattern called? What is the significance of this pattern of blood flow?
Laminar pattern (layered).

It helps keep clotting factors dispersed and inactivated.
Provide three examples that abnormal blood flow (of Virchow's triad) can produce thrombosis.
(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.
Why does endothelial damage increase the risk for thrombosis?
Because the endothelium is highly protective against the formation of a thrombus.
What does the endothelium do to protect against the formation of thrombosis?
(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.
Plasmin cleaves what?
(1) Fibrin, fibrinogen
(2) Clotting factors
(3) Blocks platelet aggregation
How is PGI2 and plasmin similar in their effect?
Plasmin has many roles, but one of them is to block PLT aggregation, which is the role of PGI2.
What are some examples of endothelial damage?
(1) Atherosclerosis.
(2) Vasculitis
(3) High levels of homocysteine
What inherited enzyme defect can cause an increase in the risk of thrombosis? What are its inheritance pattern?
Homocystinuria (Cystathionine beta synthase deficiency; CBS). AR. Deficiency of cystathionine synthase which combines homocysteine with serine to create cystathionine.
What are the ways by which we can have elevated homocysteine?
(1) Vitamin B12 or folate deficiency.
- Can no longer convert homocysteine to methionine
(1) Vitamin B12 or folate deficiency.
- Can no longer convert homocysteine to methionine
Draw a simplified scheme of the role of B12 in the body (one of its roles).
What is the life expectancy for patients with CBS?
They usually die at a young age
CBS deficiency is characterized clinically by [...]
(1) Mental retardation
(2) Vessel thrombosis
(3) Lens dislocation
(4) Long slender fingers
How can you achieve a hypercoagulable state?
Due to excessive procoagulant or defective anticoagulant proteins.
What is the classic presentation of a person with a hypercoagulable state?
They tend to have recurrent DVTs and DVTs at a young age.
In a person with a hypercoagulable state, what other sites than the deep veins of the legs would clots occur?
Hepatic and cerebral veins
Lack of what natural endogenous anticoagulants can create a hypercoagulable state? Elaborate.
Protein C and S deficiency.

(1) They normally inactivate V & VIII.
(2) Decreased negative feedback on coagulation cascade.
(3) Patients become hypercoagulable.
In protein C and protein S deficiencies, there is an increased risk for what?
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.
In warfarin therapy, what are the first factors to be degraded due to their shorter half life? What is the consequence?
Protein C and protein S. A transient hypercoagulable state.
What is factor V leiden?
Patients have a mutated form of factor V. This makes it resistant to cleavage by protein C and protein S.
What is the MC inherited cause of hypercoagulable state?
Factor V leiden
This disease is caused by a point mutation in prothrombin. What is it?
Prothrombin 20210A. Results in increased gene expression. Promotes thrombus formation.
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?
Antithrombin III deficiency. Decreases the protective effects of heparin-like molecules produced by endothelium, increasing the risk for thrombosis.
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?
Antithrombin III deficiency.
In ATIII deficiency you have to give ____________ (low/high) doses of heparin to increase PTT.
high
What drug used by sexually active women can cause a hypercoagulable state? Why does this happen?
Oral contraceptives.

Estrogen induces increased production of coagulation factors and increases the risk for thrombosis.