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Path U2 > Ch4 - 4) Thrombosis > Flashcards

Ch4 - 4) Thrombosis Flashcards

1
Q

What is thrombosis?

A

Pathologic formation of an intravascular blood clot (thrombus), Can occur in an artery or vein,

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2
Q

What is the most common location for thrombosis?

A

it is the deep veins (DVT) of the leg below the knee

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3
Q

What is thrombosis characterized by?

A

lines of Zahn and attachment to vessel wall

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4
Q

What are the lines of Zahn?

A

alternating layers of platelets/fibrin and RBCs

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5
Q

What distinguishes thrombus from a postmortem clot?

A

lines of Zahn and attachment to vessel wall

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6
Q

What are three major risk factors for thrombosis?

A

disruption in blood flow, endothelial cell damage, and hypercoagulable state (Virchow triad)

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7
Q

What is normal blood flow?

A

blood flow is normally continuous and laminar; keeps platelets and factors dispersed and inactivated

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8
Q

What happens to blood flow that causes an increase in the risk for thrombosis?

A

Stasis and turbulence of blood flow increases risk for thrombosis

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9
Q

What are some examples of disruption of normal blood flow?

A

Immobilization?increased risk for deep venous thrombosis 2. Cardiac wall dysfunction (e.g arrhythmia or myocardial infarction) 3. Aneurysm

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10
Q

How does endothelial cell damage increase the risk for thrombosis?

A

Endothelial damage disrupts the protective function of endothelial cells, increasing the risk for thrombosis

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11
Q

How do endothelial cells prevent thrombosis?

A
  1. Block exposure to subendothelial collagen and underlying tissue factor 2. Produce prostacyclin (PGI2) and NO, 3. Secrete heparin-like molecules, 4. Secrete tissue plasminogen activator (tPA) 5. Secrete thrombomodulin
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12
Q

How does endothelial cells use the secretion of tPA to prevent thrombosis?

A

converts plasminogen to plasmin, which (1) cleaves fibrin and serum fibrinogen, (2) destroys coagulation factors, and (3) blocks platelet aggregation

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13
Q

How does the secretion of thrombomodulin from endothelial cells prevent thrombosis?

A

redirects thrombin to activate protein C, which inactivates factors V and VIII

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14
Q

How do endothelial cells use the secretion of heparin-like molecules to prevent thrombosis?

A

augment antithrombin III (ATIII) which inactivates thrombin and coagulation factors

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15
Q

How does endothelial cells use the production of prostacyclin (PGI2) and NO to prevent thrombosis?

A

vasodilation and inhibition of platelet aggregation

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16
Q

What are the causes of endothelial cell damage?

A

atherosclerosis, vasculitis, and high levels of homocysteine

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17
Q

Vitamin B12 and folate deficiency result in?

A

mildly elevated homocysteine levels, increasing the risk for thrombosis.

18
Q

What does folic acid circulate as?

A

methyl-THF (tetrahydrofolate, THF) in the serum,

19
Q

How does THF participate in the synthesis of DNA precursors?

A

Methyl is transferred to cobalamin (vitamin B12) which transfers methyl to homocysteine resulting in methionine

20
Q

What does a lack of vitamin B12 or folate lead to?

A

decreased conversion of homocysteine to methionine resulting in buildup of homocysteine

21
Q

Cystathionine beta synthase (CBS) deficiency results in what?

A

high homocysteine levels with homocystinuria,

22
Q

What does CBS do?

A

CBS converts homocysteine to cystathionine

23
Q

CBS deficiency leads to?

A

homocysteine buildup

24
Q

CBS deficiency is characterized by?

A

vessel thrombosis, mental retardation, lens dislocation, and long slender fingers

25
Q

what is a hypercoagulabe state due to?

A

excessive procoagulant proteins or defective anticoagulant proteins; may be inherited or acquired

26
Q

What is the classic presentation for a hypercoagulable state?

A

recurrent DVTs or DVT at a young age, usually occurs in the deep veins of the leg; other sites include hepatic and cerebral veins

27
Q

What are some causes of a hypercoagulable state?

A

protein C and S deficiency, factor V Liden deficiency, prothrombin 20210A, ATIII deficiency, oral contraceptives

28
Q

protein C or S deficiency

A

(autosomal dominant) decreases negative feedback on the coagulation cascade (hypercoagulable state)

29
Q

Proteins C and S normally do what?

A

inactivate factors V and VIII

30
Q

Protein C and S deficiency increases the risk for what?

A

warfarin skin necrosis

31
Q

What does the initial stage of warfarin therapy result in?

A

a temporary deficiency of proteins C and S (due to shorter half-life) relative to factors II, VII, IX, and X

32
Q

In preexisting C or S deficiency, what danger does the initial stage of warfarin therapy present?

A

a severe deficiency is seen at the onset of warfarin therapy increasing the risk for thrombosis, especially in the skin

33
Q

What is Factor V Leiden?

A

a mutated form of factor V that lacks the cleavage site for deactivation by proteins C and S

34
Q

What is the most common inherited cause of hypercoagulable state?

A

Factor V Leiden

35
Q

What is Prothrombin 20210A?

A

it is an inherited point mutation in prothrombin that results in increased gene expression,

36
Q

Increased prothrombin (prothrombin 20210A) results in what?

A

increased thrombin, promoting thrombus formation.

37
Q

What does ATIII deficiency result in?

A

decreases the protective effect of heparin-like molecules produced by the endothelium, increasing the risk for thrombus

38
Q

What do heparin-like molecules normally do?

A

activate ATIII, which inactivates thrombin and coagulation factors

39
Q

What happens in ATIII deficiency?

A

PTT does not rise with standard heparin dosing.

40
Q

Pharmacologic heparin works by doing what?

A

binding and activating ATIII

41
Q

High doses of heparin in someone with ATIII deficiency results in what?

A

activate limited ATIII; Coumadin is then given to maintain an anticoagulated state.

42
Q

How are oral contraceptives associated with a hypercoagulable state?

A

Estrogen induces increased production of coagulation factors, thereby increasing the risk for thrombosis

Path U2 (25 decks)

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