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Flashcards in Thrombosis Deck (66):
1

What are the components of Virchow's triad?

Endothelial injury
Blood stasis/turbulence
Hypercoagulability

2

What are the two sites in vessels that are sites for thrombosis?

Turbulent flow
Endothelial injury

3

True or false: thrombi are usually attached to the underlying vessel

True

4

Where do arterial thrombi go? Venous?

Grow back to the heart

5

What are the cytokines that have an antiplatelet effect?

PGI2
NO

6

What are the anticoagulant properties of the endothelium?

Heparin-like molecules
Thrombomodulin activates protein C

7

What are the fibrinolytic properties of endothelium?

tPA

8

What is the protein that allows for platelets to bind?

vWF

9

What is the role of tissue factor?

Produced by endothelium, activates extrinxic pathway

10

What is the role of plasminogen activator inhibitors?

***

11

What is the drug that inhibits platelet aggregation? How?

ASA
inhibits thromboxane A2

12

What is the role of the alpha granules that are in platelets?

P selectin
Fibrinogen
Fibronectin
Factor V, VIII

13

What is in the delta graules of platelets?

ATP
AFP
Ca
Histamine
Epi

14

True or false: the platelet aggregation is reversibles

True

15

Why is it that the loss of endothelium will result in thrombosis?

Exposures of the ECM and vWF

16

True or false: turbulences enhances endothelial injury

True

17

True or false: stasis enhances endothelial injury

False--enhances venous thrombosis

18

What happens to vWF when there is increased shearing stress d/t faster blood flow?

Unfolds and becomes stickier

19

What is the role of fibrin in blood clots?

Polymerizes and crosslinks to stabilize clots

20

What begins the process of clot degradation?

Plasminogen activators convert plasminogen to plasmin

21

What is the most common cause of hypercoaguability?

Factor V leiden mutation

22

What happens in antithrombin III deficiency?

Thrombosis

23

What happens in protein C or S deficiency

Thrombosis

24

What is disease leads to secondary antiphospholipid syndrome?

SLE

25

What is the MOA of HITs?

antibodies bind to platelets and activate them

26

What is antiphospholipid syndrome?

Abs to phospholipids like cardiolipin, inducing coagulation

27

True or false: superficial thrombosis cause pain, but are not usually concerning

True

28

What is the vein that is involved in DVTs?

Popliteal, femoral, iliac

29

What is the vein that is involved in superficial venous thromboses?

Saphenous

30

True or false: most pts are symptomatic for DVTs

False--50%

31

DIC is what?

Sudden, widespread fibrin thrombi in the microciculation

32

When does DIC occur?

infx, prego

33

What are the effects of DIC?

Infarcts in kidneys, brain, lung etc

34

What does DIC lead to?

consumption of platelets and clotting factors, increasing the risk of bleeding

35

What are the four fates of thrombus?

1. Propagation
2. Embolization
3. lysis
4. Organization and recanalization (inflammation and fibrosis)

36

What is the most common preventable cause of hospital death?

PE secondary to DVT

37

What is the consequences of a medium PE?

Acute respiratory and cardiac symptoms

38

What is the consequences of a large PE?

Right heart failure and collapse

39

What is a paradoxical embolus?

Cardiac emboli passing to the right side through the septal defect

40

Venous infarcts occurs in organs with what type of blood supply?

Single venous outflow

41

How long does it take for a neuron to die from hypoxia?

3-4 minutes

42

How long does it take for the heart to die from hypoxia?

20-30 minutes

43

How long does it take for fibrous tissue to die from hypoxia?

hours

44

What are the parts of the body with dual blood supply?

Lung
Liver
Hand

45

What are the most common inciting factors for embolism?

Iatrogenic causes

46

True or false: EPO increases the risk of thrombosis

True

47

Is MTHFR a risk factor for embolism

No

48

Are there many, or is there one type of genotype for: antithrombin deficiency

Many

49

Are there many, or is there one type of genotype for: factor V leiden

One

50

What is the prevalence of thrombophilia with factor V leiden?

40-50%

51

What is the relative risk for heterozygous factor V leiden?

7x

52

What is the relative risk for homozygous factor V leiden?

80x

53

What is the relative risk of thrombosis with exogenous estrogen? How about those with factor V leiden, and exogenous estrogen?

3.7

34.7

54

True or false: you should always evaluate young pts who have thrombosis for genetic history

True

55

True or false: you should always evaluate pts who have recurrent miscarriages for genetic history of thrombosis

True

56

Neonatal purpura fulminans is caused by what?

Homozygous PC or PS deficiency

57

Is AT (III) deficiency AD or AR?

AD

58

When does AT(III) deficiency usually present?

Adolescence or earlier

59

Is PC deficiency AD or AR?

AD

60

What happens to homozygous PC or PS deficiency?

Death early

61

Warfarin necrosis is caused by what genetic disease?

PC or PS deficiency

62

Is PS deficiency AD or AR?

AD

63

What is the MOA of factor V leiden?

Slow inactivation of factor V by protein C

64

True or false: factor Va procoagulant activity is not affected by factor V leiden

True

65

What is the MOA of prothrombin G20210A mutation?

mutation in prothrombin, leading to hypercoagulability

66

One prothrombotic condition increases the risk of thrombosis how much?

5-8 x