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Hematology > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

What are the components of Virchow’s triad?

A

Endothelial injury
Blood stasis/turbulence
Hypercoagulability

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2
Q

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

A

Turbulent flow

Endothelial injury

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3
Q

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

A

True

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4
Q

Where do arterial thrombi go? Venous?

A

Grow back to the heart

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5
Q

What are the cytokines that have an antiplatelet effect?

A

PGI2

NO

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6
Q

What are the anticoagulant properties of the endothelium?

A

Heparin-like molecules

Thrombomodulin activates protein C

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7
Q

What are the fibrinolytic properties of endothelium?

A

tPA

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8
Q

What is the protein that allows for platelets to bind?

A

vWF

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9
Q

What is the role of tissue factor?

A

Produced by endothelium, activates extrinxic pathway

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10
Q

What is the role of plasminogen activator inhibitors?

A
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11
Q

What is the drug that inhibits platelet aggregation? How?

A

ASA

inhibits thromboxane A2

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12
Q

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

A

P selectin
Fibrinogen
Fibronectin
Factor V, VIII

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13
Q

What is in the delta graules of platelets?

A 
ATP
AFP
Ca
Histamine
Epi
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14
Q

True or false: the platelet aggregation is reversibles

A

True

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15
Q

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

A

Exposures of the ECM and vWF

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16
Q

True or false: turbulences enhances endothelial injury

A

True

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17
Q

True or false: stasis enhances endothelial injury

A

False–enhances venous thrombosis

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18
Q

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

A

Unfolds and becomes stickier

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19
Q

What is the role of fibrin in blood clots?

A

Polymerizes and crosslinks to stabilize clots

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20
Q

What begins the process of clot degradation?

A

Plasminogen activators convert plasminogen to plasmin

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21
Q

What is the most common cause of hypercoaguability?

A

Factor V leiden mutation

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22
Q

What happens in antithrombin III deficiency?

A

Thrombosis

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23
Q

What happens in protein C or S deficiency

A

Thrombosis

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24
Q

What is disease leads to secondary antiphospholipid syndrome?

A

SLE

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25
Q

What is the MOA of HITs?

A

antibodies bind to platelets and activate them

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26
Q

What is antiphospholipid syndrome?

A

Abs to phospholipids like cardiolipin, inducing coagulation

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27
Q

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

28
Q

What is the vein that is involved in DVTs?

A

Popliteal, femoral, iliac

29
Q

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

30
Q

True or false: most pts are symptomatic for DVTs

A

False–50%

31
Q

DIC is what?

A

Sudden, widespread fibrin thrombi in the microciculation

32
Q

When does DIC occur?

A

infx, prego

33
Q

What are the effects of DIC?

A

Infarcts in kidneys, brain, lung etc

34
Q

What does DIC lead to?

A

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

35
Q

What are the four fates of thrombus?

A
  1. Propagation
  2. Embolization
  3. lysis
  4. Organization and recanalization (inflammation and fibrosis)
36
Q

What is the most common preventable cause of hospital death?

A

PE secondary to DVT

37
Q

What is the consequences of a medium PE?

A

Acute respiratory and cardiac symptoms

38
Q

What is the consequences of a large PE?

A

Right heart failure and collapse

39
Q

What is a paradoxical embolus?

A

Cardiac emboli passing to the right side through the septal defect

40
Q

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

A

Single venous outflow

41
Q

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

A

3-4 minutes

42
Q

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

A

20-30 minutes

43
Q

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

44
Q

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

A

Lung
Liver
Hand

45
Q

What are the most common inciting factors for embolism?

A

Iatrogenic causes

46
Q

True or false: EPO increases the risk of thrombosis

47
Q

Is MTHFR a risk factor for embolism

48
Q

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

49
Q

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

50
Q

What is the prevalence of thrombophilia with factor V leiden?

51
Q

What is the relative risk for heterozygous factor V leiden?

52
Q

What is the relative risk for homozygous factor V leiden?

53
Q

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

54
Q

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

55
Q

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

56
Q

Neonatal purpura fulminans is caused by what?

A

Homozygous PC or PS deficiency

57
Q

Is AT (III) deficiency AD or AR?

58
Q

When does AT(III) deficiency usually present?

A

Adolescence or earlier

59
Q

Is PC deficiency AD or AR?

60
Q

What happens to homozygous PC or PS deficiency?

A

Death early

61
Q

Warfarin necrosis is caused by what genetic disease?

A

PC or PS deficiency

62
Q

Is PS deficiency AD or AR?

63
Q

What is the MOA of factor V leiden?

A

Slow inactivation of factor V by protein C

64
Q

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

65
Q

What is the MOA of prothrombin G20210A mutation?

A

mutation in prothrombin, leading to hypercoagulability

66
Q

One prothrombotic condition increases the risk of thrombosis how much?

Hematology (32 decks)

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