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CVR Biweekly 2 > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

mechanism to form blood clot at site of vessel damage

A

hemostasis

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2
Q

blood clot at site of vessel damage

A

thrombosis

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3
Q

blood clot that travels to a different location

A

embolus

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4
Q

2 parts of primary hemostasis

A

vascular wall
platelets

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5
Q

secondary hemostasis

A

coagulation cascade

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6
Q

vessel wall damage triggers what

A

sympathetic vasoconstriction

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7
Q

clot formation (2 main steps)

A

platelet activation
fibrin formation

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8
Q

plasma protein produced by EC’s and bind platelets

A

vWF (von willebrand factor)

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9
Q
A

normal blood smear, no platelets

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10
Q

arrows point to

A

platelets

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11
Q
A

normal parrot RBC’s

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12
Q

epi, collagen, thrombin, ADP, TXA2

A

important for platelet activation

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13
Q

what happens with platelets that leads to degranulation

A

shape changes

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14
Q

what determines successful degranulation

A

TXA2 formation from cyclooxygenase (COX)

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15
Q

blocks platelets from forming mature platelet plug

A

Aspirin

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16
Q

contents that platelets release during degranulation

A

vWF, fibrinogen, Factor V, ATP

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17
Q

what is required for platelets to aggregate

A

fibrinogen binding to platelet surface receptor GPIIb/IIIa

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18
Q

defect in GPIIb/IIIa and causes people to bleed

A

Glanzmann thrombasthenia (GT)

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19
Q

without this complex, can’t form platelet plug

A

GPIIb/IIIa

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20
Q

what can also activate platelets

A

sepsis

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21
Q

atheroma formation when macrophages can’t break down cholesterol; platelets come to damaged EC; vWF binds GP IIb/IIIa—> fibrinogen released, coagulation cascade—> more solid clot formed

A

cross talk b/t WBC’s and platelets

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22
Q

one leg larger than the other; erythema; warm; hurts to squeeze calf

A

deep vein thrombosis

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23
Q

what is the fear for deep vein thrombosis

A

pulmonary embolism

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24
Q

why is it red?

A

RBC’s trapped in platelet/fibrin net

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25
Q

how is clot fortified

A

platelet plug fortified w/ fibrin polymers

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26
Q

end result of coagulation cascade

A

fibrin formation

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27
Q

pathway that utilizes soluble factors

A

intrinsic

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28
Q

pathway that utilizes insoluble factors (tissue factor)

A

extrinsic

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29
Q

the intrinsic and extrinsic pathway join to form what

A

common pathway

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30
Q

site of coagulation cascade

A

activated platelet membrane (held together by Ca2+ ions)

31
Q

sequence of hemostasis

A

blood vessel damage
vasoconstriction
activated platelets (plug)
coagulation cascade

32
Q

factor II

A

prothrombin

33
Q

factor IIa

A

thrombin

34
Q

factor that converts prothrombin to thrombin

A

factor Xa

35
Q

converts fibrinogen to fibrin monomers

A

thrombin (factor IIa)

36
Q

factor that converts fibrin monomers to fibrin polymers

A

factor XIIIa

37
Q

body makes this to break down clots

A

D-dimer

38
Q

+ D-dimer test indicates

A

might have a blood clot

39
Q

most important pathway in secondary hemostasis

A

extrinsic pathway

40
Q

factor III

A

tissue factor

41
Q

activates extrinsic pathway in cascade

A

tissue factor (factor III)

42
Q

important in triggering inflammation, angiogenesis and carcinogenesis

A

tissue factor (factor III)

43
Q

deficiency in factor IX or VIII causes what

A

severe bleeding

44
Q

1st step in extrinsic pathway

A

tissue factor (factor III) binds and activates factor VII to VIIa

45
Q

2nd step in extrinsic pathway

A

TF:VIIa activates factor X to Xa (common pathway)

46
Q

3rd step in extrinsic/common pathway

A

factor Xa activates factor V

47
Q

role of factor V

A

prothrombin to thrombin

48
Q

what part of extrinsic pathway pulls intrinsic pathway w/ it

A

TF: VIIa activates IXaVIIIa complex

49
Q

1st step in intrinsic pathway

A

factor XII is activated (XIIa)

50
Q

2nd step in intrinsic pathway: factor XIIa activates what

A

factor XI (XIa)

51
Q

factor XIa activates what

A

factor IX (IXa)

52
Q

from both intrinsic and extrinsic pathway, what activates factor X (Xa)

A

IXa:VIIIa complex

53
Q

due to poor nutrition and blocks factor 2,7,9,10 in coagulation cascade (bleeding)

A

vitamin K deficiency

54
Q

inactivates thrombin (converts fibrinogen to fibrin)

A

anti-thrombin III

55
Q

inactivates V and VIII(stops thrombin and factor X formation)

A

Protein C and S

56
Q

breaks down clot (fibrin)

A

D-dimers

57
Q

limits excess clot formation

A

fibrinolytic cascade

58
Q

main player in lysing clots

A

plasmin

59
Q

released from EC and lyses clots

A

t-PA

60
Q

turns plasminogen into plasmin

A

t-PA

61
Q

turns fibrin into fibrin degradation products

A

plasmin

62
Q

deficiency of plasminogen leads to

A

thrombosis

63
Q

deficiency in plasminogen activator inhibitors (allowing break down of clots) leads to

A

bleeding

64
Q

normal PT (prothrombin time)

A

15

65
Q

normal PTT

A

30

66
Q

normal INR

A

1

67
Q

patients on warfarin have normal PT/INR of

A

2.5

68
Q

PT/INR of 5 worried about what

A

bleeding

69
Q

PT/INR of 0.5 worried about what

A

clotting

70
Q

PTT for what pathway

A

intrinsic to common

71
Q

PT for what pathway

A

extrinsic to fibrin clot

72
Q

how does aspirin affect bleeding time

A

increases it

73
Q

no prothrombin to thrombin

A

factor V deficient

74
Q

deficient in IX:VIII or no X activated

A

vWF disease
Hemophilia A
Hemophilia B

CVR Biweekly 2 (15 decks)

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