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CVR Biweekly 2 > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

4 main steps in hemostasis

A
  1. vasoconstriction
  2. platelet aggregation (plug)
  3. coagulation (clot)
  4. thrombolysis
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2
Q

what allows for platelet aggregation

A

platelets cross-linked by fibrinogen binding to GPIIb/IIIa

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3
Q

platelet activation happens when bound to what

A

collagen

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4
Q

only molecule of coagulation cascade made by EC

A

vWF

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5
Q

clotting factors of coagulation cascade besides vWF made by what

A

liver hepatocytes

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6
Q

direct binding of platelet to collagen by what

A

GPVI

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7
Q

indirect binding of platelet to collagen

A

vWF: GPIIb/GPIIIa

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8
Q

cytokines inhibit antithrombotic factor and promote thrombotic factors

A

septic shock thrombosis pathogenesis

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9
Q

heparan sulfate
PGI2
NO
Adenosine
t-PA
thrombomodulin

A

anti-thrombotic factors produced from EC

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10
Q

vWF
PAI1 (Ang IV receptor)
tissue factor (factor III)

A

thrombotic factors produced from EC

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11
Q

thrombin receptor that activates protein C and turns thrombin into anti-coagulant

A

thrombomodulin

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12
Q

found in blood that will be used in platelet aggregation

A

fibrinogen

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13
Q

what happens for platelets to degranulate

A

they bind with GPIIb/GPIIIa and GPVI to vWF on subendothelium

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14
Q

how platelet is activated by TXA2 and 5-HT (serotonin)

A

TXA2 and 5-HT bind Gq receptor on platelet and cause increase in Ca2+

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15
Q

increased Ca2+ from TXA2 and 5-HT binding to Gq on platelet allows for what

A

activation of GPIIb/IIIa to bind to fibrinogen

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16
Q

how ADP activates platelet

A

binds P2Y12 (Gi) and decreases cAMP and activates GpIIb/IIIa

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17
Q

crosslinking by fibrinogen via GPIIb/IIIa

A

platelet aggregation

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18
Q

tissue factor (factor III) so powerful it does what when bound to platelet

A

directly activates GPIIb/GPIIIa

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19
Q

how thrombin activates platelet

A

thrombin binds PAR1 (Gq) and leads to degranulation

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20
Q

when platelets are activated what happens

A

degranulation and ready to bind fibrinogen (step 1 achieved)

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21
Q

lack of vWF (EC problem); mucosal bleeds (nose); most common bleeding disorder; AD

A

vWD

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22
Q

nose bleeds

A

epistaxis

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23
Q

stabilizes factor VIII and protects it from inactivation by Protein C

A

vWF

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24
Q

2 main functions of vWF

A

platelet aggregation and saving factor VIII

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25
Q

lack of vWF will affect what stages of coagulation

A

increased (PTT)

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26
Q

2nd most common bleeding disorder; x-linked recessive

A

Hemophilia A

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27
Q

males of Royal family were affected by this bleeding disorder

A

Hemophilia B

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28
Q

mutation in Factor V causes it to not be inactivated by protein C; propensity to form clots (thrombosis)

A

Factor V Leiden

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29
Q

GpIb deficiency (platelet problem)

A

Bernard-Soulier

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30
Q

Gp IIb/IIIa deficiency

A

Glanzmann thromboasthenia

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31
Q

made by Stellate cells in the liver

A

ADAMTS13

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32
Q

multimeric vWF used for adhesion is degraded by what

A

ADAMTS13

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33
Q

Ab against ADAMTS13, causes accumulation of vWF and thrombosis (TTP)

A

Ticlopidine

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34
Q

abnormal function of this makes collagen (can lead to cirrhosis of liver)

A

Stellate cells of liver

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35
Q

endothelial cell exocytotic bodies

A

Weibel-Palade body

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36
Q

cAMP associated exocytosis when V2 (Gq) is bound

A

Weibel-Palade body exocytosis

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37
Q

what is carried in the Weibel-Palade body

A

vWF

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38
Q

V2 receptor agonist (increases release of vWF from EC Weibel-Palade Body)

A

Desmopressin

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39
Q

what to administer in patient w/ DIC that has no platelets available and clotting factors being used in the disseminated clots

A

Desmopressin

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40
Q

no platelets available and clotting factors being used in the disseminated clots

A

consumption coagulopathy

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41
Q

defective platelet aggregation due to absent fibrinogen

A

Afibrinogenemia

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42
Q

what test to use to tell if vWF or GpIb is deficient

A

Ristocetin induced platelet aggregation (RIPA)

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43
Q

plant based molecule that directly binds to vWF

A

Ristocetin

44
Q

no aggregation means what if both RIPA and RCA tests were used

A

vWF is absent or not active

45
Q

RIPA no aggregation, but RCA aggregation (means vWF present)

A

absent or inactive GpIb

46
Q

multiple platelets joined together

A

platelet plug

47
Q

antiaggregant drug that is a COX I/II irreversible inhibitor (blocks TXA2)

A

Aspirin

48
Q

(-GREL)

A

P2Y12 inhibitors (stops activation of GpIIb)

49
Q
A

PDE inhibitor (cAMP increased and GpIIb not activated)

50
Q

ABCIXIMAB

A

mab that blocks fibrinogen from binding GpIIb/IIIa

51
Q
A

GpIIb/IIIa inhibitors (blocks FIBrinogen from binding)

52
Q

VORAPAXAR

A

PAR1 inhibitor (prevents binding of thrombin)

53
Q

SE of Ticlopidine (P2Y12 inhibitor)

A

neutropenia, TTP

54
Q

contraindication for Clopidogrel

A

breast feeding (can get into breast milk

55
Q

most liked P2Y12 inhibitor now

A

Prasugrel

56
Q

____ when converted to ____forms the structural meshwork that consolidates an initial platelet plug into a solid hemostatic clot

A

fibrinogen to fibrin

57
Q

what is required for the clotting factors to be activated

A

factor IV (Ca2+)

58
Q

protein C can deactivate which 2 factors

A

factor VIII and V

59
Q

when deactivated by thrombomodulin, ____ can help protein C deactivate VIII and V

A

thrombin

60
Q

what factor from extrinsic side activates factor X

A

VIIa

61
Q

what factors from intrinsic side activate factor X

A

VIIIa and IXa

62
Q

way to measure functionality of extrinsic arm

A

PT (N 11-15 s)

63
Q

way to measure functionality of intrinsic arm

A

PTT (N 25-40 s)

64
Q

TT normal length (time to convert fibrinogen to fibrin)

A

<2

65
Q

INR normal length (patient PT/normal PT)

A

1

66
Q

PTT increases with what

A

vWFD, Heparin and Hemaphilia

67
Q

PT increases with what

A

Warfarin and Vitamin K deficiency

68
Q

what to check for thrombosis in the body

A

D-dimer

69
Q

vitamin K antagonist; oral anticoagulant

A

Warfarin

70
Q

ingesting Vitamin K can decrease effects of what

A

Warfarin

71
Q

very effective drugs that block factor Xa

A

Warfarin and Dicumarol

72
Q

block Epoxide reductase (VKORC1 gene); blocks formation of Vitamin K

A

Warfarin and Dicumarol

73
Q

target INR for patients on Warfarin

A

2.5

74
Q

warfarin used for

A

Atrial fibrillation

75
Q

WARNING for warfarin

A

TERATOGEN

76
Q

SE’s of warfarin

A

bleeding and skin necrosis

77
Q

how microthrombosis and then skin necrosis is induced with patient on warfarin

A

Protein C depletes before factor II or X and before warfarin can reduce their production

78
Q

what do you prescribe with warfarin to prevent microthrombosis

A

Heparin

79
Q

antidote of warfarin serious bleeding

A

FFP (fresh frozen plasma)
vitamin K

80
Q

indirect inhibitor of factor IIa (thrombin) and factor Xa

A

heparin

81
Q

indirect effect of heparin due to what

A

they amplify action of antithrombin III

82
Q

high molecular weight heparin

A

Heparin

83
Q

low molecular weight heparin

A

Enoxaparin

84
Q

minimalistic heparin

A

Fondaparinux

85
Q

main factors antithrombin III inhibits

A

IIa (thrombin)
Xa

86
Q

heparin is safe to use in patient’s with what 2 things

A

pregnancy
or
renal failure

87
Q

SE of heparin

A

heparin induced thrombocytopenia (HIT)

88
Q

antibodies against platelet 4 leads to what

A

HIT (heparin induced thrombocytopenia)

89
Q

antidote for heparin

A

protamine sulfate

90
Q

specific heparin that inactivates factor Xa

A

ENOXAPARIN

91
Q

heparins that activate antithrombin III and inhibit only Xa

A

Enoxaparin
Fondaparinux

92
Q

this specific type of heparin activates antithrombin III and inhibits Xa AND IIa

A

unfractionated heparin

93
Q

(-RUDIN)

A

inactivate IIa (thrombin)

94
Q

antidote of -RUDINs (thrombin inactivators)

A

IDARUCIZUMAB

95
Q

drug from leech saliva that blocks thrombin

A

HIRUDIN

96
Q

(-XABAN)

A

factor Xa inhibitors

97
Q

more effective and safer than warfarin

A

direct factor Xa inhibitors

98
Q

antidote for direct factor Xa inhibitors

A

ANDEXANET

99
Q

major 2 fibrinolytic agents

A

t-PA
urokinase

100
Q

clot buster

A

plasmin

101
Q

natural in our bodies and blocks plasmin

A

alpha2-antiplasmin

102
Q

inhibits t-PA and urokinase

A

PAI-1and2

103
Q

drug that inhibits plasmin

A

AMINOCAPROIC ACID

104
Q

initial Rx of venous thromboembolism

A

heparins
-RUDINS (direct IIa inhibitors)

105
Q

secondary Rx for venous thromboembolism

A

Warfarin
-XABAN (direct Xa inhibitors)

106
Q

2 main drugs used to treat arterial thrombosis

A

Aspirin
t-PA

CVR Biweekly 2 (15 decks)

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