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Pharmacology > Pharm Unit 2 - Anti-Thrombotics > Flashcards

Pharm Unit 2 - Anti-Thrombotics Flashcards

1
Q

antiplatelets

A

prevent blood clot formation

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2
Q

primary hemostasis

A

endothelial injury
adhesion
activation
aggregation

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3
Q

endothelial injury

A

exposure of collagen and vWF inside vessel

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4
Q

adhesion

A

circulating platelets bind to vWF and collagen

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5
Q

activation

A

shape change of platelets
TXA2 release
granual release
GP IIb/IIIa conformation change

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6
Q

do platelets have nucleus?

A

no

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7
Q

TXA2 function

A

thromboxane recruits more platelets to the plug
expands the clot

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8
Q

what is converted into TXA2

A

arachadonic acid –> TXA2

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9
Q

what does granule release do

A

ADP
coagulation factors

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10
Q

aggregation

A

fibrinogen cross linking between platelets’ surfaces

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11
Q

anti-thombotic therapy goals

A

prevent thrombosis
without over promotion of bleeding

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12
Q

main risk of antithrombotics

A

bleeding
increase risk of death 3-5x

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13
Q

pt monitoring during antithrombotic therapy

A

Hgb drop
bloody stools
melena
hematuria
bruising
oozing from arterial/venous puncture

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14
Q

antiplatelets drug types

A

aspirin
P2Y12 receptor antagonists
GP IIb/IIIa inhibitors
Vorapaxar

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15
Q

aspirin mechanism

A

irreversibly inhibits COX-1
prevents conversion of arachidonic acid into thromboxane
- decr platelet formation
- decr vasoconstriction

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16
Q

aspirin uses

A

prevention of DVT
prevention of ASCVD (secondary)
- MI
- angina
- stroke/TIA
- PAD
- CAD
antiypyretic
analgesic
prevention of colorectal cancer

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17
Q

what is the fastest way to get aspirin into the body?

A

chew non-enteric coated
–20 mins

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18
Q

duration of aspiring effects

A

lasts entire platelet lifespan
wears off once new plts are made

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19
Q

aspiring SE

A

GI
bleeding
allergic rxns
incr hemorrhagic stroke in men

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20
Q

aspiring drug interactions

A

NSAIDs will blunt aspirins effect
incr risk of serious GI complications

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21
Q

ADP

A

binds to P2Y1
- incr Ca2+ == shape change
binds to P2Y12
- granule release

both paths activate GPIIb/IIIa, resulting in platelet aggregation

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22
Q

which is the more dominant ADP biding site?

A

P2Y12

so drugs target P2Y12

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23
Q

P2Y12 ADP inhibitor drugs

A

clopidogrel
prasugrel
ticagrelor
cangrelor

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24
Q

what polymorphism impacts clopidogrel?

A

decr CYP2C19 function
loss of effectiveness of drug

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25
Q

clopidogrel and prasugrel bind

A

irreversibly to P2Y12 receptor

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26
Q

which is more potent: clapidogrel or prasugrel?

A

prasugrel has more potent plt inhibition w/faster onset

clopidogrel is a prodrug so must be metabolized to work == slower

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27
Q

if you inhibit CYP2C19 function, would you amplify or reduce clopidogrels anti-platelet effect?

A

reduce

clopidogrel requires CYP2C19 to convert into active form

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28
Q

clopidogrel indications

A

acute coronary syndrome
- typically DAPT w/aspirin
percutaneous coronary intervention
- prevents stent thrombosis
2ndary prevention in atherothrombotic disease
- CAD
- CVD
- PAD

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29
Q

what drug can replace aspiring in prevention of atherothrombotic disease?

A

clopidogrel

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30
Q

Prasugrel CI

A

<60 kg = half dose
Stroke or TIA history
>75 yrs old
cannot be used in CABG pts

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31
Q

Prasugrel indication

A

only pts w/PCI and stent implant

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32
Q

Ticagrelor and Cangrelor bind

A

reversibly to ADP P2Y12 receptor

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33
Q

Ticagrelor and Cangrelor are administered

A

IV only
Ticagrelor: 2x daily
Cangrelor: continous IV

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34
Q

Ticagrelor is metabolized by

A

CYP3A

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35
Q

Ticagrelor vs Clopidogrel

A

ticagrelor has:
faster onset
more potent platelet inhibition

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36
Q

What other receptor does Tacagrelor block?

A

ENT1
– incr adenosine plasma levels
– incr endothelium function
– decr HR

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37
Q

Ticagrelor SE

A

dyspnea
– P2Y12 incr neuronal signaling
– incr conductivity of pulmomnary vagal C-fibers
– incr sensation of dyspnea

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38
Q

cangrelor bleeding rates compared to clopidogrel

A

cangrelor has higher bleeding rates compared to clopidogrel

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39
Q

cangrelor SE

A

dyspnea
decr renal function (3.2%)

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40
Q

Cilostazol mechanism

A

PDE3 inhibitor
incr intraplatelet cAMP
decr Ca2+
plt inhibition

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41
Q

Cilostazol effects

A

platelet inhibition
inhibit vascular smooth muscle cell proliferation
improves peripheral BF

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42
Q

Cilostazol indications

A

PAD - claudication
PVD
stroke/TIA
post-PCI

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43
Q

Cliostazol CI

A

HF

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44
Q

most abundant receptor on platelates

A

Gp IIb/IIIa
80,000 copies/plt

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45
Q

GPIIb/IIIa inhibitor mechanism

A

binds to GPIIb/IIIa receptors
prevents formation of fibrinogen plt-plt crosslinks

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46
Q

GPIIb/IIIa inhibitor indications

A

PCI
unstable angina

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47
Q

GP IIb/IIIa inhibitors SE

A

bleeding
thrombocytopenia

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48
Q

GP IIb/IIIa drugs

A

abcimimab
eptifibatide
tirofiban

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49
Q

GP IIb/IIIa inhibitor CI

A

active internal bleeding
major surgeries
recent trauma
intracranial hemorrhage
bleeding disorders
severe hypertension

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50
Q

abciximab has a ____ % risk of thrombocytopenia

A

5% risk
1% severe risk

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51
Q

anticoagulants

A

prevent blood clots from forming by interfering with coagulation factors

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52
Q

hemostasis

A

stopping bleeding

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53
Q

primary hemostasis

A

formation of platelet plug

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54
Q

secondary hemostasis

A

coagulation

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55
Q

extrinsic pathway of secondary hemostasis

A

activated by tissue factor found outside the blood

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56
Q

intrinsic pathway of secondary hemostasis

A

factors required for activation are found in the blood

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57
Q

common pathway

A

activation of factor X
coagulation cascade

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58
Q

4 parental anticoagulants

A

unfractionated heparin
low molecular weight heparin
synthetic pentasaccharides
direct thrombin inhibitors

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59
Q

parenteral anticoagulatns indications

A

DVT
PE
initial management of ACS

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60
Q

clotting times

A

measure the time it takes plasma to clot when various substances are added

61
Q

prothrombin time (PT)

A

assesses extrinsic pathway of coagulation

INR

62
Q

activated clotting time (ACT)

A

measures time of clot formation via the intrinsic coagulation pathway

63
Q

high dose heparin monitoring uses

A

ACT

64
Q

activated partial thromboplastin time (aPTT)

A

assess intrinsic pathway of coagulation

65
Q

antifactor Xa assay

A

measures unbound Factor Xa level
assesses functional activity of anticoagulant

66
Q

unfractionated heparin mechanism

A

binds to endothelium/plasma proteins
causes a confirmational change in antithrombin
inactivates clotting factor proteases (IIa, IXa, Xa)

67
Q

which molecular weight heparin inhibits thrombin

A

High molecular weight heparin inhibits thrombin

68
Q

heparin clinical uses

A

PE
DVT
clot prevention in arterial/cardiac surgery
Afib w/embolization
ACS
MI

69
Q

Low-molecular weight heparin mechanism

A

primarily inhibit Factor Xa

70
Q

heparin SE

A

hemorrhage
heparin induced thrombocytopenia (HIT)
epidural/spinal hematoma

71
Q

HIT

A

prothrombotic

72
Q

Heparin monitoring

A

aPTT
anti-factor Xa plasma levels
ACT (high doses)

73
Q

heparin aPTT

A

2-3x normal

74
Q

heparin clearance

A

reticuloendothelial system
dose-dependent
- low = fast clearance
- high = long clearance

75
Q

heparin reversal

A

protamine sulfate

76
Q

protamine sulfate

A

highly basic (+ charge)
neutralizes heparin
better at HWMH than LWMH

77
Q

Heparin Induced Thrombocytopenia

A

antibody mediated process
PF4-heparin antibody rxn
activated plts
decr plt count
incr thrombin production
incr clotting

78
Q

occurence rate of HIT

A

5%

79
Q

HIT ocurrence timeframe

A

4-10 days post-heparin dosing

80
Q

LMWH drugs

A

enoxaparin
dalteparin
tinzaparin

81
Q

LMWH

A

longer half life
more predictable
minimal need for monitoring
kidney clearance
decr HIT risk
partial reversal by protamine

82
Q

Fondaparinux

A

synthetic indirect Factor Xa inhibitor
100% bioavailability

83
Q

Fondaparinux mechanism

A

binds antithrombin
inactivation of factor Xa

84
Q

Fondaparinux is dependent on

A

renal excretion

85
Q

renal impairment (Fondaparinux clearancce rates)

A

mild: decr clearance 25%
mod: decr clearance 40%
sev: decr clearance 55%

86
Q

Fondaparinux SE

A

thrombocytopenia
(2.9%)
severe (0.2%)
hemorrhage
epidural/spinal hematoma

87
Q

does fondaparinux cause HIT?

A

no

88
Q

LMWH/Fondaparinux CI

A

epidural indwelling catheter
NSAIDs
plt inhibitors
anticoagulants
traumatic epidurals/spinals
spinal deformity
spinal surgery

89
Q

Direct Thrombin inhibitor mechanismn

A

directly bind and inhibit unbound and fibrin-bound thrombin

90
Q

direct thrombin inhibitor drugs

A

bivalriduin
argatroban

91
Q

bivalirudin metabolism/excretion

A

met: blood proteases
excr: urine (20%)

92
Q

argatroban metabolism

A

hepatic

93
Q

bivalirudin requires does adjustment for

A

renal impairment
CrCl<30

94
Q

argatroban requires dose adjustment for

A

hepatic impairment

95
Q

direct thrombin inhibitor monitoring

A

aPTT
ACT

96
Q

argatroban does what to PT and INR

A

argatroban prolongs PT/INR

97
Q

argatroban indications

A

HIT pts

98
Q

bivalirudin indications

A

PCI (coronary angioplasty)
with or w/o HIT

99
Q

direct thrombin inhibitor side effects

A

hemorrhage

100
Q

oral anticoagulants

A

warfarin
dabigatran
direct Factor X inhbitors
– apixaban
– edoxaban
– rivaroxaban

101
Q

oral anticoagulants indications

A

DVT
PE
stroke prevention in afib pts

102
Q

Warfarin mechanism

A

inhibits conversion of Vit K into its active form
results in incomplete clotting factors that are biologically inactive in coagulation

103
Q

Active Vit K is needed for

A

the production of functional clotting factors:
II
VII
IX
X

and anticoagulant proteins:
C
S

104
Q

what polymorphisms impact warfarin clearance and dosing?

A

CYP2C9

105
Q

what polymorphisms impact warfarin anticoagulation response?

A

VKORC1

106
Q

which polymorphisms have reduced enzyme activity with warfarin?

A

CYP2C92
CYP2C93

107
Q

what polymorphism are associated with increased sensitivity to warfarin and lower dose requirements?

A

VKORC1
– G3673A
– -1639G>A

108
Q

VKORC1 G/G warfarin dosing

A

46 mg/wk

109
Q

VKORC1 G/A warfarin dosing

A

33 mg/wk

110
Q

VKORC1 A/A warfarin dosing

A

21 mg/wk

111
Q

when is the anticoagulant effect of warfarin observed?

A

after elimination of normal pre-formed clotting factors
~48-72 hrs post-administration

112
Q

how do you recover from warfarin?

A

synthesize new normal clotting factors

113
Q

which coagulation factor has the shortest half-life with warfarin?

A

shortest: F VII

FIX
FX

longest: FII

114
Q

what is the length of time to maximal effect of warfarin on Factor II?

A

7 days

115
Q

warfarin normal INR

A

2.0-3.0

116
Q

warfarin starting dose

A

5mg daily
titrate to appropriate INR

117
Q

warfarin SE

A

bleeding
skin necrosis (3-10 days)
thrombosis of microvasculature
protein C depletion

118
Q

warfarin CI

A

pregnancy

119
Q

warfarin reversal

A

Vit K (phytonadione)

120
Q

clotting factor replacements to help warfarin reversal

A

fresh frozen plasma
prothrombin complex concentrate
recombinant factor VIIa

121
Q

Direct oral anticoagulant drugs

A

dabigatran
rivaroxaban
apixaban
edoxaban

122
Q

direct oral anticoagulants inhibit what factors?

A

Factor Xa
Factor IIa

123
Q

Factor Xa inhibitors

A

rivaroxaban
apixaban
edoxaban

124
Q

Factor IIa inhibitor

A

dabigatran

125
Q

DOAC onset

A

rapid

126
Q

DOAC dosing

A

fixed

127
Q

Do you need to monitor DOACs?

A

no

128
Q

dabigatran clearance

A

renal (80%)

129
Q

which DOACs are metabolized by the liver?

A

rivaroxaban
apixaban (minor)
edoxaban (minimal)

130
Q

dabigatran SE

A

dyspepsia

131
Q

DOAC boxed warning

A

increased rate of stroke following discontinuation of DOACs
(incr risk of thrombotic events)

132
Q

dagibatran antidote

A

idarucizumab
(monoclonal antibody)

133
Q

DOAC antidote

A

decoy Factor Xa
–decr DOAC effect

134
Q

DOAC indications

A

DVT
PE
VTE (hip/knee replacements)
stroke prevention in afib

135
Q

Rivaroxaban inbdications

A

chronic CAD or PAD
– combined w/aspirin to decr risk

136
Q

thrombolytics

A

break up blood clots formed during hemostasis
restore blood flow

137
Q

thrombolytics drugs

A

alteplase
reteplase
tenecteplase
streptokinase

138
Q

which thrombolytics are derived from tPA

A

alteplase
reteplase
tenecteplase

139
Q

streptokinase is derived from

A

beta hemolytic bacteria proteins

140
Q

tPA derived-thrombolytics mechanism

A

bind to fibrin proteins
onverts plasminogen to plasmin
plasmin degrades fibrin mesh

141
Q

streptokinase mechanism

A

binds to circulating or fibrin bound plasminogen
converts plasminogen to plasmin
plasmin degrades fibrin mesh

142
Q

which thrombolytic is not selective to fibrin? what does that mean?

A

streptokinase
it impacts the entire body, not just fibrin

143
Q

thrombolytics indications

A

short term emergent mgmt of thrombosis
STEMI
DVT
PE
acute ischemic stroke
acute peripheral arterial occlusion

144
Q

thrombolytics SE

A

severe bleeding
intracranial hemorrhage

145
Q

thrombolytics CI

A

active internal bleeding
close to major surgiers
after recent trauma
suspected aortic dissection
intracranial hemorrhage
bleeding disorders
severe hypertension

146
Q

thrombotic (fibrinolytic) antidotes

A

aminocaproic acid
tranexamic acid

147
Q

aminocaproic acid mechanism

A

blocks binding of plasminogen to fibrin
blocks conversion of plasminogen to plasmin

148
Q

tranexamic Acid mechanism

A

forms reversible complex that displaces plasminogen from fibrin
inhibition of fibrinolysis

149
Q

thrombotic (fibrinolytic) antidote indications

A

fibrinolytic bleeding
hemophilia
prevention of surgical blood loss
post-trauma hemorrhage

Pharmacology (9 decks)

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