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Hematology > anticoagulants > Flashcards

anticoagulants Flashcards

anticoagulants

1
Q

Aspirin mechanism

A

inhibits platelet aggregation by inhibiting COX irreversibly via acetylation COX inhibition means that membrane arachidonic acid can’t be broken down to TXA2 which means that platelet aggregation is stopped

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2
Q

Aspirin peak platelet effect (time to)

A

1 hr or 3-4 for enteric coated

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3
Q

Aspirin oral bioavailability

A

40-50%

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4
Q

aspirin half life

A

15-20 minutes, but irreversible effect and 10-15% of circulating platelets are replaced every 24 hours

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5
Q

Aspirin adverse effects (3)

A

GI upset, ulcer, bleeding

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6
Q

aspirin indications

A

primary and secondary prevention of arterial thrombosis, disorders of placental insufficiency (ie preeclampsia) , sometimes used for VTE prevention

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7
Q

what is better for stroke prevention in afib and mechanical heart valves: aspirin or anticoagulants?

A

anticoagulants

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8
Q

NSAID mechanism

A

reversible inhibition of COX

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9
Q

Ibuprofen peak effect

A

1-2 hours

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10
Q

Ibuprofen half life

A

2 hours

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11
Q

Naproxen half life

A

12-17 hours

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12
Q

discontinue aspirin, ibuprofen, and naproxen how many days before surgery?

A

10 days, 1-2 days, and several days

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13
Q

clopidogrel metabolized by which enzyme

A

CYP3A4

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14
Q

clopidogrel metabolism inhibited by which drugs

A

atorvastatin

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15
Q

clopidogrel peak effect

A

4-6 hours after dose

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16
Q

clopidogrel half life

A

8 hours

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17
Q

clopidogrel use (2)

A

2nd prevention of arterial thrombosis and prevention of coronary stent thrombosis

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18
Q

clopidgorel adverse effects (3)

A

thrombotic thromyocytopenic purpura (TTP), rash, diarrhea

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19
Q

clopidgorel mechanism

A

irreversibly inhibits PY12 a ADP receptor

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20
Q

t/f prasugel has to be metabolized before it is activated

A

true

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21
Q

prasugrel peak effect

A

1-2 horus after oral dose

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22
Q

prasugrel half life

A

7 hours

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23
Q

prasugrel use (2)

A

management of ACS w/ PCI

prevention of coronary stent thromboisis

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24
Q

prasugrel adverse effects (2)

A

increased risk of stroke (stroke history= contraindication), TTP

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25
Q

prasugrel mechanism

A

irreversible inhibition of ADP receptor, PY12

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26
Q

ticagrelor mechanism

A

reversible inhibition of ADP recpetor, PY12

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27
Q

ticargrelor– is parent drug or metabolite active

A

both

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28
Q

ticagrelor peak effect

A

2 hours after oral dose

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29
Q

ticagrelor half life

A

7-9 hours

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30
Q

ticagrelor uses

A

prevention of CV events in patients w/ ACS

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31
Q

ticagrelor adverse effects (3)

A

dyspnea, bradycardia, gynecomastia

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32
Q

Heparin is produced by which cells

A

mast cells

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33
Q

heparin mechanism

A

inhibits coagulation via antithrombin which blocks factor 10a and thrombin

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34
Q

heparin bioavailability

A

100% when given IV , but because of plasma binding= 30-35%

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35
Q

heparin time until anticoagulant effect if IV

A

immediate

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36
Q

what decreases heparin efficacy

A

binding to plasma proteins

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37
Q

heparin route (2)

A

IV subQ

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38
Q

time until effect if heparin is given subQ

A

1-3 hours

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39
Q

unfractionated heparin clearance

A

initial rapid phase where it’s internalized by endothelial cells and macrophages where it’s metabolized to smaller forms and binds to plasma proteins second slow phase = renal

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40
Q

2 types of heparin dosing and uses of each

A

mini: subQ for thromboprophylaxis therapeutic: IV, treatment of acute thrombosis : dose adjusted by aPTT (goal is 80-114 sec at DH)

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41
Q

heparin greatest risk of osteoporosis is at what time

A

over 3 months of treatment

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42
Q

Heparin induced Thombocytopenia mechanism

A

immune mediated ( IgG) directed against heparin/ PF4 antigen on platelet surface which leads to clearance and thromboisis from activation

43
Q

Heparin Induced Thrombocytopenia usually occurs when

A

5-15 days of initiation of therapy

44
Q

is HIT a bleeding or thrombotic state

A

thrombotic

45
Q

unfractionated Heparin size

A

5000-30,000

46
Q

LMWH size

A

around 5000

47
Q

name of 4 LMWHs

A

enoxaparin, dalteparin, tinzaparin, fondaparinux

48
Q

heparin side effects

A

osteoporosis, skin lesions (urticaria, papules and plaques, necosis), hyperaldosteronism

49
Q

what is difference in bioavailability b/w unfractionated and LMWH

A

LMWH doesn’t bind as much to plasma proteins, so alsmost 100% bioavailable and there’s less interpatient variability

50
Q

unfractionated hep vs LMWH monitioring

A

UH= aPTT LMWH= anti-Xa

51
Q

risk of HIT wish UH vs LMWH

A

1-5% for UH less than 1% for LMWH

52
Q

LMWH peak effect

A

4-6 hrs after dose

53
Q

LMWH advantage (5)

A

fixed, weight based dosed
subQ admin
no routine lab monitoring needed
more predictable response
less HIT

54
Q

LMWH disadvantage (2)

A

long half life may be problem in bleeding patients b/c no antidote.
renal excretion makes use in renal insufficiency difficult

55
Q

Heparin use/ indication

A

primary prevention of venous and arterial thrombosis
stops thrombus propagation and new clot formation in case of acute venous and arterial thrombosis

56
Q

what do you give to reverse heparin if bleeding is severe and how does it work?

A

protamine sulfate
protamine is positively charged and heparin is negatively charged

57
Q

What is anticoagulant of choice in pregnancy

A

heparin

58
Q

Warfarin mechanism of action

A

vitamin K antagonist which is required as a cofactor in pathways that effects gamma carboxylation on vit-K dependent factors (2,7, 9, 10, Protein C, Protein S, and PZ)
Gamma carboxylation is necessary for coagulation factor binding to phospholipid surfaces ie long story short, inhiibts synthesis of active coagulation factors

59
Q

big mechanistic difference b/w warfarin and heparin

A

warfarin inhibits synthesis of active coagulation factors and heparin inhibits activity of preformed factors

60
Q

Warfarin time to peak activity

A

90 minutes

61
Q

warfarin route

A

oral

62
Q

does warfarin get bound to plasma proteins

A

yes

63
Q

does clearance of warfarin decrease in patients w/ renal dysfunction

A

no, but it does increase in peeps undergoing dialysis

64
Q

warfarin half life

A

33 hours

65
Q

warfarin steady state anticoagulation is reached in how long?

A

7-10 days

66
Q

how is warfarindose adjuged?

A

according to PT/INR

67
Q

what is INR range for warfarin?

A

3-Feb

68
Q

what is special issue w/ starting warfarin

A

slow onset of action so need to be used concurrently w/ fast acting anticoagulant and it’s important to overlap heparin and warfarin by 2 days once therapeutic INR has been reached

69
Q

PT/INR effect of warfarin depends on
Anticoagulant effect depends on (which factors)

A

VII which has shortest half life
IIa and Xa

70
Q

caveat w/ warfarin

A

can induce transient hypercoagulable state b/c VitK dependent Anticoag factors (Protein c and S) have shorter half life than coagulant factors

71
Q

indications for warfarin use

A

primary and secondary prevention of venous thromboembolism
primary and secondary prevention of arterial thromboisis in some circumstances (stroke prevention in Afib/ mechanical heart valves, failure of antiplatelet therapy, added to anti platelet in high risk patients)

72
Q

Warfarin side effects (2)

A

skin necrosis and teratogenic

73
Q

skin necrosis induced by warfarin use occurs when?

A

between days 3-8 of therapy

74
Q

what 3 things can reverse warfarin effect

A

vit K
fresh frozen plasma (for immediate)
prothrombin complex concentrates (for immediate)

75
Q

DTIs are used when

A

heparins are contraindicatedie HIT

76
Q

2 DTIs used in states

A

argatroban, bivalirudin

77
Q

DTI route

A

IV

78
Q

DTI half life

A

0.5-2 hours

79
Q

DTI effect is monitored how

A

PTT
goal is 1.5-3x midpoint of normal range ie 45-90 sec at DH

80
Q

in addition to being an anticoagulantargatroban is also approved for

A

treatment and prevention of thrombosis in HIT

81
Q

bivalirudin and argatroban are also approved for what scenario

A

anticoaguation during PCI in patients w/ HIT

82
Q

Dabigatran ie Pradaxa target

A

Thrombin

83
Q

Dabigatran ie pradaxa time to peak

A

2-3 hrs

84
Q

Dabigatran ie Pradaxa route

A

oral

85
Q

dabigatran is parent drug active

A

no rapidly covnerted to active by the liver

86
Q

dabigatran oral availability

A

7%

87
Q

dabigatran cleared how?

A

renal excretion

88
Q

dabigatran drug itneractions

A

verapamil, quinidine

89
Q

dabigatran monitored how?

A

thrombin time

90
Q

dabigatran side effects

A

bleeding and GI

91
Q

dabigatran use/ approved for

A

stroke prevention in A fib and acute VTE treatment

92
Q

does dabigatran have a antidote

A

yes

93
Q

Rivaroxaban ie Xarelto target

A

Xa

94
Q

Rivaroxaban ie Xarelto time to peak

A

3 hrs

95
Q

Rivaroxaban ie Xarelto bioavailability

A

80-100%

96
Q

Rivaroxaban ie Xarelto cleared how

A

renal excretion

97
Q

does Rivaroxaban ie Xarelto gave an antidote

A

no

98
Q

Rivaroxaban ie Xarelto use/ approved for

A

prevention, treatmentof acute VTE and stroke prevention in A fib

99
Q

Rivaroxaban t/f has a lot of food/drug interactions

A

false, has few

100
Q

Mechanism of tpA and urokinase plasminogen activator

A

convert plasminogen to plasmin which degrades fibrin

101
Q

Mechanism of streptokinase

A

bind to plasminogen and complex degrades fibrin

102
Q

fibrinolytic agent uses

A

ischemic stroke , arterial occlusion, PE, DVT, occluded central venous catheters

103
Q

major adverse event of fibrinolytic agents

A

bleeding

Hematology (3 decks)

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