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Heme/Lymph > Pharm: Anti Coag Anti Platelet > Flashcards

Pharm: Anti Coag Anti Platelet Flashcards

1
Q

When do we use antithrombotic therapy?

A

prevent thrombosis in pts w/acute or symptomatic venous thromboembolism

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2
Q

3 subgroups of antithrombotic agents

A

anticoagulants
antiplatelet agents
fibrinolytic agents

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3
Q

Venous thrombosis thrombi?

A

Red thrombi, RBCs enmeshed in thrombi

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4
Q

Arterial thrombosis thrombi?

A

White thrombi, platelets with little fibrin or red cells

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5
Q

Venous thrombosis risk factors?

A

immobility, surgery, cancer, pregnancy, estrogen use

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6
Q

Arterial thrombosis risk factors?

A

smoking, HTN, DM, obesity, hyperlipidemia

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7
Q

Gain of function mutations associated with venous thrombosis?

A

G20210A

factor V leiden

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8
Q

What causes primary hemostasis?

A

formation of a platelet monolayer over the subendothelial matrix
platelets are held in place by vWF

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9
Q

What receptor is necessary for platelet aggregation?

A

GPIIb/IIIa

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10
Q

What do platelets synthesize from arachidonic acid?

A

TXA2

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11
Q

What causes secondary hemostasis?

A 
coagulation cascase (conversion of soluble fibrinogen to insoluble fibrin)
clot formation
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12
Q

How to platelets activate the coagulation cascade?

A

surface phospholipids provide support on which the complexes of coag cascade are formed, allowing for calcium binding

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13
Q

Heparin mechanism

A

no intrinsic anticoag activity
binds antithrombin and thrombin simultaneously
accelerates rate of interaction of antithrombin w/Xa

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14
Q

Heparin admin

A

parenteral, immediate onset of action

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15
Q

What are the LMWHs?

A

exoxaparin

dalteparin

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16
Q

LMWH mechanism

A

potentiate factor Xa inhibition by antithrombin

not as good at inhibiting thrombin

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17
Q

LMWH admin

A

parenteral, can accumulate in pts w/renal disease

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18
Q

Heparin SEs

A

thrombocytopenia

bleeding

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19
Q

LMWH SEs

A

bleeding

lower risk of thrombocytopenia

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20
Q

What are the direct thrombin inhibitors?

A

lepirudin

bivalirudin

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21
Q

Lepirudin mechanism?

A

binds tightly to catalytic site and extended substrate recognition site of thrombin

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22
Q

Bivalirudin mechanism?

A

occupies catalytic site of thrombin

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23
Q

Direct thrombin inhibitors admin?

A

parenteral

excreted by kidneys

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24
Q

What is the direct factor Xa inhibitor?

A

Fondaparinux

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25
Q

Fondaparinux mechanism?

A

causes antithrombin mediated selective inhibition of Xa

26
Q

Fondaparinux admin?

A

subcut

Do NOT use in pts w/renal failure

27
Q

Direct thrombin inhibitor SEs?

A

bleeding if they accumulate

28
Q

Fondaparinux SEs

A

bleeding

much less likely to cause thrombocytopenia

29
Q

Warfarin mechanism?

A

inhibits vitamin K epoxide, which recycles vit K back to it’s active form

30
Q

What requires Vit K?

A

facotrs 2,7,9,10, protein C, protein S

31
Q

Which enantiomer of warfarin ia most active?

A

S

32
Q

What metabolizes warfarin?

A

CYP2C9

33
Q

Polymorphisms in which protein affects dosing?

A

VKORC1

affects the susceptibility of hte enzyme to warfarin induced inhibition

34
Q

Warfarin SEs?

A

bleeding
birth defects/abortion
skin necrosis
purple toe syndrome

35
Q

What is the oral direct thrombin inhibitor?

A

dabigatran

36
Q

Metab of dabigatran?

A

renal excretion

37
Q

What drug should NOT be administered with dabigatran?

A

rifampin

both are Pgp substrates

38
Q

Dabigatran SEs?

A

bleeding

39
Q

What is the orally available direct factor Xa inhibitor?

A

Rivaroxaban

40
Q

What does factor Xa do?

A

converts prothrombin to thrombin

41
Q

How is rivaroxaban eliminated?

A

unchanged by kidneys or metabolized by liver

42
Q

What are the thrombolytic agent?

A

alteplase

43
Q

Mechanism of alteplase?

A

plasminogen activator

44
Q

alteplase admin?

A

bolus dose over 1 min followed by infusion

45
Q

Alteplase SEs?

A

bleeding

46
Q

List the antiplatelet drugs

A

aspirin
clopidogrel/ticlopidine/prasugrel/ticagrelor
dipyridamole
abciximab/eptifibatide

47
Q

Mehcanism of aspirin

A

inhibits platelet aggregation by irreversibly inhibiting COX

block PG and TXA2 production

48
Q

Where is aspirin absorbed?

A

upper GI tract

49
Q

Aspirin SEs

A

bleeding

GI irritation

50
Q

What are the ADP receptor blockers?

A

clopidogrel, ticlopidine, prasurgrel, ticagrelor

51
Q

Mechansim of clopidogrel et al?

A

inhibit ADP from binding P2Y12

except for ticagrelor, irreversible antagonists

52
Q

What metabolises Clopidogrel/ticlopidine?

A

prodrugs, activated by CYP2C19

53
Q

What drug can potentially inhibit clopidogrel?

A

PPIs used to tx peptic ulcer (ie/ omeprazole)

54
Q

Clopidogrel SEs

A

bleeding
dyspnea (ticagrelor)
neutropenia (ticlopidine)

55
Q

What is the adenosine deaminase and phosphodiesterase inhibitor?

A

dipyridamole

56
Q

What is the end result of dipyridamole?

A

inhibits aggregation, may cause vasodilation, may also cause release of prostcyclin of PGD2, casues coronary vasodilation

57
Q

Dipyridamole SEs

A

headache, GI upset, dixxiness

58
Q

How do abciximab and eptifibatide work?

A

prevent platetlet aggregation by binding to CPIIb/IIIa to prevent fibrinogen binding/crosslinking platelets

59
Q

Is abciximab competitive?

A

no

60
Q

Is eptifibatide competitive?

A

yes

61
Q

Abciximab/eptifibatide admin?

A

IV

62
Q

Abciximab/eptifibatide SEs?

A

bleeding, thrombocytopenia
hTN
bradycardia
use caution in pts w/renal dysfunction

Heme/Lymph (18 decks)

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