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Pharmacology > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

what are the 4 phases of hemostasis

A
  • vascular spasm
  • platelet plug formation (primary hemostasis)
  • blood coagulation (2ndary hemostasis)
  • dissolution of fibrin clot (tertiary hemostasis)
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2
Q

what is Virchow’s triad and what is its importance

A

endothelial injury, abnormal flow of blood, and hypercoagulability

they predispose one to formation of a thrombus

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3
Q

classes of drugs that are used to reduce clotting

A
  • platelet aggregation inhibitors
  • anticoagulants
  • thrombolytics
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4
Q

classes of drugs that are used to treat bleeding

A
  • plasminogen activation inhibitors
  • protamine sulfate
  • vitamin K
  • plasma fractions
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5
Q

platelet aggregation inhibitor are useful in the prevention and treatment of

A

cardiovascular diseases
maintenance of vascular grafts and arterial patency
adjuncts in treatment of MI

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6
Q

what are the platelet aggregation inhibitors

A

GAAP

  • GP IIb/IIIa inhibitors: abciximab, eptifibatide, tirofiban
  • Aspirin
  • ADP receptor inhibitors: Clopidogrel, ticlopidine
  • Phosphodiesterase inhibitor: Cilostazol, Dipyridamole
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7
Q

mechanism of aspirin

A

it inhibits thromboxane synthesis by irreversible acetylation of enzyme COX hence it is a COX inhibitor

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8
Q

why is aspirin better than other NSAIDs

A

it can acetylate COX and is irreversible hence its action lasts longer than the reversible action of other NSAIDs

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9
Q

what is aspirin used for

A
  • prophylactic tx of transient cerebral ischemia
  • reduce incident of recurrent MI
  • reduce mortality in post MI patient
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10
Q

name the ADP receptor blockers and their mechanism

A

clopidogrel and ticlopidine

inhibit P2Y12 irreversibly (ADP receptor on platelet surface) –> reduced platelet aggregation

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11
Q

adverse effects of ADP receptor blockers (name the drugs again)

A

clopidogrel and ticlopidine

thrombocytopenia pupura

but ticlopidine can cause neutropenia

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12
Q

how is clopidogrel activated and what are conditions that can cause it not to be activated

A
  • it is a prodrug that is activated by CYP2C19
  • if someone is a poor metabolizer of CYP2C19 or takes omeprazole (CYP2C19 inhibitor), then they would have less of the active metabolite in their plasma
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13
Q

uses of clopidogrel and ticlopidine (more clopidogrel though)

A

reduce the rate of stroke, MI, death in pts with recent MI or stroke, established peripheral artery disease, or acute coronary syndrome

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14
Q

mechanism of dipyridamole

A

inhibits phosphodiesterase and/or blocks adenosine uptake –> increase in cAMP –> activates adenylyl cyclase –> coronary vasodilation

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15
Q

uses of dipyridamole

A
  • little to no benefit if taken alone
  • with warfarin it prevents post op thromboembolic complication of cardiac valve replacement
  • with aspirin it’s a prophylaxis for cerebrovascular disease
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16
Q

mechanism of cilostazol

A

inhibits phosphodiesterase –> vasodilation and inhibition of platelet aggregation

17
Q

what is cilostazol used for

A

intermittent claudication

18
Q

uses of platelet GP IIb/IIIa receptor blocker (name drugs agin)

A

tirofiban, eptifibatide, abciximab,

  • reduce the rate of thrombotic cardiovascular event in non-ST elevation acute coronary syndrome (NSTE-ACS)
  • adjunct to percutaneous coronary intervention (PCI) for the prevention of cardiac ischemic complications
19
Q

how does the IIb/IIIa complex function

A
  • receptor for fibrinogen and vitronectin but also for fibronectin and von willebrand factor
  • activation of this complex is the final common pathway for platelet aggregation
20
Q

condition called in those lacking the IIb/IIIa receptor

A

bleeding disorder called Glanzmann’s thrombasthenia

21
Q

direct mechanism of the IIb/IIIa drugs

A
  • tirofiban: nonpeptide tyrosine analogue that is a reversible antagonist of the complex
  • eptifibatide: cyclic peptide reversible antagonist of the receptor
  • abciximab: chimeric mouse human monoclonal antibody against the receptor
22
Q

anticoagulants can be classified into what four groups

A
  • indirect thrombin and factor X inhibitor: unfractioned standard heparin, low molecular weight heparin (Enoxaparin, Dalteparin, Tinzaparin) and fondaparinux
  • direct thrombin inhibitors: lepirudin, bivalirudin, argatroban, dabigatran
  • direct factor Xa inhibitor: apixaban and rivaroxaban
  • couramin anticoagulants: warfarin
23
Q

why are low molecular weight heparin (name them) the replacement for unfractioned heparin

A

Enoxaparin, Dalteparin, Tinzaparin

they have fewer drawback than UFH, have equal efficacy, superior bioavailability, longer half lives, less frequent dosing requirements

24
Q

mechanism of action of heparin

A

binds to anti thrombin III –> inhibits clotting factor proteases especially thrombin, IXa, Xa

25
Q

difference in mechanism of UFH and LMWH

A
  • to most efficiently inactivate thrombin by antithrombin III, heparin has to bind to both antithrombin and thrombin simultaneously
  • to inactivate factor Xa by antithrombin III, heparin only needs to bind to antithrombin III
  • LMWH inhibits Xa but not long enough to form ternary complex so no effect on thrombin but UFH efficiently inactivates Xa and thrombin
26
Q

what test is used to monitor heparin levels and prevent bleeding and what does the test check

A

aPTT

test for the integrity of the intrinsic and common pathway of coagulation

27
Q

when taking LMWH why is it not necessary to monitor blood level

A

it’s weight dosing causes predictable plasma levels with normal renal function

28
Q

when do you have to monitor LMWH

A

in those with renal insufficiency, pregnancy, and obesity

29
Q

uses of heparin

A
  • initiate tx of venous thrombosis and pulmonary embolism (warfarin started at same time then heparin discontinued after 5 days when warfarin reaches its full therapeutic effect)
  • initial management of pts with unstable angina of acute MI
  • coronary balloon angioplasty to prevent thrombosis
  • drug of choice for preggos because does not cross the placenta
30
Q

adverse effects of heparin

A
  • bleeding
  • hypersensitivity reactions
  • heparin induced thrombocytopenia (two types)
  • elevation of liver transaminases
  • osteoporosis
31
Q

how is type II heparin induced thrombocytopenia work (mechanism)

A
  • seen more commonly in UFH
  • antibodies recognize heparin and a platelet protein, platelet factor 4
  • IgG binds both heparin and PF4 forming an immune complex then binds to Fc receptor on platelets
  • Fc activation lead to platelet degranulation and aggregation
  • activated platelets release more PF4 and more immune complexes form
  • leads to thrombocytopenia and thrombosis
  • hence leading to DVT, heart attack, stroke, PE
32
Q

what is next step if excessive anticoagulant action with heparin

A

stop heparin and give direct thrombin inhibitor or fondaparinux

if bleeding give protamine sulfate though it does not reverse action of fondaparinux

33
Q

mechanism of fondaparinux and what it is mainly used for

A

selective, indirect, inhibitor of factor Xa with negligible antithrombin activity

mainly used for DVTs

34
Q

what are the direct thrombin inhibitors and how do they work

which ones are parenteral and which oral

how are they monitored

A

BALD
Bivalirudin, Argatroban, Lepirudin, Dabigatran

they directly bind to the active site of thrombin

all parenteral except for dabigatran

monitored by aPTT

35
Q

what types of patients should lepirudin be given cautiously to and why

A

those with renal insufficiency because no antidote exists

36
Q

what are the direct factor Xa inhibitors and how are they monitored

A

apixaban and rivaroxaban

like dabigatran, they do not require monitoring

Pharmacology (79 decks)

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