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Heme > Antithrombotic and hemostatic drugs > Flashcards

Antithrombotic and hemostatic drugs Flashcards

1
Q

Define/ describe the three main classes of antithrombotic drugs

A
  • anticoagulants: used to treat or prevent venous thrombosis
  • antiplatelets: used to prevent arterial thrombosis
  • thromboyltic agents: used to acutely reverse thrombosis
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2
Q

What is the mechanism of the anticoagulant effect of heparin?

A

accelerates inhibition of coagulation proteases Xa and IIa (thrombin) by antithrombin

heparin binds to antithrombin and induces a conformational change that accelerates the rate of protease inhibition

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3
Q

What property in addition to anticoagulation is notable in heparin?

A

anti-inflammatory

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4
Q

Describe the pharmacology of unfractionated heparin

A
  • unpredictable kinetics, monitor with aPTT
  • can inhibit Xa and IIa
  • side effects: bleeding, HIT, osteoporosis
  • neutralized by protamin
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5
Q

Describe the pharmacology of low molecular weight heparin

A
  • effects on Xa> IIa (thrombin)
  • does not reliably prolong aPTT
  • cleared mainly by kidneys
  • only partially neutralized by protamine
  • no need for routine monitoring and fewer complications
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6
Q

Describe the pharmacology of fondaparinux

A
  • specifically inhibits Xa
  • longer half life
  • does not require monitoring
  • eliminated by kidneys
  • can be used in HIT
  • not neutralized by protamine
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7
Q

List indications for use of heparins

A
  • LMWH is DOC for DVT/PE, can transition to warfarin
  • prevention of post-op thrombosis and during acute MI
  • UFH in dialysis and cardiopulmonary bypass machines
    _LMWH is DOC in pregnancy
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8
Q

Describe the mechanism of action of warfarin

A

Warfarin acts by interfering with the vitamin K-dependent gamma carboxylation of glutamines within
the amino-terminus “Gla domain” of the coagulation proteases

Interferes with reduction of vitamin K and depletes the body of this vitamin

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9
Q

Warfarin is monitored using the

A

PT/INR, goal is 2.0-3.0

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10
Q

List indications for warfarin

A
  • prevent recurrence of VTE, give for 3-6 months after an event
  • reduce risk of stroke and arterial emboli in atrial fibrillation or artificial valves
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11
Q

What can be given to reverse a warfarin overdose?

A

Vitamin K

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12
Q

Warfarin should never be given to __________

A

pregnant women

can cross placenta

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13
Q

_________ is a complication of warfarin thought to be due to suppression of protein C

A

warfarin induced skin necrosis

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14
Q

List some drugs that potentiate the effects of warfarin

A
  • inhibitors of warfarin metabolism: phenytoin, metronidazole, chloramphenicol, cimetidine, disulfiram, acute EtOH
  • displacement of warfarin from albumin: aspirin, clofibrate
  • inhibition of platelet aggregation: aspirin, clobidogrel
  • decreased vitamin K synthesis: antibiotics
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15
Q

List drugs that decrease warfarin effects

A
  • drugs that stimulate warfarin metabolism: barbiturates, rifampin, chronic EtOH
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16
Q

List and describe three direct thrombin inhibitors

A
  • argatroban: monitor by aPTT
  • bivalirudin: IV drug cleared by kidneys, used in percutaneous coronary angioplasty and HIT
  • dabigatran: oral alternative to warfarin, no routine monitoring and no antidote
17
Q

List a drug that is a direct factor Xa inhibitor

A

rivaroxaban: used to prevent VTE in orthopedic surgeries, stroke prevention in atrial fibrillation, tx of VTE

18
Q

Describe the mechanism of action of aspirin

A

inhibits platelet activation by irreversibly inhibiting COX-1 which prevents conversion of arachidonic acid to TXA2

19
Q

How do other NSAIDs that reversibly inhibit COX interact with aspirin?

A

compete with aspirin for binding to COX1, they can interfere with the anti-platelet effects
of aspirin

20
Q

List indications for aspirin use

A 
unstable angina
prevention of thrombosis after CABG
Coronary angioplasty
prevention of thrombosis in artificial heart valves
prevention of acute MI
TIA prophylaxis
21
Q

List side effects of aspririn

A

GI or cerebral bleed, rash, tinnitis

22
Q

What is the mechanism of action of clopidogrel

A

inhibits ADP-dependent platelet aggregation by binding to the ADP receptor

23
Q

20-30% of people have a CYP2C polymorphism that results in lower production of the active metabolite of _____, resulting in non-response

A

clopidogrel

24
Q

List indications of clopidogrel

A

TIA- may be superior to aspirin
Acute coronary syndrome
Prevention of coronary stent occlusion

25
Q

List major side effects of clopidogrel

A

immune mediated thrombocytopenia, neutropenia
hemorrhage
drug interactions

26
Q

List two drug names that are LMWH

A

enoxaparin, dalteparin

27
Q

What is the mechanism of action of abciximab?

A

inhibits platelet aggregation by inhibiting binding of fibrinogen and vWF.
monoclonal antibody against GpIIb/IIIa

28
Q

List indications for abciximab

A

adjunct therapy to percutaneous coronary intervention

useful in unstable angina if not responding to conventional therapy

29
Q

What is the mechanism of action of eptifibatide and tirofiban?

A

Mimic a peptide that is a ligand for GpIIb/IIIa, thus inhibiting fibrinogen binding and preventing aggregation of platelets

30
Q

What is the mechanism of action of reteplase and alteplase?

A

tPA recombinant forms, work by converting plasminogen to plasmin so it can digest the fibrin thrombus

31
Q

List some indications for fibrinolysis (reteplase and alteplase)

A 
acute MI
acute peripheral arterial obstruction
ischemic stroke
massive PE with hemodynamic compromise
massive proximal DVT
32
Q

List factors that determine the success of thrombolytic therapy

A

time to administration
character of the thrombus
re-occlusion

33
Q

List three indications for DDAVP

A

A hemostatic drug used in type I vWF, mild hemophilia, and thrombocytopenia

34
Q

List indications for amicar

A

Hemostatic drug that inhibits plasminogen activation

used for post-op bleeding, to reduce bleeding in coronary bypass, to reverse bleeding due to thrombolytic drugs

35
Q

What are indications for recombinant factor VIIa?

A

hemophilia if inhibitors have developed against replacement coagulation factors

uncontrolled hemorrhage

Heme (9 decks)

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