100114 anti thrombotic pharm

Question 1

STEMI treatment

Answer 1

immediate reperfusion therapy

antiplatelet/antithrombotic agents, statin, aspirin, beta adrenergic blockers, nitrates

Question 2

NSTEMI and UA treatment

Answer 2

antiplatelet/antithrombotic agents, statin, aspirin, beta adrenergic blockers, nitrates

Question 3

alteplase MOA

Answer 3

plasminogen activator

Question 4

adverse effects of fibrinolytic therapy

Answer 4

bleeding

Question 5

contraindications to thrombolytic therapy

Answer 5

about 30% of pts unsuited for thrombolytics

situations where drug therapy could impair necessary fibrin clots within circulation

active peptic ulcer, recent stroke, recovering from recent surgery

Question 6

anticoagulants’ goals

Answer 6

inhibit activation of thrombin by Xa
directly inhibit thrombin
decrease production of functional prothrombin

Question 7

unfractionated heparin MOA

Answer 7

catalyzes antithrombin’s actions on Xa and thrombin

Question 8

low molecular weight heparin MOA

Answer 8

catalyzes antithrombin’s action on Xa

enoxaparin, dalteparin

Question 9

fondaparinux

Answer 9

catalyzes antithrombin’s action on Xa

Question 10

unfractionated heparin, LMWHs, fondaparinux are all administered how?

Answer 10

parenterally

Question 11

side effects of unfractionated heparin

Answer 11

heparin induced thrombocytopenia

Question 12

LMWH and fondaparinux have an advantage over UFH how?

Answer 12

they have longer half lives and more predictable bioavailability (less bleeding, less risk of thrombocytopenia)

Question 13

direct thrombin inhibitor

Answer 13

bivalirudin
inhibits independently of antithrombin
acts on both circulating and clot bound thrombin

no thrombocytopenia

unstable angina pts undergoing PCI

Question 14

MOA of thienopyridines

Answer 14

prevent ADP and P2Y12/P2Y1 interaction so that platelet cannot have increased Ca and be activated

Question 15

GP IIb/IIIa receptor antagonists MOA

Answer 15

prevent fibrinogen binding in the GP IIb/IIIa

Question 16

aspirin MOA

Answer 16

irreversibly actylates COX-1 in platelet. blocks production of thromboxane, which activates platelets and helps with platelet aggregation

platelets lack nuclei so permanent effect of aspirin

endothelial cells (which produce prostacyclin downstream of COX) do not experience loss of prostacyclin like platelets experience loss of thromboxane because endothelial cells have nuclei

Question 17

aspirin uses

Answer 17

UA, acute MI, history of MI

chronic stable angina without history of MI

pts who’ve had minor stroke or transient cerebral ischemia

pts who have undergone coronary artery bypass

should not be used for primary prevention to completely healthy ppl

Question 18

which thienopyridines are irreversible

Answer 18

clopidogrel, prasugrel

Question 19

advantage of reversible platelet inhibitor

Answer 19

if pt requires surgery (like coronary bypass) and is taking drug like clopidogrel or aspirin, you have to wait for platelet fxn to return to normal (platelet life span is 7-10 days)

Question 20

side effects of thienopyridines

Answer 20

bleeding

GI related symptoms

Question 21

clopidogrel is metabolized by

Answer 21

CYP2C19

Question 22

effectiveness of thienopyridines compared to aspirin

Answer 22

as monotherapy, are modestly superior to aspirin in reducing risk of MI

Question 23

glycoprotein IIb/IIIa receptor antagonists examples

Answer 23

abciximab, eptifibatide

Question 24

glycoprotein IIb/IIIa inhibition is reversible or irrev?

Answer 24

reversibly inhibit the final common pathway of platelet aggregation-binding of GPIIb/IIIa receptor to fibrinogen and vWF. so platelets cannot stick to each other and you don’t get formation of the hemostatic plug

Question 25

rivaroxaban MOA

Answer 25

inhibits Xa

Question 26

dabigatran MOA

Answer 26

inhibits thrombin