Pharmacology

Question 1

major categories of anticoagulants

Answer 1

heparin (UFH)
enoxaparin (LMWH)
warfarin
dabigatran
rivaroxaban

Question 2

major categories of antiplatelet agents

Answer 2

aspirin
clopidrogel
GIIB/GIIIa inhibitors (abciximab, eptifibatide, tirofiban)

Question 3

major categories of thrombolytic agents

Answer 3

tissue plasminogen activator/variants

Question 4

MOA - heparin

Answer 4

combines with antithrombin III to inhibit activated clotting factors (IIa, IXa, Xa, XIa, XIIa) in plasma
can be measured by aPTT

Question 5

MOA - enoxaparin

Answer 5

combines with antithrombin III to inactivate factor Xa not IIa (thrombin)

Question 6

MOA - warfarin

Answer 6

acts in liver to prevent synthesis of Vit-K dependent clotting factors (II, VII, IX, X)
monitor with PT

Question 7

MOA - dabigatran

Answer 7

Acts in plasma to directly inhibit activity of thrombin (Factor IIa)
monitor with ECT

Question 8

MOA - rivaroxaban

Answer 8

Acts in plasma to directly inhibit activity of factor Xa

Question 9

MOA - aspirin

Answer 9

inhibition of COX-1, platelet aggregation

Question 10

MOA - clopidrogel

Answer 10

inhibits ADP receptor to interfere with ADP-induced platelet aggregation

Question 11

MOA - GIIB/GIIIa inhibitors

Answer 11

blocks IIb/IIIa receptors on platelet
prevent integrin and fibrinogen binding that facilitates aggregation
blocks all pathways of platelet activation

Question 12

Pharmacokinetics - heparin

Answer 12

does NOT cross placenta
IV or SC
if give IM – hematoma risk

Question 13

MOA - thrombolytic agents

Answer 13

increase formation of plasmin from plasminogen

Question 14

Pharmacokinetics - enoxaparin

Answer 14

IV or SC
first order renal elimination kinetics
does NOT cross placenta

Question 15

Pharmacokinetics - warfarin

Answer 15

100% oral absorption

crosses placenta

Question 16

Pharmacokinetics - dabigatran

Answer 16

polar drug, poor oral
prodrug rapidly absorbed from GI
renal excretion 80%

Question 17

Pharmacokinetics - rivaroxaban

Answer 17

oral

hepatic metabolism and renal excretion

Question 18

Pharmacokinetics - aspirin

Answer 18

orally

Question 19

Pharmacokinetics - clopidogrel

Answer 19

orally 1x

Question 20

Pharmacokinetics - GIIB/GIIIa

Answer 20

IV infusion

Question 21

Pharmacokinetics - thrombolytic agents

Answer 21

?

Question 22

major determinants of myocardial O2 supply

Answer 22

coronary blood flow (major)
-perfusion pressure (aortic pressure)
-length of diastole
-decreased by increased LVEDP
oxygen extraction
inversely proportional to coronary vascular resistance
-control by metabolites (major)
-damage to endothelium
-neural/hormonal control of vascular tone (small)

Question 23

major determinants of myocardial O2 demand

Answer 23

contractile state
heart rate
myocardial wall tension

Question 24

angina - cause

Answer 24

imbalance btw O2 supply and demand

Question 25

angina - goal of therapy

Answer 25

improve coronary blood flow (MBF) (surgically-bypass grafts or angioplasty or pharmacologically - vasodilators) reduction of MVO2 (pharmacologically - vasodilators and negative ionotropic/chronotropic agents)

Question 26

stable angina - define

Answer 26

classic/exertional angina fixed stenotic endothelialized atheromatous plaque imbalance when O2 demand increases; O2 supply can't increase treat - reduce O2 demand with nitrates, Ca++ channel blockers, beta-blockers

Question 27

variant (prinzmetal) angina

Answer 27

coronary vasospasm +/- atheromatous plaque imbalance as O2 supply decreases treat - reverse/prevent vasospasm, increase supply with vasodilators (nitrates, Ca++ channel blockers)

Question 28

unstable angina

Answer 28

ruptured atheromatous plaque with subocclusive thrombus MI risk; angina at rest treat acutely - clot (aspirin, heparin, CPIIB-IIIa inhibitors, PTCA/CABG, fibrinolytics), arrhythmias (beta blockers), pain (NTG, morphine) treat post-MI - ACEIs, statins, beta blockers, aspirin, clopidrogel (if post-stent)

Question 29

MOA - nitrates

Answer 29

converted to NO --> increase in cGMP --> relaxation of smooth muscle NO = vasodilator decreases LVEDP, systemic vascular resistance, wall tension --> decreases MVO2 requirement

Question 30

Pharmacokinetics - nitrates

Answer 30

low oral bioavailability (sustained release) sublingual - rapid therapeutic level transdermal

Question 31

Uses - nitrates

Answer 31

acute angina | prophylaxis - chronic angina

Question 32

Adverse rxns - nitrates

Answer 32

direct extension of therapeutic vasodilation (headache, orthostatic hypertension, reflex tachycardia, facial flushing) tachyphylaxis (tolerance) with continuous exposure

Question 33

MOA - Ca++ channel blockers

Answer 33

block of L-type Ca++ channels (vascular smooth muscle, arterioles > veins)

Question 34

Pharmacokinetics - Ca++ channel blockers

Answer 34

AVOID short acting dihydropyridines

Question 35

purpose of anticoagulants

Answer 35

prevention/treatment of venous thromboembolism prevention of cardioembolic events in atrial fibrillation arterial thrombosis

Question 36

purpose of antiplatelet agents

Answer 36

prevention/treatment of arterial thrombosis

Question 37

what is a venous thrombus made of?

Answer 37

fibrin + RBC with few platelets

Question 38

what is an arterial thrombus made of?

Answer 38

platelet aggregates; small amounts of fibrin