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CVPR Cardio 2 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

major categories of anticoagulants

A 
heparin (UFH)
enoxaparin (LMWH)
warfarin
dabigatran
rivaroxaban
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2
Q

major categories of antiplatelet agents

A

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

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3
Q

major categories of thrombolytic agents

A

tissue plasminogen activator/variants

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4
Q

MOA - heparin

A

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

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5
Q

MOA - enoxaparin

A

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

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6
Q

MOA - warfarin

A

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

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7
Q

MOA - dabigatran

A

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

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8
Q

MOA - rivaroxaban

A

Acts in plasma to directly inhibit activity of factor Xa

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9
Q

MOA - aspirin

A

inhibition of COX-1, platelet aggregation

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10
Q

MOA - clopidrogel

A

inhibits ADP receptor to interfere with ADP-induced platelet aggregation

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11
Q

MOA - GIIB/GIIIa inhibitors

A

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

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12
Q

Pharmacokinetics - heparin

A

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

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13
Q

MOA - thrombolytic agents

A

increase formation of plasmin from plasminogen

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14
Q

Pharmacokinetics - enoxaparin

A

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

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15
Q

Pharmacokinetics - warfarin

A

100% oral absorption

crosses placenta

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16
Q

Pharmacokinetics - dabigatran

A

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

17
Q

Pharmacokinetics - rivaroxaban

A

oral

hepatic metabolism and renal excretion

18
Q

Pharmacokinetics - aspirin

A

orally

19
Q

Pharmacokinetics - clopidogrel

A

orally 1x

20
Q

Pharmacokinetics - GIIB/GIIIa

A

IV infusion

21
Q

Pharmacokinetics - thrombolytic agents

A

?

22
Q

major determinants of myocardial O2 supply

A 
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)
23
Q

major determinants of myocardial O2 demand

A

contractile state
heart rate
myocardial wall tension

24
Q

angina - cause

A

imbalance btw O2 supply and demand

25
Q

angina - goal of therapy

A

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

26
Q

stable angina - define

A

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

27
Q

variant (prinzmetal) angina

A

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

28
Q

unstable angina

A

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)

29
Q

MOA - nitrates

A

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

30
Q

Pharmacokinetics - nitrates

A

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

31
Q

Uses - nitrates

A

acute angina

prophylaxis - chronic angina

32
Q

Adverse rxns - nitrates

A

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

33
Q

MOA - Ca++ channel blockers

A

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

34
Q

Pharmacokinetics - Ca++ channel blockers

A

AVOID short acting dihydropyridines

35
Q

purpose of anticoagulants

A

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

36
Q

purpose of antiplatelet agents

A

prevention/treatment of arterial thrombosis

37
Q

what is a venous thrombus made of?

A

fibrin + RBC with few platelets

38
Q

what is an arterial thrombus made of?

A

platelet aggregates; small amounts of fibrin

CVPR Cardio 2 (2 decks)

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