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Year 2 CV > Exam3 Antianginals- Martin > Flashcards

Exam3 Antianginals- Martin Flashcards

1
Q

What nitrates do we use to tx angina

A

nitroglycerin
isosorbide dinitrate
isosorbide dinatrate

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2
Q

what CCBs do we use to Tx angina

A

verapamil, diltiazem

DHPs: nifedipine, amlodipine, felodipine

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3
Q

what Beta blockers do we use to Tx angina

A

atenolol, metoprolol, propranolol

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4
Q

what antiplatelets do we use to Tx angina

A

aspirin, clopidogrel, prasugrel

IIa/IIIb inhibitors: abciximab, tirofiban, eptifibatide

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5
Q

what anticoagulants can we use for angina

A

heparin, UHF, and LMWH

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6
Q

What drugs do we use for chronic CAD, stable angina

A

aspirin, Beta antagonists

nitrates, CCBs, ACEI, ranolzine

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7
Q

what drugs do we use for acute coronary syndromes

A

aspirin, Beta blockers and nitrates

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8
Q

What causes angina

A

the reversible imbalance between myocardial O2 supply and demand

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9
Q

what increases demand in angina pectoris and what decreases supply

A

increased demand from increase in HR, increase ventricular contraction and increased wall tension (afterload)
decreased supply from decreased coronary blood flow, O2 carrying capacity of blood or both

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10
Q

What is the sensation of angina

A

heavy pressing substernal discomfort
radiating left shoulder, flexor aspect of left arm, jaw or epigastrum
signigicant minority of patients describe different location of character

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11
Q

When does typical angina occur

A 
exertional
from fixed atherosclerotic narrowing of coronary artery so with increase O2 demand have Sx
relieved by rest or NTG
last no more than 15 min 5-15 x /week
ST segment depression
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12
Q

what is atypical angina

A

angina at rest
variant, vasospastic, prinzmetals
focul or diffuse coronary vasospasm episodically reduces coronary flow
transient ST elevation during angina

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13
Q

what can cause unstable angina

A

rupture of atherosclerotic plaque with platelet adhesion and aggregation that decrease coronary blood flow
impending MI
if not relieved by 3 NTG in 15 minutes, call 911

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14
Q

What are the therapeutic approaches to angina

A

increased O2

decrease O2 demand (decrease work and increase blood flow)

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15
Q

What are the Tx options of choice for typical angina

A

main goal is to decrease demand
beta blocker and aspirin
beta blocker and aspirin and long acting nitrate
nitrate for subacute (NTG)
ACEI for DM or L ventricular dysfunction
long acting CCBs DHPs or long acting nitrates when beta blocker contraindicated

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16
Q

What are the Tx options for unstable angina

A

MI so MONA
morphine, O2 NTG, aspirin

usually want beta blocker too
if beta blocker contraindicated use verapamil or dilitiazem if no LV dysfunction
use aspirine and hepatin to decrease thrombus
surgery if needed
thrombolytics “plase”

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17
Q

what is the mechanism of organic nitrates (nitroglycerin)

A

provide NO

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18
Q

what are the effects of organic nitrates

A

decrease preload and afterload
relax vascular smooth muscle(large veins which dec VR thus preload)
dilate coronary aa, especiallly subendocardial regions
increase O2 supply (transient)

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19
Q

why is sublingual NTG more effective then direct infusion into heart

A

vascular effect

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20
Q

what are the routes of admin for NTG

A 
sublingual or spray (PRN)
sustained release capsules BID or QID
gel 3-5 hr
ointment 4-8 hr
dermal patch 12-16 hr
21
Q

what are the routes of admin for isosorbide dintrate

A

long acting
sublingual Q2-3 hr
oral tablets Q2-3 hr
sustained release tablet Q12 hr

22
Q

what are the adverse effects of organic nitrates

A

HA, facial flush, dizziness
orthostatic hypotension (alcohol makes it worse
Tolerance!! dec effectivness with use
dose/frequency dependent
have to give yourself a drug free period. skip certain doses

23
Q

when are nitrates to be avoided

A

in acute MI if right ventricular infarction because higher R sided filling Pressures are needed
If patient on viagra! sildenafil, tadalafil, cardenafil

24
Q

What CCBs have prominent cardiac effects

A

non DHPs

verapamil and diltizem

25
Q

What are the CCBs with arteriolar vasodilation effects

A

DHPs

nifedipine, amlodipine, felodipine etc

26
Q

How do CCBs work

A

bind to L type Ca Ch at different sites

27
Q

what occurs with CCBs when block Ca entry in L type channels

A

relaxation of arteriolar smooth muscle decreasing afterload and O2 demand
increases supply by dilating coronary arteries

28
Q

what are the effects of CCBs in cardiac cells

A

Ca binds troponin and releaves inhibition allowing contraction usually. so block Ca decreases the inotropic effects
however! since dec TPR, baroReceptor will negate the inotrpic effects

29
Q

How do non DHPs affect electrical components of heart

A

block channel and relay recovery so they decrease the rate of SA node depolarizaiton and slow AV node conduction

30
Q

the nodal effects of nonDHPs make them useful in treating what condition

A

supraventricular arrhythmias

31
Q

describe pharmacokinetics of CCBs

A

good oral absorption but high 1st pass effect
amlodipine, felodipine, isradipine slowly absorbed, long t 1/2 is advantage
verapamil soemtimes used IV

32
Q

what are adverse effects of CCBs

A

excessive vasodilation leading to dizziness, hypotension, HA, flushing and nausea
constipation (verapamil)
peripheral edema, coughin, wheezing, pulmonary edema
coronary steal - worsens agnina

33
Q

use of verapamil of diltiazem is contraindicated with use of what other cardaic drug and why

A

beta blocker because potential AV block

34
Q

What type of patients whould you not use verapamil/diltiazem

A

pts with ventricular dysfuntion, SA or AV nodal conduction defects and systolic BP< 90mmHg

35
Q

what are the effects of beta blockers in anginal therapy

A

decreased HR(major effect)
decreased contractility
decreased cardiac work, decrease O2 demand
decreased TPR

36
Q

what are the most commonly used cardioselective beta blockers

A

atenolol and metoprolol

37
Q

what are indications to use beta blocker for chronic stable angina

A

monotherapy fo rmild to moderate angina of effort
combination with long acting nitrate or DHP CCB (exertional)
after MI

38
Q

when should you not use beta blocker for chronic stable

A

bradyarrhythmias or AV block
compensated CHF
asthmatics and DM

39
Q

what is the dosage for aspirin for Tx of angina

A

once per day 85-325 mg

40
Q

how does aspirin work

A

blocks productions of PGs, irreversibly inhibits cyclooxygenase
platelets have no nuclei and cannot produce new cyclooxygenase

41
Q

hwo does clopidogrel (plavix) work

A

selectively inhibits ADP binding to platelet R and thus activation of glycoprotein GpIIb/IIIa complex

42
Q

when is clopidogrel used

A

unstable angina, prophylaxis and Tx of TIA and completed stroke
udnergoing stent placement

43
Q

What drug is used during angioplasty

A

Abciximab

44
Q

how does abciximab work

A

monoclonal Ab against IIb/IIIa R inhibiting platelet aggregation

45
Q

how do Tirofibana nd eptifibatide work

A

inhibit ligand binding to IIb/IIIa R

46
Q

what drugs are used during angioplasty or atherectomy

A

abciximab, tirofiban and eptifibatide

47
Q

what is Tx for acute angina single attacks

A

NTG

48
Q

what are Tx choices for maintenacnce therapy of chronic stable angina

A

B blockers, CCBs or long duration nitrates

and combinations

49
Q

what is used for vasospastic angina

A

CCBs or nitrates

Year 2 CV (31 decks)

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