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Flashcards in Exam3 Antianginals- Martin Deck (49):
1

What nitrates do we use to tx angina

nitroglycerin
isosorbide dinitrate
isosorbide dinatrate

2

what CCBs do we use to Tx angina

verapamil, diltiazem
DHPs: nifedipine, amlodipine, felodipine

3

what Beta blockers do we use to Tx angina

atenolol, metoprolol, propranolol

4

what antiplatelets do we use to Tx angina

aspirin, clopidogrel, prasugrel
IIa/IIIb inhibitors: abciximab, tirofiban, eptifibatide

5

what anticoagulants can we use for angina

heparin, UHF, and LMWH

6

What drugs do we use for chronic CAD, stable angina

aspirin, Beta antagonists
nitrates, CCBs, ACEI, ranolzine

7

what drugs do we use for acute coronary syndromes

aspirin, Beta blockers and nitrates

8

What causes angina

the reversible imbalance between myocardial O2 supply and demand

9

what increases demand in angina pectoris and what decreases supply

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

10

What is the sensation of angina

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

11

When does typical angina occur

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

12

what is atypical angina

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

13

what can cause unstable angina

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

14

What are the therapeutic approaches to angina

increased O2
decrease O2 demand (decrease work and increase blood flow)

15

What are the Tx options of choice for typical angina

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

16

What are the Tx options for unstable angina

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"

17

what is the mechanism of organic nitrates (nitroglycerin)

provide NO

18

what are the effects of organic nitrates

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)

19

why is sublingual NTG more effective then direct infusion into heart

vascular effect

20

what are the routes of admin for NTG

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

21

what are the routes of admin for isosorbide dintrate

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

22

what are the adverse effects of organic nitrates

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

when are nitrates to be avoided

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

24

What CCBs have prominent cardiac effects

non DHPs
verapamil and diltizem

25

What are the CCBs with arteriolar vasodilation effects

DHPs
nifedipine, amlodipine, felodipine etc

26

How do CCBs work

bind to L type Ca Ch at different sites

27

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

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

28

what are the effects of CCBs in cardiac cells

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

How do non DHPs affect electrical components of heart

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

30

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

supraventricular arrhythmias

31

describe pharmacokinetics of CCBs

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

32

what are adverse effects of CCBs

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

33

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

beta blocker because potential AV block

34

What type of patients whould you not use verapamil/diltiazem

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

35

what are the effects of beta blockers in anginal therapy

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

36

what are the most commonly used cardioselective beta blockers

atenolol and metoprolol

37

what are indications to use beta blocker for chronic stable angina

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

38

when should you not use beta blocker for chronic stable

bradyarrhythmias or AV block
compensated CHF
asthmatics and DM

39

what is the dosage for aspirin for Tx of angina

once per day 85-325 mg

40

how does aspirin work

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

41

hwo does clopidogrel (plavix) work

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

42

when is clopidogrel used

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

43

What drug is used during angioplasty

Abciximab

44

how does abciximab work

monoclonal Ab against IIb/IIIa R inhibiting platelet aggregation

45

how do Tirofibana nd eptifibatide work

inhibit ligand binding to IIb/IIIa R

46

what drugs are used during angioplasty or atherectomy

abciximab, tirofiban and eptifibatide

47

what is Tx for acute angina single attacks

NTG

48

what are Tx choices for maintenacnce therapy of chronic stable angina

B blockers, CCBs or long duration nitrates
and combinations

49

what is used for vasospastic angina

CCBs or nitrates