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Pharm II > drugs for ischemic heart dz > Flashcards

drugs for ischemic heart dz Flashcards

1
Q

evidence based tx for ischemic heart disease

A

Lipid-lowering drugs Anti-platelet agents
ACEI (HOPE and PEACE trials - CAD without HF)
Beta-blockers – reduce mortality post-MI

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2
Q

SX control for ischemic heart disdease

A

Nitrates Calcium antagonists

Beta-blockers

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3
Q

what two things do you need to consider when tx ischemic heart dz

A

reducing disease process and sx control

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4
Q

sxs of myocardial ischemia is usually secondary to

A

atherosclerosis of the coronary arteries

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5
Q

prinzmetals variant angina

A

normal coronary arteries but with spasms

seen in younger women in the morning

can be seen with CAD variant

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6
Q

New angina at rest or an increase in angina intensity, frequency, or duration

A

Unstable angina:

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7
Q

Occurs in patients without coronary artery disease and is due to a spasm of the coronary artery resulting in decreased myocardial blood flow

A

Classic Prinzmetal’s variant angina or vasospastic angina:

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8
Q

Coronary vasospasm occurring at the site of a fixed atherosclerotic plaque

A

Mixed angina:

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9
Q

Transient change in myocardial perfusion, function, or electrical activity; can be detected on an ECG in most anginal patients; patient does not experience chest pain or other signs of angina

A

Silent myocardial ischemia:

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10
Q

<50% asthersclerotic plaques will present with what sxs

A

Usually asymptomatic < 50%
Symptomatic at >70% obstructed
50-70% obstructed +/- sx

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11
Q

most txs for ischemic heart dz work by

A

decreasing oxygen demand

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12
Q

myocardial oxygen demand is determined by

A

wall stress
heart rate
and contractility

which are all variants of workload

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13
Q

wall stress that determines work load

A

Intraventricular pressure = blood pressure

Wall force – ventricular volume

Wall thickness

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14
Q

MLCK

how does it work and what drugs act on this

A

myosin-LC kinase when active can promote the phosphorylation of myosin LC and when phosphorylated they combine with actin to cause contraction

dephosphorylation causes relaxation

Ca activates this phosphorylation
which is how CCB and BB work in this way as well

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15
Q

how do nitrates work

A

increase cycle cGmP and increase dephosphorylation of myosin –> vasodilation

Decreasing intracellular Ca++ -
increase dephosphorylation

cause vasodilation

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16
Q

if we can block calcium in the cell what effect will it have on the cell

A

decrease contractily

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17
Q

alpha 1

A

heart

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18
Q

alpha 2

A

all over

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19
Q

beta 2

A

increase deactivation and cause vasodilation

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20
Q

Nitrates cause what effect in the body

A

Decrease venous return to heart, and therefore decrease workload
Promote coronary vasodilation, even with atherosclerosis

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21
Q

nitrates contraindicated with viagra why?

A

sidenafil increases cGMP
through another mechanism

can’t take with nitrates b/c of unsafe drops in blood pressure

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22
Q

BB would cause a higer risk or orthostatic HTN with nitrates because

A

blocks compensatory tachy response

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23
Q

sxs of nitrates

A

Orthostatic hypotension, syncope, temporal artery pulsations, throbbing headache d/t meningeal artery pulsations, compensatory sympathetic response (tachycardia, increased cardiac contractility), compensatory renal response (Na and water retention)

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24
Q

Isosorbide mononitrate

A

metabolite of isosorbide dinitrate

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25
Q

Amyl nitrite

adm and onset

A

onset .5 mins

duration
3-5 mins

inhalent

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26
Q

Nitroglycerin

routes of adm

A

IV
sublingual
translingual

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27
Q

Isosorbide dinitrate

A

sublingual 2-5 minutes

lasts 1-2 hours

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28
Q

NTG

A

Topical Ointment
30 - 60
2 – 12 hr

Transdermal
30 - 60
up to 24h

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29
Q

Isosorbide mononitrate

routes of adm

A

PO, SR
this is what most people use

onset 30-60 minutes

duration 12-24 hrs

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30
Q

short acting nitrates are used to

A

Short acting used to abort acute anginal episodes

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31
Q

long-acting nitrates are used for

A

Long-acting formulations used as to prevent angina (maintenance therapy)

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32
Q

what is nitrates used for in unstable angina

A

Both reduced cardiac workload and coronary artery dilation and redistribution of coronary blood flow to ischemic areas

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33
Q

instructions for use of NTG

A

Sit down
Place tablet under tongue; do not swallow; may tingle
Pain usually relieved in 3-5 minutes; if not, seek emergent medical care (call 9-1-1); may take second tablet
May repeat every 5 minutes for total of 3 doses over 15 minutes

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34
Q

Optimal NTG Sl dose should relieve pain and produce objective hemodynamic response seen as what bp change

A

Optimal NTG Sl dose should relieve pain and produce objective hemodynamic response: 10 mmHg fall SBP or 10 beat/min increase HR

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35
Q

MOA of NTG

A

NTG is broken down to NO and NO activates GMP in smooth muscle which leads to an increase in cGMP which acts to relax muscle contraction and leads to vasodilation

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36
Q

when should you replace NTG

A

befor 6 months

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37
Q

what might you want to consider with routes of administration for older pts

A

older people with tremors can have difficulty with pills

spray can be helpful

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38
Q

NTG IV dose

A

5 mcg/min, titrate by 5-10 mcg/min to effect

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39
Q

NTG Sl dose

A

0.3 – 0.6 mg/tab

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40
Q

Transdermal dose NTG

A

0.1 – 0.8 mg/hr release rate

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41
Q

why do you want to take nitrate breaks

A

only wear patch when you see most common angina attacks

need break because people build up tolerance

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42
Q

ADE of NTG

A

” Orthostatic hypotension (d/t diifulties maintaining venous tone, especially when stands up) , severe in ETCH
“ Syncope
“ Temporal artery pulsations (increase HR reflex d/t decrease vagal tone)
“ Throbbing HA, compensatory sympathetic and renal responses
“ PD5s will potentiate Nitrates hypotensive effect

SL:
  • Warmth
  • Flushing, lightheadedness, faint,
  • Tachycardia
  • HA (sot start low & slow), sublingual burn
43
Q

Drug interactions with NTG

A

alcohol
hottub
PD5s

44
Q

other uses for nitrates besides angina

A

Ointment used topically for anal fissures and hemorrhoids

45
Q

MOA of CCB

A

“Binds L-type Ca channel in cardiac and smooth muscle

  • ->reduction in Ca current
  • -> relaxed smooth muscle (↓afterload!), ↓contractility, ↓HR (SA & AV node via T-type)

varaible effects at the heart

Areterioles > veins

46
Q

which two CCB have greater cardiac effect

A

Diltiazem, verapamil greater decrease in HR

47
Q

NTG more vein or arteriole dilation

A

more vein dilation

48
Q

CCB more veins or arteriole dilation

A

arterioles

49
Q

which two CCB are more selective for cerebral blood vessels

A

Nimodipine, nicardipine more selective for cerebral blood vessels – nimodipine not available in US

50
Q

CCB are used for

A

HTN and angina

Raynaud’s (off label)
HA (off label)
Reduces myocardial oxygen demand
“

51
Q

Raynauds

A

in Raynaud’s phenomenon, smaller arteries that supply blood to the skin constrict excessively in response to cold, limiting blood supply to the affected area

52
Q

why do we see increased contractility in some CCB

which one do you see this with the most

A

reflex response

seen most common in Nifedipine

53
Q

ADE of CCB

A 
"	All from vasodilating effect:
"	     Peripheral edema
"	       HA
"	       Dizziness
"	       Nausea
"	       Constipation (30% 
                 w/rapper)
"	        Bradycardia
"	
"	DO NOT USE diltiazem or verapamil in CHF d/t decrease myocardial contractility
54
Q

pathophys of CCB

A

reduces oxygen demand through peripheral vascular resistance

can reduce spasms in arteries

55
Q

names of CCB

A

V-rapper
verapamil

Dil pickle
Diltiazem

Nimodepine
knee moped

Knee fed pine
Nifedpine

Felod pine

56
Q

which CCB should you not use in HF and why?

A

” DO NOT USE diltiazem or verapamil in CHF d/t decrease myocardial contractility

57
Q

CCB: Drug Interactions CI

A

Beta-adrenergic blockers: cardiac effects of both drugs may be increase

Digoxin: DIGOXIN effects may be enhanced. Increased
DIGOXIN levels and toxicity could occur. Verapamil > diltiazem.

HMG-CoA RI: Plasma concentrations of certain HMG-CoA REDUCTASE INHIBITORS may be elevated, increasing the risk of toxicity (eg, rhabdomyolysis, myositis).

Quinidine: Hypotension, bradycardia, ventricular tachycardia and AV block may occur (verapamil > diltiazem)
Carbamazepine: Serum

CARBAMAZEPINE levels may be increased, resulting in an increase in pharmacologic and toxic effects

Rifampin: Loss of clinical effectiveness of oral VERAPAMIL or DILTIAZEM; due to increased first-pass hepatic metabolism

58
Q

drug interactions with verapmil

A

Calcium products: pharmacologic antagonism; Clinical effects and toxicities of VERAPAMIL may be reversed by CALCIUM
Ethanol: Increased and prolonged CNS effects of ETHANOL affecting coordination and judgment. Possibly due to inhibition of ethanol metabolism

59
Q

Diltiazem CI

A

Aminophylline: The pharmacologic and toxic effects of THEOPHYLLINES may be increased.

60
Q

Nifedipine, felodipine CI

A

Barbiturates: decreased serum NIFEDIPINE and FELODIPINE concentrations, possibly reducing efficacy. Enhanced metabolic clearance caused by enzyme induction.

Cimetidine: the effects of NIFEDIPINE and FELODIPINE may be increased. hepatic metabolism of NIFEDIPINE may be decreased.

Melatonin: may interfere with the antihypertensive effect of NIFEDIPINE.

61
Q

Felodipine

CI

A

Grapefruit juice: Serum FELODIPINE concentrations may be elevated, producing an increase in both pharmacologic and adverse effects.
Erythromycin: The pharmacologic and adverse effects of FELODIPINE may be increased.
HYDANTOINS: The pharmacologic effects of FELODIPINE may be decreased. The metabolism of FELODIPINE may be increased because of induction of mixed-function oxidases by HYDANTOINS, causing an increase in first-pass metabolism and decreased bioavailability.

62
Q

MOA of BB

A

Competitively inhibit beta adrenergic receptor

63
Q

three main CV effects of BB

A

Lower BP; negative inotropic and chronotropic effects resulting in reduced cardiac output ( heart primarily beta 1 receptors, 10-40% beta 2 receptors)

Vascular effects: Oppose beta 2-mediated vasodilation
Antagonize release of renin
(neurohormonal)

64
Q

Respiratory BB effects

A

blockade of beta2 receptors may increase airway resistance

65
Q

eye effects of bb

A

beta receptor blockade reduces IOP by decreasing aqueous humor production

66
Q

Metabolic effects of BB

A

Inhibit sympathetic nervous system stimulation of lipolysis
Glycogenolysis in liver partially inhibited; may impair recovery from hypoglycemia
Lipids: increased TG and decreased HDL; less with ISA

67
Q

BB problem with hypoglycemia

A

will block feelings of hypoglycemia

68
Q

how do BB help with angina ?

A

Reduced cardiac workload and oxygen demand
Slowing and regularization of heart rate may contribute – improved coronary artery filling during diastole

Timolol, propranolol and metoprolol prolong survival following myocardial infarction

69
Q

which three BB prolong survival following MI

A

Timolol, propranolol and metoprolol

70
Q

what tx should you use first for long term tx of angina

A

bb Generally should be used before nitrates and CCB for long-term tx

71
Q

____ more effective at lowering incidence of anginal episodes

A

BB more effective at lowering incidence of anginal episodes

72
Q

____ most effective at preventing silent ischemia

A

BB most effective at preventing silent ischemia

73
Q

___lower mortality in HTN, HF, post-MI

A

BB lower mortality in HTN, HF, post-MI

74
Q

What BB have been indicated for angina

A

atenolol, metoprolol, nadolol, propranolol

75
Q

What BB have been indicated for HTN

A

all except sotolol and esmolol

76
Q

BB for SVT, sinus tachycardias, intraoperative HTN/tachycardia:

A

SVT, sinus tachycardias, intraoperative HTN/tachycardia: esmolol (IV), others PO

77
Q

BB for Ventricular arrhythmias

A

sotolol

78
Q

bb for SVT and ventricular arrhythmias:

A

propranolol

79
Q

BB for Migraine prophylaxis

A

: propranolol, timolol (also atenolol, metoprolol, nadolol)

80
Q

BB Post-MI

A

: atenolol, metoprolol, propranolol, timolol

81
Q

Systolic HF BB

A

metoprolol, carvedilol, bisoprolol

Others:

82
Q

ISA

A

intrinsic sympathomimetic activity

partial agonist

but antagonist

83
Q

which BB reduces late Na current that facilitates Ca entry via Na-Ca exchanger and has nitric oxide-induced vasodilatory properties

A

Nebivolol

84
Q

BB w/ alpha-1 adrenergic blocking effect

A

Carvedilol**

85
Q

this BB can be titrated quickly to manage bp due to quick half life and RBC esterase metabolism

A

Esmolol

86
Q

ADE of BB

A 
Bradycardia, will worsen HF if we don't go low and slow
Bronchospasm
Impaired peripheral circulation
"	↓exercise tolerance
"	Worsening angina if abrupt D/C
"

Worsening HF if dosed incorrect

” Well tolerated
“ HA, nausea, bradycardia

87
Q

would caution use of BB in DM pt on

A

sulfonaurias or insulin

88
Q

BB di

A

Cimetidine, quinidine, diphenhydramine, food

NSAID’s

Clonidine

Agents that induce hepatic enzymes (rifampin, barbiturates):

Verapamil, diltiazem: heart block

Sympathomimetics, ergot derivativeS

89
Q

Sympathomimetics, ergot derivatives DI with BB

A

: unopposed alpha adrenergic-mediated or ergot-mediated vasoconstriction

90
Q

Agents that induce hepatic enzymes (rifampin, barbiturates) are CID w/ BB b/c

A

decrease efficacy of hepatically metabolized

beta blockers

91
Q

clonidine is CI w/ BB b/c

A

additive bradycardia; beta-blocker inhibition of beta2 receptor mediated vasodilation leaves peripheral alpha receptor mediated vasoconstriction unopposed during clonidine withdrawal. Management:Closely monitor blood pressure after initiation or discontinuation of clonidine or a beta-blocker when they are given concurrently. Discontinue either agent gradually; preferably, discontinue the beta-blocker first.

92
Q

why is NSAID CI with BB

A

additive bradycardia; beta-blocker inhibition of beta2 receptor mediated vasodilation leaves peripheral alpha receptor mediated vasoconstriction unopposed during clonidine withdrawal. Management:Closely monitor blood pressure after initiation or discontinuation of clonidine or a beta-blocker when they are given concurrently. Discontinue either agent gradually; preferably, discontinue the beta-blocker first.

93
Q

why is Cimetidine, quinidine, diphenhydramine, food CI w/ BB

A

: increase efficacy of hepatically metabolized  -blockers (CyP2D6)

94
Q

“Third generation” cardioselective beta-blocker

A

Nebivolol (Bystolic)

95
Q

Ranolazine Extended-Release Tablets (Ranexa) indication

A

Chronic angina – often used for cases where other antianginals have been inadequate

96
Q

MOA of Ranolazine Extended-Release Tablets (Ranexa)

A

reduces late sodium current that facilitates calcium entry via Na-Ca exchanger –> reduces diastolic tension, cardiac contractility, and work

97
Q

CI of Ranolazine Extended-Release Tablets (Ranexa)

A 
Existing QT prolongation; Concurrent use of QT prolonging drugs 
Potent and moderate CYP450 3A inhibitors
Liver impairment (Child-Pugh A, B, C)
98
Q

ADE of ranolozine

A

Dizziness, headache, constipation, nausea, asthenia, syncope, palpitations
Tinnitus, vertigo
Abdominal pain, vomiting, dry mouth
Peripheral edema, dyspnea
Bradycardia, hypotension, tremor, blurry vision, hypoesthesia, hematuria
Transient eosinophilia, decreased hematocrit

99
Q

Ivabradine MOA

A

” I-funny inhibition

100
Q

Ivabradine indications

A

Reduces HR

Recently approved for chronic heart failure; studied for angina

101
Q

ADR of ivabradine

A

atrial fibrillation(8%), bradyarrhythmia (10%)

102
Q

DI in ivabradine

A

Drugs that prolong QT: fluoroquinolones, dronedarone, ziprasidone, mesoridazine
CyP3A4 inhibitors: nelfinavir, ritonavir, nefazodone, conivaptan

103
Q

1st line in Variant angina

A

CCB often used first-line (antispasmodic effect, low ADE); may add on nitrate; BB may cause vasoconstriction

104
Q

tx of acute unstable

A

BB and nitrates acutely

CCB if poor response

anti-plt (chewable ASA)

Pharm II (16 decks)

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