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Cardiac Pharmacology > Deck 1 > Flashcards

Deck 1 Flashcards

1
Q

How does Digoxin work?

A
  • it is an Na/K+ ATPase blocker that increases Na+ concetration, which exchanges for Ca2+. This leads to an increase in Ca+ increases heart contractility, and positive inotropy
  • has parasympathommetic effects via direct stimulation of the vagus nerve, leading to AV nodal inhibition
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2
Q

digoxin is used to treat

A

chronic systolic HF and atrial arrythmias like Afib and Aflutter

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3
Q

does digoxin reduce mortility?

A

no!

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4
Q

when do you give digoxin

A

when ace inhibitors and diuretcs have failed

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5
Q

side effects if digoxin

A

hyperkalemia, PVCs, St scopps, bradychardia, AV nodal block / heart block , GI symptoms, yellow vision

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6
Q

what are the EKG change shown with digitalis poisoning

A

scooped concave ST segments

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7
Q

do not use digoxin in

A

pts w significant SA or AV nodal block
on b-blockers
pts w hypokalemia
renal dysf(x)

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8
Q

Milrinone - how does it work?

A

is a phosphodiesterase inhibitor that leads to the breakdown of cAMP

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9
Q

effects of Milrinone

A

Milrinone is inotropic and vasodillitory (decreased after load)

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10
Q

main side effect to watch out for with milrinone:

A

hypotension

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11
Q

Nesiritde is a synthetic form of and does what in a cell

A

BNP, which increases cGMP, which leads to a relaxation of smooth muscle

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12
Q

nesiritde effect

A

venous AND arterial vasodillation, and increases natriuresis. reduces pre load and afterload, along with Na+ excretion

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13
Q

ACE inhibitors act how

A

block the concersion of Angiotensin I –> ATII

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14
Q

down stream effects of ACE

A

decreased BP –> low arteriolar resistance, high venous capacitance and low CO

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15
Q

do ace inhibitos prevent cardiac remodeling?

A

yes

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16
Q

who do you not give ACE inhibitors to

A

pregnant nasty women, patients with chronic renal disease and patients with CHF

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17
Q

side effects of ACE inhibitors

A

dry cough due to bradykinin buildup and angioedema

hypokalemia

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18
Q

Aliskiren works how

A

it is an angiotensin inhibitor that blocks renin, so angiotensinogen cannot be converted to angioensin I

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19
Q

what do all angiotensin receptor blockers end in

A

“sartan”

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20
Q

what do all ace inhibitors end in

A

pril

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21
Q

Calcium channel blockers / dihydropyridines target

A

L-type calcium channels in smooth muscle. They reduce the frequency of Ca channgel opening, leading to relaxation of the muscle and in cardiac musle

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22
Q

duhydropyridines are used to treat

A

hypertension, reynauds

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23
Q

use nifedipine

A

in pregnant women w HTN

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24
Q

what is the caveot of amlodipine?

A

it takes a long time to take efect, so you have to use others until it starts working

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25
Q

non-dyhidropyridines do what

A

target calcium channels in the AV an SA node in the heart

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26
Q

which calcium channel blocker is used to treat antiarrhythmias

A

verapamil

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27
Q

side effects of non-dihydropyrimidines

A

constipation

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28
Q

side effects of calcium channels

A

flushing dizziness, peripheral edema

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29
Q

Furosimide is a

A

Loop Diuretic that is K+ wasting

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30
Q

how does furosimide work

A

causes net excretion of Na+, K+ and Mg+ and Ca+ excretion

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31
Q

side effect of furosimide

A

metabolic acidosis and more renal stones

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32
Q

Chlorothiazide and hydrochlorothiazide are

A

Thiazide diuretics, K+ wasting that block a pump in the PCT to resorb NaCl

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33
Q

thiazide diuretics are helpful in pts w

A

hypercalcemia w recurrent urinary stones

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34
Q

be careful using what drugs in gout

A

thiazide diuretics due to hypruricemia

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35
Q

what are the three K+ sparing diuretics that we care about

A

Spiroolactone, eplerenone and triamterene

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36
Q

spironolactone and eplerenone work on

A

an ATP dependent pump on interstitial side –> inability to reabsrob Na and retention of K

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37
Q

side effect of spironolactone

A

takes a few days to start working and gynecomastia

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38
Q

how does triamterene work

A

blocks Na_ influx into the cell

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39
Q

Methylopa is an

A

alpha 2 agonist that decreases sympathetic stimuli from the brain

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40
Q

how does methyldopa work

A

is replaces precursors of NE with breakdown products of methyldopa, which produces an altered neurotransmitter –> stimulation of alpha 2 receptors

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41
Q

use methydopa in patients with

A

parkinsons and pregnany patients with hypertension

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42
Q

side effects of methydopa

A

sedation, nightmares, depressio vertigo, + coombs test

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43
Q

Clonidine acts how and are used in what

A

alpha 2 agonist, leading to decreased NE,

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44
Q

effects of clonidine

A

decreases BP and HR

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45
Q

do not use clonidine in pts with

A

taking tricyclic antidepressants

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46
Q

side effect of clonidine

A

depression

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47
Q

Guanethidine ats how

A

blocks the release of NE from the SNSnby replacing it in the vesicle

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48
Q

which drugs block the action of guanethidine

A

cocaine, amphetamine and tricyclic antidepressants since they block the uptake of the drug in the first place q

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49
Q

side effects of guanethidine

A

postural hypotension, retrograde ejaculation, hypotenie crisis

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50
Q

how does resperine work

A

it blocks vesicle membrane associated transport (VMAT) that takes up bioenic amines, IRREVERSIBLY. so you get less sympathetic action through a1 receptors

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51
Q

Phentolamine is a

A

non-selectie alpha blocker, REVERSIBLE

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52
Q

give phentolamine to pateints with

A

pheochromocytoma

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53
Q

side effect of resperine

A

reflex tachyardia

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54
Q

phenoxybenzamine is a

A

aLPHA blocker, IRREVERSIBLE

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55
Q

selective alpha 1 antagonists end in

A

OSIN, example tamsulosin

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56
Q

selective apha 1 antagonists cause

A

vasodilation

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57
Q

tamsulosin is used for

A

BPH

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58
Q

which b blocker is used first line for HTN in pregnancy

A

labetolol

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59
Q

how does labetalol work

A

alpha and beta: but more b blockade than a blockade, so vasodillator effects due to a1 blocking while also blocking b1/b2

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60
Q

what is cervedilol

A

nonselective peripheral alpha and beta blocking agent. PERIPHERAL. leads to vasodilation

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61
Q

wht do we use cervedilol in

A

CHF

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62
Q

Hydralzine

A

dillates the arteries only

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63
Q

use hydralazine in pts w

A

HTN or HF

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64
Q

have to use hydralazine in combination w

A

nitrates

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65
Q

minoxodil is a

A

arterial vasodillator

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66
Q

how does minoxodil work

A

it opens K+ channels leading to hyperpolarization of the smooth muscle and less depolarization

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67
Q

side effects of minoxodil

A

hair growth

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68
Q

what drugs would you give alone w minoxodil

A

loop diuretics

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69
Q

notroprusside acts on what

A

acts on veins and arteries, but mainly arteries

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70
Q

how does nitroprusside work

A

NO –> guanylte cyclase –> cGMP –> kinases and relaxation of ARTERIAL smooth muscle

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71
Q

side effects of nitroprusside

A

cyanide toxicity which leads to bradycardia, acidosis, convulsions and confusion arrhythmias
hiocynate toxicity –> nausea and vomiting

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72
Q

diazoxide is

A

a vasodillator of arteries and veins

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73
Q

diazoxide is used when and how

A

IV in the ICU during a hypertensive crisis

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74
Q

what is the vasodillator that is best used in African American

A

hydralazine

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75
Q

what vasodillator so we use to treat insulin secreting tumors in the pancreas

A

diazoxide

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76
Q

Fenoldopam does what

A

dillates arteries and veins by acting as a D1 dopamine receptor agonist

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77
Q

avoid fendolopam in

A

patients with glaucoma

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78
Q

B1 receptors

A

increase HR, contractility and conduction speed

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79
Q

B2 receptors induce

A

fight or flight!

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80
Q

A1 receptors lead to

A

vasoconstiction

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81
Q

A2 receptors

A

tone town the SNS tone in the CNS

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82
Q

treat general population >60 when

A

SBP> 150 or DBP >90

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83
Q

in population <60 initiate treatment when

A

SBP>140 or DBP >90

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84
Q

in pts w diabetes initiate treatment when

A

SBP> 140 or DBP>90

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85
Q

avoid non-dihydropyrimidines in

A

heart failure, sick sinus syndrome or heart block

86
Q

regression of fibrosis in the liver, heart and lung have been found due to what drug

A

ARBs

87
Q

three major indications for the use of BB

A

cardiac arrhythmias, protecting from a 2nd MI, control of HTN

88
Q

what 2 beta blockers also have vasodillatory effects

A

carvedilol and labetalol

89
Q

Clonidine

A

centrally acting a2 adrenergic agonists –> decrease in SNs tone and decrease in peripheral vascular resistance

90
Q

drugs to use in treating HTN in pregnancy

A

hydralazine, methyldopa, labetalol

91
Q

avoid aspirin use in patients with

A

severe hepatic failure because it is metabolized in the iver by CYP2C9 (also metabolizes warfarin)

92
Q

clopidogrel

A

is a P2Y12 inhibitor, so block GPiib/IIIa for the rest of the platelet lifespan

93
Q

clopidogrel is metabolized by

A

CYP2C19

94
Q

eptafibitide is a

A

GP IIb/IIIa inhibitor with immediate activity

95
Q

abciximab is a

A

GP IIb/IIIa inhibitor

96
Q

wht patients are given GPiib/iiia inhibitors

A

high risk patients

97
Q

Bivalirusin works by

A

direct thrombin inhibitor, it binds to thrombin and preents cleavage of fibrinogen –> fibrin

98
Q

Fondaparinux

A

ATIII mediated inhibition of factor Xa

99
Q

what does tPa do?

A

it activates plaminogen into plasmin which cleaves fibrin

100
Q

door - needle time for thrombolytics

A

30

101
Q

door- balloon time for PCI

A

90 mins

102
Q

major contraindiciations for beta blockers

A

heart failure, heart block, asthma, hypotension, significnt bradychardia

103
Q

way to remeber types of antiarrhythmics

A

Some Block Potassium Channels

Na blocker, B Blockers, K+ blocker, Ca L-type blocker

104
Q

in general, what do type I antiarrhythmcs do?

A

they slow the upstroke of the AP by blocking the fast Na+ channels that allow for depolarization

105
Q

what do class I antiarrhythmics bind to

A

open or inactivated Na+ channels

106
Q

explain use dependence in the context of type I antiarrhythmic drugs

A

type 1 = Na+ channel blockers, which can bind in the open or inactivated state. this includes phase 0, 2 and 3. As the HR increases, the heart spends more time in phase 0,2 and 3 and less in the closed state. So tissues undergoing constant depolariztions are more susceptible to blockage

107
Q

which type of drugs exhibit use dependence?

A

type I antiarrhythmics

108
Q

what will you see on an ECG as a result of a type I antiarrhythmic

A

slow down the depolarization and decrease conduction velocity, leading to widened QRScomplex

109
Q

Class Ia drugs

A

Quinidine, Procainimide and disopyramide

110
Q

sodium channel binding strentgh of clss Ia srugs in order

A

1c>1a>1b

111
Q

class Ia antiarrhythmics result in

A

medium binding, intermediate use dependence and moderate slowing of AP

112
Q

Quinidine is used to treat

A

supraventricular and ventricular arrhythmia

113
Q

what other channel, in addition to Na+ channels do type Ia antiarrhythmics block?

A

K+channels

114
Q

what is the ultimate effect of quinidine

A

prolonged QT interval and wide QRS

115
Q

side effects of quinidine

A

tinitus, thrombocytopenia, GI side effects

116
Q

ultime effect of procainamide on EKG

A

prolongs to AP and QT interval

117
Q

Procainamide is used to treat

A

Afib in WPW syndrome

118
Q

side effects of procainamide

A

drug induced lupus

119
Q

Disopyramide can excacerbate

A

heart failure

120
Q

general risk of type I antiarrhythmics

A

toursades de pointe syndrome due to prolonging QT interval from the K+ current inhibition

121
Q

how do you reveal brugada syndrome

A

by giving procainimide in the presence of brugada syndrome can lead to ST elevations in V1, V2, V3

122
Q

wha tis brugada syndrome

A

K+ channel deficiency that makes you susceptible to long QT syndrome and sudden death

123
Q

class Ib antiarrhythmics

A

Lidocaine, phenytoin and Mexiiletine

124
Q

class Ib antiarrhythmics have a _____ affinity for Na+ channels

A

very low

125
Q

what do class Ib do to an EKG

A

they shorten the phase 3 repolarization by blocking Na+ curent during the action potential and decrease QT interval

126
Q

type Ib most useful in treating

A

ischemia induced ventricular arrhythmias

127
Q

the side effects of 1b antiarrhythmics are

A

neurological

128
Q

type Ic antiarrhythmics are

A

flecainimide and propafenone

129
Q

class Ic bind _____ to na+

A

strongly and exhibit the strongest use dependence

130
Q

class Ic effect on EKG

A

have the largest QRS duration, in a rate dependent manner

131
Q

use Ic to treat

A

atrial fibrillation

132
Q

do not give 1c to patients with

A

Heart failure or coronary artery disease, or ANY history of any heart disease since they can cause a delay in production speed, leading to arrhythmias in patients with ischemia

133
Q

what are the class III antiarrhythmics

A

defetilide, ibutilide , sotolol, amniodarone

134
Q

class III antiarrhythmics treat

A

supraventricular and ventricular arrhythmis

A fib

135
Q

which b blocker do you use for long QT syndrome and sudden death syndromes

A

Nadolol

136
Q

class III toxicities (amniodarone)

A

neurological toxicity, gray corneal sunglasss, hypothyroidism or hyperthyroidism, pulmonary fibrosis (most important), heart block, heart failure with rapid IV admin, hepatitis, grey-blue skin discoloration / photodermatitis, toursades

137
Q

which drug can cause either hypo or hyper thyroidism

A

amniodarone

138
Q

amniodarone can decrease the metablism of

A

warfarin through P450 interactions

139
Q

prolongation of the QT interval is associated with and caused by what drugs

A

toursades, polymophc ventricular tachycardia, due to Class III drugs ibutilide and deftilide, and sotolol and Class1a

140
Q

diltiazem and verapamil are used to treat

A

supraventricular arrhythmias since they work on the AV and SA node Ca channels

141
Q

does digoxin do rate or rhythm control?

A

rate control since it delays conduction through the AV node

142
Q

use magneium to treat

A

Toursades rhythm

143
Q

hyperkalemia EKG changes

A

tall peaked T waves with a shortened QT interval

144
Q

hypokalemia EKG changes

A

decrease in the amplitude of P waves, and a U wave at the end of the t wave, for two bumps after the QRS

145
Q

Adenosine acts how

A

it activates inhibitory A1 receptors on the myocardium and at the SA and AV nodes. causes an outwad K+ current leading to hyperpolarization. mostly @the AV node, to increase AV nodal refractory period

146
Q

adenosine causes

A

transient heart block

147
Q

adenosine used to treat

A

supraventricular arrhythmias

148
Q

epinephrine main effects

A

a1 agonist, leading to vasoconstriction
B1 agonist, leading to increased HR
increased HR + vasoconstriction

149
Q

Ne main effects

A

a1 agonist: vasoconstriction (less potent than Epi)

b1 agonist: tachycardia

150
Q

phenylephrine effects

A

a1 agonist only –> vasoconstriction

151
Q

what vasopressor works well in acidotic pateints

A

vasopressin

152
Q

if i only want to increase SVR and not increase Hr, what drug do i give?

A

phenylephrine

153
Q

dopamine does what

A

increases CO, contractility through a1, and peripheral vasodilltion through b1. also increases HR

154
Q

what does dobutamine do

A

mostly B1 effects –> increases HR,

vasodillation through B2

155
Q

milrinone does what

A

is a PDEIII inhibitor that is inotropic thorough a1 and vasodilitory. drops the BP alot. small impact on HR

156
Q

Nitroglycerin does what

A

it is a venous dillator, not really much arterial dillation

157
Q

Nitroprusside is a _____ dillator

A

arterial dillator

158
Q

when do you find fibrinous necrosis

A

in malignant HTN, where the HTN increases rapidly and uncontrolled

159
Q

Metoprolol is a

A

beta 1 antagonist

160
Q

Metoprolol is used to treat

A

bradycardia, arrhythmias and heart block

161
Q

tizanidine works as an ____ and is used to treat_____

A

alpha 2 agonist used to treat HTN

162
Q

Modafinil acts how

A

it displaces catecholamines to increase catecholamines in the synapse

163
Q

modafinil used to treat

A

narcolepsy

164
Q

epinephrine acts as a

A

at low doses acts on beta –> incr HR, contracility

at high doses acts on alpha —> vasconstriction and MAP

165
Q

isoproterenol is a

A

Beta 1 and 2 agonist that increases HR, and decreases diastolic pressure

166
Q

dobutamine is used to treat

A

cardiogenic shock and heart failure

167
Q

isoprenterol works as a

A

beta 1 and 2 agonist

168
Q

NE is a ______ agonist

A

alpha 1 and 2, beta 1 agonist

169
Q

phenylephrine is a

A

alpha 1 agonist

170
Q

side effect of phenylephrine

A

reflex bradychardia

171
Q

side effect of NE

A

reflex tachycardia

172
Q

oxybutynin acts as an ____ leading to treatent for _____

A

M3 antagonist, –> bladder control

173
Q

tiotropium is an

A

M3 agonist

174
Q

effects of tiotropium

A

M3 antagonist that leads to bronchodilation and reduction of bronchia seretions

175
Q

scopalamine is a

A

M1 agonist

176
Q

scopalamine used to treat

A

sea sickness

177
Q

Atropine is

A

muscarining 1, 2 and 3 antagonist leading to iincreased HR, increased sweating, bronchodilation

178
Q

side effects of atropine

A

mad as a hatter, dry as a cracker, how as a haire, blint as a bat

179
Q

rivastigmine acts as a

A

indirect cholinomimetiv where it binds to Achase –> Ach breakdown and increase of Ach at the junction

180
Q

what b blockers can be used in hypertensive emergencies

A

esmolol and meoprolol can be adminisered IV

181
Q

side effect of hydralazine

A

reflex tachycardia and exacerbation of angina

lupus

182
Q

fenoldipams most important role is to

A

dilate renal arteries

183
Q

suffix of all of the ACHase inhibitor drugs

A

STIGMINE

184
Q

most important use of acetylcholinesterase inhibitors is for the treatment of

A

myasthenia gravis

185
Q

ACHase inhibitors to treat MG

A

edrofonium, pyridostigmine, and neostigmine

186
Q

use what drug to diagnose if its a cholinergic crisis or MG

A

edrophonium

187
Q

depolarizing neurouscular blockade caused by

A

succinylcholine

188
Q

neostigmine is used to treat

A

postoperative bladder distention

189
Q

physostigmine is used to

A

treat atropine overdose - atropine is a muscarinic antagonist, so my using physostigmine to block ACHase which increases ACH, this blockade can be overcome

190
Q

if you see THIO in a drug think

A

that it is an insecticide and also a cholinesterase inhibitor

191
Q

rivastigmine, galanthastigmine and doneprezil are all

A

ACHase inhibitors that can pentrate the CNS to treat alzheimers

192
Q

is aspirin reversible or irreversible

A

irreversible

193
Q

mechanism of aspirin

A

it irreversible blocks cox1 and cox2 so you get decreased prostaglandins and thromboxane

194
Q

what does the P2Y12 receptor do

A

it is involved int he ADP dependent activation of GPIIb/IIIa

195
Q

major side effect of thienopyradines

A

bleeding

196
Q

metabolism of clopidogrel

A

it is a prodrug, the requires transofrmation by CYP2C19 - delayed onst

197
Q

the newer classes of thienopyridines are assocaited wtih

A

more intense platelet inhibition and associated higher risks of bleeding

198
Q

onset of prasugrel?

A

rapid and higher level of platelet inhibition

199
Q

what special about ticragrelor? and what is it

A

it is a P2Y12 inhibitor, that is reversivle

200
Q

when is ticragrelor better to use than clopidogrel

A

in acute coronary syndrome

201
Q

when do you use a GP11a/IIIb inhibitor?

A

when you already have ASA and a P@Y12 on board and still not responding and on way to cath kab

202
Q

what is eptafibitide

A

it is a gpIIb/IIIa inhibitor

203
Q

what is abcixumab

A

a IIb/IIIa inhibitor

204
Q

onset of action of eptifibitide

A

immediate

205
Q

contraindications to eptafibitde administration

A

renal disease

206
Q

take home point: what should a high risk patient w a UA/STEMI be treated with

A

ASA, clopidogrel and a IIb/IIIa inhibitor like abcixumab or eptafibitide

207
Q

a direct thrombin inhibitor is

A

bivalirudin,

208
Q

want to give pateints who have had an MI ACE inhibitors in what time period

A

NOT FIRST 24 HRS afterna MI

209
Q

metolazone is a

A

thiazide-like diuretic

210
Q

lupus is induced by

A

hydralazine, procainimie and methyldopa

Cardiac Pharmacology (3 decks)

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