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PHARM > heart meds > Flashcards

heart meds Flashcards

1
Q

Nitroglycerin MOA

A

Forms free nitric oxide (NO) which activate guanylate cyclase (GC) to increase cGMP resulting in smooth muscle relaxation. Aldehyde dehydrogenase-2 (ALDH2) is the enzyme that releases the NO from organic nitrates. This enzyme can get depleted resulting in “nitrate tolerance” requiring nitrate holiday

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2
Q

NG ADR

A

Headache, syncope, hypotension, reflex tachycardia,
methemoglobinemia (increased affinity of hemoglobin for ferric iron versus ferrous iron)

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3
Q

NG dental implications

A

Xerostomia- normal salivary flow resumes upon discontinuation
Monitor for orthostatic hypotension

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4
Q

Isosorbide mononitrate
(ISMN) (Imdur) MOA

A

Forms free nitric oxide (NO) which activate guanylate cyclase (GC) to increase cGMP resulting in smooth muscle relaxation. Aldehyde dehydrogenase-2 (ALDH2) is the enzyme that releases the NO from organic nitrates. This enzyme can get depleted resulting in “nitrate tolerance” requiring a nitrate holiday.
long acting oral formulation

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5
Q

Isosorbide mononitrate ADRs

A

Headache, syncope, hypotension

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6
Q

Isosorbide mononitrate dental implications

A

none

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7
Q

Isosorbide dinitrate
(ISDN/Isodril) MOA

A

Forms free nitric oxide (NO) which activate guanylate cyclase (GC) to increase cGMP resulting in smooth muscle relaxation. Aldehyde dehydrogenase-2 (ALDH2) is the enzyme that releases the NO from organic nitrates. This enzyme can get depleted resulting in “nitrate tolerance” requiring a nitrate holiday. Intermediate-acting oral formulation

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8
Q

Isosorbide dinitrate ADRs

A

Headache, syncope,
hypotension

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9
Q

Isosorbide dinitrate dental implications

A

Xerostomia- normal salivary flow resumes
upon discontinuation

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10
Q

Sodium Nitroprusside
(Nitropress)
Only available in what form

A

IV form

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11
Q

Sodium Nitroprusside
(Nitropress) MOA

A

Direct donates a NO molecule, which activate guanylate cyclase (GC) to increase cGMP resulting in smooth muscle relaxation. Does not require ALDH2.

Does not exhibit tolerance

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12
Q

Sodium Nitroprusside
(Nitropress) ADRs

A

Severe hypotension, flushing, reflex tachycardia, methemoglobinemia, thiocyanate toxicity.

Thiocyanate can form in the parenteral fluid due to
exposure to light, product MUST BE PROTECTED form
light. This is more common with higher doses and longer durations of administration

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13
Q

Sodium Nitroprusside
(Nitropress) dental implications?

A

none

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14
Q

Ranolazine (Ranexa) MOA

A

Inhibition of late inward sodium current (Ina). Does not affect heart rate or blood pressure

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15
Q

Ranolazine (Ranexa) ADRs

A

QT prolongation, torsade de pointes, bradycardia,
hypotension, xerostomia
Usually does not affect hemodynamic parameters

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16
Q

Ranolazine (Ranexa) dental implications

A

Xerostomia- normal salivary flow resumes
upon discontinuation

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17
Q

Ivabradine (Corlanor) approval in US?

A

Not approved for angina in the United
States- only approved for HF

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18
Q

Ivabradine (Corlanor) MOA

A

Inhibited the If (funny) channel in the SA node resulting in a reduction in heart rate, without a change in blood pressure

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19
Q

Ivabradine (Corlanor) ADRs

A

Bradycardia, atrial fibrillation, phosphenes

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20
Q

Ivabradine (Corlanor) dental implications

A

none

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21
Q

b1 selective blockers

A

acebutolol
esmolol
atenolol
betaxolol
metopolol
nebivolol

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22
Q

Acebutolol (Sectral) MOA
exhibits what activity?

A

Competitively blocks β1 adrenergic receptors with little
to no effect on β2 adrenergic receptors.
Exhibits intrinsic sympathomimetic activity

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23
Q

Acebutolol (Sectral) ADRs

A

Bradycardia, hypotension, dizziness

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24
Q

B1 specific blockers dental implications

A

Cardio selective beta-blockers do not interact with local anesthetics.

NSAIDs can reduce antihypertensive effects of beta-blockers. Short-term use of NSAIDs (i.e. 3 days) is safe

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25
Q

Atenolol
(Tenormin) MOA

A

Competitively blocks β1
adrenergic receptors with little
to no effect on β2 adrenergic
receptors

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26
Q

atenolol ADRs

A

Bradycardia,
hypotension,
dizziness,
AV node block,
fatigue,
Raynaud’s phenomenon,
impotence

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27
Q

betaxolol MOA

A

Competitively blocks β1
adrenergic receptors with little
to no effect on β2 adrenergic
receptors

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28
Q

betaxolol ADRs

A

Bradycardia, hypotension, dizziness, AV node block, fatigue, impotence

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29
Q

Esmolol (Brevibloc)
Only available as?

A

Only available IV:
Short acting (t1/2= 5 mins

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30
Q

esmolol MOA

A

Competitively blocks β1
adrenergic receptors with little
to no effect on β2 adrenergic
receptors

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31
Q

esmolol ADRs

A

Hypotension, bradycardia,
infusion site reaction

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32
Q

metoprolol forms

A

(Lopressor)- immediate release
(Toprol XL)- extended release

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33
Q

metoprolol MOA

A

Competitively blocks β1
adrenergic receptors with little
to no effect on β2 adrenergic
receptors at doses < 100mg
daily

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34
Q

metoprolol ADRs

A

Bradycardia,
hypotension,
dizziness,
AV node block,
fatigue,
impotence

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35
Q

Nebivolol (Bystolic) MOA
also produces what effect?

A

Competitively blocks β1 adrenergic receptors with little to no effect on β2 adrenergic receptors.
**Also produces nitric oxide dependent vasodilation **

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36
Q

nebivolol ADRs

A

Bradycardia, hypotension,
dizziness, fatigue,
impotence

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37
Q

non selective B blockers

A

carteolol
penbutolol
pindol
propranolol
timolol

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38
Q

Carteolol
(Ocupress) only formulation

A

opthalmalic

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39
Q

carteolol MOA

A

Blocks both β1 and β2 adrenergic
receptors. Reduces intraocular
pressure

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40
Q

carteolol ADRs

A

Conjunctival hyperemia
(no systemic ADRs noted)

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41
Q

carteolol dental implications

A

none

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42
Q

Penbutolol
(Levatol) MOA

A

Blocks both β1 and β2 adrenergic receptors.
**Exhibits mild intrinsic sympathomimetic activity

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43
Q

penbutolol ADRs

A

Bradycardia,
hypotension,
fatigue,
dizziness,
impotence

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44
Q

penbutolol dental implcations

A

Xerostomia- normal salivary flow resumes upon discontinuation

Non-selective beta blockers may enhance the pressor response to epinephrine resulting in hypertension and bradycardia.

NSAIDs can reduce antihypertensive effects of beta-blockers. Short-term use of NSAIDs (i.e. 3 days) is safe.

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45
Q

pindolol MOA

A

Blocks both β1 and β2 adrenergic receptors.
**Exhibits mild intrinsic sympathomimetic activity **

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46
Q

pindolol ADRs

A

Bradycardia,
hypotension,
fatigue,
dizziness,
impotence

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47
Q

pindolol dental implications

A

Non-selective beta blockers may enhance the pressor response to epinephrine resulting in hypertension and bradycardia.

NSAIDs can reduce antihypertensive effects of beta blockers. Short-term use of NSAIDs (i.e. 3 days) is safe

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48
Q

Propranolol (Inderal LA)/ (Hemangeol) MOA
can work where else? how?

A

Blocks both β1 and β2 adrenergic receptor
Reduce portal pressure by producing splanchnic vasoconstriction

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49
Q

propranolol ADRs

A

Bradycardia,
hypotension,
fatigue,
dizziness,
impotence

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50
Q

propranolol dental implications

A

Non-selective beta blockers may enhance the pressor response to epinephrine resulting in hypertension and bradycardia.

NSAIDs can reduce the antihypertensive effects of beta-blockers. Short-term use of NSAIDs (i.e. 3 days)
is safe

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51
Q

timolol formulations

A

(Timoptic)- ophthalmic formulation
(Betimol)

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52
Q

timolol MOA

A

Blocks both β1 and β2 adrenergic
receptors.
Reduces intraocular pressure

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53
Q

timolol ADRs

A

Ophthalmic- burning eyes
Bradycardia,
hypotension,
fatigue,
dizziness,
impotence

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54
Q

timolol dental implications

A

Xerostomia- normal salivary flow resumes upon discontinuation

Non-selective beta blockers may enhance the pressor response to epinephrine resulting in hypertension and bradycardia

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55
Q

carvediolol formulations

A

(Coreg)- immediate release
(Coreg CR)- extended release

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56
Q

carvediolol MOA

A

Blocks both β1 and β2 adrenergic receptors.
Also blocks α1 adrenergic receptors.

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57
Q

Non-selective beta blockade with alpha blocking (β1 = β2 ≥ α1 > α2)

A

carvediolol and labetolol

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58
Q

carvediolol ADRs

A

Bradycardia,
hypotension,
fatigue,
dizziness,
impotence

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59
Q

carvediolol dental implications

A

Orthostatic hypotension, use caution when changing position.

NSAIDs can reduce antihypertensive effects of beta-blockers. Short-term use of NSAIDs (i.e. 3 days) is safe

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60
Q

Labetalol
(Trandate) MOA

A

Blocks both β1 and β2 adrenergic receptors.
Also blocks α1 adrenergic receptors.
The ratio of alpha to beta blockade is 1:3 following
oral administration

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61
Q

labetalol ADRs

A

Bradycardia,
hypotension,
fatigue,
dizziness,
impotence

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62
Q

labetalol dental implications

A

Taste disorder

NSAIDs can reduce antihypertensive effects of beta-blockers. Short-term use of NSAIDs (i.e. 3 days) is safe

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63
Q

Dihydropyridine Rx’s

A

all end in -pine

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64
Q

Amlodipine (Norvasc) MOA

A

Inhibits calcium ions influx through L-type or “slow”
calcium channels”
Selective for vascular smooth muscle
same as all -pine Rx

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65
Q

amlodipine ADRs

A

Reflex tachycardia, flushing, hypotension,
peripheral edema, gingival hyperplasia

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66
Q

Dihydropyridine Rx’s dental implications

A

Monitor of gingival
hyperplasia, usually
resolves upon
discontinuation

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67
Q

Clevidipine
(Cleviprex)
Only available as?

A

IV form

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68
Q

clevidipine MOA

A

Inhibits calcium ions influx
through L-type or “slow”
calcium channels”
Selective for vascular smooth
muscle

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69
Q

clevidipine ADrs

A

Reflex tachycardia,
flushing,
hypotension,
peripheral edema
Gingival hyperplasia not reported probably due to shorter duration of administration

70
Q

felidipine MOA

A

Inhibits calcium ions influx
through L-type or “slow”
calcium channels”
Selective for vascular smooth
muscle

71
Q

felodipine ADRs

A

Reflex tachycardia,
flushing,
hypotension,
peripheral edema,
gingival hyperplasia

72
Q

Isradipine
(DynaCirc CR) MOA

A

Inhibits calcium ions influx
through L-type or “slow”
calcium channels”
Selective for vascular smooth
muscle

73
Q

isradipine ADRs

A

Reflex tachycardia,
flushing,
hypotension,
peripheral edema
Information is sparse as to whether isradipine causes
gingival hyperplasia

74
Q

Nicardipine
(Cardene)
Available in?

A

PO and IV
formulations

75
Q

nicardipine MOA

A

Inhibits calcium ions influx
through L-type or “slow”
calcium channels”
Selective for vascular smooth
muscle

76
Q

nicardipine ADRs

A

Reflex tachycardia,
flushing,
hypotension,
peripheral edema,
gingival hyperplasia

77
Q

nicardipine dental implications

A

Xerostomia (normal salivary flow resumes upon discontinuation)

Monitor of gingival hyperplasia, usually resolves upon discontinuation

78
Q

Nifedipine MOA

A

Inhibits calcium ions influx
through L-type or “slow”
calcium channels”
Selective for vascular smooth
muscle

79
Q

nifedipine ADRs

A

Reflex tachycardia,
flushing,
hypotension,
peripheral edema,
gingival hyperplasi

80
Q

nifedipine ADR

A

Gingival hyperplasia (10%
incidence with doses of
30-100mg/day). Effects
present after 1-9 months
of treatment. Usually
resolves upon
discontinuation

81
Q

nimodipine MOA

A

Inhibits calcium ions influx
through L-type or “slow”
calcium channels”
Selective for vascular smooth
muscle

82
Q

nimodipine ADR

A

Reflex tachycardia,
flushing,
hypotension,
peripheral edema
No reports of gingival hyperplasia with nimodipine

83
Q

nimodipine dental implications

A

Possibly gingival
hyperplasia- although no
known cases

84
Q

nisoldipine MOA

A

nhibits calcium ions influx
through L-type or “slow”
calcium channels”
Selective for vascular smooth
muscle

85
Q

nisoldipine ADRs

A

Reflex tachycardia,
flushing,
hypotension,
peripheral edema
Information is sparse as to whether nisoldipine causes
gingival hyperplasi

86
Q

nisoldipine dental

A

Xerostomia (normal salivary flow resumes upon discontinuation)
Possibly gingival hyperplasia- information is sparse

87
Q

Non-Dihydropyridine Rx

A

selective for myocardium
Diltiazem and vermapril

88
Q

Diltiazem MOA

A

inhibits calcium ions influx through L-type or “slow” calcium channels”
Selective for myocardial calcium channels
Slows impulse conduction through the AV node

89
Q

diltiazem ADRs

A

Constipation,
dizziness,
lightheadedness,
hypotension,
bradycardia,
gingival hyperplasia

90
Q

diltiazem dental

A

gingival hyperplasia
usually resolves
upon discontinuation

91
Q

Verapamil MOA
where are impulses slowed in the cardiac conduction?

A

inhibits calcium ions influx through L-type or “slow”
calcium channels”
Selective for myocardial calcium channels
Slows impulse conduction through the AV node

92
Q

verapamil ADRs

A

Constipation,
dizziness,
lightheadedness,
hypotension,
bradycardia,
gingival hyperplasia

93
Q

verapamil dental

A

gingival hyper

94
Q

class Ia anti-arrhytmatics

A

moderate sodium channel blockers

95
Q

Quinidine MOA

A

moderate na channel block

96
Q

quinidine ADRs

A

abdominal pain and cramps, nausea, vomiting, diarrhea

Cinchonsim- “overdose” (symptoms include: ringing in ears, blurred vision, hearing loss)

Cardiac- QT prolongation

97
Q

quinidine dental

A

May consider semisupine
chair position to minimize
GI distress if occurs

98
Q

procainamide MOA

A

moderate Na blocker

99
Q

procainamide ADRs

A

Lupus-like syndrome
Skin rash
QT prolongation

100
Q

procainamide dental

A

dysguesia

101
Q

dysopyramide MOA

A

moderate na blocker

102
Q

dysopyramide ADRs

A

Anticholinergic-Dry mouth, constipation, urinary hesitancy
Cardiac- QT prolongation

103
Q

dysopryamide dental

A

xerostomia- done with discontinuation

104
Q

class Ib agents

A

weak na blockers
lidocaine
tocanide
mexilitine
phenytoin

105
Q

lidocaine mech

A

weak na block

106
Q

lido ADRS

A

Neuro- Agitation, anxiety, hallucinations, seizures
(toxic)
Bradycardia

107
Q

lido dental

A

metalic taste

108
Q

tocainide MOA

A

weak na block

109
Q

mexilitine MOA

A

weak na block

110
Q

mexilitine ADRs

A

GI- nausea, vomiting, heartburn
Neuro- dizziness, light-headedness, tremors, convulsion (toxic

111
Q

mexitiline dental

A

Xerostomia- normal salivary flow resumes upon discontinuation

112
Q

phenytoin MOA

A

weak na blocker

113
Q

phenytoin ADRs

A

Ataxia, cardiovascular side
effects with IV
administration

114
Q

phenytoin dental

A

Gingival hyperplasia is
common during the first 6
months of treatment

115
Q

class Ic

A

strong na block
moricizine
flecainide
propafenone

116
Q

moricizine moa

A

strong na block

117
Q

flecainidea moa

A

strong na block

118
Q

flecainide ADRs

A

Dizziness and visual disturbances

119
Q

flecainide dental;

A

none

120
Q

Propafenone moa

A

strong na block

121
Q

propafenone ADRs

A

Unusual taste (3-23%)
Nausea/vomiting
Blurred vision (1-6%)
Dizziness

122
Q

propafenone dental

A

unusual taste, also xerostomia a possibility

123
Q

class III antiarrhytmatics

A

amiodarone
donfetilide
dronedarone
ibutilide
satalol

K channel block

124
Q

amiodarone moa

A

K+ channel blocker
Also blocks Na+ and Ca2+
channels, B receptors

125
Q

amiodarone adrs

A

eyes- blurred vision
Lungs- pulmonary fibrosis
Heart- hypotension (IV formulation)
Thyroid-hypo/hyperthyroidism
Liver- elevated LFTs
GI- nausea and vomiting
Skin-photosensitivity/blue skin

126
Q

amiodarone denta;l

A

abnormal salivation and taste

127
Q

donfetilide moa

A

k channel blocker

128
Q

donfetilide adr

A

QT prolongation/Torsades de pointes
Minimal other ADRs

129
Q

dronedarone moa

A

K+ channel blocker
Also blocks Na+ and Ca2+
channels, B receptors
Similar to Amiodarone

130
Q

dronedarone adr

A

QT prolongation/Torsades de pointes
Elevations in serum creatinine
Acute hepatic failure inpost-marketing

131
Q

ibutilide moa

A

k channel block

132
Q

ibutilide adr

A

QT prolongation/Torsades
de pointes

133
Q

salatol moa

A

K+ channel blocker
Also blocks both β1 and β2
adrenergic receptors

134
Q

salatol adr

A

QT prolongation/Torsades de pointes
Bradycardia, hypotension, fatigue, dizziness

135
Q

salatol dental

A

Related to beta blocking activity.

Non-selective beta blockers may enhance the pressor response to epinephrine resulting in hypertension and bradycardia

NSAIDs can reduce antihypertensive effects of beta-blockers. Short-term use of NSAIDs (i.e. 3 days) is safe.

136
Q

positive ionotropic meds

A

digoxin
dobutamine
milrinone
levosemnderin

137
Q

digoxin moa for HF and SV arrhythmias

A

Heart failure: inhibition of the sodium/potassium ATPase pump in myocardial cells resulting in an increase of intracellular sodium which promotes calcium influx via the sodium-calcium exchange pump
leading to increased contractility

Supraventricular arrhythmias: direct suppression of the AV node conduction to increase effective refractory period and decrease conduction velocity

138
Q

digoxin adr

A

nausea, vomiting, diarrhea, bradycardia, heart block, visual disturbances

139
Q

digoxin dental

A

increased gag reflex may make dental procedures, such as taking radiographs or impressions difficult

Avoid dental light in patient’s eye/offer dark glasses

140
Q

dobutamine moa

A

Stimulates myocardial B1-adrenergic receptor. Results in increased contractily

141
Q

dobutamine adr

A

increased heart rate and blood pressure,
arrhythmias, chest pain, localized phlebitis

142
Q

milrinone moa

A

Selective phosphodiesterase -3
inhibitor (PDE3) in cardiac and
vascular tissue, resulting in
vasodilation and increased
contractility

143
Q

milrinone adr

A

Decreased blood pressure,
arrhythmias, chest pain

144
Q

levosimendan moa

A

Sensitize troponin to Ca2+
(inotropy) and KATP channel
activation in smooth muscle
(vasodilation

145
Q

levosimendan uses

A

none, not available here

146
Q

what adrs can we see with all nitrates

A

headache, syncope, hypotension

147
Q

which nitrates can cause methemoglob

A

NG and Na nitroprusside

148
Q

which nitrate can cause thioocyante toxicity

A

Na nitroprusside

149
Q

which nitrates can cause xero

A

NG, iso dinitrate, ranolazine

150
Q

which Rx can cause phosphenes

A

ivabradine

151
Q

common adrs of all b blocks

A

hypo, dizzy, fatique

152
Q

which b block can cause raynauds

A

atenolol

153
Q

which b blockers can cause AV block

A

atenolol, betaxolol, metoprolol

154
Q

which b blockers do not cause impotence?

A

acebutolol, esmolol, carteolol

155
Q

which b blockers can cause xero

A

penbutolol, timolol

156
Q

which b blocker can cause taste disorder?

A

labetalol

157
Q

which b blocker can cause NO dependent vasodialtion

A

nebivolol

158
Q

which b blocker exhibit mild intrinsic sympathomeitic activity

A

penbutolol, pindolol

159
Q

which b blocker reduces portal pressure

A

propranolol, causes splanchnic vasoconstriction

160
Q

dihydropyradine common adrs

A

reflex tachy, flushing, hypo, edema, ging hyper (usually)

161
Q

which dihydropyradines may not have ging hyper

A

clevidipine, isradipine, nimodipine, nislodipine

162
Q

which dihydropyradines may cause xero

A

nicardipine and nislodipine

163
Q

what are the common adrs of non-dihydropyradines

A

constipation, lightheaded, dizzy, hypoten, bradycardia, ging hyper

164
Q

which Rx may increase gag

A

digoxin

165
Q

what rx should you avoid light in eyes

A

dogoxin and amiodarone

166
Q

which class 3 drugs also block other channels/receptors

A

amiodarone and dronedarone

167
Q

which class 3 drugs can cause QT prolong and TdP?

A

donfetilide, dronedarone, ibutilide, sotalol

168
Q

which Rx can cause acute hepatic failure

A

dronedarone

169
Q

which class I agents may alter taste

A

procainamide
lidocaine
propafenone

170
Q

which class I Rx’s may cause xero?

A

disopyramide, mexilitine, propafenone

PHARM (15 decks)

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