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M2 Pharmacology Jen > Adrenergic > Flashcards

Adrenergic Flashcards

1
Q

Norepinephrine: Class

A

Pharm: direct acting adrenergic agonist
Ther: vasopressor/vasoconstrictor

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2
Q

Norepi: PD

A

-stimulates peripheral alpha1 adrenoceptors –> venoconstriction, vasoconstriction, cardiac stimulation.
incr CO, incr SVR, incr MAP.
decr blood flow to skin/muscle/kidney
-stimulates B1 receptors in heart, incr HR and contractility.

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3
Q

Norepi: PK

A

F = 100%
IV only
metabolized by COMT and MAO, mainly in liver
matabolites excreted in urine
half life 1-2 min (titrate quickly by IV)
crosses placenta but not BBB

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4
Q

Norepi: tox

A 
excessive vasoconstriction in mesenteric vessels and peripheral arterioles --> ischemia, infarct, gangrene. 
reflex bradycardia (in resp to high MAP)
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5
Q

Norepi: monitor

A

BP, HR, infusion site, evidence of extravasation

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6
Q

Norepi: special issues

A

correct volume depletion before giving
careful with infusion site because of extravasation
continuous monitoring of BP in ICU
caution in peds/gers

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7
Q

Norepi v Epi: which has more activity on B receptors?

A

Epi

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8
Q

Epi: classes

A

direct acting adrenergic agonist
vasopressor, cardiac stimulant, bronchodilator
adjunct to local anesthetics, anti-anaphylaxis

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9
Q

epi: PD

A

alpha1 adrenergic receptors -> veno and vaso constriction
B1 leading to tachy and incr contractility
B2 -> bronchodilation
stabilizes mast cells!

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10
Q

Epi: PK

A 
IV = immediate
IM = variable
SC 5-15 min
inh 1-5 min
opthalmic topical
metabolized by COMT and renally excreted
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11
Q

Epi: tox

A

excessive vasoconstriction, HTN, hemorrhagic stroke, angina, arrhythmias,
risk of excessive HTN in pts taking propanolol

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12
Q

Epi: special issues

A

drug of choice in anaphylaxis

useful/added to local anesthetics because of vasoconstriction: limits blood loss, increases duration of anesthetic.

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13
Q

Epi: monitor

A

BP, HR, rhythm, infusion site, extravasation

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14
Q

Dopamine: class

A

direct acting non-selective adrenergic and dopaminergic agonist
catecholamine
inotropic agent and vasopressor

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15
Q

Dopamine: PD

A

activates Beta1 AR and Alpha1 receptors at different concentrations
Acts on D1 receptors in renal vessels (relax) and incr renal flow

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16
Q

Dopamine: PK

A

IV only
acts within minutes
half life = just minutes –> continuous infusion

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17
Q

Dopamine: tox

A

ectopy (disturbance of heart rhythm). tachycardia, angina

nausea

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18
Q

Dopamine: special issues

A

correct hypovolemia before giving

administer thru large vein and monitor patient

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19
Q

Dobutamine: class

A

adrenergic
cardiac stimulant
very sim to Dopamine

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20
Q

Dobutamine: PD

A

sim to Dopamine but with less ability to cause vasoconstriction
more specific for Beta1 receptors

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21
Q

Isoproterenol: class

A

non-selective B-AR agonist

Rx for bradycardia

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22
Q

Isoproterenol: PD

A

vasodilator, incr HR

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23
Q

Isoproterenol: tox

A

tachycardia, BP, arrhythmias

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24
Q

General receptor action at molecular level: Alpha1

A

Works through PLC/PIP2 –> IP3, incr Ca2+ intracellularly, which incr contractility

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25
Q

General receptor action at molec level: Beta1

A

GPCR, Gs so ATP –> cAMP via increased activity of Adenylyl cyclase –> incr PKA, incr Ca in cell –> incr contractilty

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26
Q

Phenylephrine: class

A

relatively pure Alpha1-AR agonist

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27
Q

Phenylephrine: PD

A

potent constrictor, nasal decongestant, mydriatic (dilates pupil) with no affect on accomodation, BP maint during surgery.

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28
Q

Phenylephrine: PK

A

not inactivated by COMT
causes release of Ca2+ from SR -> incr contractility
give intranasally or topically (eye)
half life = 3h

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29
Q

Phenylephrine: tox

A

HTN, reflex bradycardia

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30
Q

Clonidine: class

A

central alpha-2 agonist

antihypertensive, adjunct to Rx of opioid withdrawal, prophylaxis of migraine

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31
Q

Clonidine: PD

A

stimulates alpha-2 adrenoceptors in brainstem, thereby leading to down-regulation of sympathetic output

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32
Q

Clonidine: PD

A

Onset 1 h, duration 8 h, F~85%, also available as cutaneous patch

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33
Q

Clonidine: tox

A

withdraw gradually because of risk of rebound HTN; risk of bradycardia in sinus node disease; lethargy, fatigue, depression

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34
Q

Clonidine: interactions

A

additive effects with most other antihypertensives; additive sedation with other CNS drugs

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35
Q

Clonidine: special considerations

A 
Pregnancy class C; avoid in patients with renal insufficiency
If pt has first or 2nd AV block, do not give. Give an EKG to most patients to make sure no block, no LVH.
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36
Q

Clonidine: monitor

A

follow BP and HR, fatigue

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37
Q

Ibuprofen: class

A

NSAID

Analgesic, anti-pyretic (fever), anti-inflammatory, anti-gout, anti-dysmennorhea

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38
Q

Ibuprofen: PD

A

involves inhibition of prostaglandin synthetics via COX1 and COX2

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39
Q

Ibuprofen: PK

A

F =80%
some excreted unchanged in urine
extensive metabolism in liver
half life 2-4 h

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40
Q

Ibuprofen: tox

A

“allergies” to aspirin
use caution in pts with renal compromise, ulcer disease
causes fluid retention in CHF patients

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41
Q

Ibuprofen: special considerations

A

more side effects in geriatrics

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42
Q

Ibuprofen: interactions

A

with warfarin, aspirin, diuretics, anti-hypertensives

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43
Q

Albuterol: Class

A

pharmacologic class: selective β-2 AR agonist (SABA: short acting beta2 agonist)
Therapeutic class: bronchodilator for asthma/COPD

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44
Q

Albuterol: PD

A

binds to beta-2 receptors and relaxes smooth muscle of airway, causing bronchodilation

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45
Q

Albuterol: tox

A

tachycardia, tremor, tolerance

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46
Q

Albuterol: mechanism of delivery

A

nebulizer or MDI

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47
Q

Amphetamine: classes

A

indirectly-acting adrenergic agonist. sympathomimetic

CNS stimulant ==> used for appetite suppression, ADHD, and narcolepsy.

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48
Q

Amphetamine: PD

A 
release of biogenic amines from storage (noradrenaline)
Alpha1 -> vasoconstiction, inc BP
Beta2 -> bronchodilation
Beta1 -> inc HR
CNS stimulant
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49
Q

Amphetamine: PK

A

plasma half life approx 12h

excreted unchanged in urine

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50
Q

Amphetamine: tox

A

restlessness, tremor, irritability, insomnia, dependency, tolerance, inc BP, tachycardia, psychosis if excessive dose

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51
Q

Amphetamine: special issues

A

tolerance, dependance, addiction can develop (unlike ephedrine)

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52
Q

Ephedrine: class

A

Pharmacologic class: Indirect adrenergic, stimulates NE and dopamine release
Therapeutic class: decongestant, anti-hypotension
Also potent CNS stimulants used for ADHD and appetite suppression

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53
Q

Ephedrine: PD

A

↑ NE and dopamine release and direct effects on α and β

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54
Q

Ephedrine: PK

A

Prolonged duration of action

55
Q

Ephedrine: tox

A

HTN, tachyphylaxis

insomnia

56
Q

Ephedrine: special

A

ephedrine-containing herbal products have been banned in the US, Pseudoephedrine is a restricted OTC substance because it can be used to make meth

57
Q

Pseudophedrine: class

A

Pharmacologic class: Indirect adrenergic, stimulates NE and dopamine release
Therapeutic class: decongestant only (not antihypotension as is Ephedrine)
Also potent CNS stimulants used for ADHD and appetite suppression

58
Q

Pseudophedrine: PD

A

↑ NE and dopamine release and direct effects on α and β

59
Q

Pseudophedrine: PK

A

Prolonged duration of action

60
Q

Pseudophedrine: tox

A

HTN, tachyphylaxis

insomnia

61
Q

Pseudophedrine: special

A

ephedrine-containing herbal products have been banned in the US, Pseudoephedrine is a restricted OTC substance because it can be used to make meth

62
Q

Tyramine: class

A

Pharmacologic class: indirectly-acting adrenergic agonist, stimulates NE and dopamine release
Therapeutic class: None.

63
Q

Tyramine: PD

A

↑ Release of biogenic amines from storage, including dopamine in the CNS

64
Q

Tyramine: PK

A

Byproduct of tyrosine metabolism ==> metabolized by liver MAO

65
Q

Tyramine: tox

A

Can cause MAOI hypertensive crisis

66
Q

Tyramine: special issues

A

use of MAO inhibitors and severe HTN, and tachypylaxis

67
Q

Tyramine: interactions

A

caution with MAO inhibitors ==> can cause HTNsive crisis

68
Q

Cocaine: class

A

Pharmacologic class: indirect-acting agonist via blocking Uptake 1 pathway leading to inc NA effects (vasoconstriction)
Therapeutic class: CNS stimulant, musical inspiration, song title by Eric Clapton
Local anesthetic, vasoconstrictor, drug of abuse

69
Q

Cocaine: PD

A

blocks NE and dopamine reuptake via Uptake 1 pathway

Shorter lasting than amphetamine, more intense

70
Q

Cocaine: PK

A

Smoked, snorted or injected for rapid effect

71
Q

Cocaine: tox

A

Hypertension, AMI, arrhythmias, seizures. if snorted can lead to nasal septal necrosis due to vasoconstriction

72
Q

Phentolamine: class

A 
alpha blocker (reversible)
Hypertensive crisis
73
Q

Phentolamine: PD

A

blocks both Alpha1 and Alpha2.
Alpha1: block smooth muscle contraction -> vasodilation and postural hypotension
Alpha2: block leads to tachycardia and inc CO

74
Q

Phentolamine: adverse effects

A

postural hypotension, tachycardia

75
Q

Phenoxybenzamine: PD

A

blocks both Alpha1 and Alpha2.
Alpha1: block smooth muscle contraction -> vasodilation and postural hypotension
Alpha2: block leads to tachycardia and inc CO

76
Q

Phenoxybenzamine: class

A 
alpha blocker (IRreversible)
Hypertensive crisis
77
Q

Phenoxybenzamine: adverse effects

A

postural hypotension, tachycardia

78
Q

Prazosin: class

A

a1 blocker

79
Q

Prazosin: indications

A

antihypertensive, treatment of BPH, treatment of Raynaud’s syndrome, treatment for kidney stones

80
Q

Prazosin: PD

A

blocks alpha-1 receptors on arterioles and veins, thereby inhibiting NE-mediated vasoconstriction and venoconstriction

81
Q

Prazosin: PK

A

available po or transdermal; variable oral bioavailability (~60%), onset 2 h, duration 12-24 h

82
Q

Prazosin: tox

A

excessive hypotension with passing out, especially orthostatic, especially in patients on diuretics

83
Q

Prazosin: excr

A

extensively metabolized in liver

84
Q

Prazosin: interactions

A

additive effects with most other antihypertensives, especially diuretics

85
Q

Prazosin: special

A

start gradually, and at bedtime, to avoid first-time passing out; male patients with BPH?

86
Q

Prazosin: monitor

A

BP, weight, edema

87
Q

Propanolol: class

A

b blocker (1 and 2)

88
Q

Propanolol: indication

A

Antihypertensive, antianginal, antiarrhythmic, MI

89
Q

Propanolol: PD

A

binds directly to beta-receptors, with a preference for beta-1 over beta-2, leading to lower blood pressure via several potential mechanisms (less cardiac output, less activation of the RAA system); recent evidence suggests less effective in preventing strokes than other drugs

90
Q

Prolanolol: PK

A

available po or iv; variable oral F; onset 1-2 hours h, duration 12-24 h; can be given once per day; renally excreted (longer half-life)

91
Q

Propanolol: tox

A

excessive hypotension; bradycardia; heart block can worsen severe CHF (but indicated for mild to moderate CHF); worsen bronchospasm in severe asthmatics (bc not perfectly B1 selective, will block 10% of B2s)

92
Q

Propanolol: interactions

A

additive effects with most other antihypertensives, additive AV block with CEB’s

93
Q

Propanolol: special

A

may be especially useful in HTN patients with exertional angina, MI, atrial fibrillation; watch out for abrupt withdrawal; may no longer be “first line” drug unless other indications exist (recent data)

94
Q

Propanolol: monitor

A

BP, HR, exercise tolerance

95
Q

Timolol: class

A

same class as propanolol, non-specific b blocker

96
Q

Timolol: indication

A

Open angle glaucoma, antihypertensive, MI prevention

97
Q

Pindolol: class

A

same as propanolol. nonspecific b blocker & partial agonist

98
Q

Pindolol: indication

A

Antihypertensive, antianginal, antiarrhythmic

99
Q

Pindolol: PD

A

some degree of beta-1 activation is maintained while the cardiac response to increased sympathetic activity is blunted

100
Q

Sotalol: class

A

K channel blocker & b blocker

101
Q

Sotalol: indication

A

Antiarrhythmic Class III, antihypertensive

102
Q

Sotalol: PD

A

prolongs cardiac action potential; blocks K+ channels

103
Q

Metoprolol: class

A

b1 blocker (specific)

104
Q

Metoprolol: indication

A

Antihypertensive, antianginal, antiarrhythmic, CHF

105
Q

Metoprolol: PD

A

binds directly to beta-receptors, with a preference for beta-1 over beta-2, leading to lower blood pressure via several potential mechanisms (less cardiac output, less activation of the RAA system); recent evidence suggests less effective in preventing strokes than other drugs

106
Q

Metoprolol: PK

A

available po or iv; variable oral F; onset 1-2 hours h, duration 12-24 h; can be given once per day; renally excreted (longer half-life)

107
Q

Metoprolol: tox

A

excessive hypotension; bradycardia; heart block can worsen severe CHF (but indicated for mild to moderate CHF); worsen bronchospasm in severe asthmatics (bc not perfectly B1 selective, will block 10% of B2s)

108
Q

Metoprolol: interactions

A

additive effects with most other antihypertensives, additive AV block with CEB’s

109
Q

Metoprolol: special

A

may be especially useful in HTN patients with exertional angina, MI, atrial fibrillation; watch out for abrupt withdrawal; may no longer be “first line” drug unless other indications exist (recent data)

110
Q

Metoprolol: monitor

A

BP, HR, exercise tolerance

111
Q

Atenolol: class

A

b1 blocker

112
Q

Atenolol: indication

A

Antihypertensive, antianginal, antiarrhythmic, anti-MI

113
Q

Atenolol: PD

A

binds directly to beta-receptors, with a preference for beta-1 over beta-2, leading to lower blood pressure via several potential mechanisms (less cardiac output, less activation of the RAA system); recent evidence suggests less effective in preventing strokes than other drugs

114
Q

Atenolol: PK

A

available po or iv; variable oral F; onset 1-2 hours h, duration 12-24 h; can be given once per day; renally excreted (longer half-life)

115
Q

Atenolol: tox

A

excessive hypotension; bradycardia; heart block can worsen severe CHF (but indicated for mild to moderate CHF); worsen bronchospasm in severe asthmatics (bc not perfectly B1 selective, will block 10% of B2s)

116
Q

Atenolol: interactions

A

additive effects with most other antihypertensives, additive AV block with CEB’s

117
Q

Atenolol: special

A

may be especially useful in HTN patients with exertional angina, MI, atrial fibrillation; watch out for abrupt withdrawal; may no longer be “first line” drug unless other indications exist (recent data)

118
Q

Atenolol: monitor

A

BP, HR, exercise tolerance

119
Q

Labetalol: class

A

a1 and b blocker

120
Q

Labetaolol: indication

A

antihypertensive, treatment of CHF, pheochromocytoma

121
Q

Labetalol: PD

A

reduces BP by blocking access of NE to beta-receptors and alpha-1 receptors, thereby lowering BP by several different mechanisms; patients differ in degree of beta-blockade vs alpha-blockade

122
Q

Labetalol: PK

A

excellent absorption but high first-pass effect, leading to F~25%; onset 1-2 hours after po, 2-5 minutes when given iv; extensively metabolized in liver by IID6

123
Q

Labetalol: tox

A

avoid in patient with bradycardia, heartblock, CHF, asthma, shock; use with caution in patients with cardiomyopathy, pheochromocytoma: Pregnancy Class D

124
Q

Labetalol: interactions

A

additive effects with most other antihypertensives

125
Q

Labetalol: special

A

use reduced doses in patients with impaired liver function; dizziness is most troubling early side effect; most often used for hypertensive crises (as with nitroprusside)

126
Q

Labetalol: monitor

A

BP, HR

127
Q

Carvedilol: class

A

a1 and b blocker, antioxidant

128
Q

Carvedilol: indication

A

CHF

129
Q

Carvedilol: PD

A

reduces BP by blocking access of NE to beta-receptors and alpha-1 receptors, thereby lowering BP by several different mechanisms; patients differ in degree of beta-blockade vs alpha-blockade

130
Q

Carvedilol: PK

A

excellent absorption but high first-pass effect, leading to F~25%; onset 1-2 hours after po, 2-5 minutes when given iv; extensively metabolized in liver by IID6

131
Q

Carvedilol: tox

A

avoid in patient with bradycardia, heartblock, CHF, asthma, shock; use with caution in patients with cardiomyopathy, pheochromocytoma: Pregnancy Class D

132
Q

Carvedilol: interactions

A

additive effects with most other antihypertensives

133
Q

Carvedilol: special

A

use reduced doses in patients with impaired liver function; dizziness is most troubling early side effect; most often used for hypertensive crises (as with nitroprusside)

134
Q

Carvedilol: monitor

A

BP, HR

M2 Pharmacology Jen (11 decks)

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