Adrenergics Flashcards

1
Q

Epinephrine.

A

non selective (all receptors)
heart, lungs, vasculature
MCU: cardiac arrest, anaphylaxis
MO: (+) CO (B1), (+)BP (A1)

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2
Q

Norepinephrine.

A

all receptors except beta2

MCU: hypotension

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3
Q

phenylephrine.

A

selective A1 agonist
vasculature
MCU: hypotension (also nasal congestion)

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4
Q

clonidine.

A

selective A2 agonist
vasculature
MCU: hypertension
MO: (-) NE; works centrally post synaptic A2, decreasing sympathetic outflow

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5
Q

brimonidine

A

selective A2 agonist
eyes
MCU: glaucoma
MO: (-) aqueous humors

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6
Q

isoproterenol.

A

non selective Beta agonist
heart
hypotension
(+) CO (B1); also relaxes GI and lungs; COMT degrated

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7
Q

terbutaline.

A

selective agonist
lungs
MCU: asthma
MO: bronchodilation (B2); better than isoproterenol since fewer cardiac se

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8
Q

albuterol.

A

selective agonist
lungs
MCU: asthma
MO: bronchodilation (B2); better than isoproterenol since fewer cardiac se; most common

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9
Q

cocaine.

A

indirect sympathomimetic
CNS
psychostimulant
inhibits NET

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10
Q

imipramine.

A

indirect sympathomimetic
CNS
antidepressant

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11
Q

methylphenidate (Ritalin)

A

indirect sympathomimetic
CNS
ADHD

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12
Q

amphetamine.

A

indirect sympathomimetic
CNS
psychostimulant
note: tachyphylaxis

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13
Q

ephedrine.

A

indirect sympathomimetic
CNS
psychostimulant
alpha and beta agonist; also releases NE

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14
Q

tyramine.

A

indirect sympathomimetic
false transmitter
note: hypertensive crisis results when tyramines can’t be broken down by MAO (release of NE)

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15
Q

MAO inhibitors

A

indirect sympathomimetic

note: hypertensive crisis results when tyramines can’t be broken down by MAO (release of NE)

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16
Q

phenoxybenxamine.

A

non competitive, irreversible alpha blocker
vasculature
MCU: hypertension

17
Q

phentolamine.

A

competitive alpha blocker
vasculature
MCU: hypertension
also has PSmimetic GI tract stimulation and releases histamine

18
Q

prozasin.

A

competitive alpha 1 blocker
MCU: hypertension
95% bound to plasma protein
postural hypotension

19
Q

yohimbine.

A

competitive alpha 2 blocker

increases sympathetic outflow from CNS to increase BP, HR

20
Q

propranolol

A
  • first generation beta blocker (B1 and B2) along w timolol, pindolol
  • first pure beta antagonist
  • lipid soluble, well absorbed from gut, liver metabolism, short plasma half life
  • structure: have substituted amine connected by short hydrocarbon chain in ester linkage to ring
  • reduces CO and causes bronchoconstriction
21
Q

timolol.

A
  • first generation beta blocker (B1 and B2) along w -propranolol, pindolol
  • lipid soluble, well absorbed from gut, liver metabolism, short plasma half life
  • short acting
22
Q

atenolol.

A
  • 2nd generation B blocker (B1 selective) w acebutalol and metoprolol
  • decreases CO; no long side effect
  • long acting
23
Q

acebutalol

A
  • 2nd generation B blocker (B1 selective) w atenolol and metoprolol
  • decreases CO; no long side effect
  • partial agonist
24
Q

metoprolol

A
  • 2nd generation B blocker (B1 selective) with atenolol and acebutalol
  • decreases CO; no long side effect
25
Q

carvedilol.

A
  • 3rd generation beta blocker (produces vasodilation in additino to cardiac effect) w celiprolol, nebivolol
  • alpha 1 blocker
  • MCU: hypertension
26
Q

celiprolol

A
  • 3rd generation beta blocker (produces vasodilation in additino to cardiac effect) w carvedilol and nebivolol
  • partial beta 2 agonist
  • MCU: hypertension
27
Q

nebivolol

A
  • 3rd generation beta blocker (produces vasodilation in additino to cardiac effect) with carvedilol and celiprolol
  • release of NO by endothelial cells
  • MCU: hypertension
28
Q

metyrosine

A
  • adrenergic blocker
  • blocks tyrosine hydroxylase (– NE, –E)
  • MCU: hypertension
29
Q

pindolol.

A
  • first generation beta blocker (B1 and B2) along w timolol, propranolol
  • partial agonist
  • lipid soluble, well absorbed from gut, liver metabolism, short plasma half life
  • structure: have substituted amine connected by short hydrocarbon chain in ester linkage to ring
  • reduces CO and causes bronchoconstriction
30
Q

methyldopa.

A

false transmitter for NE and (++) alpha 2
competes for dopa decarboxylase
-MCU: hypertension

31
Q

reserpine

A

(–) NE vesicular uptake by VMAT
(1 dose can deplete NE storage in 24h)
-MCU: hypertension