Adrenergics Flashcards
Epinephrine.
non selective (all receptors)
heart, lungs, vasculature
MCU: cardiac arrest, anaphylaxis
MO: (+) CO (B1), (+)BP (A1)
Norepinephrine.
all receptors except beta2
MCU: hypotension
phenylephrine.
selective A1 agonist
vasculature
MCU: hypotension (also nasal congestion)
clonidine.
selective A2 agonist
vasculature
MCU: hypertension
MO: (-) NE; works centrally post synaptic A2, decreasing sympathetic outflow
brimonidine
selective A2 agonist
eyes
MCU: glaucoma
MO: (-) aqueous humors
isoproterenol.
non selective Beta agonist
heart
hypotension
(+) CO (B1); also relaxes GI and lungs; COMT degrated
terbutaline.
selective agonist
lungs
MCU: asthma
MO: bronchodilation (B2); better than isoproterenol since fewer cardiac se
albuterol.
selective agonist
lungs
MCU: asthma
MO: bronchodilation (B2); better than isoproterenol since fewer cardiac se; most common
cocaine.
indirect sympathomimetic
CNS
psychostimulant
inhibits NET
imipramine.
indirect sympathomimetic
CNS
antidepressant
methylphenidate (Ritalin)
indirect sympathomimetic
CNS
ADHD
amphetamine.
indirect sympathomimetic
CNS
psychostimulant
note: tachyphylaxis
ephedrine.
indirect sympathomimetic
CNS
psychostimulant
alpha and beta agonist; also releases NE
tyramine.
indirect sympathomimetic
false transmitter
note: hypertensive crisis results when tyramines can’t be broken down by MAO (release of NE)
MAO inhibitors
indirect sympathomimetic
note: hypertensive crisis results when tyramines can’t be broken down by MAO (release of NE)
phenoxybenxamine.
non competitive, irreversible alpha blocker
vasculature
MCU: hypertension
phentolamine.
competitive alpha blocker
vasculature
MCU: hypertension
also has PSmimetic GI tract stimulation and releases histamine
prozasin.
competitive alpha 1 blocker
MCU: hypertension
95% bound to plasma protein
postural hypotension
yohimbine.
competitive alpha 2 blocker
increases sympathetic outflow from CNS to increase BP, HR
propranolol
- 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
timolol.
- 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
atenolol.
- 2nd generation B blocker (B1 selective) w acebutalol and metoprolol
- decreases CO; no long side effect
- long acting
acebutalol
- 2nd generation B blocker (B1 selective) w atenolol and metoprolol
- decreases CO; no long side effect
- partial agonist
metoprolol
- 2nd generation B blocker (B1 selective) with atenolol and acebutalol
- decreases CO; no long side effect
carvedilol.
- 3rd generation beta blocker (produces vasodilation in additino to cardiac effect) w celiprolol, nebivolol
- alpha 1 blocker
- MCU: hypertension
celiprolol
- 3rd generation beta blocker (produces vasodilation in additino to cardiac effect) w carvedilol and nebivolol
- partial beta 2 agonist
- MCU: hypertension
nebivolol
- 3rd generation beta blocker (produces vasodilation in additino to cardiac effect) with carvedilol and celiprolol
- release of NO by endothelial cells
- MCU: hypertension
metyrosine
- adrenergic blocker
- blocks tyrosine hydroxylase (– NE, –E)
- MCU: hypertension
pindolol.
- 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
methyldopa.
false transmitter for NE and (++) alpha 2
competes for dopa decarboxylase
-MCU: hypertension
reserpine
(–) NE vesicular uptake by VMAT
(1 dose can deplete NE storage in 24h)
-MCU: hypertension
