Autonomic Drugs Overview Flashcards by Christine P

Direct acting cholinergic drugs are either ____ or ____

muscarinic agonist or nicotinic agonist

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muscarinic agonists include

acetylcholine, muscarine, pilocarpine, bethanechol

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nicotinic agonists include

acetylcholine, nicotine, succinylcholine, varenicline

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indirect acting cholinergic drugs are either ____ or ____

AChE Inhibitors that are reversible or irreversible

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reversible AChE inhibitors include

edrophonium, neostigmine, pyridostigmine, physostigmine, donepezil

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irreversible AChE inhibitors include

echothiophate
organophosphate insecticides
Sarin nerve gases

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is edrophonium long, intermediate, or short acting?

short

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is neostigmine long, intermediate, or short acting?

intermediate

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Acetylcholine

quaternary ammonium
short duration
has nicotinic and muscarinic activity

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MOA AChE inhibitors (indirect)

bind to active site and inhibit AChE

prevents ACh from binding so increases the ACh concentration, t 1/2, and activity

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is edrophonium an alcohol or carbamate?

alcohol

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is neostigmine an alcohol or carbamate?

carbamate

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Clinical uses for AChE inhibitors

reverseal of NM blockade by nondepolarizing drugs, myasthenia gravis diagnosis and treatment, glaucoma, ileus, postop urinary retention, Alzheimer’s

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AChE inhibitors effects

autonomic nervous system = increased secretions, increased GI motility, bronchoconstriction, bradycardia, hypotension, miosis

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AChE inhibitors adverse effects

if given in large doses = depolarizing block

toxicity = excitation (convulsion) then depression (unconscious)

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which reversible AChE inhibitors are quarternary amines and what is the significance of that?

edrophonium and neostigmine

polar = don’t cross BBB

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which reversible AChE inhibitors are tertiary amines and what is the significance of that?

physostigmine

nonpolar = crosses BBB

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onset and DOA for edrophonium

onset: 30-60 seconds
DOA: 10 minutes

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onset and DOA for neostigmine

onset: 10 -30 minutes
DOA: 2- 4 hours

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onset and DOA for physostigmine

onset: 3- 8 minutes
DOA: 1 hour

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Cholinergic crisis toxicity mnemonic

DUMBBELLS
D - diarrhea, diaphoresis
U- urination
M - miosis
B - bradycardia
B- bronchoconstriction
E - excitation, emesis
L - lacrimation
S - salivation, sweating

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What is the antidote for muscarinic toxicity?

atropine

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What is the antidote for AChE Inhibitor toxicity?

atropine or pralidoxime (have to give early)

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which muscarinic agonist is typically used for treatment of bladder and GI hypotonia?

betanechol (stimulates motility)

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what do muscarine, pilocarpine, oxotremorine, and cevimeline have in common?

muscarinic receptor specificity

muscarinic agonist effects (parasympathomimetic)

``` decrease HR, CO, and arterial pressure vasodilation via nitric oxide increase GI motility contracts bladder bronchoconstriction increase secretions miosis, decrease intraocular pressure ```

clinical uses for muscarinic agonists

glaucoma, ileus, urinary retention, xerostomia (Dry mouth)

mnemonic for muscarinic agonist GI/GU effects

``` SLUDGE s- salivation l - lacrimation u - urination d - diarrhea g - GI upset e - emesis ```

nicotinic nerve agonists effects

stimulation of post ganglionic neuronal activity, CNS stimulation

nicotinic nerve agonists clinical use

smoking cessation

nicotinic nerve agonists adverse effects

CNS stimulation, skeletal muscle depolarization/blockade, HTN, increase HR, N/V/D

nicotinic muscle agonist effects

activation of NM endplates, contraction

nicotinic muscle agonist clinical uses

depolarizing skeletal muscle paralysis

anticholinergics are either ____ or _____

muscarinic antagonist or nicotinic antagonist

nonselective muscarinic antagonist examples

atropine, glycopyrrolate, scopolamine

nicotinic nerve ganglionic blocker example

hexamethonium (historical)

nicotinic muscle NM blocker examples

atracurium, cisatracurium, vecuronium, rocuronium, pancuronium

muscarinic antagonist effects

increase HR, bronchodilation, decreased GI/GU, decrease glands/secretions, decrease sweating, mydriasis, sedation

would you expect effects at the blood vessels with muscarinic antaognists?

would you expect effects at the skeletal muscle with muscarinic antagonists?

clinical uses of muscarinic antagonists

motion sickness, parkinson's, COPD, asthma, excessive secretions, GI hypermotility, urinary urgency, bradycardia

which muscarinic antagonists are tertiary amines and what is the significance of that?

atropine and scopolamine | crosses BBB

half life of atropine

about 4 hours in elderly - 10 hours eye effects may last days

half life, onset, DOA of scopolamine

1-4 hours (IV), onset 10 minutes, DOA 2 hours (IV)

glycopyrrolate half life, onset, DOA

1 hour, onset 1 minute, DOA 7 hours

memory aid for anticholinergic effects

Dry as a bone, hot as a pistol, red as a beet, blind as a bat, mad as a hatter

medication classes with anticholinergic activity

antihistamines, antispasmodics, antiparkinson drugs, skeletal muscle relaxants, antipsychotics, antidepressants, antimuscarinics for urinary incontinence

which patient population is especially susceptible to anticholinergic toxicity

elderly

nicotinic muscle antagonists effects and clinical uses

effects: competitive antagonism at skeletal muscle, non depolarizing uses: skeletal muscle relaxation for surgical, intubation, and ventilation control

nicotonic nerve antagonist effects and uses

effects: blocks ganglionic output uses: historical, hypertensive emergency

direct acting adrenergic agonists include

alpha agonists, beta agonists, mixed alpha and beta agonists

indirect acting adrenergic agonists include

NT releasers, NE reuptake inhibitors, MAO inhibitors

nonselective alpha agonist

norepinephrine

alpha 1 agonist

phenylephrine

alpha 2 agonist

clonidine, dexmedetomidine

nonselective beta agonist

isoproterenol

beta 1 agonist

dobutamine

beta 2 agonist

albuterol

mixed alpha/beta agonist

epinephrine, norepinephrine

epinephrine receptors

alpha 1 and 2, beta 1 and 2

norepinephrine receptors

alpha 1 and 2 and beta 1

neurotransmitter releasers

amphetamine and ephedrine

norepi reuptake inhibitors

cocaine, SNRI

MAO inhibitors

tranylcypromine, selegiline

dopamine receptors

alpha 1, beta 1, dopamine 1 and 2

endogenous catecholamines

dopamine, epi, norepi

why don't we give catecholamines PO?

they are polar, poor CNS penetration

ephedrine, pseudoephedrine

displaces/releases stored catecholamine NT | some agonist activity

amphetamine

displaces/releases stored catecholamine NT, inhibits catecholamine reuptake

cocaine

blocks NE reuptake, blocks sodium channels

tyramine

displaces/releases stored catecholamines | in fermented foods and interact with MAOIs (HTN crisis)

alpha 1 agonist effects

vasoconstriction smooth muscle contracts expect in GI GI/GU sphincters contract mydriasis

alpha 2 agonist effects

decreases NE release, inhibit sympathetic outflow | platelet aggregation, decrease insulin

beta 1 agonist effects

increase HR and contractility increase renin release trophic effect

beta 2 agonist effects

bronchodilation, vasodilation, most smooth muscle relaxes, tremors, GI/GU relax, glycogenolysis

low dose epinephrine

beta effects

high dose epinephrine

alpha effects

epinephrine effects with local anesthetics

causes vasoconstriction to keep LA in the desired area and prevent systemic effects

low dose dopamine

Dopamine 1 in renal, mesenteric, coronary vascular beds

medium dose dopamine

Beta 1

high dose dopamine

alpha 1

which drug has the highest affinity for alpha receptors?

epinephrine

which drug has the highest affinity for beta receptors?

isoproterenol

nonselective alpha adrenergic blocker

phenoxybenzamine | phentolamine

alpha 1 adrenergic blocker

prazosin

alpha 2 adrenergic blocker

yohimbine

nonselective beta blocker

propranolol

beta 1 blocker

metoprolol | esmolol

why don't we have beta 2 blockers?

would cause bronchoconstriction (no real good reason to do that)

a beta 2 receptor agonist would NOT

stimulate renin release | beta 1

the effects of isoproterenol could be blocked by a

nonselective beta adrenergic receptor antagonist

what would be expected upon administration of a muscarinic agonist drug, but NOT with parasympathetic nerve stimulation?

vasodilation

cholinergic receptors would be found at all of the following sites except

juxtaglomerular cells