ANS Flashcards
Main activities of the ANS
regulation of smooth muscles
regulation of the heart
regulation of secretory glands
primary ANS neruotransmitters
Acetylcholine, norepinephrine, epinephrine
all drugs work either by increasing or decreasing receptor activation
acetylcholine
used at most junction of peripheral nervous system
undergoes reuptake to be stroed for reuse
Acetylcholinesterase
enzyme that breaks down Ach
psuedocholinesterase
destroys Ach
norepinephrine
released by most postgaglionic neurons
most adrenergic agonist drugs inhibit NE reuptake or inactivation or promote release
MAO
enzyme that destroys NE
COMT
enzyme that destroys NE usually in the blood stream
Epinephrine
made in adrenal medulla
released into blood stream and traveks to target organs
termination by hepatic metabolism
works on all 4 receptors
SNS nerve fibers
short preganglionic and long postganglionic nerve fibers
one preganglionic fiber activates many postganglionic fibers
Fight/flight response
SNS CV regulation
maintaing blood flow to the brain, redistributing blood, compensating for the loss of blood
SNS body temp regualtion
regulates blood flow to the skin
promotes secretion of sweat
induce piloerection (hair standing on edge)
SNS CV effects
increases heart rate
increases BP
increases contraction
SNS bronchiole effecs
bronchodilation
SNS skin effect
increases sweating
SNS eye
pupil dilation
SNS pancreas
decreased insulin
increased blood sugar
SNS GI
decreased peristalsis
SNS GU
relaxes smooth muscle, constricts sphincter, inhibits voiding
SNS peripheral blood vessels
vasoconstriction
SNS respiratory
increases rate and depth of respiration
alpha 1 receptors/ responses
in smooth muscle, (eye, blood vessles, sex organs, bladder) on postsynaptic membrane
respond to all 3 NT
constriction of blood vessels, dilation of pupil, ejaculation, contraction of bladder neck and prostate
activation increases vascular smooth muscle
alpha 2 receptor
on presynaptic membrane
inihibitory- specifically of norepinephrine
minimal clinical significance
Beta 1 receptorsd
in heart- increased rate, force of contration, AV conduction
In kindey- Renin release which causes vasoconstriction
Beta 2 receptors
arterioles in heart, lung, skeletal muscles- Dilation
bronchi- Dilation
uterus- Releaxtion
Liver- Glyconeolysis
Direct acting adrenergic agonists MOA
affect post synaptic alpha 1 and beta receptors on target organs
Indirect-acting adrenergic agonists MOA
stimulation of alpha 1, beta 1, beta 2 receptors indirectly
cause release of norepinephrine in synapse or prevent reuptake of norepinephrine
Alpha-1 Agonists
P- Phenylephrine (neo-synephrine)
naphazoline hydrochloride (allrest, cleareyes)
Alpha-1 agonists Indications
hypotension during shock- increase heart rate and vasoconstriction
nasal pharygeal mucous congestion
dilation of pupil for eye procedures (eye drops)
alpha 1 receptor agonist
generally prescripbed for nasla congestion and hypotension
hemostasis, prolong anesthesia, mydriasis during opthalmic exams
Alpha-2 Agonists
P- clonidine (catapress)
methyldopa (aldomet)
clonidine indications
blood pressure
clonidine MOA
stimulate alpha 2 receptros which inhibit sympathatic NS
block norepinephrine to reduce blood pressure
clonidine kinetics
40-60% eliminated unchanged in kidneys
Alpha-receptor 2 agonists
receptrors in preiphery and CNS
for treatment of hyperternsion and severe pain
Clonidine side effects
drowsiness, rebound hypertension, Dry mouth, CNS effects
Beta 1 adrenergic agonists
P- dopamine
dobutamine
Beta 1 receptor agonists
effects on heart
Used in critical care setting for cardiac arrest, heart attack, heart failure, shock, AV heart Block, profound hypotension
Dopamine MOA
stimulates beta 1 and dopamine receptors (and A1 at high doses)
Beta 1 stimulation produced increased cardia output by increasing force of the contration adn heart rate, leading to increased O2 need in myocardial muscles
dilates renal and mesenteric arteries
Dopamine side effects
ectopic beats
NV
tachycardia, angine, palpitation, vasoconstriction
high doses: ventricular rhythm and dilated pupils
From heart stimulation
Beta 2 receptor agonists
for asthma, reduce preterm labor contraction of uterus
Beta 2 actrivatio adverse effect
w/ higher doses
tremor, tachycardia
Hyperglycemia
Beta 2 activation causing hyperglycemia
receptors activated in liver and skeletal muscles
breakdown glycogen into glucose
only in pts with diabetes, otherwise insulin will prevent
Non selective Adrenergic Agonists
P- epinephrine
norepinephrine (levophed)
isoproterenol (Isuprel)
Epinephrine MOA
stimulates all adrnergic receptors throughout body
greatest effects on cardiovascular system and CNS
creates”fight or flight”
Epi kinetics
absorption: very fast, orally, topically, inhaltion ,IM SC
duration: 1-4 hourds
Metabolized: in the liver w/ half life 2 min
Excreted: kidneys
Epi therapeutic uses
treatment of choice for Shock
CPR, superficial bleeding control, asthma, hypotension, dysrhythmias
Epi indications
all forms of shock with inadequate tissue perfusion
vasoconstricitve/ hemostatic purposes
sinus congestion
Epi effects
increases BP, HR
relaxtion of bronchial smooth muscles
vasoconstriction in peripheral blood vessels
inhibitis insulin secretion, increased glucose
Epi adverse effects
fatigue, sleep disturbance, tremor, weakness, dizziness, cardiovascular stimulation, dysrhythmias, increased blood glucose levels, cerebral hemorrhage, hypertensive crisis, angina
Epi contraindications
hypersensitivity, active labor, closed angle glaucoma, sulfite sensitivity, dysrhythmias, CAD labor HTN or hyperthyroidism
Epi drug interactions
MOA inhibitors, tricyclic antidepressants, general anesthetics, alpha/beta adrenergic blocking agents
Nursing responsibilites w/ epi
establish baseline vital signs
resp status, BP, i/os, hyperglycemia, mucosa
Epi-pen use
single use, still need to seek emergency treatment
Adrenergic Antagonists
block or decrease effects of the sympathetic nervous system
can occur by blocking alpha 1 receptors post synaptically or stimulate presynaptic alpha2 receptors which results in return of norepinephrine to presynaptic site
adrenergic antagonist effects
dilation of arterioles and veins, decrease blood pressure, cardiac output decreases, pupillary constriction, increased GI tract motility, smooth muscle relaxation of prostate and bladder
Alpha Adrenerguc antagonist
class of adrenergic antagonists
P- prazosin (minipress)
doxazosin
tamusosin
terzosin
alpha1 adrenergic antagonists
receptors located on smooth muscle of heart, genitourinary, and GI systems and brain
most important action of these agents is on arterial smooth muscle and CV system
Blockade of alpha reeptors dilates blood vessels causing lowering of BP
Prazosin MOA
selective blockade of alpha1
dilates blood vessels
relaxes smooth muscle in bladder and prostate
approved only for treating HTN
can also benefit benign prostatic hypertension
what are alpha blockers used to treat
Hypertension- vasodilation lowering BP
BPH- reduce the contraction of smooth muscle in prostate and bladder neck
Raynaud’s disease- causes vasodilation
reversal of toxicity of alpha 1 agonistsPrazosin
prazosin kinetics
administration: oral
metabolized: liver
excreted: bile, feces, urine
peak 1-3 hrs
duration 10 hrs
half life 2-3 hrs
alpha blockers adverse effects
orthostatic hypotension: blockade of alpha receptors on veins, reduced muscle ton ein venous walls, upon standing blood pools in the veins
reflex tachycardia: reflex to increase heart rate via the autonomic nervous system
nasal congestion: dilates the blood vessels of the nasal mucosa
inhibition of ejaculation: alpha1 activation required for ejaculation. impotence is reversible; resolves when drug is discontinued
sodium retention and increased blood volume: Reduced blood pressure promotes renal retention of sodium and water. Usually combined with diuretic when used for hypertension
prazosin contraindications and precautions
hypersensitivity; use caution with angina because hypotension may worsen with condition
first dose effect
prazosin Adverse effects
orthostatic hypotension
light-headedness dizziness
reflex tachycardia
nasal congestion
prazosin drug interactions
other antihypertensive medications
beta adrenergic antagonists
class of adrenergic atangonists
P- metoprolol
atenolol
propranolol
beta adrenergic blocker indications
cardiac, glaucome, migraines, off label for sweating, anxiousness, PTSD
beta adrenergic blockers adverse effects
lower heart rate
lower BP
bronchoconstriction
hypoglycemia
parasympathetic nervous system nerve fibers
long preganglionic and short postganglionic nerve fibers
ration of preganglionic to postganglionis fibers is high
enegry conservation
types of cholinergic receptors
Nicotinic N receptors ( found in all ANS neruons, and in adrenal medulla which releases Epi)
Nictonic M receptors ( found in neruomuscular junction which cause contration of skeletal muscles
Muscarinic receptors ( founf in PSNS cells and sweat glands)
what do all cholinergic receptors respond too
achetylcholine
what do nicotinic receptors primarily respond to
nicotine
cholinergic drugs
stimulate parasympathtic nervous system in the same manner as acetylcholin
may stimulate cholinergic receptors directly or slow acetylcholine metabolism at synapse
what cholinergic receptor is effected first with a redommendd dose
muscarinic, nictoinic receptors are only effected with higher doses
direct acting muscarinic agonists
class of cholinergic agonists
P- bethanechol
pilocarpine
carbachol
Bethanechol
selective agonist at muscarinic cholinergic receptors
bethanechol indication
urinary retention (post op/partum)
GI uses like post op abdominal distention
bethnechol effects
bradycardia
bronchial constriction
increased GI tone and motility
increased urination
increased sweating,salivation, bronchial and gastric acid secretions
miosis
relaxation of blood vessels
hypotension
direct acting cholinergic drug effects
decreased HR, vasodilation
Increased gastric secretion, GI motility
helps empty bladder, relax urinary sphincter
increased salivary and sweat glands
bronchial constriction, narrowed airways, increased respiratory secretions
pupil constriction and contraction of ciliary muscle. Reduce intraocular pressure, which is good for glaucoma. Focuses the eye for near vision
direct acting cholinergic drugs in asthma/ COPD pt
contraindicated due to increased respiratory secretions
SLUDGE
cholinergic effects are ‘wet’
salvate lacrimate urinate defecate gastrointestinal cramps, emesis
cholinergic drug side effects
a result of overstimulation of PSNS
hypotensions, conduction abnormalities, arrest, extreme slow down of heart rate
headache, dizziness, convulsions
abdominal cramps, increased secretions, N/V
increased bronchial secretions, bronchospasms
lacrimation, sweating, salvation, miosis
what should be assessed before use of a cholinergic
allergies
presence of GI or GU obstruction
asthma, COPD, broncho restriction disease
peptic ulcer disease
coronary artery disease
do not abruptly stop meds
direct- acting nicotinic agonists
class of cholinergic agonists
P- nictotine
for smoking sensation
indirect-acting cholinergic agonists
cholinesterase inhibitors
class of cholinergic agonists
P- neostigmine (prostigmin)
tacrine (cognex)
donepezil (aricept)
creates increase of acetylcholine by preventing breakdown
cholinesterase inhibitors
inhibits enzyme acetylcholinesterase
results in decrease destruction of Ach, which means more Ach, resulting in increase in cholinergic action
indirect acting cholinergic drugs therapeutic uses
causes skeletal muscle contractions
myasthenia gravis
reverse neuromuscular blocking agents
alzhemiers
prophylaxis of nerve gas poisoning
glaucoma
indirect acting cholinergic agonists
Gi obstruction or ileus
urinary tract obstruction
peptic ulcers
cardiac patients
respiratory patients
hyperthyroidism
cholinergic overdose
muscarinic poisoning from direct acting muscarinic and cholinesterase inhibitors and certain mushrooms
overdosing can cause life threatening problems
sign/symptoms: profuse salivation, lacrimation, visual disturbance, bradycardia, hypotension, abdominal cramps, diarrhea, difficulty breathing
antidote: atropine, usually for bradycardia
cholinergic antagonists
drugs that inhibit or block the actions of acetylcholine in the parasympathetic nervous system
P- atropine
hyoscamine (cystospaz)
ipratropium bromide (atrovent)
scopolamine
Atropine MOA
competitive antagonists
compete with Ach
Block Ach at muscarinic receptos in the PSNS
so Ach is unable to bind and cause the cholinergic effect
atropine therapeutic uses
bradycardia, asystole, CPR
preop to decrease resp secretions
operatively: blockcardiovagal reflexes, arrhythmias
GI with duodenal ulcers, IBS
cycloplegia- paralysis of ciliary muscles
asthma
Effects of anticholinergics
increases heart rate
disorientation, hallucinations, delerium, mild CNS excitation
dilated pupils
decreasey motility, peristalsis, intestinal and gastric secretions
urinary retention
dilated bronchial airways
decreased bornchial secretions
decrease saliva and sweating, exocrine secretions
therapeutic indications for anticholinergics
preanesthetic medication
disorders of the eye
bradycardia
intesstinal hypertonicicyt and hypermotility
muscarinic agonit poisoning
peptic ulcer disease
asthma
atropine adverse effects
blurred visions, dry mouth, urinary retention, constipation, tahcycardia, increased IOP, anhidrosis
atropine drug interactions
avoid using with other anticholinergics
avoid other cholinergic drugs
cholinergic antagonists assessment
allergies, CHF fiatal hernia, GI/GU obstruction, BPH, glaucoma, tachycardia
may cause blurred visions, avoid machinery, may be photosensitive
higher risk of heat stroke
