2 | Autonomic Nervous System
Terms in this set (74)
sympathetic nervous system (SNS)
fight or flight/aroused
parasympathetic nervous system (PNS)
rest & digest/calmed
what does the ANS control?
visceral/automatic functions of the body (ex. arterial pressure, GI motility, sweating, body temp)
symptoms of SNS
- relaxes bronchiolar smooth muscle
- contracts GI & bladder sphincters
- stimulates adrenal gland
- decreased secretions (except diaphoresis)
symptoms of PNS
- smooth muscle in GI wall contracts
- GI sphincters relax
- GI secretions increase
- bladder wall contracts
- bladder sphincter relaxes
increased heart rate
decreased heart rate
what is vasovagal syncope?
a sudden drop in heart rate and blood pressure leading to fainting
what causes vasovagal syncope?
loss of balance btwn PNS & SNS
- in anticipation of stressful event, SNS surges
- in rapid response, PNS launches compensation & "overshoots" = bradycardia, hypotension, cerebral hypoperfusion (lack of blood flow to brain)
what are the major regions of the spine?
cervical, thoracic, lumbar, sacral, coccyx
origin of SNS nerve fibers?
thoracic & lumbar regions (aka thoracolumbar)
origin of PNS nerve fibers?
cranial nerves (brainstem) & sacral region (aka craniosacral)
first set of neurons that originates from the CNS
second set of neurons that connects to the effector/target organ
lengths of pre/postganglionic neurons in SNS
why are SNS preganglionic fibers considered an "exception"?
they run all the way to the adrenal glands & release epinephrine and norepinephrine into blood
lengths of pre/postganglionic neurons in PNS
neurochemicals used in SNS
ACh (acetylcholine) @ pre/post synapse
NE (norepinephrine) @ target organ
why are sweat glands an exception to the neurochemicals used in SNS?
they are under SNS control but use ACh @ target organ
neurochemicals used in PNS
ACh (acetylcholine) @ pre/post synapse
what removes ACh from the synaptic cleft? how?
- acetylcholinesterase (AChE)
- splits ACh into acetyl group & choline, then taken back up into neuron that released it
what removes NE from the synaptic cleft?
- some are cleared via enzymatic breakdown or diffusion away from the cleft
a protein that receives a signal & uses it to communicate info to cell = triggers downstream effect
what receptor does ACh bind to?
what receptor does NE bind to?
found on skeletal muscles & postganglionic neurons of BOTH SNS & PNS fibers
found on target cells of ONLY PNS postganglionic fibers
α₁ adrenergic receptor: where is it found?
target cells of postganglionic SNS fibers
α₁ adrenergic receptor: associations? preferences?
- associated w/ constriction of smooth muscle
- prefers NE
α₂ adrenergic receptor: where is it found?
presynaptic postganglionic membranes
why is the α₂ receptor different from the other receptors?
it's located at the end of postganglionic fibers instead of at the target organ
what mechanism controls the α₂ receptor?
β₁ adrenergic receptor: where is it found?
heart muscle & kidney
β₂ adrenergic receptor: where is it found?
certain blood vessels & smooth muscles
chronic inflammatory disorder where airways have increased responsiveness/sensitivity to different stimuli
3 steps in treating asthma
1. alleviate bronchoconstriction
2. decrease secretions
3. decrease inflammation
β adrenergic (anything similar to NE/Epi) looks similar & stimulates effect
albuterol: side effects
heart palpitations, shakiness
why isn't albuterol a great solution?
it's meant only to stimulate the β₂ receptors but it also stimulates the β₁ receptors (in heart)
best treatment method(s) to alleviate bronchoconstriction
metered dose inhaler (MDI) or nebulizer
why is atrovent used to decrease secretions?
- atrovent is an anticholinergic agent
- cholinergic detects ACh
- PNS uses all ACh as transmitters
- PNS controls secretions
basal level of SNS activation that keeps our vessels partially constricted
what if the sympathetic tone was completely relaxed?
there would be no pressure to drive blood flow forward to organs
a significant imbalance btwn PNS & SNS
SNS higher than PNS
symptoms of sympathomimetic toxidrome
- warm, moist skin
- altered mental state (AMS), seizures
high body temp
causes of sympathomimetic toxidrome
- ecstasy (MDMA)
why does cocaine cause a sympathomimetic toxidrome?
blocks reuptake of NE, Epi (too much in system, can't reabsorb)
why does meth cause a sympathomimetic toxidrome?
stimulates the release of NE, Epi
why does ecstasy cause a sympathomimetic toxidrome?
mimics NE, Epi (serotonin)
sympathomimetic toxidrome treatment
- valium (diazepam): calming effect
why should beta blockers be avoided?
we don't want unopposed alpha receptors
PNS higher than SNS
symptoms of cholinergic toxidrome
- salivation, foaming at the mouth
- bronchospasm/excessive bronchial secretions
- AMS, seizures
low blood pressure
lack of control over defecation/urination
what is the main cause of death in a cholinergic toxidrome?
causes of cholinergic toxidrome
nerve agents (Tabun, Sarin, Soman, VX)
- contains acetylcholinesterase inhibitors (AChEI)
what does AChEI do?
inhibits the breakdown of ACh @ synaptic cleft = excess stimulation of cholinergic receptors
cholinergic toxidrome treatment
atropine, a muscarinic (cholinergic) receptor antagonist that blocks ACh receptor & decreases received signal
PNS lower than SNS
symptoms of anticholinergic toxidrome
- hot, flushed DRY skin
- DRY mucous membranes
- urinary retention
why are things DRY in anticholinergic toxidromes?
sweat glands use ACh = no ACh means dry
causes of anticholinergic toxidrome
ACh receptor inhibition (basically atropine)
- diphenhydramine (Benadryl) = blocks ACh from binding to receptors
anticholinergic toxidrome treatment
acetylcholinesterase inhibitors (AChEI)
- ex. physostigmine = inhibits breakdown of ACh @ synaptic cleft, prolongs ACh's time @ cleft
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