Intro and PSNS Flashcards
PSNS function
rest and digest
PSNS main NT
ach
PSNS receptor target
muscarinic
PSNS effect on lens
lens convex for near vision
AChE
terminates signal by breaking down Ach into inactive form
SNS function
fight or flight (energy mobilization, increase CO, ventilation)
SNS main NTs
NE and Epi
SNS main receptor targets
alpha and beta adrenergic receptors
SNS effect on lens
flattens lens for distance vision
heart autonomic tone
dominated by PSNS
BVs autonomic tone
sympathetic innervation
4 ways drug can INCREASE activity of synapse
- increase NT release into synapse
- reduce reuptake of NT from synapse
- reduce degradation of the neurotransmitter int he synapse
- mimic activity of NT at receptor
4 ways the drug can decrease activity of a synapse
- block NT’s receptor
- inhibit synthesis of NT
- prevent release of NT
- prevent packaging in vescicles
muscarine
mushroom toxin, symptoms resemble extreme activation
even number muscarinic receptors
Gi
inhibitory - hyperpolarization (harder to get aps)
odd number muscarinic receptors
Gq
increase Ca2+ for smooth msucle contraction
cholinomimetics
effects similar t PSNS activation (enhance signalling)
effects of cholinomimetics
-decrease HR
-urination
-increase glandular secretions
-increase GI motility
-constrict airways
parasympathomimetics
mimic acts of PSNS
parasympatholytics
decrease signaling
cholinesterase
direct-acting cholinomimetics
2 types of cholinesterases
bethanechol
pilocarpine
bethanochol
-direct acting M-agonist
-treatment for post op / post partum urinary retention
-resist AchE (specific to muscarinic rec)
pilocarpine
-direct acting M agonist
-glaucoma + xerostomia
anticholinesterases
indirect-acting cholinomimetics
ache inhibitors
clinical uses for anticholinesterases
glaucoma
myasthenia gravis
anticholinesterases and insecticides
inhibit insect AchE, high concentrations cause human toxicity
symptoms of anticholinesterases
SLUDGE
overdose of anticholinesterases
respiratory effects can be lethal, irreversible, and ocular / respiratory symptoms are first to emerge
4 types of anticholinesterases
- organophosphages
- neostigmine
- pralidoxime
- atropine
organophosphates
-covalent irreversible
-chemical warfare (high potency nerve agents)
neostigmine
-covalent reversible
-slow reaction
-myasthenia gravis
pralidoxime (2-pam)
-kicks phosphorus off of AChE moleucle
-organophosphage poisoninig
atropine
-atropine + pralidoxime = antidote for insectiside poisoning
anticholinergic drug (other names)
cholinolytics or muscarinic antagonists
side effects of anticholinergic drugs
-related to blockade of muscarinic receptors
-dry mouth, blurry vision, upset stomach, headache, constipation
anticholinergic toxidrome
antihistamines, antidepressants, antipsychotics, nightshade plants
altered mental status, dilated pupil, flushed skin, dry skin, etc
atropine
-reverse bradycardia
-taken for cholinergic poisoning
-can cause mydriasis
-can be used to decrease saliva produciton
scopolamine
-blocks vestibular apparatus for motion sickness
-can cause blurry vision and dry mouth
tiotropium
-treat COPD
-prevents / reduces bronchospasm (relaxes bronchioles)
tolterodine
treats overactive bladder
M3 selective
inhibitor of ACh release
botulinum toxin a
botulinum toxin a
-cause of botulism food poisoning
-extremely lethal with small doeses
mechanism of botulinum toxin a
cleaves snare proteins
prevents NT vesicle fusion
no ach release