Neuromuscular and Ganglionic Blocking Agents
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Muscarinic agonist aka parasympathomimetic Systemic effects?
- SLUDGE (salivation, lacrimation, urinary incont, diarrhea, GI cramps, emesis)
- pupil constrict
- broncho constrict
- decrease hr and conduct
- GI/GU- increased motility and secretion, bladder contract, sphincter relax- pee
- Increased sweat and saliva
Muscarinic agonist aka parasympathomimetics
- – muscarine is a true prototype, but bethanechol is a good example of one used clinically (used for urinary retention and delayed gastric emptying)
- "bethanechol when you pee too much and dont poop at all- use bethanechol!"
Muscarinic agonist contra
- asthma- bronchoconstrict
- Acid-peptic dx- increase gastric secretion
- Coronary insuff- worsen bradycardia
- another muscarinic agonist
- for dry mouth- promotes salivation
- "pilocarpine - to start PAVLOVing"
m1, m2, m3 ,m4, m5 excite or inhibit?
- odds- excite
- even- inhibit
Muscarinic antagonist aka sympathomimetics
- – "atropine- makes your heart sing"- blocks vagal slowing on SA node- increased HR
- Pupil Dilation
- GI GU- plug up
- Lung- decrease secretions- dry up
- Tachy- dose dependent
- Glands- block sweating and salivation
- CNS (Scopalamine)- reduce parkinsonian tremor and altered vestibular function
atropine intox? aka antimuscarinic poisoning
aka- anticholinergic syndrome
- mad as a hatter
- blind as a bat
- dry as a bone (mouth)
- red as a beet (flushing)
- hot as a furnace
- use a muscarinic AGONIST- overcome muscarinic receptor blockade- Physostigmine "(antillirium)- fights atropine dilirium"
which is better?
- -COPD acts at m1,2,3- bronchodilation, BETTER
- - COPD- nonselective for m1,2,3- potential for paradoxical bronchoconstriction
Nicotinic agonist (remember cholinergic agonists are either nicotinic or muscarinic!)
2 types of Nicotinic?
- Direct– nicotine, succinycholine
- Indirect- AChEsterase inhibitor
ACh metabolism by AChE
Sites of action?
- -Anionic Site- binds ACh to enzyme
- -Esteratic Site- hydrolysis breaks ester bond
3 major groups?
Duration of action?
- AntiCholinesterase inhibitor (irreversable- need new AChE)
- Ex: echothiophate
- Anticholinesterase inhibitor (reversable)
- ex: Physostigmine- (reverse anticholinergic syndrome from atropine)
- Competitive AntiCholinesterase Inhibitor- competes for ANIONIC site
Organophosphate poisoning treatment
Symptoms of exposure
- -Atropine + Pralidoxime
Same as Parasympathetic SLUDGE + bradycardia+ muscle fasciculations+CNS slurring
Antibody made blocks ACh binding to receptor
Dx- Edrophonium test, + test shows obvious muscle strength improvement for 5 min
- Immunosupress Prednisone
Ganglionic blocker example –
mecamylamine- noncompetitive blocker- autonomic NS paralysis
DEPOLARIZING NMJ blocker
– again, like muscarine, d-tubocurarine (or curare) is a prototype not used often clinically; but if you remember that these drugs end in “onium” and “urium” you should be ok
– simple alcohol – Edrophonium (note – this one ends in “onium” but is NOT an NMJ blocker!)
– carbamate – Neostigmine
– organophosphate – Echothiophate
Alzheimers and Cholinergics
-What do muscarinic blocking agents do?
- ChAT levels and ACh?
-# of nicotinic and Muscarinic receptors
- induce memory loss
-dramatic ChAT drop- reduced ACh output
- reduced in alzheimers
blood vessels- sympathetic or par tone?
cholinergic or adrenergic?
- - sympathetic
- - adrenergic
dominant tone at rest?
sweat glands- sympathetic or para tone?cholinergic or adrenergic?
- sympathetic tone
Dominant tone?- para or sympat with addition of a muscarinic receptor agonist
para- more motility observed
Dominant tone?- para or sympat with addition of a muscarinic receptor anatagonist
- sympathetic- para is blocked
- less motility
Dominant tone?- para or sympat with addition of a nicotinic receptor antagonist
neither, both sympathetic and parasympathetic tone are blocked
Dominant tone?- para or sympat with addition of a beta adrenergic receptor agonist
- sympathetic tone is increased
- motility is decreased
Dominant tone?- para or sympat with addition of a beta adrenergic antagonist
- sym is blocked- greater motility and tone
How can a nictinic receptor agonist act as a blocker?
initial stimulation- after ion flow has occurred- unbinding of agonist has not occurred and therefore acts as a blocker
nicotinic and muscarinic- ion or g protein?
- muscle- depolarization fasciculation
- adrenal medulla- epi release- increase hr/bp
- cns- exicte, convulsion, resp stim, coma
- ganglia- depends on dom tone, secretion stim and n/v/d
nicotinic receptor anatagonist aka ganglionic blockade effect on BV?
nicotinic receptor anatagonist aka ganglionic blockade effect on sweat glands
nicotinic receptor anatagonist aka ganglionic blockade effect on heart
nicotinic receptor anatagonist aka ganglionic blockade effect on pupillary fxn and lens
mydriasis and blurred vision(cyclopegia)
nicotinic receptor anatagonist aka ganglionic blockade effect on gut
decreased tone and motility
nicotinic receptor anatagonist aka ganglionic blockade effect on bladder
nicotinic receptor anatagonist aka ganglionic blockade effect on salivary gland
ganglionic therapeutic use
- control hemorrhage in surgery
- severe htn
- dissecting aortic aneurysm
- autonomic reflexia- sc injury
- depolarizing blocker- binds to nicotinic receptors at motor end terminal
- na and ca diffuse into cell and depolarizes this is phase I blockade
- SUx is not metabolized by AChE-remains attached and channel stays open
- new action potential cannot occur until repolarization- have paralyzation because contractions cannot occur- Phase II
- sux is metabolized by palsma cholinesterase
causes hyperkalemia- worry in pts prone to this like burn victims
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