Cholinergic Antagonists Flashcards
Cholinergic Antagonists (anticholinergic)–> Muscarinic
MUSCARINIC–> antimuscarinic, blocks effects of parasympathetic autonomic discharge
ex: atropine and scopolamine
Cholinergic Antagonists–> Nicotinic
ganglionic blockers (autonomic NS)
NMJ
ex: tetraethylammonium, tubocurarine, succinylcholine
drugs block outflow past autonomic level, so you wont get any adrenergic or muscarinic action
Atropine
comes from plants, like atropa belladonna
meds with similar structure to atropine such as antihistamines, phenothiazine and tricyclic-antidepressants will have anticholinergic side fx
Actions of Atropine
Reversibly blocks muscarinic receptors (prevents ACh from binding to it.
used as an antidote if someone is exposed to a pharmacological agent that is a muscarinic agonist
tissues most sensitive to atropine are salivary, bronchial and sweat glands
Tissues affected by Atropine
Eye, CV system, respiratory system, GI tract, GU tract, sweat glands, CNS
CNS Effects of Anticholinergics
Atropine has minimal effect or use (doesnt cross BBB)
Scopolamine crosses BBB-causes drowsiness, amnesia, too much can cause toxicity
Antimuscarinics to tx Parkinsons
may be used as adjuncts to tx remor seen in parkinsons–benzotropine
in parkinsons there is an imbalance between dopamine and ACh (too much ACh) so you give something that will block the action of the ACh
Antimuscarinics to tx Motion Sickness
Scopolamine–>used to tx or prevent motion sickness. Injection, oral, or transdermal patch (lipophilicty so can be absorbed through the skin)
Effects of Antimuscarinics on the Eye
block cholinergic stimulation of pupillary constrictor muscle=pupillary dilation (mydriasis)
Prevent contraction of ciliary muscle, resulting in cycloplegia–> loss of accomidation (prevents focusing on near objects)
reduces lacrimal secretion=dry eyes
can dangerously worsen narrow angle glaucome due to lack of outflow of aqueous humor (causes high IOP)
Effects of Antimuscarinics on Cardiovascular System–low Dose (.5mg)
blocks M1 receptors only
will see bradycardia, ACh will still be bindign to M3 receptors on sinus node
Effects of Antimuscarinics on Cardiovascular System–Medium Dose (1-5mg)
Blocks M2 receptors in SA and AV node
(M2 usually slows heart rate) so blocking M2=tachycardia because of vagal slowing
Effects of Antimuscarinics on Cardiovascular System–Toxic Dose (greater than 10mg)
can cause intraventricular conduction block–inhibits electrical pulse generation in pacemaker nodes
Therapeutic uses of Antimuscarinics in CV Disorders
In acute MI–>can be used in pt’s that have bradycardia after MI, can give median dose to increase HR and C/O
Effects of Anticholinergics on Respiratory System
bronchodilation and reduce/dry up secretions
ex: Ipratropium (atrovent, spiriva)
atropine and scopolamine useful to dry upper and lower respiratory secretions prior to surgery or mechanically vented pt’s
Affects of Antimuscarinics on GI Tract
reduces GI smooth muscle motility, prolongs gastric emptying time and slowing intestinal transit time, reduces GI secretions
Antimuscarinic agents reduce salivary agents –>dry mouth (xerostomia)
Therapeutic uses of Antimuscurinics in GI Disorders
tx diarrhea (reducing GI secretions), combined with lomotil to slow down gut motility
Effects of Antimuscarinics on GU
Cause relaxation of smooth muscles in ureter and bladder (detruser muscle)–reduces voiding (runiary retention)
contraindicated in people who have BPH
Theraputic uses of Antimuscarinics in Urinary Disorders
rx urinary tract spasm associated with inflammation, surgery or neurologic conditions
Oxybutinin (Ditropan)-> used to tx urinary incontinence–> targets M3 receptor
trospium
darifenacin
solifenacin
tolterodine
Therapy for Muscarinic Toxicity
Atropine
atropine effective for central and peripheral symptoms from potent cholinomimetics (organophosphates)
pralidoxime-recycles aAChE–> allows for more breakdown of ACh to help reduce cholinergic activity
Effects of Anticholinergics on Sweat Glands
tx hyperhidrosis, especially effective on eccrine glands
Ex: glycopyrrolate (Robinul)
Anticholinergic Adverse Effects
dry mouth, mydriasis, tachycardia, hot, flushed skin, agitation, urinary retention, visual changes, constipation
Contraindicated use of Anticholinergics
glaucoma (anticholinergics will cause angle closure preventing outflow of aqueous humor
men with BPH
pt’s with gastric ulcers (because of slwoed gastric emptying will make it worse)
Presynaptic Inhibition of Cholinergic Action
clostridium botulinum
targets presynaptic proteins that block the release of ACh–>blocks release of ACh=paralysis of muscles=no more wrinkles
Ganglionic Blocking Agents
Tetraethylammonium (TEA)
Hexamethonium (C6)
Mecamylamine
Trimethaphan
block all autonomic outflow by by blocking ACh at nicotinic receptors of parasympothetic and sympathetic ganglia
Effects of Ganglionic blockers on CNS
sedation, tremor, choreiform movements, mental aberrations
Effects of Ganglionic blockers on Eye
cycloplegia, loss of accommodation, moderate dilation of pupil
Effects of Ganglionic Blockers on CV system
tachycardia
Effects of Ganglionic Blockers in GI tract
decreased secretions, decreased motility
Neuromuscular Blockers
block neuromuscular transmission between motor end plate and nicotinic receptors in skeletal muscle
Two Groups of Meruomuscular Blockers
Nondepolarizing (antagonists)
Depolarizing (agonists)
Nondepolarizing Neuromuscular Blockers
block ACh from binding to nicotinic receptors=prevents depolarization, inhibits contraction=relaxed paralyzed muscle
bind in competitive fashion (nondepolarizing blockers bind to nicotinic receptors)
can be overcome with AChE Inhibitors
Use of Nondepolarizing Neuromuscular Blockers
used in surgery to produce muscular paralysis
Ex: tubocurarine, mivacurium, atracurium, doxacurium, pancuronium, cistracurium, vecuroium, rocuronium
Depolarizing Neuromuscular Blockers
Succinylcholine–super agonist
bind to nicotinic receptors on skeletal muscle acts like ACh–> provides constant stimulation of receptor= resistant to further depolariztion and paralysis results (muscles are overstimulated and dont get a chance to depolarize again)
Therapeutic Uses of Depolarizing Neruomuscular Blockers
facilitate intubation, during electroshock therapy
