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cholinergic antagonist Flashcards

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1
Q

anticholinergics bind to the receptor and disrupt acetylcholine bind, so it is considered a ____________

A

competitive antagonist

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2
Q

antimuscarinic agents (atropine ) effect of muscarinic receptor blockade

A

Competitive antagonism at the muscarinic receptor (M1, M2 and M3)-mediated actions of acetylcholine on autonomic effectors innervated by postganglionic cholinergic nerves, as well as on smooth muscles that lack cholinergic innervation

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3
Q

antimuscarinic agents (atropine ) effect on ganglia

A

These agents have little effect on the actions of acetylcholine at the nicotinic receptor. E.g., autonomic ganglia (primarily involves ACh binding to nicotinic receptors

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4
Q

antimuscarinic agents (atropine ) effect on CNS

A

-Widespread distribution of muscarinic receptors throughout the brain
-Therapeutic doses are attributable to their central muscarinic blockade
-atropine can produce partial block (M1) only at relatively high doses

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5
Q

_____ is the oldest and most well known antimuscarinic agent that is an antagonist at M1, M2, and M3 receptors

A

atropine

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6
Q

these agents are competitive antagonists for muscarinic receptors (M1, M2, and M3) ……..

A

smooth muscle
cardiac muscle
exocrine glands

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7
Q

mechanisms of antimuscarinics agents

A

Competitive and reversible inhibition of muscarinic
receptor activation by preventing the binding of acetylcholine

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8
Q

two general classes of antimuscarinic

A

-tertiary amines: atropine (mainly used in ocular and CNS applications)
-quaternary amines: anisotropine (mainly used in GI tract and peripheral applications)

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9
Q

tertiary amines

A

-good access to the CNS
-belladonna alkaloids (long acting)
-tertiary amines derivatives (short acting)
-tertiary amines derivatives (antiparkinson use)

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10
Q

belladona alkaloids

A

atropine
scopolamine

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11
Q

tertiary amine derivatives (short acting)

A

homatropine
tropicaminde

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12
Q

tertiary amine derivatives (antiparkinson use)

A

benztropine
trihexyphenidyl

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13
Q

quaternary amines

A

-derivatives of belladonna alkaloids
-ipratropium
-tiotropium

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14
Q

long lasting tertiary amines

A

-M 1 /M 2 /M 3 non-selective
-Treat GI/urinary conditions, Motion sickness.
-Tertiary compounds therefore can affect the CNS
scopolamine has higher CNS penetration; induces greater drowsiness (low doses) or hallucinations (high doses).

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15
Q

action of scopolamine (maldemar)

A

antimuscarinic with relatively more CNS action than atropine (highly lipophilic)

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16
Q

clinical use of scopolamine (maldemar)

A

effective treatment for motion sickness (oral or transdermal administration)

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17
Q

side effects of scopolamine (maldemar)

A

dry mouth
blurred vision
sedation
high dose: confusion and psychosis

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18
Q

short acting tertiary amines

A

-homatropine and tropicamine
-used in optical applications due to short duration of action cycloplegia and mydriasis
-homatropine is less toxic; tropicamide has a shorter duration of action

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19
Q

tertiary amines used for parkinsons disease

A

-benstropine
-have sedative activity
-used as an adjunct therapy with L-DOPA in PD patients (to achieve better balance between dopaminergic and cholinergic neurotransmission)
-Similar potency to atropine

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20
Q

quaternary amines for COPD

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A

atropine and ipratropium
-longer acting analog: tiotropium

21
Q

action of ipratropium

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A

Antimuscarinic with receptor activity similar to atropine. M 3 antagonist blocks ACh-mediated constriction and open the airways

22
Q

clinical use of ipratropium

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A

-Less effective as a monotherapy, but enhances the therapeutic effect of β-adrenergic agonists in COPD.
-COMBIVENT or DUONEB (trade name) – combination of ipratropium and albuterol effective in treating COPD

23
Q

problems of ipratropium

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A

-few because of poor absorption
-toxic dose may cause hypotension (ganglionic blockade) and muscle weakness (neuromuscular blockade)

24
Q

Quaternary amines for GI disorders

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A

-glycopyrrolate and propantheline bromide
-used to treat gastric disorders (GI spasms, peptic ulcers)
-glycopyrrolate: pre-op to reduce secretions (charged N makes crossing the gut difficult)

25
antimuscarinics for overactive bladder (OAB)
tolterodine (detrol) -newer M3 selective muscarinic antagonists (Fenacin) used to treat OAB -advantages: lower incidence of constipation and confusion -beta 3 receptor agonist (mirabegron)
26
action of tolerodine
no apparent selectivity for different muscarinic receptor subtypes; however therapeutically seems to act somewhat selectively on M 3 receptor
27
clinical use of tolterodine
overactive bladder
28
problems of tolterodine
Still causes typical anticholinergic effects, but significantly lower than with previous antimuscarinic drugs
29
neuromuscular blocking drugs
look like ACh
30
blocking the nicotinic receptor
-non depolarizing blockage ("normal" antagonist) tubocurarine -depolarizing blockage (first activates, then blocks) succinylcholine
31
effects nicotine on muscles: stimulation
-The normal operation of nicotinic receptors is the rapid degradation of synaptically released acetylcholine -this allows the neuronal membrane or muscle endplate to repolarize and fast Na+ channels (responsible AP) to "reset" -The next ACh release causes another depolarization which triggers the opening of the rested Na+ channel and AP
32
effects nicotine on muscles: desensitization
-nicotinic receptors are specifically adapted to the transient nature of acetylcholine as a neurotransmitter
33
non-depolarizing neuromuscular blocker
tubocurarine
34
action of tubocurarine
nicotinic receptor competitive antagonist producing non-depolarizing blockade
35
clinical use of tubocurarine
skeletal muscle relaxation during anesthesia- particularly useful for intubation
36
problems of tubocurarine
minor
37
depolarizing neuromuscular blocker
succinylcholine (SUX)
38
action of succinylcholine
-Binds to nicotinic acetylcholine receptor -Agonist nicotinic receptor, Initial depolarization (allows ion flow) -Persistent depolarization makes the muscle fiber resistant to further stimulation by Ach (by preventing the “resetting” of voltage-gated sodium channels) -Metabolized to choline by plasma Butyrylcholinesterase -Slower than acetylcholinesterase -Choline increase BP -Muscle Fasciculation precedes paralysis -Arm, neck, leg then respiratory muscles Rapid onset (30-60 sec), short duration (5-10 min)
39
clinical use of succinylcholine
-Skeletal muscle relaxation during anesthesia – particularly useful for intubation -Also used for electro-convulsant therapy
40
problem of succinylcholine
* Muscle soreness; Avoid in hyperkalemia; cause of cardiac arrest * Malignant hyperthermia * prolonged paralysis can result in people with atypical plasma cholinesterases
41
indirect acting: inhibition of ACh release
botulinum toxin
42
action of botulinum toxin
inhibit release of acetylcholine
43
clinical use of botulinum toxin
Dystonias (uncontollred muscle spasms), cerebral palsy, spasm of ocular muscles, anal fissure, hyperhidrosis (excessive sweating)
44
problems of botulinum toxin
spread from injection site
45
ganglionic nicotinic receptor antagonist
hexamethinium
46
action of hexamethonium
Antagonist at nicotinic receptors in autonomic ganglia thus blocking all SNS and PSNS activity
47
clinical use of hexamethonium
-originally developed to treat hypertension but not used clinically due to adverse effects -Good for teaching students about the ANS
48
problems of hexamethonium
Blocking basal tone of SNS and PSNS resulting in: * Blood vessels (SNS): hypotension * Sweat glands (SNS): decreased perspiration * Other glands (PSNS): dry mouth, decreased secretions * Heart rate (PSNS): tachycardia (usually but sometimes if SNS active, will see bradycardia) * Eye (PSNS): pupillary dilation and blurred vision * Gut (PSNS): decreased tone and motility, constipation * Bladder (PSNS): urinary retention

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