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Cholinergics Flashcards

1
Q

List the two nonspecific direct acting cholinomimetics and their main clinical usage.

A

ACh

Carbachol (both topical for glaucoma)

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2
Q

List the three direct muscarinic cholinergic agonists.

A

Methacholine
Bethanechol
Pilocarpine

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3
Q

List the two direct nicotinic cholinergic agonists.

A

Nicotine

Varenicline (Chantix)

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4
Q

List one short acting cholinesterase inhibitor.

A

Edrophonium

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5
Q

List two intermediate acting cholinesterase inhibitors.

A

CARBAMATES
Neostigmine
Physostigmine

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6
Q

List five long acting cholinesterase inhibitors.

A 
ORGANOPHOSPHATES
Echothiophate
Parathion
Malathion
Sarin
Soman
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7
Q

List one presynaptic-acting cholinergic agonist.

A

Metoclopramide

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8
Q

Where are muscarinic receptors found?

A

Peripherally - cardiac and smooth muscle, glands, nerve terminals, sweat glands

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9
Q

Where are nicotinic receptors found?

A

Centrally, at neuronal (Nn) and neuromuscular junctions (Nm)

Affects both sympathetic and parasympathetic, as well as muscular transmission

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10
Q

What tissues have most access to IV injected ACh? (5, in order)

A

*Endothelial cells (M)
*Para/sympathetic effector tissues (M)
NMJ
Ganglia
CNS

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11
Q

List the symptoms of muscarinic overactivation. (10)

A

**Hypotension - from M type receptors on endothelial cells -> NO -> GC -> vasodilation

Diarrhea (increased gut motility)
Urination (contraction of detrusor muscle)
Miosis (contraction of sphincter in iris)
**Bradycardia (paradoxical - from M on SA node)
Bronchorrhea (increased secretions) and bronchoconstriction (wheezing)
Emesis (uncoordinated GI tone)
Lacrimation
Salivation
Sweating

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12
Q

List the major effects of combined muscarinic and nicotinic activation. (6)

A 
Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis
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13
Q

Why is ACh not a clinically useful drug?

A

Too many side effects, too short of a half life (destroyed by AChE)

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14
Q

Methacholine: mechanism of action, major clinical use

A

Methylated ACh - poorly absorbed

Used as aerosol challenge to diagnose bronchial hyperreactivity (-> bronchoconstriction)

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15
Q

Bethanechol: major clinical use

A

Relieve GI dysmotility syndromes (postsurgical ileus)

Not used anymore

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16
Q

Metoclopramide: mechanism of action, major clinical use

A

Stimulates presynaptic D2 receptors to trigger ACh release

Used to relieve GI dysmotility syndromes (postsurgical ileus)

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17
Q

Pilocarpine: major clinical use

A

Used topically in the eye to relieve glaucoma

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18
Q

What types of receptors are N receptors?

A

Ligand-gated Na/K channels -> depolarization

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19
Q

Nicotine: mechanism of action, major clinical use

A

Receptors in PFC -> elevated mesolimbic dopamine

Promote smoking cessation, suppress signs of nicotine withdrawal

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20
Q

List the symptoms of nicotinic overactivation.

A

Initial activation -> subsequent DEactivation (depolarization-desensitization blockade)
Muscle fasciculations (initial) -> flaccid paralysis (from deactivation, very rapid onset, can be deadly)
–Initially, also get tachycardia, hypertension, cold sweat (sympathetic) and nausea/vomiting/diarrhea, salivation, urinary incontinence (parasympathetic)

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21
Q

Varenicline: Brand name

A

Chantix

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22
Q

Varenicline: Drug class

A

Selective and potent competitive partial agonist of alpha2/beta4 nicotinic receptors

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23
Q

Varenicline: PD (2)

A

CNS mesolimbic dopamine release - prevents low dopamine and cravings
Prevents nicotine from creating dopamine surges -> no chemical reward

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24
Q

Varenicline: PK (3)

A

Well absorbed
Peak 4h, half life 24h
Excreted primarily in urine unchanged

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25
Varenicline: Toxicity/interactions
None
26
Varenicline: Special considerations (4)
Suicidal thoughts and aggressive and erratic behavior (need monitoring) Use extreme caution in psychiatric patients Contraindicated in pregnancy/lactation Causes drowsiness
27
Varenicline: Indications/dose/route
1mg PO BID for healthy adults, 0.5mg for those with renal impairment
28
Varenicline: Monitor
Neuropsychiatric symptoms
29
What's the greatest danger in AChEI overdose?
Respiratory inundation -> central respiratory arrest
30
AChE mechanism of action
Anionic site - binds cation | Esteric site - catalytic, hydrolyzes ester bond
31
Edrophonium: mechanism of action, major clinical use
Binds competitively to cation site of AChE Given IV or IM (v. short lived) Used in diagnosis of myasthenia gravis (-> rapid increase in muscle strength)
32
Briefly describe the mechanism behind myasthenia gravis.
Autoimmune disease - antibodies destroy motor end plates -> impaired neurotransmission
33
Carbamates (class): mechanism of action, two main clinical uses
Binds anionic and esteric sites of AChE for hours, until hydrolyzed Treatment of myasthenia gravis Reverse paralytic effects of nicotinic antagonists
34
Physostigmine: class, major clinical uses
Carbamate - the first one NOT for treatment of myasthenia gravis - crosses BBB and has CNS side effects Can be used to treat CNS signs of muscarinic blockers
35
Neostigmine: class, major clinical uses
Carbamate Stays in blood (has charge) Treatment of myasthenia gravis
36
Neostigmine: side effects of over/underdosing for MG, how to distinguish
Flaccid paralysis for both | Distinguish with edrophonium challenge (increased strength = low ACh)
37
Organophosphates: mechanism of action
Covalently binds esteric site -> phosphorylated enzyme, very very stable (~permanent inhibition)
38
Echothiophate: class, major clinical use
Organophosphate | Formerly used to treat narrow angle glaucoma
39
Parathion: class, usage
Organophosphate | Extremely toxic insecticide (poorly metabolized)
40
Malathion: class, usage
Organophosphate | Mammal-friendly insecticide
41
Sarin, soman: class, usage
Organophosphates | Nerve gases
42
How is organophosphate poisoning treated? (3)
``` Muscarinic blockers (atropine) Aggressive respiratory support Antidote: Pralidoxime (2-PAM) - reactivates AChE (CONTRAINDICATED in carbamate poisoning - makes it worse, adds to inhibition) ```
43
Name the one indirect acting nonspecific anticholinergic drug.
Botulinum toxin
44
Which type of muscarinic receptor is in most tissues?
M3
45
Name two M specific anticholinergics.
Atropine | Scopolamine
46
Name the Nm specific depolarizing cholinolytic agonist.
Succinylcholine
47
Name five nondepolarizing Nm specific antagonists.
BENZYLISOQUINOLINES d-Tubocurarin Cisatracurium AMINOSTEROID Pancuronium Vercuronium Rocuronium
48
Name one Nn specific anticholinergic.
Trimethaphan
49
Atropine: mechanism of action, toxicity (6)
Parasympatholytic via reversible blockade of M receptors Common cause of poisonings (belladonna -> wide pupils) --Mad as a hatter (CNS effects - confusion, delerium) --Blind as a bat (huge pupils, exacerbates glaucoma) --Dry as a bone (inhibition of salivation, sweating, lacrimation, and bronchial secretions) --Hot as a hare (no sweating) - can be life threatening in kids --Red as a beet (unclear mechanism) --Performing the pee-pee dance (blocks detrusor muscle -> urinary retention)
50
M receptor blockers: determinants of selectivity and organ specificity
Uncharged = peripheral and CNS effects Charged = peripheral effects Unique tissue response for each drug, poorly understood
51
How is atropine toxicity treated?
Adults: restraints, catheterization (not v. deadly) Peds: can be deadly, use ice baths for fever
52
Atropine: List three clinically useful effects and what syndromes they help treat.
Bronchodilation - asthma, COPD Constipation - IBS Tachycardia - bradycardia
53
Scopolamine: mechanism of action, primary clinical use, two side effects
Unknown CNS mechanism - reduces motion sickness Also used to treat vertigo and post-surgical nausea Side effects: impaired vision, delerium
54
Scopolamine: secondary clinical use
Anesthetic adjuvant - induces amnesia via CNS, reduces bronchial secretions
55
List six specific applications for M blockers and what drugs are most useful for each. (* = in red on slides)
IBS, diarrhea - dicyclomine Peptic ulcer (former usage) - methscopolamine, pirenzepine, propantheline Bladder spasms (former usage) - oxybutynin, glycopyrrolate *Dilate eyes for retinal exam - tropicamide *Prevention of synechiae (in eye post surgery) - atropine COPD/asthma - aerosol *ipratropium
56
Nm blockers: main clinical use
Inhibit skeletal muscle activity during surgery
57
List the differences between depolarizing and non-depolarizing blockers of NMJ.
Depolarizing: flaccid paralysis not easily reversed | --*Hyperkalemia is a side effect (from overactivation of muscles
58
Succinylcholine: mechanism of action, main clinical usage
Depolarizing Nm blocker with very short half life (destroyed by AChE) Used for paralysis in short surgical procedures and intubations
59
Succinylcholine: adverse effects (3)
Postsurgical pain from fasciculations * Hyperkalemia * Malignant hyperthermia (from drug-drug interaction in pts with MT RyR, esp. with halothane -> muscle rigidity/metabolism, increased temperature)
60
Succinylcholine: contraindications (4)
Family Hx of malignant hyperthermia Hyperkalemia Burns, trauma, tissue injury (hyperkalemia) Heart failure (-> arrhythmias)
61
d-Tubocurarine: mechanism of action, main clinical usage
Nondepolarizing (competitive) Nm blocker, minimal CNS effects (charged) This, and others, should NEVER be given to unanesthetized pts, and pts should wake up before paralysis has been reversed No current clinical usage...
62
What drug can you use to reverse nondepolarizing nicotinic blockers? Depolarizing?
``` Non-depolarizing = Neostigmine Depolarizing = TIME (so less useful than non-depolarizing) ```
63
What determines which non-depolarizing Nm blocker is used for paralysis during surgery?
Patient characteristics! | Each agent is cleared in a different way. Consider renal disease, liver disease, plasma ChE deficiency
64
Trimethaphan: mechanism of action, major clinical use
Non-depolarizing ganglionic blocker (blocks ALL ganglia) Charged -> minimal CNS effects Used for blocking sympathetic ganglia -> hypotension in *hypertensive crises or with *dissecting aortic aneurysms [emergencies] *Given IV, *rapid onset, cleared by liver Bad parasympathetic blocking side effects
65
Botox: mechanism of action, major clinical uses (6)
Interferes with docking of synaptic vesicles full of ACh with synaptic membrane (cleaves SNARE proteins) Used via local injection for wrinkles, axillary hyperhydrosis, strabismus (by paralyzing one eye muscle), blepharospasm (uncontrolled eyelid twitching), spasmodic torticollis, and anal achalasia to heal anal fissures

Pharmacology (10 decks)

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