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Pharmacology > Cholinergics > Flashcards

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
Q

Varenicline: Toxicity/interactions

A

None

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26
Q

Varenicline: Special considerations (4)

A

Suicidal thoughts and aggressive and erratic behavior (need monitoring)
Use extreme caution in psychiatric patients
Contraindicated in pregnancy/lactation
Causes drowsiness

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27
Q

Varenicline: Indications/dose/route

A

1mg PO BID for healthy adults, 0.5mg for those with renal impairment

28
Q

Varenicline: Monitor

A

Neuropsychiatric symptoms

29
Q

What’s the greatest danger in AChEI overdose?

A

Respiratory inundation -> central respiratory arrest

30
Q

AChE mechanism of action

A

Anionic site - binds cation

Esteric site - catalytic, hydrolyzes ester bond

31
Q

Edrophonium: mechanism of action, major clinical use

A

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
Q

Briefly describe the mechanism behind myasthenia gravis.

A

Autoimmune disease - antibodies destroy motor end plates -> impaired neurotransmission

33
Q

Carbamates (class): mechanism of action, two main clinical uses

A

Binds anionic and esteric sites of AChE for hours, until hydrolyzed
Treatment of myasthenia gravis
Reverse paralytic effects of nicotinic antagonists

34
Q

Physostigmine: class, major clinical uses

A

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
Q

Neostigmine: class, major clinical uses

A

Carbamate
Stays in blood (has charge)
Treatment of myasthenia gravis

36
Q

Neostigmine: side effects of over/underdosing for MG, how to distinguish

A

Flaccid paralysis for both

Distinguish with edrophonium challenge (increased strength = low ACh)

37
Q

Organophosphates: mechanism of action

A

Covalently binds esteric site -> phosphorylated enzyme, very very stable (~permanent inhibition)

38
Q

Echothiophate: class, major clinical use

A

Organophosphate

Formerly used to treat narrow angle glaucoma

39
Q

Parathion: class, usage

A

Organophosphate

Extremely toxic insecticide (poorly metabolized)

40
Q

Malathion: class, usage

A

Organophosphate

Mammal-friendly insecticide

41
Q

Sarin, soman: class, usage

A

Organophosphates

Nerve gases

42
Q

How is organophosphate poisoning treated? (3)

A 
Muscarinic blockers (atropine)
Aggressive respiratory support
Antidote: Pralidoxime (2-PAM) - reactivates AChE (CONTRAINDICATED in carbamate poisoning - makes it worse, adds to inhibition)
43
Q

Name the one indirect acting nonspecific anticholinergic drug.

A

Botulinum toxin

44
Q

Which type of muscarinic receptor is in most tissues?

A

M3

45
Q

Name two M specific anticholinergics.

A

Atropine

Scopolamine

46
Q

Name the Nm specific depolarizing cholinolytic agonist.

A

Succinylcholine

47
Q

Name five nondepolarizing Nm specific antagonists.

A

BENZYLISOQUINOLINES
d-Tubocurarin
Cisatracurium

AMINOSTEROID
Pancuronium
Vercuronium
Rocuronium

48
Q

Name one Nn specific anticholinergic.

A

Trimethaphan

49
Q

Atropine: mechanism of action, toxicity (6)

A

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
Q

M receptor blockers: determinants of selectivity and organ specificity

A

Uncharged = peripheral and CNS effects
Charged = peripheral effects
Unique tissue response for each drug, poorly understood

51
Q

How is atropine toxicity treated?

A

Adults: restraints, catheterization (not v. deadly)
Peds: can be deadly, use ice baths for fever

52
Q

Atropine: List three clinically useful effects and what syndromes they help treat.

A

Bronchodilation - asthma, COPD
Constipation - IBS
Tachycardia - bradycardia

53
Q

Scopolamine: mechanism of action, primary clinical use, two side effects

A

Unknown CNS mechanism - reduces motion sickness
Also used to treat vertigo and post-surgical nausea
Side effects: impaired vision, delerium

54
Q

Scopolamine: secondary clinical use

A

Anesthetic adjuvant - induces amnesia via CNS, reduces bronchial secretions

55
Q

List six specific applications for M blockers and what drugs are most useful for each. (* = in red on slides)

A

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
Q

Nm blockers: main clinical use

A

Inhibit skeletal muscle activity during surgery

57
Q

List the differences between depolarizing and non-depolarizing blockers of NMJ.

A

Depolarizing: flaccid paralysis not easily reversed

–*Hyperkalemia is a side effect (from overactivation of muscles

58
Q

Succinylcholine: mechanism of action, main clinical usage

A

Depolarizing Nm blocker with very short half life (destroyed by AChE)
Used for paralysis in short surgical procedures and intubations

59
Q

Succinylcholine: adverse effects (3)

A

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
Q

Succinylcholine: contraindications (4)

A

Family Hx of malignant hyperthermia
Hyperkalemia
Burns, trauma, tissue injury (hyperkalemia)
Heart failure (-> arrhythmias)

61
Q

d-Tubocurarine: mechanism of action, main clinical usage

A

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
Q

What drug can you use to reverse nondepolarizing nicotinic blockers? Depolarizing?

A 
Non-depolarizing = Neostigmine
Depolarizing = TIME (so less useful than non-depolarizing)
63
Q

What determines which non-depolarizing Nm blocker is used for paralysis during surgery?

A

Patient characteristics!

Each agent is cleared in a different way. Consider renal disease, liver disease, plasma ChE deficiency

64
Q

Trimethaphan: mechanism of action, major clinical use

A

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
Q

Botox: mechanism of action, major clinical uses (6)

A

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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