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Neuro II > Kruse - Cholinergic Agonists/Antagonists > Flashcards

Kruse - Cholinergic Agonists/Antagonists Flashcards

1
Q

Cholinesterase hydrolyzes at what rates?

A

ACh > methacholine > carbachol = bethanechol

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2
Q

ACh mimetics act on receptors by:

A
  • Direct acting mAChR and nAChR stimulants

- Indirect cholinesterase inhibitors

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3
Q

Two types of direct acting cholinergic agonists

A
  1. Choline esters

2. Akaloids

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4
Q

Choline ester names

A

ACh, carbachol, bethanechol

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5
Q

Alkaloid names

A

Muscarine, nictoine, policarpine

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6
Q

Choline ester:
Absoprtion -
Distribution -

A

Choline ester:
Absorption - poorly absorbed in CNS (quaternary ammonium groups)
Distribution - poorly distributed in CNS

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7
Q

Choline ester metabolism location

A

Metabolism - hydrolyzed by cholinesterase in GI

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8
Q

choline ester less active when given ___

A

PO

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9
Q

Alkaloid

Absorption -

A

Absorption - well absorbed from most sites (i.e. noctine thru skin)

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10
Q

muscarine (mushroom) ingestion is (toxic or not) and goes to what location

A

Toxic

Enters brain

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11
Q

Alkaloid metabolism

A

Kidney excretion&raquo_space; acidification of urine accelerates clearance

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12
Q

Choline ester = Type of molecule = absorbed well?

Alkaloid = Type of molecule = absorbed well?

A

Choline ester = charged quaternary amine = not well absorbed

Alkaloid = uncharged tertiary amine = well absorbed

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13
Q

M1 location

A

nerves

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14
Q

M2 location

A

HEART, nerves, smooth muscle

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15
Q

M3 location

A

glands, smooth muscle, endothelium

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16
Q

M4 location

A

CNS

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17
Q

M5 location

A

CNS

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18
Q

Nm

A

skeletal muscle NMJ

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19
Q

Nn

A

postG cell body, dendrites, CNS

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20
Q

Gq M recetors

IP3, DAG

A

M1,3,5

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21
Q

Gi M receptors

Inhibit cAMP

A

M2, 4

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22
Q

Type of receptor and its action on skeletal muscle

A

nAChR

muscle contraction

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23
Q

ParaS effect of…

A

decrease/contract everything, except:
Dilation of aa and vv.
Stimulation of bronchial glands
Detrusor contraction; trigone and sphincter relaxation
Sweat, salivary, lacrimal, naspharyngeal secretion

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24
Q

ParaS eye - contraction of relaxation of iris sphincter and ciliary mm?

A

contraction to:

increase aqueous humor&raquo_space; Schlemm&raquo_space; ant chamber drainage

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25
Q

What are all cardiac actions mediated by?

A

M2 mAChR

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26
Q

PS innervation is less in ventricle or atria?

A

ventricles (so less physiological effect when activated)

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27
Q

Muscarinic agonists release what form endothelial cells to relax smooth muscle around blood vessels?

A

Endothelium Derived Relaxing Factor (EDFR)

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28
Q

EDFR is largely ___, which activates ___, and ___cGMP in smooth muscle.
Overall effect of this is: ____

A

NO&raquo_space; activates…
GC&raquo_space;
increases cGMP»
Overall: to relax smooth muscle

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29
Q

Small doses of ACh = ____ effect on CV

Large doses of ACh = ____ effect on CV

A 
small = vasodilation = decrease BP and increased HR
large = bradycardia and decrease AV node conduction + hypOTension
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30
Q

GI:
M__ mACHR required for direct activation of smooth muscle relaxation
M__ mAChR reduces cAMP = reduces relaxation (increased contraction)

A

M2

M3

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31
Q

NO receptor on sphincters

A

M3 mAChR

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32
Q

mAChR or nAChR greater # in:

  1. Brain
  2. SC
A
  1. Brain = mAChR

2. SC = nAChR

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33
Q

inhibitory mAChR role in brain results in

A

tremors, hypothermia, analgesia

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34
Q

Activation of nAChRs is dependent upon what?

A

dose

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35
Q

Nicotine’s effect (via nAChR) in CV system are primarily sympathomimetic or parasympathomimetic?
Effects?

A

sympathomimetic

hypERtension, tachy-bradycardia alternation

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36
Q

nAChR effects in GI/GU tracts are primarily sympathomimetic or parasympathomimetic?
Effects?

A

parasympathomimetc

nausea, vom, diarr, voiding of urine

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37
Q

Major clinical uses of direct acting cholinergic agonists:

A
  1. Eye (glaucoma, accommodative esotropia)

2. GI/GU tract (post-op atony, neurogenic bladder)

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38
Q

Glaucoma -

Muscarinic stimulants cause contraction or relaxation of the ciliary body?

A

Contraction

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39
Q

Glaucoma - muscarinic stimulants are replaced by what direct acting cholinergic agonist?

A

topical beta-blockers and prostaglandin derivatives

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40
Q

Accommodative esotropia looks like what?

A

cross eyed

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41
Q

Accommodative esotropia diagnosed with what direct acting cholinergic agonist?

A

cholinomimetic agonists

42
Q

*Bethanechol is used most widely for:

A
  • post-op ileus
  • congenital megacolon
  • urinary retention
  • esophageal reflux
43
Q

*Bethanechol is what type of direct acting cholinergic agonist?

A

choline ester

44
Q

*Pilocarpine and cervimeline are used to tx what symptoms due to what disease?

A

dry mouth/Sjogren’s

45
Q

Nausea, vom, diarr, salivation, sweat, cutaneous vasodilation - are caused by what?

What is used to block them?

A

Muscarinic stimulant toxicity - Pilocarpine and choline esters

Antimuscarinics block this type of toxicity - i.e. atropine (mACHR antagonist)

46
Q

mushroom on genus Inocybe

A

cause muscarinic poisoning

47
Q

contraindiations of mAChR agonists

A

Asthma
Hyperthyroidism
Coronary insufficiency
Acid-peptic disease

48
Q

Acute toxicity of nicotine

A
  • CNS stimulation - convulsions&raquo_space; coma and respiratory arrest
  • skeletal muscle and End plate depol&raquo_space; RESPIRATORY PARALYSIS, hypERtension, cardiac arrhythmia
49
Q

Treatment for excess muscarinic stimulation from PS ganglia

A

atropine

50
Q

Treatment for excess muscarinic stimulation - CNS stimulation

A

diazepam (parenteral anticonvulsant)

51
Q

Sjogren’s syndrome tx for dry mouth

A

dry mouth - Pilocarpine and cervimeline

52
Q

Varenicline is used for _____.

A ____ type of agonist.

A 
smoking cessastion
partial agonist (alph4-beta2 nAChR)
53
Q

Varenicline’s most common side effect.

A

Nausea

possible depression/suicide

54
Q

Three types of AChE inhibitors.

A

Alcohols
Carbamic Acid Esters (carbamates)
Organophosphates

55
Q

How do you reestablish termination of ACh signaling at NMJ in organosphophate poisoning?

A

regeneration of AChE

56
Q

insecticide, CNS toxicity, lipid soluble, covalent and irreversible

A

organophosphate

57
Q

Duration of action of each AChE inhibitor.

A

Alcohol - weak interaction; 2-10 minutes
Carbamic Acid Ester - 30 minutes (2 step hydrolysis)
Organophosphate - 100s of hours “aging”

58
Q

Absorption of:

Quaternary and charged AChE inhibitors

A

relatively insoluble in lipids/skin/lungs/conjunctive

59
Q

Examples of quaternary and charged AChE inhibitors (insoluble)

A

neostigmine, pyridostigmine, edrophonium, echothiophate, ambenonium

60
Q

Absorption of tertiatry and uncharged AChE inhibitors

A

well absorbed from all sites (including oral)

61
Q

Examples of tertiary and uncharged AChE inhibitors

A

physostigmine, donepezil, tacrine, rivas tigmine, galantamine

62
Q

Absorption of organophosphates

A

Oral = well

Well absorbed from skin, lung, gut, conjunctiva

63
Q

eye, resp tract, GI, GU innervated by:

A

mAChR (paraS)

64
Q

AChR inhibitor effect on CV system (brady, CO, BP)

A

paraS tone dominates&raquo_space; CO decreases

Net: modest brady; decreased CO, moderately increased BP

65
Q

MOA of AChE inhibitors

A

ACh accumulates in body&raquo_space; activate nAChRs and mAChRs

AChE inhibitors stop AChE from breaking down ACh to increase ACh levels = increased nAChR and mAChR effects

66
Q

Reversal of pharacological paralysis:

AChE inhibitors to reverse paralysis induced by anesthesia

A

neostigmine

edrophonium

67
Q

Used to treat paralytic ileus; atony of bladder; congenital megacolon

A

AChE inhibitors

68
Q

AChE inhibitor role in glaucoma

A

reduce intraoccular pressure by stimulating mAChRs of ciliary body to contract&raquo_space; outflow of aqueous humor

69
Q

Alzheimer Disease tx and PD tx

A

tacrine and AChE inhibitors

70
Q

mechanism of anticholinergic intoxication (result-cutaneous vasodilation, anhidrosis, hyperthermia, nonreactive mydriasis, delerium, hallucinations, reduction of urination,)

A

reduced or blocked mAChR stimulation

71
Q

Antidote for anticholinergic intoxication (puts ACh back in)

A

physostigmine

72
Q

AChE inhibitor toxicity route

A

1a. Ingestion Route: GI symptoms&raquo_space;

1b. Percutanous Route: skin&raquo_space; sweat and mm fasciculations

73
Q

AChE inhibitor CNS symtoms (due to lipid soluble)

A

confusion, ataxia, respiratory coma, paralysis, convulsions

74
Q

Tx for cholinergic poisoningmm

A

mAChR antagonist = atropine

cholinesterase regenerator at NMJ (to regenerate AChE_

75
Q

In what situation are cholinesterase reactivators used and name one.

A

pralidoxime
Used to restore response to stimulation at motor nerve (NMJ, nAChR) following a dose of organophosphorus, which blocks transmission.

76
Q

nerve agent poisoning pretreatment (reduces injury)

A

pyridostigmine

77
Q

Where antinicotinic drugs elicit their effects:

A

*NMJ

nAChRs in ganglia

78
Q

mAChR-blocker (parasympatholytic) drug example

A

atropine

79
Q

atropine, tropicamide, benztropine

A

**mAChR-blocking drugs:

tertiary amines for eye and CNS effects

80
Q

ipratropium, glycopyrrolate

A

mAChR-blocking drugs:

quaternary amines; charged; affects periphery

81
Q

What mACHR-blocking drugs affects CNS more - tertiary or quaternary amines?

A

tertiary amines - atropine, tropicamide, benztropine

82
Q
  • Salivary, bronchial, and sweat glands (most or least sensitive to atropine?)
  • Acid secretion by gastric parietal cells (most or least sensitive to atropine)
A

most

least

83
Q

half life of atropine; % excreted in urine

A

2 hours

60% excreted

84
Q

Parkinson tremor is reduced by

A

centrally acting muscarinic compounds

85
Q

Ophthalmologic procedures use antimuscarinic agents to:

A

weaken contraction of ciliary muscles

86
Q

scopolamine’s CNS effects

A

drowsiness and amnesia

87
Q

mAChR-blocker effects on resp system

A

bronchodilation and decerased secretion

88
Q

mAChR-blocker effects on GI tract

A

Decreased salivary secretion

Prolonged gastric emptying time and intestinal transit time

89
Q

What can you use to treat urinary incontinence?

A

mAChR-blocker effects on GU tract - they relax smooth muscle and slow voiding

90
Q

What does atropine do to sweating (symp cholinergic nerve fibers)?

A

sppresses thrermoregulatory sweating

91
Q

Tx for PD

A 
mAChR antagonists (ATROPINE) reduce tremors
Tertiary amines - benzotropine and trihexyphenidyl
92
Q

Tx for motion sickness

A

scopolamine (PO, injection, or transdermal patch)

93
Q

Atropine in anesthesia

A

blocks vagal reflexes

94
Q

Atropine and anesthesia:

atropine or glycopyrrolate paired with neostigmine to…

A

block paraS during reversal of sk m relaxaiton

95
Q

All ganglion-blocking drugs are what type of amine?

A

Synthetic

96
Q

MOA of ganglion-blocking drugs

A

competatively block ACh and similar agonists at nAChRs of both paraS and Symp autonomic ganglia&raquo_space;
block all autonomic outflow

97
Q

what tone dominates the autonomic ns?

A

parasympathetic tone

98
Q

Charged or uncharged can cross BBB?

A

uncharged

99
Q

Mecamylamine - what type of blocker is it?

A

ganglion blocker

100
Q

Mecamylamine - what is it used to tx?

A

HTN

101
Q

Mecamylamine - what type of amine is it and why is it used?

A

tertiary amine

better absorption in GI tract

Neuro II (9 decks)

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