Cholinergic Flashcards

1
Q

Choline transporter into neuron terminal

A

Na-Dependent membrane choline receptor (CHT)

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2
Q

Potent CHT inhibitor

A

hemicholiniums

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3
Q

Enzyme that synthesizes ACh from acetyl CoA and choline

A

choline acetyltransferase (ChAT)

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4
Q

ACh transport vesicle

A

Vesicle-associated transporter (VAT)

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5
Q

Inhibitor of VAT

A

vesamicol

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6
Q

What can be stored inside VATs

A

ACh, peptides, ATP, proteoglycan

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7
Q

v-SNARE proteins on vesicles

A

synaptobrevin

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8
Q

t-SNARE proteins on neuronal cell membrane

A

syntaxin, SNAP-25

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9
Q

ACh release is dependent on

A

Calcium

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10
Q

ACh release into synaptic cleft inhibited by

A

Botulinum toxin

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11
Q

Primary terminator of ACh

A

Acetylcholinesterase

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12
Q

Muscarinic receptor signaling type

A

G-protein coupled

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13
Q

Nicotinic receptor signaling type

A

Na channels (5 subunits: 2a, B, y, d)

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14
Q

M1, M3 G protein

A

Gq

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15
Q

M2 G protein

A

Gi

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16
Q

M3 activation of papillary sphincter

A

Contraction - miosis, open Canal of Schlemm (decrease intraocular pressure)

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17
Q

M3 activation of ciliary muscle

A

Contraction - accommodation for near vision

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18
Q

M2 activation of SA/AV node

A

Decreased HR, decreased velocity, decreased ventricular contraction

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19
Q

M3 activation of bronchioles

A

Contraction - bronchospasm

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20
Q

M3 activation of glands

A

Increased secretions

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21
Q

M3 activation of stomach

A

motility, cramps

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22
Q

M3 activation of intestines

A

contraction - diarrhea, involuntary defecation

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23
Q

M3 activation of bladder

A

detrusor contraction, sphincter relaxation, voiding, incontinence

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24
Q

M3 activation of blood vessel endothelium

A

dilation

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25
Q

What receptors are found ECL cells

A

M1

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26
Q

What receptors are found on parietal cells

A

M3

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27
Q

Contraindications for treatment with cholinomimetic drugs

A

peptic ulcers, GI tract disorders, asthma

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28
Q

Why does ACh have very limited clinical use

A

Must be administered intravenously due to very rapid destruction by AChE

29
Q

Receptor type for ACh

A

nicotinic/muscarinic

30
Q

Effects of ACh

A
short lasting miosis
vasodilation, decreased TPR, reflex tachycardia
bronchial constriction/secretion
Saliva/sweat/tears
bladder constriction
31
Q

Bronchiolar hypersensitivity diagnosis

A

Inhalation of Metacholine causes bronchoconstriction at low doses

32
Q

Belladonna alkaloid poisoning diagnosis

A

subcutaneous dose of Metacholine causes sign/symptoms of muscarinic cholinoceptor activation
No response in poisoned individual

33
Q

Receptor type for Carbachol

A

nicotinic/muscarinic

34
Q

Therapeutic uses for Carbachol

A

glaucoma treatment - decrease intraocular pressure

35
Q

High doses of carbachol cause

A

Cardiac arrest

36
Q

Receptor type for Bethanechol

A

primarily M3

37
Q

Effects of Bethanechol

A

GU: increased detrusor tone
GI: increased motility/secretion

38
Q

Muscarine poisoning symptoms

A

increased saliva/sweat/tears within minutes
Larger doses cause abdominal pain, nausea, diarrhea, blurred vision, dyspnea
Symptoms subside in 2 hours

39
Q

Effects of Pilocarpine

A

Contracts iris sphincter muscle - miosis
Frees entrance to canal of Schlemm (N-A glaucoma)
Enhances tone of trabecular network (W-A glaucoma)
Contracts ciliary muscle - accommodation/loss of far vision

40
Q

Clinical uses for pilocarpine

A

glaucoma and xerostomia

Pilocarpine tests to diagnose parasympathetic dysfunction

41
Q

Direct acting cholinomimetics

A
ACh
Metacholine
Bethanechol
Carbachol
Muscarine
Pilocarpine
Nicotine
42
Q

Nicotine action on Nm receptors

A

Skeletal muscle contraction
Fasciculations
Depolarizing blockade

43
Q

Nicotine action on Nn receptors

A

Cardiac: increase HR via stimulation of renal medulla (E/NE)
Vascular: peripheral vasoconstriction
GI: increase motility/secretion
Carotid bodies: increased respiratory rate
Medullary emetic chemoreceptors: nausea/vomiting

44
Q

Edrophonium and MG

A

Improvement of MG symptoms after administration of edrophonium; negative test indicates cholinergic crisis

45
Q

AChE inhibitors as treatment for MG

A

Pyridostigmine and neostigmine - quarternary amines

46
Q

Treatment for Paralytic Ileus and Urinary Retention

A

Neostigmine - used to treat abdominal distension, atony of detrusor

47
Q

Contraindication for neostigmine

A

urinary bladder obstruction

48
Q

Treatment for Alzheimer’s

A

Tacrine and Donepezil

49
Q

AChE inhibitor intoxication symptoms

A
DUMBBELSS
Diarrhea
Urination
Miosis
Bradycardia
Bronchoconstriction
Excitation of CNS
Lacrimation
Sweat
Saliva
50
Q

AChE inhibitor intoxication treatment

A

Atropine

51
Q

Atropine relieves

A

Secretions
Bronchoconstriction
Bradycardia
CNS excitation

52
Q

AChE reactivators

A

Pralidoxime (2-PAM)

Does not work with pyridistigmine and neostigmine

53
Q

Muscarinic antagonists

A

Atropine
Ipratropium
Benztropine

54
Q

Effects of Atropine

A
Peripheral vasoconstriction
Mild vagal stimulation
Decreased secretion
Mydriasis/cycloplegia
Hyperthermia
Tachycardia
Sedation
Urinary Retention
Hallucinations
55
Q

Clinical Uses of Atropine

A

Antispasmodic, antisecretory, AChE inhibitor overdose, antidiarrheal, ophthalmology, prevent vagal reaction

56
Q

Treatment of Atropine Poisoning

A

Physostigmine

57
Q

Effects of Ipratropium

A

Decreases bronchoconstriction

Decreases bronchosecretions

58
Q

Clinical uses of Ipratropium

A

First line therapy for chronic obstructive lung disease

Second line therapy for asthma

59
Q

Effects of Benztropine

A

re-establish dopaminergic-cholinergic balance in pts with Parkinson’s
Decrease GU/GI secretions, motility and increase HR

60
Q

Ganglionic blocking agents

A

Hexamethonium and mecamylamine

61
Q

Effects of ganglionic blocking agents

A
Arterioles: vasodilation, hypotension
Veins: dilation, decreased VR, decreased CO
Heart: Tachycardia
Iris: mydriasis
Ciliary muscle: cycloplegia
GI: decreased tone/motility - constipation
Bladder: urinary retention
Salivary glands: xerostomia
Sweat glands: anhidrosis
62
Q

Non-depolarizing blocking agents action

A

prevent channel opening

63
Q

Depolarizing blocking agents action

A

prevent channel closing

64
Q

Non-depolarizing blocker

A

D-tubocurarine

65
Q

Depolarizing blocker

A

succinylcholine

66
Q

Phase 1 blockade

A

binding of depolarizing blocker to Nm receptor causes persistent depolarization - paralysis
Augmented by AChE inhibitors

67
Q

Phase 2 blockade

A

following long paralysis, endplate repolarizes but next depolarization is difficult due to channel desensitization

68
Q

Clinical uses of NM blockers

A

decrease neuromuscular transmission during anesthesia
Tracheal intubation
Control of ventilation
Treatment of convulsions

69
Q

Side effects of NM blockers

A
CV: hypotension (systemic histamine)
Hyper-K: pts with burns, nerve damage, NM disease etc respond to blockers by releasing K into blood - cardiac arrest
Intraocular pressure increase
Increased intragastric pressure
Myalgia