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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
What receptors are found ECL cells
M1
26
What receptors are found on parietal cells
M3
27
Contraindications for treatment with cholinomimetic drugs
peptic ulcers, GI tract disorders, asthma
28
Why does ACh have very limited clinical use
Must be administered intravenously due to very rapid destruction by AChE
29
Receptor type for ACh
nicotinic/muscarinic
30
Effects of ACh
``` short lasting miosis vasodilation, decreased TPR, reflex tachycardia bronchial constriction/secretion Saliva/sweat/tears bladder constriction ```
31
Bronchiolar hypersensitivity diagnosis
Inhalation of Metacholine causes bronchoconstriction at low doses
32
Belladonna alkaloid poisoning diagnosis
subcutaneous dose of Metacholine causes sign/symptoms of muscarinic cholinoceptor activation No response in poisoned individual
33
Receptor type for Carbachol
nicotinic/muscarinic
34
Therapeutic uses for Carbachol
glaucoma treatment - decrease intraocular pressure
35
High doses of carbachol cause
Cardiac arrest
36
Receptor type for Bethanechol
primarily M3
37
Effects of Bethanechol
GU: increased detrusor tone GI: increased motility/secretion
38
Muscarine poisoning symptoms
increased saliva/sweat/tears within minutes Larger doses cause abdominal pain, nausea, diarrhea, blurred vision, dyspnea Symptoms subside in 2 hours
39
Effects of Pilocarpine
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
Clinical uses for pilocarpine
glaucoma and xerostomia | Pilocarpine tests to diagnose parasympathetic dysfunction
41
Direct acting cholinomimetics
``` ACh Metacholine Bethanechol Carbachol Muscarine Pilocarpine Nicotine ```
42
Nicotine action on Nm receptors
Skeletal muscle contraction Fasciculations Depolarizing blockade
43
Nicotine action on Nn receptors
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
Edrophonium and MG
Improvement of MG symptoms after administration of edrophonium; negative test indicates cholinergic crisis
45
AChE inhibitors as treatment for MG
Pyridostigmine and neostigmine - quarternary amines
46
Treatment for Paralytic Ileus and Urinary Retention
Neostigmine - used to treat abdominal distension, atony of detrusor
47
Contraindication for neostigmine
urinary bladder obstruction
48
Treatment for Alzheimer's
Tacrine and Donepezil
49
AChE inhibitor intoxication symptoms
``` DUMBBELSS Diarrhea Urination Miosis Bradycardia Bronchoconstriction Excitation of CNS Lacrimation Sweat Saliva ```
50
AChE inhibitor intoxication treatment
Atropine
51
Atropine relieves
Secretions Bronchoconstriction Bradycardia CNS excitation
52
AChE reactivators
Pralidoxime (2-PAM) | Does not work with pyridistigmine and neostigmine
53
Muscarinic antagonists
Atropine Ipratropium Benztropine
54
Effects of Atropine
``` Peripheral vasoconstriction Mild vagal stimulation Decreased secretion Mydriasis/cycloplegia Hyperthermia Tachycardia Sedation Urinary Retention Hallucinations ```
55
Clinical Uses of Atropine
Antispasmodic, antisecretory, AChE inhibitor overdose, antidiarrheal, ophthalmology, prevent vagal reaction
56
Treatment of Atropine Poisoning
Physostigmine
57
Effects of Ipratropium
Decreases bronchoconstriction | Decreases bronchosecretions
58
Clinical uses of Ipratropium
First line therapy for chronic obstructive lung disease | Second line therapy for asthma
59
Effects of Benztropine
re-establish dopaminergic-cholinergic balance in pts with Parkinson's Decrease GU/GI secretions, motility and increase HR
60
Ganglionic blocking agents
Hexamethonium and mecamylamine
61
Effects of ganglionic blocking agents
``` 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
Non-depolarizing blocking agents action
prevent channel opening
63
Depolarizing blocking agents action
prevent channel closing
64
Non-depolarizing blocker
D-tubocurarine
65
Depolarizing blocker
succinylcholine
66
Phase 1 blockade
binding of depolarizing blocker to Nm receptor causes persistent depolarization - paralysis Augmented by AChE inhibitors
67
Phase 2 blockade
following long paralysis, endplate repolarizes but next depolarization is difficult due to channel desensitization
68
Clinical uses of NM blockers
decrease neuromuscular transmission during anesthesia Tracheal intubation Control of ventilation Treatment of convulsions
69
Side effects of NM blockers
``` 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 ```

Pharm 1 (6 decks)

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