Cholinergics Flashcards
1
Q
Acetylcholine MOA
A
Direct-acting cholinomimetic
2
Q
Bethanechol MOA
A
Direct-acting cholinomimetic
3
Q
Carbachol MOA
A
Direct-acting cholinomimetic
4
Q
Methacholine MOA
A
Direct-acting cholinomimetic
5
Q
Cevimeline MOA
A
Direct-acting cholinomimetic
6
Q
Pilocarpine MOA
A
Direct-acting cholinomimetic
7
Q
Varenicline MOA and generic name
A
Chantix, Direct-acting cholinomimetic
8
Q
Ambenonium MOA
A
Cholinesterase inhibitor
9
Q
Donepezil MOA
A
Cholinesterase inhibitor
10
Q
Echothiophate MOA
A
Cholinesterase inhibitor
11
Q
Edrophonium MOA
A
Cholinesterase inhibitor
12
Q
Galantamine MOA
A
Cholinesterase inhibitor
13
Q
Neostigmine MOA
A
Cholinesterase inhibitor
14
Q
Physostigmine MOA
A
Cholinesterase inhibitor
15
Q
Pyridostigmine MOA
A
Cholinesterase inhibitor
16
Q
Rivastigmine MOA
A
Cholinesterase inhibitor
17
Q
Tacrine MOA
A
Cholinesterase inhibitor
18
Q
Pralidoxime MOA
A
Cholinesterase regenerator
19
Q
Scopolamine MOA and clinical use
A
antimuscarinic, motion sickness and ophthalmology
20
Q
Atropine MOA and clinical use
A
antimuscarinic, GI disorders and ophthalmology, cholinergic poisoning
21
Q
Dicyclomine MOA and clinical use
A
antimuscarinic, GI disorders
22
Q
Glycopyrrolate MOA and clinical use
A
antimuscarinic, GI disorders
23
Q
Hyoscyamine MOA and clinical use
A
antimuscarinic, GI disorders
24
Q
Cyclopentolate MOA and clinical use
A
antimuscarinic, ophthalmology
25
Homatropine MOA and clinical use
antimuscarinic, ophthalmology
26
Tropicamide MOA and clinical use
antimuscarinic, ophthalmology
27
Ipratropium MOA and clinical use
antimuscarinic, resp disorders
28
Tiotropium MOA and clinical use
antimuscarinic, resp disorders
29
Darifenacin MOA and clinical use
antimuscarinic, urinary disorders
30
Fesoterodine MOA and clinical use
antimuscarinic, urinary disorders
31
Oxybutynin MOA and clinical use
antimuscarinic, urinary disorders
32
Solifenacin MOA and clinical use
antimuscarinic, urinary disorders
33
Tolterodine MOA and clinical use
antimuscarinic, urinary disorders
34
Trospium MOA and clinical use
antimuscarinic, urinary disorders
35
Benztropine MOA and clinical use
antimuscarinic, movement disorders
36
Biperiden MOA and clinical use
antimuscarinic, movement disorders
37
Orphenadrine MOA and clinical use
antimuscarinic, movement disorders
38
Procyclidine MOA and clinical use
antimuscarinic, movement disorders
39
Trihexyphenidyl MOA and clinical use
antimuscarinic, movement disorders
40
Mecamylamine MOA
ganglion blockers
41
MOA of Ach mimetics
mimic actions of ACh on nicotinic and muscarinic acetylcholine receptors
42
M1 receptor location and mechanism
nerves, GPCR - Gq
43
M2 receptor location and mechanism
heart, nerves, smooth muscle; GPCR - Gi
44
M3 receptor location and mechanism
glands, smooth muscle, endothelium; GPCR - Gq
45
M4 receptor location and mechanism
CNS, GPCR - Gi
46
M5 receptor location and mechanism
CNS, GPCR - Gq
47
Nm receptor location and mechanism
skeletal muscle, NMJ; pentamer - Na, K depolarizing ion channel
48
Nn receptor location and mechanism
Postganglionic cell body, dendrites, CNS; alpha and beta, depolarizing ion channel
49
Effects of direct-acting cholinergic agonists on skeletal muscle
nAChRs will cause muscle contraction, prolonged agonist will cause flaccid paralysis
50
Effects of direct-acting cholinergic agonists on parasympathetics
miosis, negative inotropy and chronotropy, dilation of vessels, bronchoconstriction, increased GI motility, detrusor contraction, secretion from glands increases
51
Effects of direct-acting cholinergics on eye
contraction of iris and ciliary muscle, increasing aqueous humor outflow
52
Effects of direct-acting cholinergics on CV system
reduce PVR and changes heart rate, endothelium-derived relaxing factor is released and relaxes smooth muscle
53
Effects of direct-acting cholinergics on GI and GU
increase in glandular secretions, smooth muscle contraction and smooth muscle relaxation
54
Effects of direct-acting cholinergics on CNS
moderate doses cause an increase in cognitive function, higher concentrations can cause tremors and analgesia
55
Effects of direct-acting cholinergics on PNS
activation of autonomic ganglia, sympathomimetic on CV system and parasympathomimetic on GI/GU
56
Clinical uses of direct-acting cholinergic agonists
Glaucoma, esotropia, GI/GU disorders
57
Direct-acting cholinergic agonists in glaucoma
contraction of ciliary body, facilitating aqueous humor outflow
58
Direct-acting cholinergic agonists in GI/GU disorders
Bethanechol used for postoperative ileus, megacolon, urinary retention; pilocarpine and cevimeline increase salivary secretion
59
Toxicity of muscarinic direct-acting choliniomimetics
nausea, vomiting, diarrhea, urinary urgency, salivation, sweating, bronchoconstriction
60
Major contraindications of mAChR agonists
asthma, hyperthyroidism, coronary insufficiency, acid-peptic disease
61
Acute toxicity of nicotinic stimulants
CNS stimulation, NMJ depolarization leading to resp paralysis, hypertension, cardiac arrhythmias
62
Chronic toxicity of nicotinic stimulants
increased risk of vascular disease, sudden coronary death, ulcer recurrences
63
Acetylcholine clinical use
causes miosis
64
Methacholine clinical use
bronchial airway hyperreactivity
65
Bethanechol clinical use
urinary retention and heartburn
66
Carbachol clinical use
glaucoma, produce miosis during surgery
67
Cevimeline clinical use
xerostomia in pts with Sjogrens
68
Pilocarpine clinical use
xerostomia, miosis during ophthalmic procedures, glaucoma
69
Varenicline clinical use
smoking cessation
70
Varenicline intrinsic activity
partial agonist that binds to a4B2 nicotinic receptors
71
Varenicline causes the release of what NT?
dopamine - stimulating reward pathway
72
AE of varenicline
neuropsych sxs such as agitation, depression, suicide ideation
73
Chemical subgroups of AChE inhibitors
alcohols and carbamic acid esters, which reversibly bind to AChE; organophosphates, which irreversibly bind to AChE
74
MOA of AChE Inhibitors
inhibition of AChE, resulting in ACh accumulation throughout the body and activation of nAChRs and mAChRs
75
Duration of action of AChE Inhibitors
alcohols and carbamic acid esters - short duration of action due to noncovalent bonds; organophosphates - very long duration, forms a very stable bond
76
Organ systems effected by AChE inhibitors
stimulate autonomic effector organs, stimulate CNS, depression after stimulation of CNS
77
Effects of AChE inhibitors on CV system
bradycardia, decrease in cardiac output, modest increase in BP
78
Therapeutic uses of AChE inhibitors
diseases of eye, GI and GU disorders, NMJ, heart, and Alzheimer's
79
AChE toxicity
cutaneous vasodilation, anhidrosis, anhydrotic hyperthermia, nonreactive mydriasis, delirium, hallucination
80
Common antidote for AChE Inhibitors
physostigmine
81
AChE Inhibitor interaction with succinylcholine
enhance phase 1 block, antagonize phase 2 block
82
AChE inhibitor interaction with nondepolarizing NMBA
diminish neuromuscular blockade
83
AChE inhibitor interaction with cholinergic agonists
enhance effects of cholinergic agnoists
84
AChE inhibitor interaction with B-blockers
enhance bradycardic effects
85
AChE inhibitor interaction with systemic corticosteroids
enhance muscle weakness
86
Acute intoxication of AChE inhibitors
miosis, salivation, sweating, bronchial constriction, vomiting, diarrhea; CNS involvement may follow rapidly
87
Antidote for AChE Inhibitor poisoning
atropine, cholinesterase regenerator
88
Cholinesterase regenerator MOA
regenerate active enzyme from organophosphorus-cholinesterase complex via removal of phosphorous group
89
Prophylactic agent for AChE inhibitor
pyridostigmine
90
Pyridostigmine side effects
stomach cramps, diarrhea, nausea, frequent urination, HA, dizziness, SOB, peptic ulcer, blurred vision, watery eyes
91
MOA of mAChR blockers
parasympatholytic, block effects of PS autonomic discharge
92
Clinical use of tertiary amines - mAChR-blockers
eye or CNS
93
Clinical use of quaternary amines - mAChR-blockers
peripheral nervous system
94
Half life and excretion of atropine
2 hours; 60% excreted in urine, 40% eliminated by phase I and II reactions
95
Intrinsic activity of atropine
reversible antagonist
96
Tissues most sensitive to atropine
salivary, bronchial, sweat glands
97
mAChR blockers on CNS
longer lasting sedative effect, can reduce tremor associated with Parkinson's disease, prevents motion sickness
98
mAChR blockers on eye
block papillary constrictor muscle resulting in dilation, weaken contraction of ciliary muscle which prevents accommodation, and reduces lacrimal secretion
99
mAChR blockers on CV system
tachycardia may occur, no significant changes
100
mAChR blockers on respiratory
bronchodilation and reduced secretion
101
mAChR blockers on GI
decrease salivary secretion, other GI secretions are most unaffected, gastric emptying is prolonged, smooth muscle relaxation
102
mAChR blockers on GU
relax smooth m. of ureters and bladder to slow voiding
103
mAChR blockers on sweat glands
suppression of thermoregulatory sweating, inhibits sympathetic cholinergic nerve fibers
104
Cholinergic antagonists for parkinson disease
reduce tremor, benzotropine and trihexyphenidyl
105
Cholinergic antagonists for motion sickness
vestibular disorders, scopolamine
106
Cholinergic antagonists for anesthesia
atropine blocks vagal reflexes
107
Cholinergic antagonists for ophthalmologic disorders
retina examination facilitated by mydriasis
108
Cholinergic antagonists for respiratory disorders
ipratropium used as first-line therapy, tiotropium may also be used
109
Cholinergic antagonists in CV disorders
atropine used for symptomatic bradycardia and hyperactive carotid sinus reflexes
110
Cholinergic antagonists in GI disorders
travelers diarrhea, conditions of hypermotility
111
Cholinergic antagonists in urinary disorders
relief of urinary urgency; generally will be selective for M3 receptor
112
cholinergic poisoning antidote
pralidoxime
113
AE of mAChR antagonists
block of parasympathetic function, hyperthermic effects
114
Contraindication of mAChR antagonists
glaucoma, men with prostatic hyperplasia, acid-peptic diseases (can slow gastric emptying)
115
Pirenzepine selectivity and MOA
M1, inhibits gastric secretion by acting at the ganaglia
116
Chemistry of ganglion-blocking drugs
synthetic amines
117
MOA Ganglion-blocking drugs
block action of ACh and similar agonists at nAChRs of both parasympathetic and sympathetic autonomic ganglia, block autonomic outflow
118
Nerve effects of ganglion-blocking drugs
enhance sympathetic tone, sedation, tremor, choreiform movements, mental aberrations
119
Eye effects of ganglion-blocking drugs
cycloplegia with loss of accommodation, moderate dilation of pupil
120
CV system effects of ganglion blocking drugs
decrease in vascular tone, decrease in BP, diminished contractility, moderate tachycardia
121
GI effect of ganglion blocking drugs
reduced secretion and inhibited motility
122
GU effect of ganglion blocking drugs
urination retention or hesitancy, erection may be prevented
123
Clinical applications of ganglion blocking drugs
may be used for hypertension, but patients are not typically willing to use them due to toxicity
