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Fundamentals 2 > Cholinergics > Flashcards

Cholinergics Flashcards

1
Q

hemicholinium

A

blocks choline transport into the terminal, not pharmacologically useful because it blocks all cholinergic functions

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2
Q

choline cotransports

A

with Na+, rate limiting step

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3
Q

CAT

A

choline + acetylCoA –> Ach inhibitors are not effective

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4
Q

ACh is stored

A

in presynaptic vesicles

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5
Q

ACh structure

A

quarternary amine, positively changed, has an ester bond prone to rapid degredation

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6
Q

uptake

A
  1. choline 2. ACh synthesis, 3. vesicle storage
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7
Q

black widow

A

alpha latrotoxin, causes over release of ACh

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8
Q

botulinum toxin

A

blocks Ach release

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9
Q

release of ACh

A

basic depolarization-induced excretion-secretion coupling (calcium dependent vesicle fusion with pre synaptic membrane)

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10
Q

botox is used for

A

strabismus, blapharospasm, hyperhidriosis, focal distonia, migraine, cosmetic treatment

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11
Q

d-tubocurarine function

A

blocks nicotinic receptors (non-depolarizing neuromuscular blocker)

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12
Q

cholinomimetic

A

cholinergic agonist ‘mimicry’

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13
Q

botulinum neurotoxins

A

7 types of protease, cleave VAMP/SNAP-25/syntaxin (proteins required for fusion and exocytosis of ACh synaptic vesicles)

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14
Q

botulinum neurotoxins have selective

A

activity at NMJ and cause flaccid paralysis, effects last for weeks and cause muscle atrophy

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15
Q

botulinum neurotoxin precaution

A

systemic spread can block crucial functions such as respiration

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16
Q

removal of ACh

A

flashlike suddeness, shorter than time to make an action potential (you’ve got one shot)

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17
Q

BChE

A

pseudocholinesterase, non specific…, serum cholinesterase, prefers butyrylcholine as a substrate, generally distributed

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18
Q

reversible ACE inhibitors

A

physostigmine, neostigmine

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19
Q

irreversible ACE inhibitors

A

organic phosphates

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20
Q

electric fish

A

contain tissue rich in nicotinic receptors (packed with ACh receptors)

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21
Q

poisonous snakes

A

contain α toxins (peptides) that interact with cholinergic receptors in a way that causes irreversible antagonism

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22
Q

structure of the nicotinic receptor

A

5 subunits (α, α, β, δ, γ) in a circular array, the center is a gated ion channel

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23
Q

myastenia gravis is caused by

A

antibodies to ones own nicotinic receptors

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24
Q

nicotinic receptors require the binding of

A

TWO ACh molecules (causes positive ion influx), all or none switch

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25
Q

goal of nicotinic receptor activation

A

is depolarization

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26
Q

dual response

A

continuous or massive nicotinic receptor stimulation causes desensitization or a failure to repolarize (initial stimulation followed by cessation)

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27
Q

N(g) blocker

A

6, hexamethonium (ganglionic synapses and adrenal medulla)

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28
Q

N(m) blocker

A

10, decamethonium (neuromuscular junctions of somatic system)

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29
Q

methonium compounds

A

variation in chain length, block various nicotinic receptors with specificity

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30
Q

all nicotinic receptors require

A

two α subunits for ACh binding

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31
Q

ganglionic nicotinic receptor subunits

A

2α3, 3β4

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32
Q

muscarinic receptor structure

A

integral membrane proteins with a single membrane spanning polypeptide (seven times)

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33
Q

M2, M4

A

G(i) inhibition of cAMP, increased K+ currents

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34
Q

M1, M3, M4

A

G(q), increase in intracellular Ca2+

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35
Q

muscarinic receptor effect

A

slow, graded response, synapses less structured, Ach degredation is slwoer (used to regulate organ intrinsic activity)

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36
Q

muscarinic receptor blocker

A

atropine

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37
Q

utility of agents depends on

A

specificity of receptor subtype, availability (ability to penetrate to desired sites)

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38
Q

penetration to CNS

A

tertiary amines, hydrophobic compounds (un charged)

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39
Q

lots of Ach

A

causes the activation of nicotinic receptors (and therefore, sympathetic system as well)

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40
Q

lots of ACh and atropine

A

increase in autonomic ganglia firing rate and an increase in BP and heart rate

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41
Q

ACh as a drug

A

is not much use due to rapid degredation

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42
Q

methacholine

A

is resistant to hydrolysis, used opthalmologically, and has muscarinic and nicotinic effects

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43
Q

bethanechol

A

muscarinic agonist, resistant to degradation, pronounced in GI and UT smooth muscle, NO NICOTINIC EFFECTS

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44
Q

ACE inhibitor and bethanechol

A

additive effects

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45
Q

Methacholine and ACE inhibitor

A

synergistic effects

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46
Q

bethanecol administration

A

orally or subcutaneously, IV/IM negates specificity (toxic)

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47
Q

bethanecol structure and purpose

A

quarternary amine; used to treat urinary retention, GI stasis (post-op), diagnosis of anti-cholinergic intoxication (there are better agents), locally for the eye

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48
Q

contraindications for muscarinic agonists

A

asthma, hypothyroidism, coronary insufficiency, peptic ulcer, physical obstruction (bronchioconstriction, hypotension, gastric secretion)

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49
Q

muscarine

A

muscarinic agonist, quaternary amine, found in mushrooms

50
Q

pilocarpine

A

muscarinic agonist, tertiary amine, rarely used systemically, potent diaphoretic

51
Q

pilocarpine clinical uses

A

topical: treatment of acute glaucoma, xerostemia, CF sweat test, sjorgen’s syndrome

52
Q

diagnostic sweat test for CF

A

pilocarpine

53
Q

sjorgen’s syndrome

A

pilocarpine (or M3 agonist), autoimmune attack of endocrine glands

54
Q

belladonna alkaloids

A

night shade, atropine, muscarinic antagonist, highly specific, competitive, tertiary amines

55
Q

atropine

A

competitive inhibition, tertiary amines, half life 24 hours

56
Q

synthetic muscarinic antagonists

A

Tropicamide, Tolterodine, Tiotropium

57
Q

Tropicamide

A

short half life, eyes

58
Q

Tolterodine

A

selectivity for receptors,

59
Q

Tiotropium

A

quaternary amine, lungs

60
Q

indications for specific atropine use

A

cholinesterase poisoning, AHA emergency care

61
Q

M3 selective agents treat

A

incontinence in the elderly

62
Q

treatment of stable COPD

A

long acting β-adrenergic agonists and muscarinic antagonists

63
Q

treatment for anti-muscarinic intoxication

A

AChE inhibitor (physostigmine), diazapam for psychotic effects

64
Q

symptoms of muscarinic antagonist poisioning

A

cutaenous vasodilation, anhidrosis, anhydrotic hyperthermia, nonreactive mydriasis, delirium, urinary retention

65
Q

preanesthetic scopalamine is

A

better than atropine

66
Q

cholinesterase inhibitors high doses

A

can cause stimulation through natural leakage of ACh

67
Q

cholinesterase inhibitors are important for

A

Myasthenia Gravis, Alzheimer’s, opthalmology, atony, termination of competitive cholinergic blocking drugs

68
Q

ACE inhibitors toxic

A

used for insecticides and in chemical warfare

69
Q

hexamethonium

A

blocks reflex effects

70
Q

reversible competitive ACE inhibitor example

71
Q

Donepezil

A

tertiary amine, longer acting, competitive antagonist

72
Q

carbamoylating agents are

A

ACE inhibitors and are reversed by slow hydrolysis (2-6 hour half life)

73
Q

Physostigmine

A

carbamoylating agent, ACE inhibitor, tertiary amine, ordeal bean

74
Q

Neostigmine

A

carbamoylating agent, ACE inhibitor, quaternary amine

75
Q

irreversible ACE inhibitor

A

organic phosphates, turnover is fast than enzyme removal, SARIN :(

76
Q

sites of action for ACE inhibitors

A

muscarinic post-ganglionic junctions, ganglionic nicotinic junctions, nicotinic NMJs, CNS muscarinic and nicotinic junctions

77
Q

lipid soluble ACE inhibitors

A

physostigmine, donepezil, organic phosphates –> reach all sites for inhibitor

78
Q

ACE inhibitor quarternary amine

A

nesostigmine

79
Q

used for parkinson’s

A

atropine (muscarinic antagonist) - high doses lead to CNS problems

80
Q

prevents motion sickness

A

scopolamine

81
Q

rapid hydrolysis of the acetylated enzyme

A

restores the native enzyme

82
Q

organic phosphates produce

A

phosphorylated enzymes

83
Q

increased inhibition of ACE eventually causes

A

blockage of signal transduction

84
Q

vagotomy

A

neostigmine is no long effective after this procedure

85
Q

acute attacks of glaucoma are treated with

A

physostigmine (ACE inhibitor)

86
Q

given for relief of abdominal distension

A

neostigmine

87
Q

ACE inhibitor with good CNS penetrance

A

Donepezil (theoretically good for Alzhimer’s)

88
Q

ACh increase effect on skeletal muscle

A

facilitation followed by paralysis

89
Q

AChE inhibitor in myastenia gravis

A

too little = myastenia crisis, too much = cholinergic crisis

90
Q

why is neostigmine good for myastenia gravis?

A

longer acting, carbomylating, quaternary amine

91
Q

edrophonium test

A

you know why

92
Q

other treatments for myastenia gravis

A

immunosuppression, plasma exchange, thymectomy (ACE inhibitors treat the symptoms, not the disease)

93
Q

lipophilic agents

A

easily pass into the brain

94
Q

lipophilic agent used for Alzhimer’s

95
Q

effects can be local or general (ACE inhibitor poisoning)

A

dermal vs. pulmonary exposure

96
Q

miosis

A

pupil pinpointing

97
Q

diazapam

A

alleviates convulsions in ACE inhibitor poisoning

98
Q

cholinesterase reactivator

A

pralidoxime, must be given before the phosphorylated enzyme ages! ONLY effective against phosphorylating enzyme

99
Q

muscarinic antagonist

100
Q

hexamethonium

A

selectively blocks ganglionic receptors

101
Q

central effects of nicotine

A

sharpening of attention, development of dependence

102
Q

nicotine stimulation of

A

nucleus accumbens and prefrontal cortex when activate release dopamine (reward perception)

103
Q

why do plants make nicotine?

A

as a defense mechanism

104
Q

nicotine poisoning

A

empty stomach via activated charcoal, DONT USE basic solution

105
Q

varenicline

A

partial agonist for α4β2 nicotinic receptors

106
Q

trimethaphan

A

quarternary sulfonium, inhibit nicotinic ganglionic receptors

107
Q

sympathetically lead effects of nicotinic ganglion receptors

A

arterioles and veins are dominant tone, therefore blocking causes vasodilation

108
Q

mydriasis

A

pupil dilation

109
Q

nicotinic ganglionic blocker used for

A

hypertensive crisis, controlled hypotension, upper spinal cord injury hyperreflexia control

110
Q

neuromuscular blocking agents

A

curare, methonium (2 quarternary amine dichotomy allows for activation of both receptors at one time) produce flaccid paralysis

111
Q

competitive inhibition of NMJ

A

d-tubocurarine, vecuronium <– bulky, nonflexible,

112
Q

depolarizing agents (NMJ blocking)

A

methonium compounds, succinylcholine <— long and slender molecular configuration

113
Q

depolarizing agents block function in two phases

A
  1. persistent depolarization 2. receptor desensitization
114
Q

depolarizing agent vs. competitive inhibitor sequence of paralysis

A

limbs/neck, diaphragm last; comp. small rapid muscles first, depolarization. small rapid muscles after neck

115
Q

densensitization

A

postsynaptic membrane is repolarized but the nicotinic receptors do not respond to agonists, recovery is slow

116
Q

during phase I there can be

A

significant loss of K+ from muscle

117
Q

succinylcholine

A

characterized by fast action, depolarizing agent, rapidly hydrolyzed by butyryl cholinesterase

118
Q

use of neuromuscular junction blockers

A

muscle relaxation as a surgical anesthesia adjunct, orthopedic procedures, intubation, electroshock therapy

119
Q

neuromuscular blocking agent drug interactions

A

ACE inhibitors, inhalation anesthetics, certain antibiotics, calcium channel blockers

120
Q

neuromuscular agent disease interactions

A

reduced cholinesterase, malignant hyperthermia, soft tissue damage (hyperkalemia), muscular disorders

121
Q

reduced plasma cholinesterase and succinylcholine

A

prolonged apnea

122
Q

overdose of NMJ blocker

A

prolonged apnea, CV collapse, histamine release

Fundamentals 2 (7 decks)

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