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Pharm module 4 CNS I > Cholenergic agonist > Flashcards

Cholenergic agonist Flashcards

1
Q

What type of neurologic function is not under direct control

A

autonomic

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2
Q

What does the autonomic nervous system have control over

A

Visceral functions necessary for life
-Cardiac output
-blood flow distribution
-digestion

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3
Q

What causes neurologic function

A

Chemical transmission that occurs between nerve and effector cells

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4
Q

What tissues are effected by the autonomic nervous system

A

Cardiac muscle
smooth muscle
vascular endothelium
exocrine glands
presynaptic nerve terminals

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5
Q

How is the autonomic nervous system divided

A

Sympathetic and parasympathetic

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6
Q

Which nerve fibers leave the CNS via the thoracic, lumbar, and sacral spinal nerves

A

Sympathetic preganglionic fibers

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7
Q

Which nerve fibers leave the CNS via the cranial nerves

A

Parasympathetic preganglionic nerve fibers

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8
Q

What is the enteric nervous system

A

The third division of the ANS

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9
Q

What are the primary neurotransmitters in the body

A

norepinephrine
Acetylcholine

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10
Q

What are cholinergic fibers

A

Fibers that work by releasing acetylcholine

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11
Q

A large number of peripheral ANS fibers are what type of fiber classification

A

cholinergic

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12
Q

What are the types of cholinergic fibers

A

all Preganglionic efferent autonomic fibers (non-autonomic)

all somatic motor fibers (skeletal muscle)

Most parasympathetic postganglionic fibers

Some sympathetic post ganglionic fibers

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13
Q

What do most postganglionic sympathetic fibers release and what type of fiber are they

A

Most commonly noradernergic fibers

Release norepinephrine

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14
Q

Which autonomic receptors are non-specific

A

Nicotinic

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15
Q

Which autonomic receptors work almost exclusively with the parasympathetic system

A

Muscarinic

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16
Q

What do adrenergic receptors respond to

A

Catecholamines (Norepinephrine)

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17
Q

What do cholinoceptors respond to

A

Acetycholine

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18
Q

What are the adrenoreceptors broken down into

A

alpha
beta
dopamine receptor types

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19
Q

A drug that blocks action potential propagation (local anesthestic) is selective or non-selective and why

A

non-selective because it acts on a process common to all neurons

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20
Q

Drugs that act on the biochemical processes involved in transmitter synthesis and storage are selective or non-selective and why

A

More selective because the biochemistry of each transmitter is different

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21
Q

Which classes of drugs make up a large group that mimics acetylcholine

A

Acetylcholine-receptor stimulants
Cholinesterase inhibitor

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22
Q

What are cholinomimetics

A

Drugs that mimic acetylcholine

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23
Q

how are cholinomimetics classified and why

A

by MOA because some bind directly to cholinoreceptors and some act indirectly by inhibiting the hydrolysis of endogenous acetylcholine

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24
Q

What do cholinesterases do

A

Allow for acetylcholine to remain activated

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25
Q

What is the MOA for direct active cholinomimetic agents

A

They bind directly to and activated muscarinic or nicotinic receptors

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26
Q

What is the MOA for indirect acting cholinomimetics

A

Inhibit acetylcholinesterase which hydrolyzes acetylcholine and acetic acid which then increases endogenous acetylcholine concentration in the synaptic cleft and neuroeffector junctions

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27
Q

What are the effects on the eye from muscarinic agonists

A

Miosis
accommodation

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28
Q

What are the cardiovascular effects from muscarinic agents

A

Decrease in slow inward Ca current

Increase in K in current cells of SA, AV, purkinje fibers

Reduction in current for diastolic depolarization

all this = Bradycardia

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29
Q

What respiratory effect happen with muscarinic agonists

A

Contraction of bronchial tree

Increased glandular secretion in tracheobrochial tree

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30
Q

What are the GI effects with muscarinic agonist

A

Increased motor and secretory activity
Stimulation of salivary and gastric glands

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31
Q

What are the effects of the GU system from muscarinic agonists

A

Stimulation of detrusor muscle
Relaxation of trigone and sphincter muscles

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32
Q

What are the cholinergic agonist effects on the body

A

Diarrhea
diaphoresis
miosis
nausea
Urinary urgency

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33
Q

What are the effects on the CNS from indirect acting cholinomimetics

A

Diffuse EEG activation and alert response improvement

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34
Q

What are the cardiovascular effects from indirect acting cholinomimetics

A

Vagal nerve activation in the heart

Negative chronotropy, dromotropy, inotropy (cardiac output falls)

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35
Q

What are the effects of the NMJ from indirect acting cholinomimetics

A

Increased strength of skeletal muscle contraction

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36
Q

How would acetylcholine act as a direct acting cholinergic agent

A

Binds to both nicotinic and muscarinic receptors which means that it would have wide spread systemic effects leaving it with limited utility

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37
Q

What would the side effects of acetylcholine be

A

Brief decrease in HR and Cardiac output

Vasodilation

Activation of muscarinic receptor M3 that causes endothelial release of nitric oxide

Increase salvation is intestinal motility

Increase bronchial secretion

detrusor muscle action

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38
Q

What are some direct acting cholinergic agents

A

Bethanechol

Pilocarpine

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39
Q

Does bethanechol act on nicotinic or muscarinic receptors

A

Muscarinic

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40
Q

What disease is bethanechol most commonly used on

A

GU diseases

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41
Q

What is the MOA of bethanechol

A

Stimulated the detrusor muscle of the bladder and relaxes the trigone and sphincter muscles which allow for urination

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42
Q

How is bethanechol used in postpartum and post-operative settings

A

to stimulate an atonic bladder

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43
Q

Is pilocarpine muscarinic or nicotinic

A

Muscarinic

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44
Q

What setting is pilocarpine most commonly used in

A

Ophthalmology

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45
Q

What is the MOA of pilocarpine

A

Apply topically to the eye

produces rapid mitosis and contraction of the cilliary muscles

Promotes salivation in those with xerostoma

46
Q

What drug is very useful in glaucoma treatment and why

A

pilocarpine because it can lower intraoccular pressure

47
Q

What drug is very useful in those with sjogrens syndrome or who have undergone head/neck radiation

A

Pilocarpine because it can help increase salivation

48
Q

What is occurring with open angle glaucoma

A

there is increased resistance to aqueous humor drainage through the trabecular meshwork

49
Q

What is occurring in closed angle glaucoma

A

Obstruction of drainage pathways by the iris

50
Q

How does pilocarpine help in closed angle glaucoma

A

Acts of muscarninc receptor -> iris contracts

Pupil then constricts and will move the iris away from the angle

This allows opening of the trabecular meshwork around the canal of schlemm= decrease in intraoccular pressure

51
Q

What are some indirect-acting cholinergic agents

A

Edrophonium
Pyridostigmine/Neostigmine
Physostigmine
Echotrophate

52
Q

What in the MOA of edrophonium

A

Binds reversibly to the active center of acetylcholinesterase, preventing the hydrolysis of Ach

This will increase the concentration of Ach in the NMJ to rapidly increase muscle strength

53
Q

What is edrophonium primarily used for

A

Diagnosis of M. Gravis

54
Q

What causes M. Gravis

A

Autoimmune disease caused by antibodies to the nicotinic receptor in the NMJ

Antibodies then breakdown the receptors so less can interact with Ach

55
Q

Which drugs are used in the chronic management of M. Gravis

A

Pyridostigmine (USA)
neostigmine (Canada)

56
Q

What is the down side to taking pyridostigmine

A

works for 3-6 hours and thus needs to be taken 4-5 times a day for therapeutic effect

57
Q

What is the MOA for physostigmine

A

Binds with acetylcholinesterase, making it reversibly inactivated

This stimulated the muscarinic & nicotinic sites of the ANS and nicotinic receptors of NMJ

58
Q

What is physostigmine primarily used for

A

atropine overdose

59
Q

What are the side effects of physostigmine

A

Miosis
hypotension
bradycardia

*high doses=convulsions

60
Q

What is unique about echothiophate

A

Irreversibly binds to a phosphate group on AChE to permanently inactivate it

61
Q

How is echothiophate used therapeutically

A

Treatment of ocular hypertension in chronic glaucoma

62
Q

If echothiophate is used topically on the eye, what is the side effect

A

Intense miosis

63
Q

If echothiophate is used in high doses, what can happen

A

Cataracts can be caused

64
Q

What can be taken to reverse symptoms of echothiophate

A

High dose atropine

65
Q

How are most organophosphate compounds used outside of echothiophate

A

Insecticides
chemical warfare

66
Q

What symptoms occur with anticholinesterase toxicity

A

Increased urination
bradycardia
excessive secretions
pupillary constriction

67
Q

What can be given to reverse anticholinesterase toxicity

A

Pralidoxime

68
Q

How does pralidoxime work

A

Reactivates AChE in the periphery but it is unable to reverse the CNS effect

69
Q

What group of cholinoceptor blocking drugs have a preference for nicotinic receptors

A

Ganglionic blockers

70
Q

What group of cholinoceptor blocking drugs are useful for operative settings

A

Neuromuscular blocking agents (nicotinic antagonists)

71
Q

What is the MOA for Neuromuscular blocking agents

A

Interfere with transmission of efferent impulses on skeletal muscle

72
Q

What is atropine

A

A prototype anti-muscarinic drug

Highly selective muscarinic receptor

73
Q

What does atropine have an effect on

A

Salivary, bronchial and sweat glands

*Little to no effect on skeletal NMJ

74
Q

What type of effect does atropine have on the CNS

A

minimal

75
Q

What effect does atropine have on the eye

A

Reduces lacrimation
Causes mydriasis, cycloplegia

76
Q

What is mydriasis and cycloplegia

A

Inability to focus for near vision

77
Q

What effect does atropine have on the respiratory system

A

Bronchodilation
Reduces airway secretions

78
Q

What effect does atropine have on the cardiovascular system

A

Tachycardia (no BP effect)
Reduces PR interval
Blocks vasodilation of coronary arteries

79
Q

What effect can low dose atropine have on the heart initially

A

bradycardia

80
Q

What effect does atropine have on the GI system

A

Decrease salivary secretion
prolongs gastric emptying and intestinal transit time

81
Q

What effect does atropine have on the GU system

A

Relaxes arterial / bladder wall smooth muscle
May cause urinary retention

82
Q

What are the general side effects of cholinergic antagonists

A

Blurry vision, mydriasis
Decreased lacrimation, salivation, sweating
Confusion
Constipation
urinary retention

“Mad as a hatter, hot as hell, red as a beet, dry as a bone, blind as a bat”

83
Q

How can topical atropine be used

A

To induce mydriasis and cycloplegia to measure refractory errors in the lens

84
Q

How is IV atropine used therapeutically

A

Reversal of dangerous bradycardia

Reverse organophosphate toxicity / mushroom poisoning

blocks secretions in the upper and lower respiratory tract before surgery

85
Q

What are some types of antimuscarinic agents

A

Scopolamine
ipatropium / tiotropium

86
Q

What is scopolamine used for

A

Combat motion sickness

87
Q

How is scopolamine administered

A

A patch

88
Q

How is scopolamine different from atropine

A

Greater CNS effects

89
Q

What is a side effect of scopolamine

A

Can be sedating

90
Q

What are synthetic analogs of atropine

A

Ipatropium and tiotropium

91
Q

How are ipatropium and tiotropium administered and why

A

Administered via aerosol route to allow for maximum targeting of bronchial tissue and reduce systemic effects

92
Q

What are ipratropium and tiotropium used to treat

A

COPD either alone or with long acting beta adrenoreceptor agonist

93
Q

What is the difference between ipratropium and tiotropium

A

Tiotropium is a long acting form of ipratropium

94
Q

What are ganglionic blockers

A

Agents that block nicotinic receptors for both sympathetic and parasympathetic autonomic ganglia

95
Q

What drug in the ganglionic blockers actually have therapeutic use

A

Nicotine

96
Q

What is the MOA for Nicotine

A

Depolarizes the autonomic ganglia resulting in stimulation and then paralysis of all ganglia

causes release of dopamine and norepinephrine (pleasure and appetite suppression)

97
Q

How can nicotine be administered and why

A

Gum, lozenges, MDI, transdermal patch to replicate drugs effects without smoking tobacco

98
Q

Why are neuromuscular blockers useful during surgery

A

To facilitate tracheal intubation and provide complete muscle relaxation which allows for more rapid recovery of anesthesia

99
Q

What is the MOA of neuromuscular blockers

A

Block cholinergic transmission between motor nerve ending and nicotinic receptors on skeletal muscle

100
Q

How do neuromuscular blockers act on the different receptors

A

Antagonistic of Ach on nicotinic receptors(non-depolarizing)

agonist that causes desensitization of ACh at the NMJ endplate receptors (depolarizing)

101
Q

What are examples or non-depolarizing neuromuscular blockers

A

Tubocurarine
rocuronium
vercuronion

102
Q

What is the MOA of non-depolarizing blockers

A

They block ACH receptors and prevent depolarization of cell membrane which inhibits muscle contraction

103
Q

Which muscles are paralyzed first with non-depolarizing blockers

A

smaller muscles (facial / ocular), then fingers, neck….

Respiratory effected last

104
Q

What are some antidotes of non-depolarizing blockers

A

Neostigmine
edrophonium

105
Q

How are non-depolarizing blockers administered and why

A

IV or IM

minimal bioavailability if taken orally

106
Q

Do non-depolarizing blockers effect CNS or BBB

A

NO

107
Q

What is the only depolarizing blocker in use today

A

succinylcholine

108
Q

What is the MOA of succinylcholine

A

Causes cell membrane depolarization which produces transient fasciculations in the muscle followed by flaccid paralysis and then keeps ACh receptors desensitized to allow for continued paralysis

109
Q

When is succinylcholine useful

A

Rapid ET intubation or ECT treatment

110
Q

Complications for succinylcholine

A

Malignant hyperthermia
Apnea from prolonged paralysis
Hyperkalemia

Pharm module 4 CNS I (2 decks)

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