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Systemic Pharm I > Modulation of the Parasympathetic System and NMJ > Flashcards

Modulation of the Parasympathetic System and NMJ Flashcards

1
Q

Direct acting cholinomimetics

A

acetylcholine, bethanechol, carbachol, cevimeline, nicotine, pilocarpine, varenicline

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2
Q

Short acting anticholinesterase

A

edrophonium

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3
Q

Intermediate acting anticholinesterase

A

donepezil, galantamine, neostigmine, physostigmine, pyridostigmine, rivastigmine

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4
Q

Long acting anti cholinesterase

A

echothiophate, malathion, parathion, sarin

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5
Q

Reactivation of acetylcholinesterase

A

pralidoxime

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6
Q

Cholinoceptor blocking drugs

A

atropine, cyclopentolate, dicyclomine, homatropine, ipratropium, oxybutynin, scopolamine, tiotropium, tropicamide

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7
Q

Which neurotransmitter is used at the presynaptic terminal of para and sympathetic systems?

A

acetylcholine

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8
Q

What receptor is found at the post synaptic terminal of both para and sympathetic systems?

A

nicotinic

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9
Q

Which neurotransmitter is found at the parasympathetic effector cell?

A

acetylcholine

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10
Q

Which neurotransmitter is found at the sympathetic effector cell?

A

norepinephrine

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11
Q

Which receptor is found at the parasympathetic effector organ?

A

muscarinic

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12
Q

Which receptor is found at the sympathetic effector organ?

A

adrenergic

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13
Q

What do cholinesterase inhibitors do?

A

inhibit the hydrolysis of endogenous acetylcholine thereby increasing the availability of naturally occurring ACh in the synapse

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14
Q

All cholinergic agonists are metabolized by cholinesterase in what three places?

A

at the receptor, in the blood, and in the liver

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15
Q

ACh, Carbachol, and Bethanechol pharmokinetics

A

not lipid soluble/highly charged, often have to inject it where you want it, ACh is rapidly broken down while the other two have a longer duration

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16
Q

Pilocarpine, nicotine, and muscarine pharmokinetics

A

readily absorbed from most sites of administration, excreted by kidney

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17
Q

Which direct cholinomimetic is not seen clinically because of toxicity and crossing the BBB?

A

muscarine

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18
Q

What receptor is on the presynaptic nerve terminal of para and sympathetic systems?

A

muscarinic receptor, activation cause inhibition of neurotransmitter release

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19
Q

T/F muscarinic receptors are g protein coupled and produce 2nd messenger cascade that directly affects organ function

A

true

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20
Q

T/F nicotinic receptors are ion channel and activation produces depolarization of the nerve cell or NMJ

A

true

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21
Q

What is the result of prolonged agonist binding to the nicotinic post ganglion neuron?

A

desensitization/depolarizing blockade, prevents recovery

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22
Q

What is the muscarinic effect on the eye?

A

miosis (contraction of sphincter), accommodation, opening of TM (lower IOP)

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23
Q

What is the muscarinic effect on the heart?

A

decrease in heart rate (hyperpolarization of SA and AV node)

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24
Q

What is the muscarinic effect on blood vessels?

A

indirect vasodilation and decrease in peripheral resistance (in atherosclerosis will cause vasoconstriction)

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25
Q

What is the muscarinic effect on the respiratory system?

A

contraction of bronchial smooth muscle aka broncho-constriction and increased mucous secretion

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26
Q

What is the muscarinic effect on the GI tract?

A

increase smooth muscle motility and relax most sphincters, stimulate salivary and gastric glands to secrete

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27
Q

What is the muscarinic effect of the urinary tract?

A

stimulate detrusor and relax trigone and sphincter aka promote urination

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28
Q

What is the muscarinic effect on other glands?

A

SECRETION sweat, lacrimal, nasopharyngeal

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29
Q

T/F activation of nicotinic receptors often resembles simultaneous discharge on both para and sympathetic system

A

true be careful of drug side effects

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30
Q

Activation of nicotinic receptors in autonomic ganglia cause simultaneous…

A

sympathomimetic cardiovascular activity (increase HR and BP) AND parasympathomimetic GI and Urinary activity (nausea, vomiting, diarrhea, and urination)

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31
Q

What is the nicotinic effect at the NMJ?

A

depolarization followed by depolarization blockage aka desensitization

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32
Q

T/F most indirect acting cholinomimetics are simple alcohols or esters

A

true

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33
Q

T/F derivatives of phosphoric acid (organophosphates) have the shortest duration of action

A

false

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34
Q

What is the administration of indirect cholinomimetics?

A

any including IV

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35
Q

Where are organophosphates absorbed from?

A

skin, lung, gut, and conj – dangerous to humans

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36
Q

Which intermediate indirect drug is well absorbed from all sites and can be used topically in the eye?

A

physostigmine

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37
Q

T/F organophosphates are distributed to the CNS

A

true, CNS toxicity is common

38
Q

Which organophosphate does not cross the CNS?

A

echothiophate

39
Q

Why is edrophonium short acting?

A

forms a reversible bond with the enzyme but is not actually a substrate for ACh-esterase

40
Q

What is the MOA of intermediate acting drugs?

A

neostigmine, physostigmine, and pyridostigmine are resistant to part of the enzyme action so it takes longer

41
Q

What is the MOA of echothiophate, malathion, parathion, and sarin?

A

forms phosphorylated enzyme complex that strengthens the bond with the drug aka completely deactivates ACh-ase

42
Q

What effect do low concentrations of indirect acting drugs have?

A

alerting response

43
Q

What effect do high concentrations of indirect acting drugs have?

A

convulsions

44
Q

What happens to the cardiovascular system when indirect acting drugs are used?

A

increased activity in both sympathetic and parasympathetic ganglia as well as increased activity at muscarinic receptors

45
Q

Which system dominates the cardiovascular response to indirect acting cholinergic agonists?

A

parasympathetic because of direct muscarinic innervation aka decreased HR and decreased cardiac output

46
Q

What is the indirect cholinergic agonist effect at the NMF?

A

prolong and intensify actions of acetylcholine, strengthen muscle contraction=helpful in myasthenia gravis

47
Q

T/F the NMJ can be desensitized by high or prolonged concentrations

A

true

48
Q

Which cholinomimetics can treat glaucoma?

A

carbachol, pilocarpine, echothiophate(obsolete)

49
Q

Which cholinomimetic treats urinary retention?

A

bethanechol or neostigmine

50
Q

Which cholinomimetic treats dry mouth?

A

cevimeline, pilocarpine

51
Q

Which cholinomimetics treat myasthenia gravis?

A

edrophonium (diagnosis) and pyridostigmine maybe neostigmine

52
Q

T/F cholinomimetics may help treat alzheimer’s?

A

true (donepezil, galantamine, rivastigmine)

53
Q

How do cholinomimetics work in the eye?

A

cause contraction of the ciliary body +miosis to increase aqueous outflow

54
Q

What cholinomimetic can reverse neuromuscular blockage produces during surgical anesthesia?

A

neostigmine and edrophonium

55
Q

What are adverse effects of direct acting cholinomimetics?

A

nausea, vomiting and diarrhea (increase GI activity) urinary urgency, salivation and sweating (increase secretions) flushing of skin from vasodilation and bronchial constriction

56
Q

What are adverse effects of cholinesterase inhibitors?

A

same as direct + muscle weakness (NMJ), convulsions (CNS) and respiratory failure

57
Q

What are symptoms of organophosphate poisoning?

A

same as cholinesterase inhibitors

58
Q

What are the effects of cholinergic blockers (muscarinic antagonists)?

A

interrupt parasympathetic nerve impulses and prevent ACh from stimulating cholinergic receptors

59
Q

T/F Cholinergic blockers can be divided into muscarinic and nicotinic subgroups

A

true

60
Q

What is an example of a naturally occurring muscarinic antagonists?

A

atropine, derived from nightshade plant

61
Q

What is an example of a synthetic muscarinic antagonist?

A

tropicamide

62
Q

What is the absorption of cholinergic blockers?

A

most are well absorbed in the gut, conj and across skin

63
Q

What is the distribution of cholinergic blockers?

A

widely distributed with CNS penetration

64
Q

Where are muscarinic antagonists eliminated?

A

kidney

65
Q

What is the MOA of cholinergic blockers?

A

block acetylcholine action at muscarinic receptors, moderately selective for receptor subtypes

66
Q

Is atropine selective or nonselective?

A

nonselective, useful in treating cholinomimetic toxicity like from organophosphates

67
Q

Which muscarinic antagonist has minimal CNS effects and which has marked effects?

A

minimal atropine, marked scopolamine

68
Q

What are scopolamine’s side effects and why does it have them?

A

drowsiness and amnesia, also reversal of vestibular disturbances, side effect because it crosses the BBB

69
Q

What are cholinergic blocker effects on the cardiovascular system?

A

increased HR

70
Q

What are cholinergic blocker effects on the eye?

A

mydriasis from blocking muscarinic activation of pupillary constrictor muscle allowing unopposed sympathetic dilator activity— also cycloplegia from weakening ciliary muscle– and reduction in lacrimal secretion

71
Q

What are muscarinic antagonist effects on the respiratory system?

A

bronchodilation and decrease in secretions

72
Q

What are muscarinic antagonist effects on GI tract?

A

decreased salivation and stomach acid, decreased smooth muscle tone and less propulsive movements

73
Q

What are cholinergic blocker effects on the urinary tract?

A

relax bladder smooth muscle which slows voiding

74
Q

What do cholinergic blockers do to sweat glands?

A

reduces sweating and can induce fever in younger patients

75
Q

What CNS disorders are antimuscarinic drugs used for?

A

parkinsons and treatment of motion sickness

76
Q

What antimuscarinic drugs are used for accurate refraction?

A

cyclopentolate or homatropine

77
Q

What antimuscarinic drugs are used for dilated fundus exam?

A

tropicamide or cyclopentolate

78
Q

What antimuscarinic drugs are used for uveitis and prevention of synechia?

A

homatropine or cyclopentolate

79
Q

What are characteristics of iris synechia?

A

irregular pupil and increased IOP possible

80
Q

What is the duration of eye drop dilation effects?

A

atropine 7-10 days, homatropine 1-3 days, cyclopentolate 1 day, tropicamide 6 hours

81
Q

What antimuscarinic drugs are used as pre-anesthesis to prevent airway secretions?

A

atropine or scopolamine

82
Q

What antimuscarinic drugs treat COPD and asthma because of bronchodilation?

A

ipratropium or tiotropium

83
Q

What antimuscarinic drugs treat urinary urgency or bladder spasm?

A

oxybutynin

84
Q

T/F antimuscarinic drugs treat bradycardia and some arrhythmias

A

true

85
Q

What is cholinergic poisoning?

A

long acting indirect poisoning

86
Q

What drug has an antimuscarinic effect used to treat cholinergic poisoning?

A

atropine because its nonspecific, multiple doses required

87
Q

What cholinesterase regenerator can treat cholinergic poisoning if used rapidly?

A

pralidoxime because it can regenerate phosphorylated enzyme

88
Q

What are adverse effects of antimuscarinic drugs?

A

mydriasis and light sensitivity, decreased accommodation, dry mouth, tachycardia, flushed skin, agitation, delirium, elevated body temp

89
Q

T/F Cholinoreceptor agonists cause SLUD

A

true, salivation, lacrimation, urination, diarrhea

90
Q

What are the cholinoreceptor antagonists? (opposite effect of SLUD)

A

dry mouth, dry eyes, urinary retention, constipation

Systemic Pharm I (13 decks)

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