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Pharmacology I > Lecture 11/12 - Cholinergic Agonists > Flashcards

Lecture 11/12 - Cholinergic Agonists Flashcards

1
Q

What are the direct acting cholinergic agonists? (six)

A 
ACh 
Muscarine 
Nicotine 
Carbachol 
Bethanechol 
Pilocarpine
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2
Q

What are the cholinesterase inhibitors? (six)

A 
Edrophonium 
Neostigmine 
Pyridostigmine 
Physostigmine 
Organophosphates 
Pralidoxime
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3
Q

What abnormality inhibits ACh release?

A

Botulism

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4
Q

What can prolong the effects of ACh?

A

AChE inhibitors

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5
Q

What does ACh stimulate?

A

M + N

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6
Q

Where are muscarinic receptors located?

A

PNS effector organs

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7
Q

What is M1+3 linked to?

A

Gq

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8
Q

What is M2 linked to?

A

Gi

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9
Q

Where are muscarinic receptors where the PNS is not?

A

Sweat glands

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10
Q

What do nicotinic receptors respond to?

A

ACh + Nicotine

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11
Q

What is a special characteristic of nicotinic recptors?

A

Rapid desensitization

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12
Q

Where are nicotinic receptors found?

A

Brain
Adrenal medulla
Autonomic ganglia
NMJ

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13
Q

Why can drugs select between NMJ and autonomic nicotinic receptors?

A

Both have different structures

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14
Q

What is direct action?

A

Agonist binds and stimulates receptor

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15
Q

What is indirect action?

A

Molecule binds to enzyme or other part of pathway that leads to a different effect of NT

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16
Q

What will happen with ACh injection/

A

Slowing of HR - M2

Drop in BP - M3

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17
Q

Why can’t you give ACh orally?

A

Charged, not absorbed

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18
Q

What does bethanechol stimulate?

A

M receptors only

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19
Q

What effects predominate with bethanechol?

A

Bladder + GI

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20
Q

Does bethanechol enter the brain? Why?

A

No, charged

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21
Q

What does pilocarpine stimulate?

A

M receptors only

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22
Q

What are the distribution characteristics of pilocarpine?

A

Not charged, so taken orally

Gets into CNS

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23
Q

What is pilocarpine used for in the eye?

A

Decrease intraocular pressure (M3)

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24
Q

What is really sensitive to pilocarpine that leads to side effects? what are the effects?

A

Sweat + Salivary glands

Drooling

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25
Q

What does muscarinic stimulation do to the heart?

A

Vagal stimulation = Bradycardia (M2)
Atrial-muscarinic receptors
Conduction slowed through AV node
Pre-synaptic decrease NE = Decrease HR (M2)

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26
Q

What does muscarinic stimulation do to the blood vessels?

A

NO PNS, but M3 is present on endothelium

ACh given IV will cause vasodilation

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27
Q

How does ACh given IV cause vasodilation?

A

NO

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28
Q

What happens with release of NO from endothelial cells?

A

cGMP production + Vasodilation

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29
Q

What is the PNS tone like in the GI tract?

A

High, responsible for digestion

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30
Q

What are the effects of muscarine on the GI tract?

A

Motility + Peristalsis increase
Tone increases
Salivary + Gastric secretions increase
Sphincters relax

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31
Q

How is carbachol used with horses?

A

Treatment of colic or impactions

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32
Q

What do you have to watch out for when using carbachol in horses?

A

If obstruction is present can lead to intestinal rupture

33
Q

What is carbachol used for in cattle?

A

Rumen atony and impaction

34
Q

What does normal PNS activity do to the bladder?

A

Enhances overall activity

35
Q

What do muscarinic drugs do to the bladder?

A 
Bladder tone + peristalsis increase 
Void pressure increase 
Bladder capacity decrease 
Detrusor contracts 
Trigone and sphincter relax
36
Q

What is the basic end result of muscarinic stimulation of the bladder?

A

Increased urination

37
Q

What drug is used for bladder effects?

A

Bethanechol

38
Q

What is betahanechol used for?

A

Urinary atony in cats following urolithiasis

39
Q

What do you have to watch out for when using betanechol in cats?

A

That the urethra is patent, so they can control urine output

40
Q

What are the muscarinic effects in the eye?

A

Circular muscle contraction = Pupil smaller
Increased AH drainage = Decreased pressure
Ciliary muscle contracts = Near vision

41
Q

How is pilocarpine used in the eye?

A

KCS + Glaucoma

42
Q

What are the side effects of pilocarpine in the eye?

A

Blurred vision + Brow ache

43
Q

What are the muscarinic side effects?

A 
Nausea + V/D + Colic 
Bladder tightness = Increased urination 
Salivation 
Bronchoconstriction + increased mucus 
Blurred vision 
Constricted pupils
44
Q

What happens with muscarine toxicity?

A

Same as side effects just worse

Hypotension + Shock + Bradycardia

45
Q

What is muscarine toxicity treated with?

A

Atropine + Albuterol

46
Q

What are the three main places for nicotinic receptors?

A

Autonomic ganglia
Skeletal muscle
Brain

47
Q

What type of channel is nicotinic receptors?

A

Ligand gated Na+ channel

48
Q

What movement of ions occurs with an activated nicotinic receptor?

A 
Na/Ca = in 
K = out
49
Q

What, in the most general sense, does N activate?

A

SNS + PNS

50
Q

What are the SNS effects with nicotinic stimulation?

A

Hypertension

Tachycardia w/ vagal bradycardia

51
Q

What are the PNS effects with nicotinic stimulation?

A

Nausea + Vomiting + Diarrhea + Urination

52
Q

What happens with desensitization of the NMJ?

A

Initial muscle twitch/contraction + depolarization blockcade

53
Q

What is seen with nicotine toxicity?

A

Vomiting
Convulsion + coma + respiratory arrest
Skeletal muscle depolarization
Hypertension + Cardiac arrythmia

54
Q

What three things are done to treat nicotine toxicity?

A

Atropine + Anticonvulsants + Assist respiration

55
Q

What are the four major drugs that affect AChE? (not toxins)

A

Neostigmine
Physostigmine
Pryidostigmine
Edrophonium

56
Q

What are the five examples of Organophostphates?

A

DFP + Eschothiophate + Soman + Sarin + Malathion

57
Q

What are the distribution characteristics of neostigmine?

A

Charged, cant be taken orally + no CNS N

Acts mostly on skeletal muscle

58
Q

How does pyrdiostigmine compare to neostigmine?

A

Longer acting

59
Q

What are the general characteristics of Physostigmine?

A

Enters CNS

U-shaped response curve

60
Q

What is Physostigmine used for?

A

Atropine toxicity

61
Q

What is the duration of action for Edrophonium?

A

Very short = 5 to 10 min

62
Q

What is edrophonium used for?

A

Diagnosis of myasthenia-like syndrome

63
Q

What is used to treat myasthenia-like syndrome?

A

Neostigmine

64
Q

What is the problem with organophosphates?

A

Long-lasting effect

Due to aging, becomes irreversible

65
Q

What can stop oragnophosphate aging?

A

2-PAM, if given 3 to 4 hours post-exposure

66
Q

How does aging occur?

A

Phosphorus-Oxygen bonds breaks

Bond to AChE irreversible

67
Q

Why does 2-PAM stop the “aging” process”?

A

Strong nucleophile

Attracts organophosphate away from AChE

68
Q

What is important to remember when using 2-PAM?

A

If organophosphate not present it can inhibit AChE itseld

69
Q

What are the CNS effects of AChE inhibition?

A

Convulsions + respiratory arrest

70
Q

What are the effects of AChE inhibition on the eye?

A

Miosis

Near vision

71
Q

What are the effects of AChE inhibition on GI/bladder?

A

V/D + Abdominal cramps + Urination

72
Q

What are the effects of AChE inhibition on the respiratory system?

A

Salivation + Secretion + Bronchoconstriction

73
Q

What are the cardiovascular effects of AChE inhibition?

A

PNS dominates
Prolonged ACh = M2 stimulation
Bradycardia + Decrease contraction + Decrease CO

74
Q

What happens with low concentrations of AChE inhibitors at the NMJ?

A

Skeletal muscle strength increases

75
Q

What happens with high concentrations of AChE inhibitors at the NMJ?

A

Twitches + Fasiculation
Blockade
Paralysis

76
Q

What is myasthenia gravis?

A

Autoimmune disease
Ab’s to nicotinic receptors
Not enough ACh to stimulate
Weakness and fatigue with excercise

77
Q

What is physostigmine used for?

A

Eye = miosis + decrease pressure
Synechia = alternate with atropine
Rumen atony = in cattle

78
Q

What are the side effects of AChE inhibitor toxicity?

A

Salivation + Lacrimation + Urination + Defecation + Gastric distress + Emesis

79
Q

What is the withdrawal time in meat and milk for 2-PAM (pralidoxime)?

A

28 days for meat

6 days for milk

Pharmacology I (21 decks)

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