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Pharmacology > EXAM #1: ANS PHARMACOLOGY - CHOLINERGICS > Flashcards

EXAM #1: ANS PHARMACOLOGY - CHOLINERGICS Flashcards

1
Q

What is a direct acting cholinomimetics?

A

Drugs that bind directly to and activate muscarinic or nicotinic cholinoceptors

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2
Q

What is a indirect acting cholinomimetics?

A

Drugs that produce their effects by inhibiting AChE i.e. preventing the destruction of endogenous ACh

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3
Q

What are the two classes of indirect acting cholinomimetics? What are their basic clinical and commerical applications?

A
  • Reversible= used to treat Alzheimer’s Disease or Myasthenia Gravis
  • Irreversible= Organophosphates, commerical insecticides
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4
Q

What are the different types of direct-acting cholinomimetics?

A

1) Choline esters
2) Natural alkaloids
3) Synthetic analogs

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5
Q

List the choline esters. Generally, what type of drug are these?

A
  • Acetylcholine
  • Methacholine
  • Carbachol
  • Bethanechol

These are all “choline esters,” which are direct cholinoceptor agonists.

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6
Q

Describe ACh’s: 1) susceptibility to cholinesterase, 2) muscarinic action, and 3) nicotinic action.

A

1) High susceptibility to cholinesterase

2) Equally high muscarinic and nicotinic action

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7
Q

Describe Methacholine’s: 1) susceptibility to cholinesterase, 2) muscarinic action, and 3) nicotinic action.

A

1) Low susceptibility to cholinesterase
2) High muscarinic action (greater than ACh)
3) Low nicotinic action

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8
Q

Describe Carbachol’s: 1) susceptibility to cholinesterase, 2) muscarinic action, and 3) nicotinic action.

A

1) NO susceptibility to cholinesterase
2) Moderate muscarinic action
3) Moderately high nicotinic action

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9
Q

Describe Bethanechol’s: 1) susceptibility to cholinesterase, 2) muscarinic action, and 3) nicotinic action.

A

1) NO susceptibility to cholinesterase
2) Moderate muscarinic action
3) NO nicotinic action

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10
Q

What are the cardiovascular effects of the choline esters?

A
  • Hypotension from direct vasodilation
  • Bradycardia
  • Slowed conduction/ prolonged refractory period of AV node
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11
Q

What are the gastrointestinal effects of the choline esters? What symptoms seen with choline esters?

A
  • Increased tone and contractility of the gut
  • Increased acid secretion

Nausea, vomiting, diarrhea, and cramps

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12
Q

What are the genitourinary effects of the choline esters?

A
  • Increased bladder motility and relaxation of sphincter resulting in involuntary urination
  • Little or NO effect on UTERUS
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13
Q

What are the ocular effects of the choline esters?

A
  • Miosis (sphincter m.)

- Decreased intraocular pressure and accomodation (ciliary m.)

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14
Q

What are the respiratory effects of the choline esters?

A

Bronchoconstriction

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15
Q

What are the effects of choline esters on glands?

A

Increased secretory activity resulting in:

  • Salivation
  • Lacrimation
  • Sweating
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16
Q

How does acetylcholine need to be administered? Why?

A

IV b/c it is rapidly destroyed by AChE

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17
Q

What are the effects of ACh on the cardiovascular system at low doses vs. high doses?

A

Low=

  • Vasodilation
  • Decreased TPR b/c of M3 receptor activation on vascular endothelium
  • -> “Reflex tachycardia”

High=

  • Bradycardia
  • Decreased AV conduction
  • Negative ionotope
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18
Q

What are the nicotinic effects of ACh?

A

None–does NOT penetrate fat surrounding skeletal muscle and ANS ganglia

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19
Q

What are the clinical uses of ACh?

A

B/c of rapid degradation, clinical use is limited, but it can be used for:

1) Eye surgery for short-lasting miosis
2) Provocation test in coronary angiography

Provocation test assists in the diagnosis of coronary vasospasm

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20
Q

What are the respiratory effects of ACh administration?

A

1) Bronchoconstriction
2) Increased bronchial secretion

Thus, ACh should NOT be given to ASTHMATICS

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21
Q

What is the clinical use of methacholine?

A

Diagnosis of bronchiolar hypersensitivity

This is called a “methacholine challenge”–>M3 activation leads to transient bronchoconstriction patients with bronchiolar hypersensitivity at much lower doses than normal population

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22
Q

How does Methacholine differ from ACh?

A

Longer half-life b/c of methyl group

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23
Q

What is the clinical cuse of Carbachol?

A

Treatment of Glaucoma; it contracts the ciliary muscle, which:

1) Enlarges canal of Schlemm
2) Increases drainage of aqueous humor
3) Decreases intraocular pressure

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24
Q

What receptors are activated by therapeutic doses of Carbachol?

A

BOTH nicotinic and muscarinic cholinoreceptors

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25
Q

What is the danger associated with high doses of Carbachol?

A

May induce cardiac arrest

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26
Q

What are the clinical indications for Bethanechol?

A

1) Gastric atony
2) Gastric emptying abnormalities
3) Urinary retention (w/out obstruction)

Bethanechol increases Lower Esophageal Sphincter (LES) tone; this can reduce symptoms of reflux s/p vagotomy

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27
Q

What are the predominate Gu and GI effects of Bethanechol? Drug interaction with which type of receptor mediates these effects?

A

GU=

  • Increased detrusor tone
  • Decreased outlet resistance of internal sphincter

GI= increased motility and secretion

M3 receptor mediated

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28
Q

What are the two direct acting muscarininc alkaloids?

A

Muscarine

Pilocarpine

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29
Q

What are the symptoms of muscarine poisoning?

A
  • Salivation, lacrimation, and sweating initially
  • Abdominal pain, nausea, diarrhea, blurred vision, and dyspnea

Effects typically subside within 2 hours

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30
Q

What are the clinical uses of Pilocarpine?

A
  • Glaucoma- this is the drug of choice (topically)
  • Xerostomia (orally)
  • Test on autonomic state/ PNS dysfunction
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31
Q

What effects of Pilocarpine predominate? What receptor type are these effects mediated by?

A

Opthalmic (M3)

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32
Q

What the mechanism of action of Pilocarpine on the eye?

A

1) Contracts sphincter muscle to produce MIOSIS
2) Contracts ciliary m. to free entrance into Canal of Schlemm (narrow angle Glaucoma)
3) Enhances tone of trabecular network (wide angle glaucoma)

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33
Q

What are the contraindciations to direct-acting cholinoceptor agonists?

A

1) Peptic ulcers
2) GI tract disorders
3) Asthma

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34
Q

What drugs interact with direct-acting cholinoceptor agonists?

A

Drugs with antimuscarinic properties:

  • Quinidine (antiarrhythmic)
  • Procainamide (antiarrhythmic)
  • Tricyclic antidepressants

All can block the intended effects of cholinoceptor agonists

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35
Q

What are the two nicotinic alkaloids?

A

Nicotine
Succinylcholine

These are direct acting nicotinic receptor agonists. Note that b/c of dramatic long term receptor activation, Succinylcholine function as a nicotinic receptor antagonist

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36
Q

What are the actions of nicotine on Nm receptors?

A
  • Skeletal muscle contraction
  • Fasiculations/ spasm
  • Depolarizing blockade (similar to succinylcholine)
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37
Q

Generally, what is the action of nicotine on Nn receptors?

A

Stimulation of BOTH SNS and PNS post-ganglionic neurons

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38
Q

What is the action of nicotine on Nn subtype receptors in the heart?

A

Increased heart rate

39
Q

What is the action of nicotine on Nn subtype receptors in the vascular system?

A

Peripheral vasoconstriction

40
Q

What is the action of nicotine on Nn subtype receptors in the GI tract?

A

Increased gut motility and secretion

41
Q

What is the action of nicotine on Nn subtype receptors in the carotid bodies?

A

Increased respiratory rate

42
Q

What is the action of nicotine on Nn subtype receptors in the medullary emetic chemoreceptors?

A

Nausea and vomiting

43
Q

What is the clinical indication for nicotine prescription?

A

To assist with smoking cessation

44
Q

List the reversible cholinesterase inhibitors.

A 
Edrophonium 
Neostigmine 
Pyridostigmine 
Phyostigmine 
Donepezil 
Tacrine
45
Q

What is the important characteristic of Edrophonium?

A

Short-acting

46
Q

What is the clinical use of Edrophonium?

A

Diagnosis of Myasthenia Gravis

*****It can be difficult to differentiate the symptoms/ etiology of myasthenia gravis. Blocking AChE leads to the specific improvement of MG symptoms and can thus be useful diagnostically.

47
Q

What is are important characteristics of Neostigmine and Pyridostigmine?

A
  • Quaternary amines= no CNS entry
  • Intermediate-acting

**Inability to penetrate the CNS keeps the action of these drugs confined to the periphery hence their utility in treating MG.*

48
Q

What are the clinical uses of Neostigmine and Pyridostigmine?

A

These are the standard AChE inhibitors used to treat Myasthenia Gravis. Other uses include:

1) Ileus
2) Urinary retention
4) Reversal of non-depolarizing NM blockers

49
Q

What are the important characteristic of Physostigmine?

A
  • Tertiary amine= ENTERS CNS

- Intermediate acting

50
Q

What are the clinical uses of Physostigmine?

A
  • Glaucoma

- Antidote in atropine overdose

51
Q

What is the important characteristic of Donepezil and Tacrine?

A

Lipid soluble i.e. enters the CNS

52
Q

What is the clinical use of Donepezil and Tacrine?

A

Alzheimer’s disease

There is a deficiency in intact cholinergic neurons in AD; thus these drugs, which DO cross the BBB are used.

53
Q

What are the important characteristics of Organophosphates?

A

1) Lipid-soluble
2) Long-acting
3) Irreversible inhibitors of AChE

54
Q

What are the clinical uses for the Organophosphates?

A

1) Glaucoma
2) Insecticide
3) Nerve gas

55
Q

What is the mnemonic to remember the symptoms of cholinesterase inhibitor intoxication?

A

DUMBBELSS

D= Diarrhea 
U= Urination
M= Miosis 
B= Bronchoconstriction
B= Bradycardia 
E= Excitement 
L= Lacrimation 
S= Sweating 
S= Salivation
56
Q

List the muscarinic receptor antagnoists.

A

Atropine
Ipratropium
Benztropine

57
Q

What are the characteristics of atropine?

A
  • Tertiary amine; thus, it enters the CNS (but not readily at therapeutic doses)
  • Competes with ACh at M receptors
  • Does NOT distinguish between M1, M2, and M3 receptors
58
Q

What are the pharmacologic effects of atropine?

A

1) Decreased secretions
2) Mydriasis and cycloplegia
3) Hyperthermia
4) Tachycardia
5) Sedation
6) Urinary retention and constipation
7) Behavioral excitation and hallucinations

*****Note that these effects are listed in order of increasing dose.

59
Q

What drug will completely counteract peripheral vasodilation caused by choline esters?

A

Atropine

60
Q

Does atropine effect blood pressure when given alone?

A

NO

This is due to lack of significant cholinergic innervation most vascular beds

61
Q

What are the indications for atropine?

A
  • Antispasmodic
  • Antisecretory
  • Management of AChE inhibitor overdose
  • Antidiarrheal
  • Ophthalmology
  • Prevention of vagal reaction e.g. in pericardiocentesis
62
Q

What drug can be used to counteract acute intoxication of atropine?

A

Physostigmine

63
Q

What are the clinical uses of Ipratropium?

A

1) First line therapy for COPD

2) Asthma (2nd line)

64
Q

What are the properties of Ipratropium?

A
  • Nonselective muscarinic antagonist
  • Mainly acts on bronchial SMC/ glandular M3 receptors when inhaled
  • Quaternary amine= no CNS effects
65
Q

What are the effects of Ipratropium?

A

1) Decreased bronchoconstriction

2) Decreased bronchial secretions

66
Q

What are the clinical uses of Benztropine?

A
  • Parkinson’s Disease (2nd or 3rd line therapy)

- PD secondary to an antipsychotic medication

67
Q

What are the properties of Benztropine?

A
  • Tertiary amine= CNS absorption

- Acts on muscarinic receptors in the brain

68
Q

What are the effects of Benztropine?

A

1) Re-establishment of DA-ACh balance in patients with PD
- Decreased GI/GU secretions and motility
- Increased HR

69
Q

What are the two nicotinic receptor antagonists?

A

Hexamethonium

Mecamylamine

70
Q

What are the pharmacologic effects of nicotinic receptor antagonists?

A
  • Reduce the predominant ANS tone
  • Prevent baroreceptor reflex changes in HR

**Most are no longer available clinically b/c of toxicity

71
Q

What is the effect of nicotinic receptor antagonists on the arterioles? Which system (PNS or SNS) is being antagonized?

A

SNS

- Vasodilation and hypotension

72
Q

What is the effect of nicotinic receptor antagonists on the veins? Which system (PNS or SNS) is being antagonized?

A

SNS

  • Dilation
  • Decreased venous return
  • Decreased CO
73
Q

What is the effect of nicotinic receptor antagonists on the heart? Which system (PNS or SNS) is being antagonized?

A

PNS

- Tachycardia

74
Q

What is the effect of nicotinic receptor antagonists on the iris? Which system (PNS or SNS) is being antagonized?

A

PNS

- Mydriasis

75
Q

What is the effect of nicotinic receptor antagonists on the ciliary muscle? Which system (PNS or SNS) is being antagonized?

A

PNS
- Cycloplegia

Cycloplegia is the paralysis of the ciliary muscle of the eye, which results in a loss of accommodation.

76
Q

What is the effect of nicotinic receptor antagonists on the GI tract? Which system (PNS or SNS) is being antagonized?

A

PNS

  • Decreased tone and motility
  • Costipation
77
Q

What is the effect of nicotinic receptor antagonists on the bladder? Which system (PNS or SNS) is being antagonized?

A

PNS

- Urinary retention

78
Q

What is the effect of nicotinic receptor antagonists on the salivary glands? Which system (PNS or SNS) is being antagonized?

A

PNS

- Xerostomia

79
Q

What is the effect of nicotinic receptor antagonists on the sweat glands? Which system (PNS or SNS) is being antagonized?

A

SNS
- Anhidrosis

Ahidrosis is the abnormal lack of a sweating response.

80
Q

What is the non-depolarizing neuromuscular blocking agent?

A

D-tubocurarine

81
Q

What is the depolarizing neuromuscular blocking agent?

A

Succinylcholine

82
Q

What are the neuromuscular blocking drugs clinically used for?

A

Used as adjuncts during general anesthesia to:

1) Facilitate tracheal intubation
2) Optimize surgical conditions while ensuring adequate ventilation

83
Q

What is D-tubocurarine’s mechanism of action? What is the difference between small and large doses?

A

Prevention of ion channel opening when bound to the Nm receptor

  • Low dose= compete with ACh
  • High dose= enters the Nm channel pore
84
Q

What is phase 1 of depolarizing neuromuscular blocking agents?

A

1) Drug binds Nm receptor causing depolarization
2) Persistent depolarization leads to paralysis

*****Note that this effect can be augmented by the administration of AChE inhibitors

85
Q

What is Phase 2 blockade of depolarizing neuromuscular blocking agents?

A

Repolarized occurs but the receptor is “desensitized” and not easily depolarized again

86
Q

In what sequence do muscles respond Succinylcholine administration? In what order do they recover?

A
  • Larger muscles are more resistant than smaller ones
  • Diaphragm responds last
  • Larger muscles recover first
87
Q

Aside from facilitating airway management, what else can neuromuscular blocking agents be used for?

A

Treatment of convulsions

Note that these agents DO NOT enter the CNS and thus only decrease the MUSCULAR manifestations of a seizure

88
Q

What are the side effects of the neuromusclar blockers?

A
  • Hypotension
  • Hyperkalemia
  • Increased intraocular pressure
  • Increase intragastric pressure
  • Muscle pain
89
Q

Why does hypotension follow neuromuscular blocker administration? What can be given to prevent this?

A
  • Tubocurarine can produce systemic histamine release that results in hypotension
  • Anti-histamines can prevent this effect
90
Q

Describe the structure of the choline esters. What is clinically important about their structure?

A

All are “cationic quaternary ammonium compounds”

*****Thus, all are INSOLUBLE in lipids and DO NOT enter the CNS

91
Q

Which two choline esters have an extended half-life compared to ACh? What is the structural basis for this difference?

A

1) Methacholine
2) Bethanechol

BOTH have a longer half life b/c of the addition of a methyl group

92
Q

Outline the management of cholinesterase inhibitor intoxication.

A

1) Symptom management including:
- Airway support
- Cardiovascular support
2) Antidote= ATROPINE
3) PRALIDOXIM (2-PAM)= regeneration of AChE

Atropine is a a muscarinic receptor antagonist that can block M receptors from high ACh conentrations. AChE inhibitors phosphorylate AChE. 2-PAM reverses that phosphorylation.

93
Q

What is Myasthenia Gravis?

A

NM disorder caused by autoimmune attack of the ACh receptor on post-junctional endplate, which causes:

  • Weakness
  • Fagitability of skeletal muscle

Fgitability is an increased susceptibility to fatigue.

94
Q

What is the difference between the mechanism of action of a depolarizing vs. a non-depolarizing NM-blocking agent?

A

Non-depolarizing= prevents Nm Na+ channel opening

Depolarizing= prevents Nm Na+ channel opening

Pharmacology (64 decks)

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