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Pharmacology > Cholinergic Pharmacology > Flashcards

Cholinergic Pharmacology Flashcards

1
Q

2 types of cholinergic receptors

focus on muscarinic

A

Muscarinic and Nicotinic

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2
Q

Location of muscarinic receptors

A

M1: CNS neurons, sympathetic postganglionic neurons, some presynaptic neurons
M2: MYOCARDIUM (heart)
M3: Exocrine glands, vessels (smooth muscle & endothelium)
M4: CNS neurons
M5: Vascular endothelium; cerebral vessels

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3
Q

A muscarinic receptor associated with the heart

A

M2

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4
Q

Examples of direct-acting cholinergic drugs

Direct-acting: Binds directly to Ach receptors

A

Alkaloids: Pilocarpine, Muscarine, Nicotine, Arecoline

Choline esters: Acetylcholine, Bethanechol, Carbachol, Methacholine

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5
Q

Examples of indirect-acting cholinergic drugs

Indirect-acting: Inhibit degradation of Ach

A

All are cholinesterase inhibitors:
-Anticholinesterases

Reversible:
Carbamates: Neostigmine
Acridine: Tacrine

Irreversible:
Organophosphates: Malathion, Parathion, Sarin
Carbamates: Carbaryl

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6
Q

Neurotransmitter of cholinergic

A

-Acetylcholine
(All preganglionic autonomic fibers, all postganglionic parasympathetic fibers, and a few postganglionic sympathetic fibers)

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7
Q

The action of the M2 receptor decreases the contractility of the atrial.

Why it does not decrease the contractility of vesicles?

A

There is no muscarinic receptor on vesicles. The receptors only involve atrial.

NO RECEPTOR, NO EFFECT!

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8
Q

Which is muscarinic receptor causing contraction of bronchiolar smooth muscle (bronchoconstriction)?

A

M3 receptor

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9
Q

Which receptors are inhibitory and stimulatory?

A

M1, M3, M5: Stimulatory (increased intracellular calcium)

M2, M4: Inhibitory (Inhibition of adenylyl cyclase)

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10
Q

Nicotinic

A

NN: Postganglionic neurons, some presynaptic cholinergic terminals
NM: Skeletal muscle neuromuscular endplates

[Opening of Na+, K+ channels, depolarization]

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11
Q

Cholinergic receptor type primarily localized at skeletal muscle neuromuscular junctions:

A

Nicotinic N*M

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12
Q

Cholinergic drugs mimic or

block the action of _____.

A

Acetylcholine

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13
Q

Acetylcholine is rapidly inactivated by synaptic

_____.

A

Acetylcholinesterase

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14
Q

Anticholinesterases

A

Reversible:

  • Short-acting (ionic binding to the anionic site)
  • Medium-acting (carbamylated enzyme is much slower to hydrolyzed)

Irreversible:

  • Phosphorylation of the serine group
  • Long-acting as the phosphorylated enzyme is very stable
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15
Q

Ileus

A

The inability of the intestine to contract normally leading to a build-up of food material.

Symptoms:

  • Inability to fart
  • Nausea
  • Vomiting
  • Abdominal discomfort
  • Constipation
  • Loss of appetite
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16
Q

List 4 Indirect Cholinergic agonists
(REVERSIBLE inhibitors of ChE)

ChE = cholinesterase which breaks down ACh

A 
Reversible inhibitors of ChE: 
neostigmine
physostigmine
pyridostigmine
edrophonium

P/S: 3 ends with “stigmine”

17
Q

What are the clinical effects at the PNS, CNS, and NMJ?

NMJ: neuromuscular junction
CNS: central nervous system
PNS: peripheral nervous system

A

Eye:
Sphincter muscle of IRIS- contraction (miosis)
Ciliary muscle- contraction for near vision

Miosis: Reduction in pupil size caused by the contraction of the pupillary constrictor muscle (muscarine receptor-mediated)

Heart:
SA- decrease in the rate (-ve chronotropy)
Atria- decrease in contractile strength (-ve inotropy), decrease in refractory period
Ventricles- small decrease in contractile strength
AV- decrease in conduction velocity (-ve dromotropy), increase in refractory period

18
Q

cont;

What are the clinical effects at the PNS, CNS, and NMJ?

A

Blood vessels:
Arteries, veins- dilation (via EDRF), constriction (high-dose direct effect)

Lung:
Bronchiol muscle- contraction (bronchoconstriction)
Bronchiol glands- stimulation

GIT:
Motility: increase
Sphincters: relaxation
Secretion: stimulation

19
Q

cont;

What are the clinical effects at the PNS, CNS, and NMJ?

A

Urinary bladder:
Detrusor- contraction
Trigon & sphincter- relaxation

Glands:
Sweat, salivary, lacrimal, nasopharyngeal- secretion

20
Q

NEOSTIGMINE

A

Used to reverse neuromuscular blockade induced by certain neuromuscular blocking agents.

Pharmacokinetics:-
Bioavailability: 1-2% (PO)
Onset: 1-20 mins (IV), 20-30 mins (IM)
Duration: 2.5-4H (IM), 1-2H (IV)
Protein bound: 15-25% to albumin (PO)
t1/2: 47-60 mins (IV), 51-90 mins (IM), 42-60 mins (PO)
21
Q

Arrange the duration of action of indirect ACh agonists

longest to shortest

A

Longest duration:

  1. Physostigmine
  2. Pyridostigmine
  3. Neostigmine
  4. Edrophonium; shortest duration
22
Q

True/ False:

Both Neostigmine & Physostigmine effective given orally, but Neostigmine easily penetrates BBB (causes CNS effects).

A

FALSE!!!

Both Neostigmine & Physostigmine effective given orally, but PHYSOSTIGMINE easily penetrates BBB (causes CNS effects).

23
Q

BETHANECHOL

Direct-acting choline esters

A
  • Pure muscarinic agonist
  • Used as treatment of bladder and gastrointestinal hypotonia

Pharmacokinetics:
Oral & parenteral, duration: 30 mins
Not enter CNS
Toxicity: Excessive parasympathomimetic effects, especially bronchospasm in asthmatics
Interactions: Additive with other parasympathomimetics

24
Q

​BETHANECHOL

Mechanism of action, Effects

A

Muscarinic agonist; negligible effect at nicotinic receptors

Effects:

  • Activates M1 through M3 receptors in all peripheral tissues
  • Causes increased secretion, smooth muscle contraction (except vascular smooth muscle relaxes), and changes in heart rate
25
Q

CARBACHOL

A

Nonselective muscarinic and nicotinic agonist; otherwise similar to bethanechol
Used tropically almost exclusively for GLAUCOMA

26
Q

PILOCARPINE

Mechanism of action, Effects

A

Partial muscarinic agonist; negligible effect at nicotinic receptors

Effects:

  • Activates M1 through M3 receptors in all peripheral tissues
  • Causes increased secretion, smooth muscle contraction (except vascular smooth muscle relaxes), and changes in heart rate
27
Q

PILOCARPINE

Clinical use, Pharmacokinetics

A
  • Treat Glaucoma (A condition where the eye’s optic nerve, which provides information to the brain, is damaged with or without raised intraocular pressure)
  • For xerostomia in Sjogren’s syndrome

Pharmacokinetics:
-Oral lozenge and topical
Toxicity: Excessive parasympathomimetic effects, especially bronchospasm in asthmatics
Interactions: Additive with other parasympathomimetics

28
Q

Xerostomia

A

Dry mouth, a condition in which the salivary glands in your mouth don’t make enough saliva to keep your mouth wet

29
Q

Name naturally occurring alkaloid which is a directly-acting cholinergic agonist
-producing all parasympathomimetic effects
-used topically to reduce intraocular pressure in canine
glaucoma therapy.

A

PILOCARPINE!!!

  • topically to reduce intraocular pressure in canine
    glaucoma therapy.
  • primarily a muscarinic agonist
30
Q

What do these compounds have in common?

  • Muscarine
  • Arecoline
  • Pilocarpine
A

All naturally occurring, direct-acting cholinergic AGONISTS

MAP “Directs u to nature’s cholon”
ine

31
Q

ATROPINE

A

Non-selective antagonist
Well absorbed orally
CNS stimulant

Clinical uses:
Adjunct for anesthesia (reduced secretions, bronchodilations)
Anticholinesterase poisoning Bradycardia
Gastrointestinal hypermobility (antispasmodic)

32
Q

ATROPINE

A

Main side effects:
urinary retention, dry mouth, blurred vision
Dicycloverine (dicyclomine) is similar and used mainly as an antispasmodic agent

Belladonna alkaloid
t1/2: 4 hours

33
Q

ATROPINE (Opthalmology)

A

Mechanism of action:
Competitive antagonism at all M receptors

Effects:
Causes mydriasis and cycloplegia

Clinical uses:
Retinal examination
Prevention of synechiae after surgery

Pharmacokinetics:
Uses as drops; long (5-6 days) action
Toxicity: increased intraocular pressure in closed-angle glaucoma
Interaction: with other antimuscarinics

34
Q

PIRENZIPINE

A

Pharmacokinetics:

  • Selective for M1 receptors
  • Inhibits gastric secretion by action on ganglion cells
  • Little effect on smooth muscle or CNS

Clinical use:
Peptic ulcer treatment

  • Fewer side effects than other muscarinic antagonists
  • Largely superseded by other antiulcer drugs
35
Q

Name 2 synthetic anti-muscarinic drugs (atropine-like agents)

A

Pirenzepine

Telenzepine

36
Q

IPRATROPIUM

A
  • Derivative of atropine
  • Produce bronchodilation, tachycardia & inhibition of secretion similar to atropine but with less inhibitory effect on mucociliary clearance
  • Side effect: dry mouth
  • Administered as an aerosol or solution for inhalation
  • Maximal responses: 30-90 mins
  • Effects: 4-6 hours
37
Q

IPRATROPIUM

Respiratory; asthma, COPD

A
  • Competitive, nonselective antagonist at M receptors

Mechanism of action: reduces/ prevents bronchospasm

Effects: prevention & relief of acute episodes of bronchospasm

Pharmacokinetics: Aerosol canister, up to qid
*qid: quarter in die, 4 times a day
Toxicity: Xerostomia, cough
Interactions: with other muscarinic

38
Q

PRALIDOXIME

A

Mechanism of action: very high affinity for phosphorus atom but does not enter CNS

Effects:

  • Regenerates active AChE (acetylcholinesterase)
  • Can relieve skeletal muscle & plate block

Clinical use:
Usual antidote for early-stage (48 hours) cholinesterase inhibitor poisoning

Pharmacokinetics:

  • Intravenous every 4-6 hours
  • Toxicity: Can cause muscle weakness in overdose

Pharmacology (8 decks)

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