CHOLINERGIC SYSTEM

AND
CHOLIMIMETIC DRUGS

Dr. SHARATH KM

Doctor of Pharmacy,

Physician Asst., FMMCH,

Mangalore
 CHOLINERGIC AGENTS
INTRODUCTION Direct Acting Cholinergics
Cholinergic medications are a category of pharmaceutical agents
that act upon the neurotransmitter acetylcholine, the primary
neurotransmitter within the parasympathetic nervous system
(PNS).

• There are two broad categories of cholinergic drugs: direct-

acting and indirect-acting.
The direct-acting cholinergic agonists work by directly binding
to and activating the muscarinic receptors.

• Examples of direct-acting cholinergic agents include:

1. Choline esters (acetylcholine, methacholine, carbachol,
bethanechol) and
2. Alkaloids (muscarine, pilocarpine, cevimeline).
 INTRODUCTION TO INDIRECT ACTING CHOLINERGICS
• Indirect-acting cholinergic 1. Reversible Agents:
agents increase the availability
Physostigmine: Neostigmine Bromide: Pyridostigmine Bromide:
of acetylcholine at the
cholinergic receptors.
 These include reversible agents:
1. Physostigmine,
2. Neostigmine,
3. Pyridostigmine,
4. Edrophonium,
5. Rivastigmine,
6. Donepezil, 2. Irreversible Agents:
7. Galantamine
Echothiophate: Pralidoxime Chloride:
 Irreversible agents:
1. Echothiophate,
2. Parathion,
3. Malathion,
4. Diazinon,
5. Sarin and Soman.
 CHOLINERGIC SYSTEM
1. Acetylcholine (ACh) is the major neurotransmitter of parasympathetic nervous system
(PSNS).
2. Cholinergic nerves: Synthesize, store and release ACh.
3. Important ACh release sites:
a. Ganglia: All preganglionic ANS (SNS and PSNS) fibers.
b. Postganglionic parasympathetic nerve terminals.
c. Adrenal medulla.
d. Brain and spinal cord.
e. Neuromuscular junction (NMJ).
f. Sympathetic postganglionic nerve terminals of sweat
glands (this is an unconventional site).
 SYNTHESIS/TRANSMISSION/METABOLISM OF ACETYLCHOLINE (ACH):

• Acetyl CoA + Choline Acetylcholine

Choline Acetyl Transferase (CAT)

• Acetylcholine is stored in vesicles in cholinergic nerve terminals.

• Action potential at presynaptic membrane
• Release of ACh in synaptic cleft
• ACh binds and stimulates postsynaptic cholinergic receptor
• Depolarization of postsynaptic membrane
• Metabolism of ACh by acetylcholinesterase (AChE) in synaptic cleft
• Repolarization of postsynaptic membrane
TRANSMISSION OF ACETYLCHOLINESTERASE (ACH)
 CHOLINESTERASES

1 ACh is degraded to choline + Acetic acid by enzyme Acetylcholinesterase(AChE).

2 There are two types of AChE:

a. True
b. Pseudo

3 Cholinergic Receptors
1. Cholinergic receptors are of two types:
• Muscarinic
• Nicotinic

• Muscarinic receptors are of five subtypes, i.e.

M1, M2, M3, M4 and M5. Its effector pathways
• Nicotinic are of two subtypes, i.e.,
nicotinic neuronal (Nn) and nicotinic muscle (Nm).
 4. Muscarinic receptors are G protein coupled receptors.

5. Nicotinic are ion (Na+) channels and have 5 subunits, i.e. 2α,1β,1γ,1δ:
• M1 receptors are present in → autonomic ganglia, gastric glands and central nervous system
(CNS)
• M2 receptors are present in → heart, smooth muscles
and nerves
1 CHOLINERGIC DRUGS: These are 2 Classification:
medications that affect the cholinergic 1. Choline esters → Acetylcholine,
system, which involves the methacholine, carbachol, bethanechol
neurotransmitter acetylcholine.
1. Act at same site, i.e. ACh. 2. Cholinomimetic alkaloids →
2. Mimic actions of ACh. pilocarpine, muscarine
Therefore called ‘Cholinomimetics’ or
‘Parasympathomimetics’
 CLASSIFICATION

1 2

3. Anticholinesterases:

• Reversible → Neostigmine,
physostigmine, pyridostigmine, REVERSIBLE ANTICHOLINESTERSES
edrophonium (short acting),
rivastigmine, galantamine, donepezil
[(CNS action, i.e. for treatment of
Alzheimer’s disease)]

• Irreversible → Organophosphates
→ echothiophate,
malathion, toxic nerve gases (sarin,
tabun). IRREVERSIBEL CHOLINESTEREASES
MUSCURANIC AND NICOTINIC AGONISTS AND ANTAGONISTS
 MECHANISM OF ACTION
Actions of Acetylcholine (ACh):
1. Muscarinic actions: It resembles
alkaloid muscarine present in
mushrooms, due to stimulation of
muscarinic receptors (M1–M3):
a. Heart:
• Resemble vagal stimulation
• Inhibits sinoatrial (SA) and
atrioventricular (AV) node
• Hence, increases in heart rate (HR) and
force of contraction (FOC) →
Bradycardia.
b. Blood vessels:
• Dilatation
• Due to release of nitric oxide/endothelium
derived relaxing factor (EDRF).
c. Smooth muscles:
• Increases tone of all nonvascular smooth
muscles
• Gastrointestinal tract (GIT): Increases
tone and peristalsis, relaxes sphincters, hence
there is propulsion and evacuation of GI
contents
• Urinary bladder: Detrusor contracts,
trigone relaxes, hence it promotes evacuation
of urine.
 MECHANISM OF ACTION

d. Secretory glands: Increases secretion of all glands viz. lacrimal, salivary, tracheobronchial,
nasopharyngeal, gastric, intestinal and sweat.

e. Eye :

i. Constriction of sphincter pupillae leads to miosis.

ii. Increases drainage of aqueous humor, hence increases Intra-Ocular Pressure (IOP).

iii. Ciliary muscle contraction causes spasm of accommodation.

 2. Nicotinic actions: It resemble, action of alkaloid nicotine due to stimulation of
nicotinic receptor, i.e. Nn and Nm:

1 a. Neuro-Muscular Junctions:
i. Contraction of skeletal muscles (Nm receptors).
ii. Higher doses result in persistent contraction, thus causing spastic paralysis.

2 b. Autonomic ganglia:
i. Activates both sympathetic and parasympathetic
ganglia.
ii. Activates adrenal medulla.

3 c. CNS:
i. Stimulates several sites.
ACTIONS OF CHOLINERGIC AND ANTICHOLINERGIC DRUGS
 CHOLINERGIC DRUGS AND THEIR TYPES
1 • Cholinergic drugs are medications that
affect the cholinergic system, which
involves the neurotransmitter
acetylcholine. These drugs either
mimic the action of acetylcholine or
inhibit its breakdown, leading to
increased cholinergic activity.
• The cholinergic system is involved in
various physiological processes,
including muscle contraction, heart
rate regulation, and cognitive function.
2 1. Cholinergic Agonists: These drugs
stimulate cholinergic receptors, leading
to increased acetylcholine activity.
• Examples include drugs like
pilocarpine (used for conditions like
glaucoma) and bethanechol (used for
urinary retention).
2. Cholinesterase Inhibitors: These
drugs prevent the breakdown of
acetylcholine by inhibiting the enzyme
acetylcholinesterase.
• Examples include medications like
donepezil, rivastigmine, and
galantamine, which are used in the
treatment of Alzheimer's disease.
 ACETLYCHOLINE AND THEIR USES

Uses of ACh:

• Cholinergic agonists may be used to stimulate smooth muscle contractions,

increase secretions, or lower intraocular pressure.

• Cholinesterase inhibitors are often used to enhance cholinergic activity in

conditions associated with acetylcholine deficiency, such as Alzheimer's disease.
1. Rapidly metabolized in gut and plasma (by pseudocholinesterase) and at site of action
(by true cholinesterase).
2. Hence, not used therapeutically.
3. Rarely used as 1% eye drops for miosis during some eye Operations.
 CHOLINOMIMETICS AND THEIR USES

• Uses of other Cholinomimetics:

1. Carbachol/Bethanechol resistant to metabolism by both cholinesterase's, hence acts on a long
duration of action.
2. Carbachol - used in glaucoma.
3. Bethanechol:
• Used in urinary bladder hypotonia
• Used in urinary retention
• Used in postoperative paralytic ileus
• Used in xerostomia (alternative to pilocarpine).
ADVERSE DRUG REACTIONS OF CHOLINERGICS
Side Effects:
• Common side effects of cholinergic drugs may include increased salivation, sweating,
gastrointestinal disturbances, and, in some cases, bradycardia (slowed heart rate).
• Excessive cholinergic stimulation can lead to adverse effects, and dosages need to be carefully
managed.
• Adverse Reactions of Cholinomimetics
• (Mnemonic SLUDGE’)
i. S: Salivation iv. D: Diarrhoea
ii. L: Lacrimation v. G: GI/GU Cramps
iii. U: Urination vi. E: Emesis/ Eye (Miosis)
 CHOLINOMIMETIC ALKALOIDS
• Cholinomimetic Alkaloids:
1. Pilocarpine
• Source - Pilocarpus microphyllus.
• Has prominent muscarinic actions.
• Actions on eye
i. Miosis
ii. Spasm of accommodation topically
iii. Decreases IOP (Intra Ocular Pressure).
• Increases sweating (diaphoresis).
• Increases salivary secretion (sialagogue).
• Side effects:
i. Brow ache and headache due to spasm of accommodation
and miosis
ii. Corneal edema
iii. Retinal detachment (on long-term use).
• Uses:
a. Glaucoma—as ocusert, a novel delivery system, which releases
pilocarpine for 7 days.
b. Alternatively with mydriatics (pupillary dilators) to
prevent/break adhesions between iris and lens.
c. Xerostomia (Sjogren’s syndrome).
 CHOLIMIMETIC ALKALOIDS AND THEIR THERAPEUTIC USES
• Glaucoma:
1. Increase in Intra-Ocular Pressure (IOP)
beyond 21 mm Hg.
2. Aqueous humor is produced by ciliary body.
3. It drains via canal of Schlemm.
4. Increase in IOPs, which leads to optic nerve
degeneration, therefore causes blindness.
.
5. There are two types of glaucoma:
a. Acute congestive/angle closure/narrow angle:
i. In this type, the iris blocks canal of
Schlemm.
ii. Should be treated urgently.
b. Chronic simple/open angle/wide angle:
i. Has a slow onset.
ii. Long-term
treatment is required.
iii. Surgical treatment is usually preferred.
DRUGS USED TO TREAT GLAUCOMA:
A. Drugs decreasing formation of aqueous humor
(all topical):
i. Beta blockers: Timolol, Betaxolol,
Levobunolol (first-line drugs).
ii. Adrenergic agonists: Adrenaline, dipivefrin
(usedwith beta blockers)
iii. α2 adrenergic agonists: Apraclonidine,
brimonidine.
iv. Carbonic anhydrase inhibitors:
Dorzolamide, acetazolamide (oral).
B. Drugs increasing drainage of aqueous humor:
i. Cholinergics: Pilocarpine, carbachol,
physostigmine, echothiophate.
ii. Prostaglandine analogues: Latanoprost,
Bimatopros (adjuvants).
C. Beta blockers in glaucoma:
a. For example, timolol.
b. They are first-line drugs.
c. They decrease aqueous production.
d. They block βreceptors in ciliary body.
e. There is no miosis, hence there is no headache,
brow
ache (unlike pilocarpine), therefore: It is preferred.
f. Causes a smooth and sustained decrease in IOP.
DRUGS USED TO TREAT GLAUCOMA:
D. Adrenergic agonists in glaucoma:
a. For example, dipivefrin (a prodrug
of adrenaline), apraclonidine
(analogue of clonidine, brimonidine).
b. Decreases IOP by reducing ciliary
body blood flow (due to α1induced
vasoconstrictions).
c. Also reduces uveoscleral blood
flow.
d. Adrenaline cannot cross cornea,
but dipivefrin
penetrates cornea and is converted to
adrenaline.
E. Miotics:
a. For example, pilocarpine, physostigmine.
b. They constrict pupils, thus opens up canal of
Schlemm, hence increases drainage.
F. Prostaglandin analogues:
a. For example, latanoprost.
b. It is a prodrug of PGF2α.
c. It increases drainage by relaxing ciliary muscle.
d. They are used as adjunct.
DRUGS USED TO TREAT GLAUCOMA:

11. Carbonic anhydrase inhibitors (CAI’s):

a. For example, dorzolamide (topical), acetazolamide (oral).

b. Aqueous humor formation requires HCO3 –.
c. HCO3 – are produced by carbonic anhydrase.
Carbonic anhydrase
↓
H2 CO3 → H+ + HCO- 3
d. CAI’s by inhibiting the enzyme carbonic anhydrase
decreases HCO –3, thus decreases IOP.
e. Oral acetazolamide leads to Hypokalaemia, Anorexia, Drowsiness.
f . Hence, topical dorzolamide is preferred.
CLASS OF DRUGS USED TO TREAT GLAUCOMA:
 ANTI-CHOLINESTERASES
Anticholinesterases (Anti-ChE): Classification of Anti-ChE:
• Reversible:
• Inhibits enzyme cholinesterase (AChE)
Acetylcholine → Acetic acid + choline I. Carbamates → Physostigmine,
↑ neostigmine, pyridostigmine,
AntiChE inhibits→ AChE edrophonium, donepezil, rivastigmine,
tacrine,
• Anticholinesterases are structural analogs of Ach Galantamine

• They bind to cholinergic receptors and inactivates them
• Therefore, ACh is not metabolized and accumulates at
Synapse
• Therefore, their actions are similar to Ach
• AChE has two sites → anionic and esteratic.
II. Insecticides → Propoxur (baygon),
carbaryl, aldicarb.
• Irreversible:
I. Organophosphates → Echothiophate,
malathion, toxic nerve gases (sarin, tabun).
 CLASSIFICATION OF ANTICHOLINESTERASES

• Physostigmine: • Neostigmine:
1. Source – natural alkaloid of Physostigma 1. Neostigmine is synthetically produced.
venenosum. 2. It is a quaternary ammonium compound,
2. It is a tertiary ammonium compound, hence has a hence has
high lipid solubility. poor lipid solubility.
3. Thus, it has a better oral, CNS, tissue penetration:
3. Uses:
4. Uses: a. Myasthenia gravis (as it has additional direct
a. Glaucoma (with pilocarpine nitrate).
action
b. Atropine poisoning.
on NMJ).
b. Postoperative paralytic ileus.
5. Adverse drug reactions (ADRs):
a. Brow ache.
c. Urinary bladder atony.
b. Retinal detachment.
c. Cataract.

6. Availability—topical (0.1–1%), IV injection.

 CLASSIFICATION AND MECHANISM OF ANTICHOLINESTERASES
Mechanism of anticholinesterases
• Edrophonium
1. It is rapid and short-acting.

2. Uses:
• To differentiate between myasthenia
crisis v/s cholinergic crisis.
• IV for snake bite, curare poisoning.

• Rivastigmine, Donepezil, Galantamine,

Tacrine:

Specifically used in the treatment for Alzheimer’s

disease (AD)
 USES OF REVERSIBLE ANTI-CHOLINERGICS
As a miotic:
a. In glaucoma with pilocarpine.
b. Alternating with mydriatics to prevent/break
adhesions between lens and iris.
2. Myasthenia gravis:
a. Myasthenia gravis (MG) is a chronic autoimmune
disorder.
b. Characterized by Nicotinic receptor (NMJ)
antibodies, which decreases NMJ receptor mass.
c. Leads to progressive skeletal muscle weakness
and easy fatigability.
d. Diagnosed by IV edrophonium.
e. Treatment is neostigmine 15 mg qds.
f. Neostigmine increases ACh concentration at NMJ.
g. Neostigmine additionally has direct stimulant
action on NMJ.
h. Hence, muscle power improves.
i. Excessive muscle weakness (due to infection, surgery,
stress) can lead to myasthenia crisis.
j. Excessive muscle weakness (due to increase dose of
Anti-ChE, i.e. neostigmine) can lead to cholinergic
crisis.
k. Crisis differentiated by IV edrophonium 2 mg.
l. IV edrophonium in myasthenia crisis → patient
improves.
m. IV edrophonium in cholinergic crisis → patient
worsens.
n. Treatment of myasthenia crisis → increase dose of
AntiChE.
o. Treatment of cholinergic crisis → decrease dose of
AntiChE, atropine.
p. Other treatment of myasthenia gravis:
i. Glucocorticoids to decrease antibodies.
ii. Immunosuppressants, e.g. azathioprine, cyclosporine,
decreases antibodies
 USES OF REVERSIBLE ANTI-CHOLINERGICS
3. Anticholinergic poisoning:
a. Atropine poisoning.
b. Toxicity of drugs with anticholinergic actions,
e.g. Anti-Histaminic, Tricyclic antidepressants and
Phenothiazine.
c. Physostigmine preferred, since it has good tissue
penetration (as it is a tertiary amine), crosses BBB,
hence it neutralizes CNS toxicity also.
4. Curare poisoning:
a. Neostigmine is preferred as it has additional
direct NMJ action besides Anti-ChE
action.
5. Postoperative paralytic ileus.
6. Urinary bladder atony/retention.
7. Cobra bite, since bite releases neurotoxin which
paralyses skeletal muscles.
8. Alzheimer’s disease:
a. To improve cholinergic deficiency in CNS.
b. Specifically rivastigmine, tacrine, donepezil.
9. Irreversible AntiChE:
a. Echothiophate eye drops for glaucoma.
 IRREVERSIBLE ANTI-CHOLINERGICS
Irreversible Anti-ChE
(Organophosphorus Compounds):
6. Edrophonium binds to only anionic site, hence
action is quickly reversible and short acting.
1. Organophosphorus, compounds.
7. All OP compounds (except echothiophate) are
2. They are powerful, irreversible inhibitors of highly lipid soluble.
anti-ChE.
8. Hence, can be absorbed from all routes, including
3. Binding is covalent to only esteratic site and intact skin.
enzyme is phosphorylated.
9. Thus, OP poisoning can also occur by spraying of
agricultural pesticides/insecticides.
4. Hence, binding is stable and irreversible.
10. Only echothiophate binds to both anionic and
5. Reversible anti-ChE (except edrophonium) esteratic site.
binds to both anionic and esteratic site.
 ORGANOPHOSPHOROUS POISINING
Organophosphorus Poisoning: 5. Treatment:
a. Poisoning via skin:
1. OP compounds are used as agricultural i. Remove clothing.
insecticides/ pesticides. ii. Wash skin with soap and water.

2. Hence, poisoning is frequent. b. Poisoning via oral route.

i. Gastric lavage.
3. Poisoning could be accidental/suicidal/homicidal. c. Maintain BP and airway patency.

4. Signs/Symptoms: d. Atropine IV 2 mg every 10 minutes. Till pupil dilates/dryness

a. Similar to cholinergic (muscarinic, nicotinic, CNS)
hyperactivity.
b. For example, SLUDGE (salivation, lacrimation,
urination,
diarrhoea, GI/GU cramps, emesis/eyemiosis).
c. Sweating, increased tracheobronchial secretions,
increased GI secretions, bronchospasm, hypotension,
convulsions and coma.
d. Respiratory paralysis can cause death.
of mouth (drug of choice).
e. Cholinesterase reactivators, e.g. pralidoxime:
i. Pralidoxime combines with cholinesterase—OP
complex.
ii. Releases binding, frees AChE enzyme.
iii. Administered within minutes of poisoning
(maximum 12–24 hours).
iv. Since delay leads to ‘ageing’ of enzyme hence cannot be
freed.
 ANTICHOLINERGICS

1. Also called antimuscarinics, para-sympatholytics or cholinergic blocking drugs.

2. They block the effects of ACh on muscarinic receptors.
3. Drugs that block nicotinic receptors are ganglionic blockers or neuromuscular blockers.

Classification
1. Natural alkaloids → atropine (prototype), obtained from Atropa belladonna, DOC for OP poisoning →
hyoscine (scopolamine) for motion sickness).

2. Semisynthetic derivatives → Homatropine (mydriatic) → Ipratropium bromide, Tiotropium bromide

(both for bronchial asthma).

3. Synthetic substitutes:
→ Mydriatics: Tropicamide, Cyclopentolate.
→ Antispasmodic: Antisecretory, Dicyclomine, Propantheline,
Glycopyrrolate, Telenzepine, Tolterodine.
→ Antiparkinsonian: Benztropine, Benzhexol,
Trihexyphenidyl.
 MECHANISM OF ACTION OF ANTICHOLINERGICS
1. Cardiovascular system (CVS): 3. Smooth muscles:
a. Increases heart rate, causes tachycardia. a. GIT:
b. Large doses leads to hypotension. i. Decreases tone and motility, hence causes
constipation.
2. Secretions: ii. Relieves spasm.
a. Decrease all secretion, i.e. lacrimal, salivary,
gastric, b. Genitourinary:
tracheobronchial, nasopharyngeal, except milk. i. Relaxes ureters.
b. Decreases sweating results in fever, atropine ii. Relaxes urinary bladder.
fever. iii. Hence, they can cause urinary retention,
c. Decreased salivary secretions lead to dry especially
mouth, in elderly males with benign prostate hypertrophy
dysphagia. (BPH).
d. Decreased lacrimal secretions lead to dryness
of eyes. c. Bronchi:
i. Bronchodilation.
ii. Decrease tracheobronchial secretion.
iii. Provides symptomatic relief in (COPD)
 MECHANISM OF ACTION OF ANTICHOLINERGICS

d. Biliary tract:
i. Relaxes smooth muscle.
ii. Hence, relieves spasm.

4. Eye:
a. Topical application blocks muscarinic receptors
on sphincter pupillae, which causes mydriasis → increased IOP.
b. Ciliary muscle are paralyzed, paralysis of accommodation leads to cycloplegia (blurring of
vision).

5. Central nervous system (CNS):

a. High doses of atropine causes CNS stimulation leading to anxiety, restlessness, hallucination,
delirium.
b. Scopolamine (hyoscine) causes CNS depression hence causes sedation and drowsiness.
 REPORTED ADR’S OF ANTICHOLINERGIC TOXICITY
Adverse Effects:

• Dry mouth

• Dysphagia

• Constipation

• Urinary retention

• Blurring of vision

• Tachycardia, palpitations

• Restlessness, hallucinations, delirium

• Toxicity is treated with IV physostigmine.

 USES OF ANTICHOLINERGIC AGENTS
Uses
1. Antispasmodic:
a. Renal colic along with morphine.
b. Biliary colic.
c. Abdominal colic along with loperamide.
d. Irritable bowel syndrome.
e. Nocturnal enuresis.
f. Post urological surgeries.
2. Mydriatic and cycloplegic:
a. Therapeutic:
i. Iritis, iridocyclitis, keratitis, following
iridectomy (to provide rest to eye).
b. Diagnostic:
i. Fundoscopy.
ii. Testing errors of refraction.
c. Alternating with miotics (e.g. pilocarpine,
physostigmine) to prevent/break adhesions between
lens and iris.
3. Preanesthetic:
a. Atropine 30 minutes before anaesthesia.
b. Decreases salivary, tracheobronchial and gastric
secretions.
c. Prevents laryngospasm.
d. Additional bronchodilatory property.
e. Prevents vasovagal attack.
f. Glycopyrrolate is preferred.
4. Organophosphorus (OP) poisoning:
a. Drug of choice (DOC).
b. 2 mg IV every 10 minutes till pupil
dilates/dryness of mouth.
 USES OF ANTICHOLINERGIC AGENTS

5. Motion sickness:
a. Transdermal (behind ear, on mastoid) scopolamine 30 minutes before journey.

6. Bronchial asthma and COPD:

a. Ipratropium/Tiotropium bromide.
b. Causes bronchodilation.
c. Does not depress mucociliary clearance (unlike atropine), hence there is no inspissation of mucus in
respiratory passage.

7. Peptic ulcer:
b. M1 blockers such as pirenzepine/telenzepine.

8. Antiparkinsonian/Drug-induced parkinsonism:
a. Centrally acting anticholinergics.
b. For example, benztropine, benzhexol, trihexyphenidyl.
 OTHER USES OF ANTICHOLINERGICS
Atropine Substitutes
Quaternary Compounds
1. Hyoscine butyl bromide—20–40 mg oral/IM:
• Use: Oesophageal, gastrointestinal (GI) spastic
conditions.
2. Atropine methonitrate—2.5–10 mg orally/IM:
• Use: Abdominal colic and hyperacidity.
3. Ipratropium bromide—40–80 mg inhalational:
Use: COPD and bronchial asthma.
4. Glycopyrrolate—0.1–0.3 mg IM, 1–2 mg/oral:
• No central effect
• Potent and rapidly acting antimuscarinic
• Use: For preanesthetic medication and during
anaesthesia
5. Propantheline, clidinium and oxyphenonium
• Use: Peptic ulcer, gastritis, irritable bowel
syndrome,
colic and GI hypermotility.
Tertiary Amines
1. Dicyclomine: 20 mg oral/IM:
a. Direct smooth muscle relaxant action.
b. Antispasmodic action.
c. Antiemetic.
• Use: Dysmenorrhea, irritable bowel syndrome,
motion sickness and morning sickness.
2. Pirenzepine: Used to relieve peptic ulcer pain.
 OTHER USES OF ANTICHOLINERGICS
Vasicoselective Drugs: 2. Homatropine:
• 10 times less potent than atropine
• Oxybutynin • Dilatation takes 45–60 minutes last for 1–3 days.
• High affinity for receptors of urinary bladder and
salivary glands. 3. Cyclopentolate:
Uses: Neurogenic bladder, spina bifida, nocturnal • Potent and fast acting (dilatation 30–60 minutes
enuresis and last for 1 day)
and overactive bladder, urinary urgency, frequency, • Preferred for cycloplegic refraction, uveitis and
dysuria. iritis
• Adverse effects—transient behavioural
Mydriatics abnormalities.
1. Atropine:
• Potent 4. Tropicamide:
• Slow and longer acting a. Quickest (onset 20–40 minutes, brief duration for
• Undesirable for refraction testing 3–6 hours).
• Pupils dilates in 30–40 minutes, cycloplegia in 1–3 b. Satisfactory for refraction testing in adults and
hours last for a week. for fundoscopy.
CLASSES, USES AND ACTIONS OF ANTICHOLINESTERASES
THE END