Cholinergic Drugs - Pharmacology B. Pharma 5th Semester PDF Notes

Cholinergic Drugs



       Cholinergic drugs

       Pharmacology of acetylcholine

       Organophosphorous poisoning and its treatment

Intended Learning Outcomes

At the end of this lecture, student will be able to

       List the cholinergic drugs

       Explain the pharmacology of acetylcholine

       Describe pharmacokinetic of Ach

       Explain organophophorous poisoning

       Describe treatment of poisoning

Cholinergic Drugs (Parasympathomimetics)

       + effector cells innervated by cholinergic nerves

       Ester of choline

      Acetylcholine, methacholine, carbachol, bethanechol

       Cholinomimetic alkaloids

      Pilocarpine, muscarine, arecholine

       Choline esterase inhibitors (Anticholine esterase)

      Physostigmine, neostigmine, organophosphorous compounds

Pharmacological Actions of Acetylcholine



      + vagus nerve

      Depress SA Node: negative chronotropic

      Decrease FOC:  negative Inotropic

      May cause AV block

      Increase CV

       Blood vessels

      Dilate skin, mucous membrane blood vessels

      M3 – R: release NO

      Dilates coronary arteries

      Doubtful effect: cerebral, pulmonary vessels

      IV: transient flushing, sense of warmth in skin, throbbing headache

      Decrease PR – BP Falls

Smooth muscle

       GIT: increase tone and peristalsis

       Gall bladder: Contraction

       Bladder: Detrusor muscle contraction, trigonal sphincter relaxation

       Bronchial smooth muscle: constriction, bronchospasm

       Ureter: usually contraction

       Uterus: inconsistent response


       Increase gastric, intestinal, pancreatic, bronchial, salivary, lacrimal, nasopharyngeal

       Increase bronchial secretion: accompanied by bronchospasm

       May result in cough and dyspnea

       Salivary: profuse and watery

       Sweat glands: increase sweating


       Instillation – no effect

       Intracarotid injection: miosis

       Contraction of circular muscle fibers

       Decrease IOP

       Increase the drainage of ocular fluid through canal of Schlemm

       Contraction of ciliary muscle

       Relaxation of suspensory ligaments

       Lens bulge into anterior chamber

       Increase thickness, decrease focal length

       Vision fixed for short distance

       Spasm of accomodation

Autonomic ganglia

       Ach + ganglia

       Post ganglionic site: Increase NA/ Ach

       NA:   BP- Peripheral vasoconstriction

       Large dose: Adrenal medulla +

       Sustained increase in BP

Myoneural Junction

       Contraction of skeletal muscle

       High conc: paralysis by persistent depolarisation


       Essential for normal behaviour and cognition

       Does not cross BBB


       Extreme transient action

       Not used in clinical practice

       Substitutes : Effective orally

       More selective in actions

Cholinergic Drugs

Cholinomimetic alkaloids

       Pilocarpine (P. microphyllus, P. jaborandi)

       Muscarine (Amanita muscaria)

       Arecholine (Areca catechu)


      M3 agonist

      Incerase salivary and lacrimal secretion

      Used in dry mouth  

Choline esterase inhibitors (Anticholine esterases)

       Inhibits true and peudo choline esterase

       Prevent inactivation of Ach

Reversible choline esterase inhibitors

       Natural: Physostigmine

       Synthetic: Neostigmine, pyridostigmine, ambenonium, demecaium, edrophonium, tacrine, rivastigmine

Irreversible choline esterase inhibitors


       Useful: Di isopropyl fluorophosphate, metrifonate, echothiophate

       Insecticides: Fenthion, malathion, sumithion, monocrotophos, octamethyl pyrophosphotetramide

Uses of reversible Anti ChE


       For decurarisation, Curare poisoning


       GIT: Post-operative paralytic ileus

       Urinary retention (Rare)


       Snake venom poisoning

Irreversible Anti ChE

       Absorbed by all the routes

       Cross BBB

       Glaucoma: echothiophate

       Worm infestation: dichlorovos, dichlorofos (Not used)

       Toxicological importance

OPC Poisoning

Muscarinic effects

       Eyes: Miosis, spasm of accomodation, head ache, conjunctival hyperemia

        inhalation: bronchospasm, cough, increases secretions, tightness in chest

       Ingestion: anorexia, nausea, vomitting, abdominal cramps, tenesmus and diarrhoea

       Severe bronchospasm, pulm. edema - fatal

Nicotinic effects

       Fasciculations, twitching, generalised weakness, depolarisation type paralysis

Central effects

       Giddiness, anxiety, confusion, ataxia, hypotension, respiratory depression, convulsion, coma

       Death – due to respiratory paralysis

Neurotoxic effects

       Demyelination of nerve tracts in CNS & PNS

       Permanent functional derrangements

       Not related to ChE inhibition

       Weakness, fatiguability, twitching, loss of tendon reflexes

Treatment of acute OPC Poisoning

       Remove soiled clothes

       Wash soiled skin/ eyes

       Nurse in prone position

       Clear mouth, throat

       Insert airway/ intubate

       Gastric lavage

       Atropine in sufficient qty.

       ChE activator: Pralidoxime (1-2 g)

       Supportive measures: Oxygen, shock treatment

       Convulsion: Diazepam

       Vigilance for delayed toxicity

       Note: Mouth to mouth respiration to be avoided


       Cholinergic drugs stimulate effector cells innervated by cholinergic nerves

       Cholinergic drugs: Ester of choline, Cholinomimetic alkaloids, Choline esterase inhibitors (Anticholine esterase)

       Acetylcholine actions - mostly inhibitory; stimulatory on digestion and exocrine glands

       Pralidoxime is the antidote for OPC poisoning

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