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![CHOLINERGIC DRUGS
[PARASYMPATHOMIMETICS]
DR. RAMESH KRISHNAN
MD,PHARMACOLOGY[2 ND YEAR]](https://image.slidesharecdn.com/cholinergicramesh-170719142000/85/Cholinergic-ramesh-1-320.jpg)
![CHOLINERGIC DRUGS
[PARASYMPATHOMIMETICS]
DR. RAMESH KRISHNAN
MD,PHARMACOLOGY[2 ND YEAR]](https://image.slidesharecdn.com/cholinergicramesh-170719142000/75/Cholinergic-ramesh-1-2048.jpg)
Uploaded byDr Ramesh Krishnan
Cholinergic ramesh
This document discusses cholinergic drugs, which act on the parasympathetic nervous system. It describes two main types: direct-acting cholinergics (acetylcholine and related agonists) and indirect-acting cholinergics (cholinesterase inhibitors). The direct-acting drugs include acetylcholine, pilocarpine, and muscarine. The indirect-acting drugs inhibit the enzyme acetylcholinesterase, increasing cholinergic activity. Examples given are physostigmine, neostigmine, pyridostigmine, and organophosphate nerve agents. The document outlines the mechanisms and uses of these drugs in conditions like glaucoma, myasthenia gravis,
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- 1. CHOLINERGIC DRUGS [PARASYMPATHOMIMETICS] DR. RAMESHKRISHNAN MD,PHARMACOLOGY[2 ND YEAR]
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- 7. Action Potential Na+ aab ACh Acetylcholinesterase Na+ Parasympathetic GanglionicSynapse Preganglionic neuron Postganglionic neuron Receptor
- 9. nicotine muscarine muscarinic receptor The ‘master key’for both types of ‘lock’ ACh ACh Acknowlegement-Dr.Kumarasingam
- 12. M1 Location 1) Gastricparacrine glands 2) CNS (Cortex, hippocampus, striatum 3) sympathetic ganglia Molecular mechanism Activation of PLC : ↑ IP3 & DAG :↑ Ca2+ & PKC Functional response ↑ acid secretion ↑ cognitive function(learning &memory) ↑ depolarisation of autonomic ganglia Agonists Oxotremorine Antagonists Pirenzepine,Telenzepine
- 14. M2 Location 1)Heart 2)Smooth muscle 3)Nerveterminal 4)CNS Molecular mechanism (-) of adenyl cyclase – ↓cAMP , Activation of K+channel Functional response HEART -SA node -↓ HR : AV node - ↓ conduction Atria - ↓contraction : Ventricle- ↓ contraction Smooth muscle - ↑contraction Agonists Methacholine Antagonists Methoctramine, Tripitramine
- 16. M3 Location 1)Glands 2)Smooth muscle 3)Iris,ciliary muscle 4)CNS Molecular mechanism Similar to M1 Functional response Smooth muscle contraction Blood Vessel-relaxation Pupil constriction , ciliary contraction Agonists Bethanechol Antagonists Darifenacin
- 22. M4 Location CNS(forebrain) Molecular mechanismSimilar to M2 Functional response Inhibit transmitter release Analgesia Location Substantia nigra Molecular mechanism Similar to M1 & 3 Functional response Cerebral vasodilatation Facilitates DA release M5
- 23. Ach actions – Nicotinic 1.Autonomic ganglia: – Both Sympathetic and parasympathetic ganglia are stimulated – After atropine injection Ach causes tachycardia and rise in BP 2. Skeletal muscle – IV injection – no effect – Application causes contraction of skeletal muscle 3. CNS: – Does not penetrate BBB
- 25. Classification Cholinoceptor stimulants Direct-acting (receptor agonists) Indirect-acting (cholinesteraseinhibitors) Muscarinic Nicotinic Choline esters Alkaloids Ganglionic Neuromuscular
- 26. DIRECTLY ACTING CHOLINERGICS CHOLINEESTERS • Acetylcholine • Bethanechol • Carbachol • Methacholine ALKALOIDS • Muscarine • Pilocarpine • Arecoline
- 27. Acetylecholine:- Is the neurotransmitterof the parasympathetic N.S and cholinergic nerves, it is therapeutically of no importance due to: • 1. Multiplicity of actions. • 2. Rapid inactivation by acetyl-cholinesterase. • 3. Has both muscarinic and nicotinic activity.
- 30. CHOLINOMIMETIC ALKALOIDS PILOCARPINE • Obtainedfrom leaves of Pilocarpus Microphyllus • Tertiary amine Crosses BBB • Dominant – M3 & NN • Too toxic for systemic use • ADR – ↑ sweating, salivation & other secretions • Small doses ↓ BP High doses ↑ BP
- 31. USES 1. EYE -Penetrates cornea – Miosis, Ciliary muscle contraction, ↓IOP lasting 4 – 8 hrs • 3rd line drug - Primary open angle Glaucoma –S/E : Initial stinging , –Painful spasm of accomodation • To counteract Mydriatics • Prevent adhesions of Iris with lens/ cornea 2. As SIALOGOGUE
- 32. MUSCARINE • Obtained frompoisonous mushrooms • Amanita muscaria & Inocybe • Has only muscarinic actions • No therapeutic indications • Quarternary alkaloid ↓ BBB penetration
- 33. ARECOLINE • Betel nut •Predominant M + slight N • Prominent CNS effect
- 34. CEVIMELINE • Direct actingat M3 • Lacrimal & Salivary gland epithelium • Longer lasting Sialogogue action than pilocarpine • ↑ lacrimal secretion in Sjogrens syndrome
- 35. INDIRECTLY ACTING PARASYMPATHOMIMETICS ANTI CHOLINEESTERASES REVERSIBLE NATURAL SYNTHETIC CARBAMATES ACRIDINE IRREVERSIBLE OP CARBAMATES
- 36. ANTI CHOLINE ESTERASES NATURAL •Physostigmine • Galantamine SYNTHETIC CARBAMATES ACRIDINE Neostigmine Tacrine Pyridostigmine Edrophonium Donepezil Rivastigmine REVERSIBLE
- 37. IRREVERSIBLE Organophosphates • Ecothiophate • Isoflurophate •Parathion • Malathion • Diazinon NERVE GASES • Tabun , Sarin , soman CARBAMATES • Carbaryl • Propoxur
- 38. ACh is brokenby AChE
- 40. Mechanism of action:- • 1.Acetylcholinesterase inhibitors - inhibit the AChE, responsible for breakdown of ACh • 2.increased cholinergic activity -both nicotinic and muscarinic receptors
- 41. Mechanism of actionof phosphates:- AchE + phosphates Phosphorylated enzyme Ageing-Loss of alkyl gp-resistant to hydrolysis (extremely slow reaction)
- 42. Mechanism of actionof carbamates:- AchE + carbamates Carbamylated enzyme + H2O Free enzyme + carbamic acid (slow reaction) ½ life of reactivation - carbamylated enzyme - 30 mins -less than synthesis of fresh enzyme
- 51. USES OF ANTICHOLINESTERASEDRUGS 1.MIOTIC A) GLAUCOMA • ↑ tone of ciliary muscle ( attached to scleral spur) & • ↑ tone of Sphincter pupillae pull on & improve alignment of trabeculae outflow facility is ↑ • Physostigmine (0.1 %) B ) TO REVERSE EFFECT OF MYDRIATICS C ) TO PREVENT ADHESIONS OF IRIS WITH CORNEA / LENS
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- 54. 3.POST OPERATIVE PARALYTICILEUS / URINARY RETENTION • Neostigmine 4.POST OPERATIVE DECURARIZATION • Atropine (Block M) Followed by Neostigmine 5.COBRA BITE • Neostigmine + Atropine prevent Respiratory Paralysis 6.ANTI CHOLINERGIC OVERDOSAGE • TCA, Phenothiazine, Anti Histamine – Physostigmine.
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- 59. Management of OPPoisoning :- • Termination of further exposure fresh air, wash the skin & mucosa with soap & water, gastric lavage • Maintain airway- PPV if its failing • Supportive measures – Maintain BP – Hydration – control of convulsions -diazepam
- 60. 1. Atropine • Highlyeffective, it counteract Muscarinic symptoms, higher doses antagonise central effects • 2 mg IV repeated every 10 minutes till dryness of mouth • Dilatation of pupil and HR up to 140 • Does not reverse peripheral muscle paralysis
- 61. CHOLINE ESTERASE REACTIVATORS 2.OXIMES •Phosphorylated enzyme reacts very slowly with water • Hydrolysis occurs a million times faster if more reactive OH groups in the form of oximes are given. • PRALIDOXIME • Quarternary N : Attaches to Anionic site – which remains unoccupied in OP poisoning