Anticholinesterases
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This document discusses anticholinesterases, which are drugs that inhibit the enzyme cholinesterase. They work by preventing the breakdown of acetylcholine, leading to increased cholinergic effects. Some key points covered include: - Examples of natural and synthetic anticholinesterases discussed include physostigmine, neostigmine, and organophosphate nerve agents. - They work by amplifying endogenous acetylcholine levels through inhibiting its breakdown by cholinesterase. - Effects include stimulation of muscarinic, nicotinic and ganglionic receptors leading to actions like increased secretions, muscle fasciculations, and CNS effects in some cases. - Clinical
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Anticholinesterases
- 2. ANS 1. General Considerations 2. Cholinergic and Anticholinergic Drugs 5. Drugs acting on the ganglia 6. Adrenergic and Antiadrenergic Drugs
- 3. 1. CholinergicSystem 2.Ganglia 3.AdrenergicSystem 1. CholinergicTransmission/ Cholinergic Receptors/ Cholinergic Drugs 2. Anticholinesterase Drugs / OP Poisoning 3. Anticholinergic Drugs
- 4. A cholinesterase or choline esterase (ChE) is an esterase enzyme that lyses choline-based esters Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications
- 5. 1. Central Nervous System
- 7. Agents which inhibit ChE, protect ACh from hydrolysis – persistence of the action produce cholinergic effects in vivo and potentiate ACh both in vivo and in vitro Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications
- 11. Physostigmine Physostimine Neostigmine Rivastigmine Nerve Gases OP Poison Calabar beans, West Africa
- 12. Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications PK & PD Pharmacodynamic properties are almost identical. Chief differences between members of the group - chemical and pharmacokinetics.
- 13. Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications Mechanism of action • Amplifiers of endogenous ACh. • Primary effects are at the active site of this enzyme.
- 15. Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications Pharmacological Actions Actions - amplification of endogenous ACh. qualitatively similar – DCA BUT Relative intensity of action on muscarinic, ganglionic, skeletal muscle and CNS sites varies
- 16. Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications Lipid-soluble agents • Marked muscarinic and CNS effects • Stimulate ganglia • Action on skeletal muscles is less prominent Lipid-insoluble agents • Marked effect on the skeletal muscles stimulate ganglia, • Muscarinic effects are less prominent. • Do not penetrate CNS • No central effects.
- 17. Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications Pharmacological Actions • Ganglia: stimulation through muscarinic receptors • CVS: Depends on the individual drug
- 18. Skeletal muscle 1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications Single nerve impulse ACh release No immediate destruction rebinds to the same receptor, diffuses to act on neighbouring receptors activates pre-junctional fibres repetitive firing twitching and fasciculations. Higher doses: Persistent depolarization
- 19. Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications CNS • Lipophilic anti-ChEs • generalized alerting response • Cognitive function may improve • Higher doses: excitement, mental confusion, disorientation, tremors and convulsions followed by coma.
- 20. Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications Physostigmine Neostigmine and congeners Organophosphates Rapidly absorbed - g.i.t. and parenteral sites poorly absorbed orally Absorbed from all sites including intact skin and lungs Crosses blood-brain barrier & Cornea do not effectively penetrate cornea or cross blood-brain barrier Crosses all the barriers Hydrolysis by ChE Partially hydrolysed and partially excreted unchanged in urine hydrolyzed as well as oxidized in the body and little is excreted unchanged.
- 22. Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications Other drugs Pyridostigmine - resembles neo in all aspects Less potent, longer acting less frequent dosing in myasthenia Ambenonium- longer acting congener used in MG Edrophonium- short action – diagnostic agent MG
- 23. Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications 1.As miotic- In glaucoma- pilocarpine preferred Physostigmine used to supplement pilocarpine To reverse the effect of mydriatics To prevent formation of adhesions between lens & iris or cornea & iris 2. Postoperative paaralytic ileus/ urinary retention- Neostigmine0.5-1mg/s.c
- 24. Autonomic Nervous System1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications 4. Postoperative decurarization-Neostigmine 0.5-2mg i.v., preceded by atropine for reversal of muscle paralysis 5. Cobra bite- neostigmine + atropine prevent respiratory paralysis 6. Belladona poisoning-physostigmine 0.5-2mg i.v.,specific antidote 7. Over dosage of drugs like- tricyclic antidepressants, phenothiazines antihistaminics
- 26. - Senile dementia - deposition of amyloid plaques in the hippocampus (Presence of neurofibrillary tangles). - Loss of cholinergic neurons in the brain - Anticholinesterases that can cross the blood brain barrier are the mainstay of treatment of this disease 1. Description 2. Mechanism 3. Management Alzheimer's Disease
- 27. https://www.youtube.com/watch?v=zTd0-A5yDZI 1. Central Nervous System 1.Sedative–HypnoticDrugs 2.Parkinsonism 3.OtherNeurodegenerative Disorders 4.AntiepilepticDrugs 5.AntipsychoticDrugs 6.AntidepressantDrugs 7.Antianxietydrugs 8.Alcohol 9.Opioids a. Alzheimer's Disease
- 28. 1. Description 2. Mechanism 3. Management a. Alzheimer's Disease
- 29. - Auto immune disorder - Development of auto antibodies - nicotinic receptors at the muscle endplate - free Nm cholinoceptors to 1/3 of normal or less and structural damage to the neuromuscular junction. - weakness and easy fatigability on repeated activity, with recovery after rest. 1. Description 2. Mechanism 3. Management MYAESTHENIA GRAVIS
- 31. https://www.youtube.com/watch?v=zTd0-A5yDZI 1. Central Nervous System 1.Sedative–HypnoticDrugs 2.Parkinsonism 3.OtherNeurodegenerative Disorders 4.AntiepilepticDrugs 5.AntipsychoticDrugs 6.AntidepressantDrugs 7.Antianxietydrugs 8.Alcohol 9.Opioids a. Alzheimer's Disease
- 32. 1. Description 2. Mechanism 3. Management MYAESTHENIA GRAVIS
- 33. Autonomic Nervous System 1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications 4. Poisoning OP POISONING • Irritation of eye, lacrimation, salivation, sweating, copious tracheo-bronchial secretions, miosis, blurring of vision, bronchospasm, breathlessness, colic, involuntary defecation and urination. • Fall in BP, bradycardia or tachycardia, cardiac arrhythmias, vascular collapse. • Muscular fasciculations, weakness, respiratory paralysis (central as well as peripheral). • Irritability, disorientation, unsteadiness, tremor, ataxia, convulsions, coma and death. • Death is generally due to respiratory failure
- 35. Autonomic Nervous System 1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications 4. Poisoning Treatment 1. Termination of further exposure to the poison— fresh air, wash the skin and mucous membranes with soap and water, gastric lavage according to need. 2. Maintain patent airway, positive pressure respiration if it is failing. 3. Supportive measures—maintain BP, hydration, control of convulsions with judicious use of diazepam.
- 36. Autonomic Nervous System 1.cholinesterases 2.Anticholinesterases 3.Therapeutic Implications 4. Poisoning 4. Specific antidotes— (a) Atropine (b) Cholinesterase reactivators: OXIMES
- 37. 37 西安交大医学院药理学系 曹永孝 yxy@xjtu.edu.cn; 029-82655140 西安交大医学院药理学系 曹永孝 yxy@xjtu.edu.cn; 029-82655140