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Review of Pharmacology - 9E (2015)

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<strong>Review</strong> <strong>of</strong> <strong>Pharmacology</strong><br />

Autonomic Nervous System<br />

Oximes should not be given in<br />

carbamate poisoning.<br />

• Except ecothiophate these are not used therapeutically. Ecothiophate is useful in glaucoma.<br />

• Other drugs are used as insecticides and are important due to their potential to cause<br />

poisoning.<br />

• Symptoms <strong>of</strong> anti-cholinesterase poisoning are simply the extension <strong>of</strong> the<br />

pharmacological actions <strong>of</strong> ACh and are manifested as pin-point pupil, salivation,<br />

lacrimation, sweating, bronchoconstriction, diarrhea, urination, bradycardia, hypotension<br />

and coma. Blood pressure and heart rate may increase rarely due to stimulation <strong>of</strong><br />

nicotinic receptors.<br />

• Atropine is an antidote <strong>of</strong> choice for both organophosphate and carbamate poisoning.<br />

• Enzyme reactivators like pralidoxime, obidoxime and diacetylmonoxime can be used<br />

to regenerate AChE in the organophosphate poisoning but are contra-indicated in<br />

the carbamate poisoning. Principle indications <strong>of</strong> oximes are muscle weakness and<br />

respiratory depression.The site on which oximes bind and reactivate the enzyme<br />

(anionic site) is occupied by carbamates whereas it is free in the organophosphate<br />

poisoning. (organophosphates binds to esteritic site only whereas carbamates bind<br />

to both esteritic as well as anionic sites) Further oximes themselves possess weak AChE<br />

inhibitory action. Due to these two reasons, oximes should not be given in carbamate<br />

poisoning.<br />

• Diacetylmonoxime can cross BBB and regenerate AChE in the brain whereas<br />

pralidoxime and obidoxime cannot cross BBB.<br />

• Chronic exposure to certain organophosphates e.g. triorthocresyl phosphate<br />

(additive in lubricating oils) may cause:<br />

––<br />

Delayed neuropathy (appear 1-2 weeks after exposure) associated with<br />

demyelination <strong>of</strong> axons. It is not caused by cholinesterase inhibition but rather<br />

by NTE (neuropathy target esterase) inhibition.<br />

––<br />

Intermediate syndrome (occurs after 1-4 days) caused by cholinesterase inhibition.<br />

60<br />

Glaucoma<br />

• Glaucoma is characterized by progressive damage to optic nerve associated with<br />

raised intraocular pressure (> 21 mm Hg). Rise in intraocular tension is either due<br />

to excessive production or due to less drainage <strong>of</strong> aqueous humor. So, the drugs<br />

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