Toxicology (Part-13) Insecticide Poisoning and Organophosphorus Poisoning Treatment | Antidote Drugs

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Organophosphate compounds are used as commercial insecticides (disulfoton, phorate, dimethoate, ciodrin, dichlorvos, dioxathion, ruelene, carbophenothion, supona, TEPP, EPN, HETP, parathion, malathion, ronnel, coumaphos, diazinon, trichlorfon, paraoxon, potasan, dimefox, mipafox, schradan, sevin, and dimetonor) in chemical warfare (nerve gases such as tabun and sarin) and are applied as aerosols or dusts. They can be rapidly absorbed through skin and mucous membranes or by inhalation.
Organophosphates are also used in ophthalmology - echothiopate is used to treat glaucoma.
mechanism of Toxicity = Acetylcholine is the neurotransmitter at the cholinergic synaptic areas. And acetylcholinesterase enzyme degrades acetylcholine following stimulation of a nerve. Organophosphates are acetylcholinesterase inhibitors and they form a stable irreversible covalent bond to the enzyme. Organophosphates mediated inhibition of acetylcholinesterase causes acetylcholine to accumulate and results in initial excessive stimulation followed by depression.
In cholinergic junctions of the nervous system including postganglionic parasympathetic junctions (sites of muscarinic activity), autonomic ganglia and the neuromuscular junctions (sites of nicotinic activity) and certain synapses in the CNS all get affected by overstimulation by excessive acetylcholine.
Sign and Symptoms- (1) Muscarinic signs = (SLUDGE) salivation, lacrimation, urination, diaphoresis, gastrointestinal upset, emesis and progressing to bronchospasm, bronchorrhea, blurred vision, bradycardia or tachycardia, hypotension, confusion, and shock.
(2) Nicotinic effects = Skeletal muscle initially exhibits fasciculation (involuntary irregular, violent muscle contractions) followed by the inability to repolarize cell membranes resulting in weakness and paralysis. Severe reactions can lead to ventilatory failure and death (cholinergic crisis).
(1) Termination of the exposure including removing all soiled clothing. Gently cleanse with soap and water to hydrolyze organophosphate solutions. (2) Airway control and adequate oxygenation. Intubation may be necessary in cases of respiratory distress due to laryngospasm, bronchospasm, bronchorrhea, or seizures. Immediate aggressive use of atropine may eliminate the need for intubation. Succinylcholine should be avoided because it is degraded by AChE and may result in prolonged paralysis (3) Continuous cardiac monitoring and pulse oximetry should be established; an ECG should be performed. Torsades de Pointes should be treated in a standard manner. The use of intravenous magnesium sulfate has been reported as beneficial for organophosphate toxicity. The mechanism of action may involve acetylcholine antagonism or ventricular membrane stabilization. (4) Irrigate the eyes of patients who have had ocular exposure using isotonic sodium chloride solution or lactated Ringer’s solution. Morgan lenses can be used for eye irrigation.
(5) IV atropine- it is a competitive inhibitor. (6) IV pralidoxime- it reactivates acetylcholinesterase.
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[@chaitanyac.1148]

Sir apne whiteboard presentation me batya hai ki Tachycardia and Mydriasis are nicotinic effects... As per my knowledge there are no any nicotinic receptor in heart and eye....Then sir how it is ? Please explain....🙏

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In our house we spray organophosphorus insecticides for terminite . Is it dangerous. What is affect withdrawal period of this insecticides

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Is mouth to mouth or mouth to nose resuscitation safe in poisoning ?

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Actylcholine bradycardia krta ha if receptors bind hota ha apne bataya tachycardia

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Watch the video first and then comment

[@kmpooja4112]

Sir online test me ek question thik nahi laga mujhe jisme effect nicotinic ke pucha h par symptoms muscarinic ke diye h ... last wala question h sir i am sorry sir par confuse hun to puch liya

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2nd

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