Agricultural poisons

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24 Terms

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Insecticides:organophosphorous, carbamates, organochlorines

Rodenticides: Phosphorous, anticoagulants, strychnine

Herbicides

Fungicides

Nematicides

Acaricides

Types of agricultural poisons

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Alkyl -

HETP

OMPA

TEPP

Malathion

Trichlorfon

Demeton

Dimefox

Isopestox

Aryl- Parathion, Paraoxon, Methyl-parathion, Chlorothion, Diazinon

Types of organophosphate compounds

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<p></p>

Action of OP

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Acute cholinergic syndrome(<1day)

Intermediate Syndrome (1-4 days)

Delayed Polyneuropathy(1-4weeks)

Signs and symptoms of OP is divided as

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Muscarinic-

DUMBBELS

diarrhea, urination, miosis, bradycardia, bronchorrhea, emesis, lacrimation(chromodacryorrhea-red tears due to protoporphyrin excretion), salivation

Nicotinic effects-

MATCH

Muscle weakness and fasciculation

Adrenal medulla activity increase

Tachycardia

Cramps in muscle

Hypertension

CNS effects- irritability, apprehension, convulsions, restlessness, fine fibrillary tremors in hands, eyelids, face

Features of acute cholinergic syndrome

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due to release of OP stored in fat tissue

includes proximal muscle weakness and the neck flexors muscles——areas innervated by cranial nerves

cranial nerve palsies

Intermediate syndrome includes

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<p>due to the inhibition of the enzyme neurotoxic esterase with nerve demyelination</p><p>paralysis is usually limited to distal muscles of the limbs, cranial nerves and proximal muscles are sparede</p><p>-foot drop</p><p>-flaccid symmetrical paralysis</p><p>-muscle wasting</p>

due to the inhibition of the enzyme neurotoxic esterase with nerve demyelination

paralysis is usually limited to distal muscles of the limbs, cranial nerves and proximal muscles are sparede

-foot drop

-flaccid symmetrical paralysis

-muscle wasting

Delayed polyneuropathy is

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History

Clinical features

Cholinesterase level:Rbc cholinesterase and plasma cholinesterase—-<50% fall.

Colorimetric method

Paper chromatography

P-nitrophenol test

Thin layer chromatography

Gas chromatography

Gas chromatography-mass spectrometry

High performance liquid chromatography

ECG-Right axis deviation, ST depression, T wave inversion

Diagnosis of OPP

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PM findings of OP poisoning

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Stabilisation

Decontamination

Antidote_atropine sulfate-reverses the muscarininc effect but cannont reverse nicotinic effect.2-4 mgIV

Oximes-regeneration of acetylcholinesterase at the muscarinic, nicotinic and CNS sites. Pralidoxime-500mg/20ml infusion at a dose of 1-2gm.

For convulsions-diazepamm

Antibiotics

Oxygen administraion, ventilator

Treatment of Opp

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insecticides

include carboaryl,carbfuran, methomyl, popoxur, aldicarb, triallate

causes reversible inhibition of ACE by binding to its anionic site

What are carbamates

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-anionic site is not available for oximes to bind and they themselves have anticholinesteric efffect hence not given

Why is oxime not given in carbamates poisoning

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Respiratory failure

Cerebral hypoxia

Hyperthermia

Hepatic failure

Renal failure

Causes of death in OP poisoning

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Organochlorines are chlorinated hydrocarbons used for pesticides

They include

-DDT
-Benzene hexachloride group-BHC, Lindane

-Cyclodienes-endosulfan,endrin,dieldrin

-Toxaphene and related compounds

What are organichlorines

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DDT——> blocs sodium channels and sodium conductance across the axons

Lindanes and Cyclodienes inhibit GABA-medicated chloride channels.

MOA of organochlorines are

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<p>mydriasis</p>

mydriasis

Clinical features of Organochlorine poisoning

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when it comes in contact with water it produces phosgene gas. phosgene gas is absorbed and itis a protoplasmic poison which inhibits cytochrome oxidase.

Aluminium phosphide moa

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Weaknes

Ataxia

Tremors

Weight loss

Pseudotumor cerebri

Abnormal mental changes

Oligospermia

Thrombocytopenic purpura

Aplastic anemia

Liver cancer

Leukaemia

Chronic poisoning with organochlorines causes

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term image

clinical features of AP poisoning

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Garlicky odour breath

Abnormal LFT

Urinalysis- occult blood, glucose, albumin, bilirubin

ABG- Metabolic acidosis

Silver nitrate test- black color

Diagnosis of aluminium phosphide poisoning

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Undergoes nicotinamide dependent reduction to form free radiacals which inturn combines with o2 to form cations. superoxide free radicals and hydroxyl radicals are produced which disrupts cellular function, structure and death.

MOA of paraquat

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Prolongs the inactivation of sodium channels by binding to it in the open state.

MOA of pyrethrin compounds

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