Give easy to remember notes in this text for mbbs exams More than thousand chemicals are currently used as dipending on the toxicity. VIRTUALLY HARMLESS: (1) Phenoxyacetic acid plant wermones, e.g., M.C.P.A., D.C.P.A., T.C.P.A. They are used for dock and time-sulphur washes, used as orchard fungicides. (4) Petroleum washes, datle control. (2) Copper oxides, oxychlorides, used as fungicides. (3) ed as orchard insecticides. (5) Tar-oil emulsion, used as orchard ced as weed-killer. (2) Sodium chlorate used as mass herbicide for roads Il COMPARATIVELY HARMLESS: (1) Sulphuric acid (20%), (III) MILDLY TOXIC: (1) Chlorinated hydrocarbon insecticides: (a) DDT. (b) Gammexane. (c) Methoxachlor. (d) Chlordan, aldrin insecticides and cattle disinfestors. and dieldrin. They are used to control fly, louse, tick, as agricultural arsenite. (b) Lead and calcium arsenate. (c) Paris green. They (V) HICHLY TOXIC: (1) Arsenical compounds: (a) Sodium are used as weed-killers and orchard insecticides. (2) Nicotine, sulphates, tannates. They are used as horticultural insecticides. (3) Hydrocyanic acid, KCN, NaCN. They are used as a disinfestor and raticide. (4) Dinitro compounds, e.g., D.N.P. (dinitrophenol), D.N.O.C. (dinitro-orthocresol). They are used as selective weed-killers, ovicides and insecticides. (5) Organic polyphosphates: (a) HETP (hexaethyltetraphosphate). (b) TEPP (tetraethyl-pyrophosphate). (c) OMPA (octamethylpyrophosphoramide). (d) Parathion (diethyl nitrophenyl thiophosphate). They are used as insecticides and acaricides. CLASSIFICATION: (1) INSECTICIDES OF VEGETABLE ORIGIN: They are nicotine, pyrethrins and rotenone. 2) CHEMICAL INSECTICIDES: (I) Inorganic: They are phosphorus and compounds of antimony, arsenic, barium, mercury, thallium, zine and fluorides. (3) SYNTHETIC ORGANIC CHEMICAL INSECTICIDES: They can be divided into: (1) Phosphate esters. (2) Carbamates. (3) Chlorinated hydrocarbons: (a) Indane derivatives (chlordane, heptachlor, aldrin, dieldrin, endrin, diendrin). (b) Chlorobenzene derivatives: (DDT, chlorophenothane). Fatal dose: 150 mg/kg. body weight. (c) Benzene hexachloride (lindane, gammexane). Fatal dose: 15 8• (d Chlorinated camphenes. (toxaphene, strobane). Fatal dose: 2 g. ORGANOPHOSPHORUS POISONS They are esters of phosphoric acid and form two series of compounds. (A) Alkyl phosphates: (1) HETP. (2) TEPP (Tetron). (3) OMPA. (4) Dimefox. (5) Isopestox. (6) Malathion (Kill bug; Bugsoline). (7) Sulfotepp. (8) Demeton. (9) Trichlorton. (B) Aryl phosphates: (1) Parathion (nitrostigmine) (Follidol; Kill phos; Ekato). (2) Paraoxon. (3) Methyl-parathion (Metacide). (4) Chlorthion. (5) Diazinon (Diazion; Tik 20). They are available as dusts, granules and liquids. Absorption: They are absorbed by inhalation, through the skin, mucous membranes and the gastrointestinal tract. They are widely distributed in the body and readily cross placenta. Excretion is prolonged over a week. When sprayed in air, absorption in the plants occurs through leaves and stems. Metabolism occurs in the liver. Detoxification occurs via cytochrome P15o monooxygenase. The aryl organophosphates require liver activation to become toxic. Excretion of metabolites occurs in the urine. They are mixed with a solvent, usually aromax, which is responsible for kerosene-like smell in the body cavities, stomach contents, vomit, froth, etc. Some of the solvents used are odourless. Action: Acetylcholine is produced at the myoneural junction, and acts as a chemical signal transmitter at synapses (neurotransmitter) which is hydrolysed to choline and acetic acid spontaneously. Hydrolysis is greatly increased by cholinesterases, which are present in plasma and on the membranes, or within the cytoplasm of many cells. Organophosphorus compounds are powerful inhibitors of carboxylic esterase enzymes, including acetylcholinesterase (true cholinesterase found in red cells, nervous tissue and skeletal muscle) and pseudocholinesterase (found in plasma, liver, heart, pancreas and brain). Organophosphorus compounds bind firmly to the esterase enzyme, inactivating it by phosphorylation, at the myoneural junctions and synapses of the ganglions. A proportion of the enzyme inhibited by a single dose is restored to activity within a few hours, but some remains permanently inactivated and can only be replaced by the synthesis of new proteins. Phosphorylated acetylcholinesterase loses an alkyl group, due to which the enzyme cannot spontaneously hydrolyse and becomes permanently 396 Section 2: Toricology inactivated. They are called cholinesterase inhibitors. Organic phosphates inhibit AChE in all parts of the body, due to which acetylcholine accumulates at the parasympathetic. sympathetic and somatic sites. This produces a syndrome of overactivity due to unhydrolysed acetylcholine with continued stimulation of local receptors and eventual paralysis of nerve or muscle. The inactivation of cholinesterase enzymes becomes irreversible after 24 to 36 hours. Symptoms appear in both the sympathetic and parasympathetic nervous system. Mild poisoning usually occurs when cholinesterase activity is 20 to 50% of normal; moderate poisoning occurs when activity is 10 to 20% of normal, and severe poisoning when activity is less than 10% normal. Small repeated exposures may gradually depress the cholinesterase activity to very low levels, often resulting in minimal symptoms. Signs and Symptoms: They are similar to those resulting from overdosage of acetylcholine, pilocarpine, physostigmine or muscarine. They have three distinct toxic actions. (1) A muscarine-like effect which potentiates postganglionic parasympathetic activity. (2) Nicotine-like stimulation followed by paralysis of postganglionic and somatic motor nerves. (3) Central nervous system stimulation followed by depression. They depend on the balance between stimulation of muscarinic and nicotinic receptors in the autonomic nervous system and skeletal muscle neuroreceptors. The dose received, route and rate of absorption, and other individual factors influence this balance. Onset of systemic symptoms is most rapid following inhalation, and least rapid following absorption from the skin. Involuntary muscles and secretory glands are affected first, then voluntary muscles and finally vital brain centres. Respiratory symptoms may resemble an attack of asthma. With massive ingestion or inhalation, symptoms may begin within five minutes, or may be delayed for half to one hour and are at a maximum in two to eight hours. Signs and symptoms appear when the cholinesterase level drops to 30% of its normal activity. The respiratory or gastrointestinal symptoms are more marked depending on the route of entry. Ocular exposure causes persistent miosis. (1) Muscarinic manifestations: These symptoms can be easily remembered by the acronym SLUDGE: Salivation, lachrymation, urination, defecation, gastrointestinal distress, and emesis. (1) Bronchial tree: Bronchoconstriction, increased bronchial secretions, dyspnoea, cyanosis, pulmonary oedema. (2) G.I.T.: Anorexia, salivation, nausea, vomiting, cramps, diarrhoea, faecal incontinence, tenesmus. Pancreatitis may develop. (3) Sweat glands: Increased sweating. (4) Salivary glands: Increased salivation. (5) Lacrimal glands: Increased lacrimation. (6) C.V.S.: Bradycardia or tachycardia, arrhythmias, conduction blocks, hypotension. (7) Pupils: Miosis, occasionally unequal or dilated. (8) Ciliary body: Blurred vision. (9) Bladder: Urinary incontinence. (II) Nicotinic manifestations: (1) Striated muscle: Initial stimulus results in contraction. Later there is paralysis due to persistent depolarisation. Muscle weakness is due to accumulation of acetylcholine. Muscular fasciculations, cramps, weakness, areflexia. (2) Sympathetic ganglia: Hypertension, tachycardia, pallor, mydriasis. (ID CNS manifestations: Restlessness, emotional lability headache, tremors, anxiety, drowsiness, confusion, Slurred speech ataxia, genomlised weakness. coma, convulsions, depression o respiratory and cardiovascular centres. In some cases, only muscarinic or nicotinic or CNS effects are seen, but most cases show a combination of all three. Nicotinis effects are seen in 10 to 20% cases only. Mild poisoning (Cholinesterase activity 20 to 50% o normal. Signs and symptoms are: nausea, malaise, fatigue. minimal muscle weakness, cramping without diarrhoea. Moderate noisoning (Cholinesterase activity 10 to 20% of normal: SLUDGE and/or tremors, weakness, fasciculations. confusion, lethargy, anxiety. Severe poisoning Cholinesterase activity less than 10% of normal: SLUDGE. and respiratory insufficiency, weakness, fasciculations, coma, paralysis, seizures, autonomic dysfunction. Porphyrinaemia, resulting in chromodachryorrhoea (shedding of red tears) due to accumulation of porphyrin in the lachrymal glands is seen very rarely. commore rapidy and t The plasma ch ise plasma value will s Tered cases， : to normalise. plasma Th to demonstrated in Amperature for one to tissues stored at 4 Wered formalin and • body does no wroneural junctions 2) Diagnosis ampine. in a non But in a case of po relieved without contimatory. Treatment: exposure, the c areas are wash water, or some the conjuncti and external patent. Trac is ingested potassium 1 8/K5 or magn has occ aloria the mi perip afres d muscles, and acute respiratory paresis are seen due to prolonged cholinesterase inhibition and muscle necrosis. It does not respond to oximes or atropine. Delayed Sequelae: Delayed peripheral neuropathy can occur one to 5 weeks after exposure to certain compounds, such as parathion, malathion, trichloron, etc. It begins with paraesthesias and pain or cramps in the calves followed by ataxia, weakness, and toe drop. It rapidly progresses to a flaccid paresis which can ascend similar to Guillain-Barre syndrome. Reflexes are diminished. The disease may progress for 2 to 3 months, and muscle wasting occurs. Fatal Dose: TEPP 50 mg. i.m. or 100 mg. orally. OMPA 80 mg. i.m. or 175 mg. orally. Parathion 80 mg. i.m. or 175 mg. orally. HETP 60 mg. i.m. or 350 mg. orally. Malathion and diazinon one g. orally. Fatal Period: Death usually occurs within 24 hours in untreated cases, and within ten days in those treated cases when treatment is not successful. In non-fatal cases, the acute effects last for six to thirty hours which disappear in 2 to 3 days, but may sometimes persist for two weeks. Complete recovery occurs in ten days in patients treated early, unless hypoxic encephalopathy intervenes. Cause of Death: Death is caused by paralysis of respiratory muscles, respiratory arrest due to failure of respiratory centre, or intense bronchoconstriction. Late death, as long as 15 days after acute ingestion may be caused by ventricular arrhythmias. Diagnosis: (1) Five ml of heparinised blood should be collected for cholinesterase determination. Serum is separated and both refrigerated. Alternatively, samples can be frozen fo cholinesterase. The average normal values of cholinesteras are 77 to 142 in the red cells and 41 to 140 in the plasm RBC cholinesterase level of less than 50% of normal indica of the two, ie., if the plasma is down and red adial nore rapidly and before that of red cells. Thus, if there mated cases, plasma cholinesterase levels may require 4 wells relatively little changed, the amount of exposure is less. wools to normalise. The cholinesterase at the motor end-plate The plasma value will approach normal in 7 to 10 days. In at be demonstrated histochemically in muscles kept at room the tissues stored at 4 to 6°C. Fixation of tissue with phosphate temperature for one to two days, and up to several months in ruffered formalin and cold acetone for 24 hours or the embalming myoneural junctions. the body does not affect the cholinesterase activity at the tonine In a normal person this causes marked atropinisation. (2) Diagnosis may be confirmed by giving 2 mg. ol but in a case of poisoning by organophosphorus, symptoms ar relieved without atropinizing. Estimations of cholinesterase are confirmatory. Treatment: (1) The patient is removed from the source of exposure, the contaminated clothing removed and the exposed mons are washed with soap and water, followed by ethanol and water, or some alkaline solution. If eye 15 contaminated irrigate the coniunctival recesses, cornea, bulbar conjunctiva, internal and external palpebral surfaces. (2) The airway should be kept is ingested, the stomach should be washed with 1:5,000 patent. Tracheostomy may be required. (3) When the poison potassium permanganate solution. (4) Activated charcoal 1 g./kg. Ipecac should not be used. A cathartic, e.g., sorbitol or magnesium citrate can be given once, unless diarrhoea has occurred. (5) Avoid physostigmine, endorphonium chloride and succinylcholine. (6) Atropine sulphate arrests the muscarinic effects of postganglionic parasympathetic (peripheral) activity (muscarinic receptor antagonist) and arrests CNS effects. It has no effect on nicotinic actions. It is ineffective on respiratory centre in the presence of severe asphyxia and also if B.P. falls, Heart rate exceeding 140 beats/ min should be avoided. 2 to 4 mg. is given i.v. (paediatric dose 0.05 mg/kg.) as a test dose. If there is no effect this dose may be doubled every 10 to 15 min. until muscarinic symptoms are relieved. Atropine should be continued until the tracheobronchial tree is cleared of the secretions and most secretions are dried, but not pupillary status. The average patient requires 40 mg per day, but as much as 1000 mg/day has been used. It can be given in continuous infusion. Tachycardia is not a contraindication. Once signs of adequate atropinisation occur, the dose should be adjusted to maintain this effect for at least 24

The whole text

In the context of forensic medicine mbbs made easy to remember nites

In the context of forensic medicine mbbs made easy to remember notes inecticides and pesticides. They can be classified as follows More than thousand chemicals are currently used as dipending on the toxicity. VIRTUALLY HARMLESS: (1) Phenoxyacetic acid plant wermones, e.g., M.C.P.A., D.C.P.A., T.C.P.A. They are used for dock and time-sulphur washes, used as orchard fungicides. (4) Petroleum washes, datle control. (2) Copper oxides, oxychlorides, used as fungicides. (3) ed as orchard insecticides. (5) Tar-oil emulsion, used as orchard ced as weed-killer. (2) Sodium chlorate used as mass herbicide for roads Il COMPARATIVELY HARMLESS: (1) Sulphuric acid (20%), (III) MILDLY TOXIC: (1) Chlorinated hydrocarbon insecticides: (a) DDT. (b) Gammexane. (c) Methoxachlor. (d) Chlordan, aldrin insecticides and cattle disinfestors. and dieldrin. They are used to control fly, louse, tick, as agricultural arsenite. (b) Lead and calcium arsenate. (c) Paris green. They (V) HICHLY TOXIC: (1) Arsenical compounds: (a) Sodium are used as weed-killers and orchard insecticides. (2) Nicotine, sulphates, tannates. They are used as horticultural insecticides. (3) Hydrocyanic acid, KCN, NaCN. They are used as a disinfestor and raticide. (4) Dinitro compounds, e.g., D.N.P. (dinitrophenol), D.N.O.C. (dinitro-orthocresol). They are used as selective weed-killers, ovicides and insecticides. (5) Organic polyphosphates: (a) HETP (hexaethyltetraphosphate). (b) TEPP (tetraethyl-pyrophosphate). (c) OMPA (octamethylpyrophosphoramide). (d) Parathion (diethyl nitrophenyl thiophosphate). They are used as insecticides and acaricides. CLASSIFICATION: (1) INSECTICIDES OF VEGETABLE ORIGIN: They are nicotine, pyrethrins and rotenone. 2) CHEMICAL INSECTICIDES: (I) Inorganic: They are phosphorus and compounds of antimony, arsenic, barium, mercury, thallium, zine and fluorides. (3) SYNTHETIC ORGANIC CHEMICAL INSECTICIDES: They can be divided into: (1) Phosphate esters. (2) Carbamates. (3) Chlorinated hydrocarbons: (a) Indane derivatives (chlordane, heptachlor, aldrin, dieldrin, endrin, diendrin). (b) Chlorobenzene derivatives: (DDT, chlorophenothane). Fatal dose: 150 mg/kg. body weight. (c) Benzene hexachloride (lindane, gammexane). Fatal dose: 15 8• (d Chlorinated camphenes. (toxaphene, strobane). Fatal dose: 2 g. ORGANOPHOSPHORUS POISONS They are esters of phosphoric acid and form two series of compounds. (A) Alkyl phosphates: (1) HETP. (2) TEPP (Tetron). (3) OMPA. (4) Dimefox. (5) Isopestox. (6) Malathion (Kill bug; Bugsoline). (7) Sulfotepp. (8) Demeton. (9) Trichlorton. (B) Aryl phosphates: (1) Parathion (nitrostigmine) (Follidol; Kill phos; Ekato). (2) Paraoxon. (3) Methyl-parathion (Metacide). (4) Chlorthion. (5) Diazinon (Diazion; Tik 20). They are available as dusts, granules and liquids. Absorption: They are absorbed by inhalation, through the skin, mucous membranes and the gastrointestinal tract. They are widely distributed in the body and readily cross placenta. Excretion is prolonged over a week. When sprayed in air, absorption in the plants occurs through leaves and stems. Metabolism occurs in the liver. Detoxification occurs via cytochrome P15o monooxygenase. The aryl organophosphates require liver activation to become toxic. Excretion of metabolites occurs in the urine. They are mixed with a solvent, usually aromax, which is responsible for kerosene-like smell in the body cavities, stomach contents, vomit, froth, etc. Some of the solvents used are odourless. Action: Acetylcholine is produced at the myoneural junction, and acts as a chemical signal transmitter at synapses (neurotransmitter) which is hydrolysed to choline and acetic acid spontaneously. Hydrolysis is greatly increased by cholinesterases, which are present in plasma and on the membranes, or within the cytoplasm of many cells. Organophosphorus compounds are powerful inhibitors of carboxylic esterase enzymes, including acetylcholinesterase (true cholinesterase found in red cells, nervous tissue and skeletal muscle) and pseudocholinesterase (found in plasma, liver, heart, pancreas and brain). Organophosphorus compounds bind firmly to the esterase enzyme, inactivating it by phosphorylation, at the myoneural junctions and synapses of the ganglions. A proportion of the enzyme inhibited by a single dose is restored to activity within a few hours, but some remains permanently inactivated and can only be replaced by the synthesis of new proteins. Phosphorylated acetylcholinesterase loses an alkyl group, due to which the enzyme cannot spontaneously hydrolyse and becomes permanently inactivated. They are called cholinesterase inhibitors. Organic phosphates inhibit AChE in all parts of the body, due to which acetylcholine accumulates at the parasympathetic. sympathetic and somatic sites. This produces a syndrome of overactivity due to unhydrolysed acetylcholine with continued stimulation of local receptors and eventual paralysis of nerve or muscle. The inactivation of cholinesterase enzymes becomes irreversible after 24 to 36 hours. Symptoms appear in both the sympathetic and parasympathetic nervous system. Mild poisoning usually occurs when cholinesterase activity is 20 to 50% of normal; moderate poisoning occurs when activity is 10 to 20% of normal, and severe poisoning when activity is less than 10% normal. Small repeated exposures may gradually depress the cholinesterase activity to very low levels, often resulting in minimal symptoms. Signs and Symptoms: They are similar to those resulting from overdosage of acetylcholine, pilocarpine, physostigmine or muscarine. They have three distinct toxic actions. (1) A muscarine-like effect which potentiates postganglionic parasympathetic activity. (2) Nicotine-like stimulation followed by paralysis of postganglionic and somatic motor nerves. (3) Central nervous system stimulation followed by depression. They depend on the balance between stimulation of muscarinic and nicotinic receptors in the autonomic nervous system and skeletal muscle neuroreceptors. The dose received, route and rate of absorption, and other individual factors influence this balance. Onset of systemic symptoms is most rapid following inhalation, and least rapid following absorption from the skin. Involuntary muscles and secretory glands are affected first, then voluntary muscles and finally vital brain centres. Respiratory symptoms may resemble an attack of asthma. With massive ingestion or inhalation, symptoms may begin within five minutes, or may be delayed for half to one hour and are at a maximum in two to eight hours. Signs and symptoms appear when the cholinesterase level drops to 30% of its normal activity. The respiratory or gastrointestinal symptoms are more marked depending on the route of entry. Ocular exposure causes persistent miosis. (1) Muscarinic manifestations: These symptoms can be easily remembered by the acronym SLUDGE: Salivation, lachrymation, urination, defecation, gastrointestinal distress, and emesis. (1) Bronchial tree: Bronchoconstriction, increased bronchial secretions, dyspnoea, cyanosis, pulmonary oedema. (2) G.I.T.: Anorexia, salivation, nausea, vomiting, cramps, diarrhoea, faecal incontinence, tenesmus. Pancreatitis may develop. (3) Sweat glands: Increased sweating. (4) Salivary glands: Increased salivation. (5) Lacrimal glands: Increased lacrimation. (6) C.V.S.: Bradycardia or tachycardia, arrhythmias, conduction blocks, hypotension. (7) Pupils: Miosis, occasionally unequal or dilated. (8) Ciliary body: Blurred vision. (9) Bladder: Urinary incontinence. (II) Nicotinic manifestations: (1) Striated muscle: Initial stimulus results in contraction. Later there is paralysis due to persistent depolarisation. Muscle weakness is due to accumulation of acetylcholine. Muscular fasciculations, cramps, weakness, areflexia. (2) Sympathetic ganglia: Hypertension, tachycardia, pallor, mydriasis. (ID CNS manifestations: Restlessness, emotional lability headache, tremors, anxiety, drowsiness, confusion, Slurred speech ataxia, genomlised weakness. coma, convulsions, depression o respiratory and cardiovascular centres. In some cases, only muscarinic or nicotinic or CNS effects are seen, but most cases show a combination of all three. Nicotinis effects are seen in 10 to 20% cases only. Mild poisoning (Cholinesterase activity 20 to 50% o normal. Signs and symptoms are: nausea, malaise, fatigue. minimal muscle weakness, cramping without diarrhoea. Moderate noisoning (Cholinesterase activity 10 to 20% of normal: SLUDGE and/or tremors, weakness, fasciculations. confusion, lethargy, anxiety. Severe poisoning Cholinesterase activity less than 10% of normal: SLUDGE. and respiratory insufficiency, weakness, fasciculations, coma, paralysis, seizures, autonomic dysfunction. Porphyrinaemia, resulting in chromodachryorrhoea (shedding of red tears) due to accumulation of porphyrin in the lachrymal glands is seen very rarely. commore rapidy and t The plasma ch ise plasma value will s Tered cases， : to normalise. plasma Th to demonstrated in Amperature for one to tissues stored at 4 Wered formalin and • body does no wroneural junctions 2) Diagnosis ampine. in a non But in a case of po relieved without contimatory. Treatment: exposure, the c areas are wash water, or some the conjuncti and external patent. Trac is ingested potassium 1 8/K5 or magn has occ aloria the mi perip afres d muscles, and acute respiratory paresis are seen due to prolonged cholinesterase inhibition and muscle necrosis. It does not respond to oximes or atropine. Delayed Sequelae: Delayed peripheral neuropathy can occur one to 5 weeks after exposure to certain compounds, such as parathion, malathion, trichloron, etc. It begins with paraesthesias and pain or cramps in the calves followed by ataxia, weakness, and toe drop. It rapidly progresses to a flaccid paresis which can ascend similar to Guillain-Barre syndrome. Reflexes are diminished. The disease may progress for 2 to 3 months, and muscle wasting occurs. Fatal Dose: TEPP 50 mg. i.m. or 100 mg. orally. OMPA 80 mg. i.m. or 175 mg. orally. Parathion 80 mg. i.m. or 175 mg. orally. HETP 60 mg. i.m. or 350 mg. orally. Malathion and diazinon one g. orally. Fatal Period: Death usually occurs within 24 hours in untreated cases, and within ten days in those treated cases when treatment is not successful. In non-fatal cases, the acute effects last for six to thirty hours which disappear in 2 to 3 days, but may sometimes persist for two weeks. Complete recovery occurs in ten days in patients treated early, unless hypoxic encephalopathy intervenes. Cause of Death: Death is caused by paralysis of respiratory muscles, respiratory arrest due to failure of respiratory centre, or intense bronchoconstriction. Late death, as long as 15 days after acute ingestion may be caused by ventricular arrhythmias. Diagnosis: (1) Five ml of heparinised blood should be collected for cholinesterase determination. Serum is separated and both refrigerated. Alternatively, samples can be frozen fo cholinesterase. The average normal values of cholinesteras are 77 to 142 in the red cells and 41 to 140 in the plasm RBC cholinesterase level of less than 50% of normal indica donciation of the two, ie., if the plasma is down and red adial nore rapidly and before that of red cells. Thus, if there mated cases, plasma cholinesterase levels may require 4 wells relatively little changed, the amount of exposure is less. wools to normalise. The cholinesterase at the motor end-plate The plasma value will approach normal in 7 to 10 days. In at be demonstrated histochemically in muscles kept at room the tissues stored at 4 to 6°C. Fixation of tissue with phosphate temperature for one to two days, and up to several months in ruffered formalin and cold acetone for 24 hours or the embalming myoneural junctions. the body does not affect the cholinesterase activity at the tonine In a normal person this causes marked atropinisation. (2) Diagnosis may be confirmed by giving 2 mg. ol but in a case of poisoning by organophosphorus, symptoms ar relieved without atropinizing. Estimations of cholinesterase are confirmatory. Treatment: (1) The patient is removed from the source of exposure, the contaminated clothing removed and the exposed mons are washed with soap and water, followed by ethanol and water, or some alkaline solution. If eye 15 contaminated irrigate the coniunctival recesses, cornea, bulbar conjunctiva, internal and external palpebral surfaces. (2) The airway should be kept is ingested, the stomach should be washed with 1:5,000 patent. Tracheostomy may be required. (3) When the poison potassium permanganate solution. (4) Activated charcoal 1 g./kg. Ipecac should not be used. A cathartic, e.g., sorbitol or magnesium citrate can be given once, unless diarrhoea has occurred. (5) Avoid physostigmine, endorphonium chloride and succinylcholine. (6) Atropine sulphate arrests the muscarinic effects of postganglionic parasympathetic (peripheral) activity (muscarinic receptor antagonist) and arrests CNS effects. It has no effect on nicotinic actions. It is ineffective on respiratory centre in the presence of severe asphyxia and also if B.P. falls, Heart rate exceeding 140 beats/ min should be avoided. 2 to 4 mg. is given i.v. (paediatric dose 0.05 mg/kg.) as a test dose. If there is no effect this dose may be doubled every 10 to 15 min. until muscarinic symptoms are relieved. Atropine should be continued until the tracheobronchial tree is cleared of the secretions and most secretions are dried, but not pupillary status. The average patient requires 40 mg per day, but as much as 1000 mg/day has been used. It can be given in continuous infusion. Tachycardia is not a contraindication. Once signs of adequate atropinisation occur, the dose should be adjusted tol