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Cholinesterase inhibitors poisoning

Atropine Nonselective competitive antagonist at all muscarinic receptors in CNS and periphery Blocks muscarinic excess at exocrine glands, heart, smooth muscle Mandatory antidote for severe cholinesterase inhibitor poisoning Intravenous infusion until antimuscarinic signs appear continue as long as necessary Toxicity Insignificant as long as AChE inhibition continues... [Pg.167]

Pralidoxime Very high affinity for phosphorus atom but does not enter CNS Regenerates active AChE can relieve skeletal muscle end plate block Usual antidote for early-stage (48 h) cholinesterase inhibitor poisoning Intravenous every 4-6 h Toxicity Can cause muscle weakness in overdose... [Pg.167]

Atropine Generic Peptic ulcer, irritable bowel syndrome, neurogenic bladder, bronchospasm, preoperative antisecretory agent, cardiac arrhythmias (e.g., sinus bradycardia, postmyocardial infarction, asystole], reversal of neuromuscular blockade, antidote to cholinesterase inhibitor poisoning... [Pg.269]

The lack of classic muscarinic effects does not exelude the possibility of cholinesterase inhibitor poisoning in young children with central nervous system depression. In one ease series, tearing and diaphoresis were not observed in pediatrie patients (Lifshitz et al, 1999). Miosis was absent in a number of pediatric patient cases reported in the literature with 27% of children in one case series lacking miosis on admission (Zwiener and Ginsburg, 1988). The percentage was 20% in another case series of pediatric patients (Sofer et al, 1989). [Pg.933]

Weis OF, Muller FO, LyeU H, Badenhorst CH, van Niekerk P. Materno-fetal cholinesterase inhibitor poisoning. Anesth Analg 1983 62(2) 233-5. [Pg.3273]

For patients with bronchospasm and bronchorrhea caused by organophos-phoms or other cholinesterase inhibitor poisoning, give atropine (see p 412) intravenously. Ipratropium bromide (see 4.b) may also be helpful. [Pg.9]

A. Patients with hypertension, tachyarrhythmias, thyrotoxicosis, congestive heart failure, coronary artery disease, and other illnesses, who might not tolerate a rapid heart rate. Patients with severe cholinesterase inhibitor poisoning are often tachycardia. Atropine should not be withheld and may lower heart rate (by improving oxygenation). Glycopyrrolate may also be helpful (due to its lessened propensity to cause a tachycardia). [Pg.412]

A. Some adverse effects include dry mouth, blurred vision, cycloplegia, mydriasis, palpitations, tachycardia, aggravation of angina, and constipation. Urinary retention is common, and a Foley catheter may be needed. Duration of effects may be prolonged (several hours). Additionally, CNS anticholinergic toxicity (delirium) may occur with large doses of atropine needed to treat cholinesterase inhibitor poisoning. [Pg.412]

A. Oximes are used to treat poisoning caused by cholinesterase inhibitor insecticides and nerve agents, ie, organophosphates, mixtures of organophospho-ms and carbamate insecticides, or pure carbamate insecticide intoxication with nicotinic-associated symptoms. Because of its low toxicity, possible ineffectiveness if treatment is delayed until after the cholinesterase enzyme has aged, ability to reverse nicotinic as well as muscarinic effects, and ability to reduce atropine requirements, pralidoxime should be used early and empirically for suspected cholinesterase inhibitor poisoning. [Pg.493]

Clinically, nicotinic signs often predominate early in the course of cholinesterase inhibitor poisoning. However, concurrent nicotinic and muscarinic signs and symptoms are often present in both the PNS and CNS. Later in the course of cholinesterase inhibitor poisoning, muscarinic signs and symptoms predominate. [Pg.132]

Many pesticides are neurotoxicants poisoning the nervous system. A number of pesticides are acetyl cholinesterase inhibitors (Serat and Mengle 1973). Generally, pesticides determination has been performed by GC since the 1960 s (Morrison and Durham 1971 Fournier et al. 1978). There are no reference materials for pesticides in urine or serum, although as with PAHs there are a number biological matrices certified for the content of various pesticides available for environmental food and agriculture analysis and which may have some application in clinical chemistry. [Pg.207]

Stone, W.B. and P.B. Gradoni. 1986. Poisoning of birds by cholinesterase inhibitor pesticides. Wildl. Rehabil. 5 12-28. [Pg.826]

Perhaps the most prominent and well-studied class of synthetic poisons are so-called cholinesterase inhibitors. Cholinesterases are important enzymes that act on compounds involved in nerve impulse transmission - the neurotransmitters (see the later section on neurotoxicity for more details). A compound called acetylcholine is one such neurotransmitter, and its concentration at certain junctions in the nervous system, and between the nervous system and the muscles, is controlled by the enzyme acetylcholinesterase the enzyme causes its conversion, by hydrolysis, to inactive products. Any chemical that can interact with acetylcholinesterase and inhibit its enzymatic activity can cause the level of acetylcholine at these critical junctions to increase, and lead to excessive neurological stimulation at these cholinergic junctions. Typical early symptoms of cholinergic poisoning are bradycardia (slowing of heart rate), diarrhea, excessive urination, lacrimation, and salivation (all symptoms of an effect on the parasympathetic nervous system). When overstimulation occurs at the so-called neuromuscular junctions the results are tremors and, at sufficiently high doses, paralysis and death. [Pg.98]

The classic cholinesterase inhibitor is the alkaloid physostigmine (33), also called eserine. Investigations carried out in the nineteenth century on the ordeal poison esere, which consisted of an extract of the Calabar Bean, the seeds of Physostigma venenosum Balf, resulted in the isolation of (33)... [Pg.394]

Cholinesterase inhibitors are a very important class of compounds related to cholinomimetics. Besides their therapeutic importance, a few of them are used as pesticides in agriculture, and the most toxic are used as chemical poisoning agents. Use of these substances is based on changes that take place after inactivation of cholinesterase or pseudocholinesterase (a less specific enzyme), i.e. effects observed as a result of acetylcholine buildup in neuro-effector compounds. Cholinesterase inhibitors are classified both by their chemical structure as well as by the type of their chemical reaction with the enzyme, which determines their temporary action. [Pg.186]

Malathion is an organophosphate cholinesterase inhibitor. Up to 8% of the topically applied dose may be absorbed. Malathion is used as a treatment for head lice, body lice and scabies. It effectively kills both the eggs and the adult lice. Malathion is an insecticide of relatively low human toxicity. However if malathion is used in an indoor environment, as it breaks down into malaoxon, it can be seriously and chronically poisonous. The safety of malathion in pregnancy and in lactating women and in children has not been established. [Pg.482]

Atropine is used as an antidote in poisoning by an overdose of a cholinesterase inhibitor (see Chapter 14). It also is used in cases of poisoning from species of mushroom that contain high concentrations of muscarine and related alkaloids (e.g., Clitocybe dealbata). [Pg.138]

Severe cholinergic excess is a medical emergency, especially in rural communities where cholinesterase inhibitor insecticides are commonly used and in cultures where wild mushrooms are commonly eaten. The potential use of cholinesterase inhibitors as chemical warfare "nerve gases" also requires an awareness of the methods for treating acute poisoning (see Chapter 58). [Pg.162]

Pralidoxime (2-PAM) Organophosphate cholinesterase inhibitors Adult dose is 1 g IV, which should be repeated every 3-4 hours as needed or preferably as a constant infusion of 250-400 mg/h. Pediatric dose is approximately 250 mg. No proved benefit in carbamate poisoning. [Pg.1255]

Organophosphate and carbamate cholinesterase inhibitors (see Chapter 7) are widely used to kill insects and other pests. Most cases of serious organophosphate or carbamate poisoning result from intentional ingestion by a suicidal person, but poisoning has also occurred at work (pesticide application or packaging) or, rarely, as a result of food contamination or terrorist attack (eg, release of the chemical warfare nerve agent sarin in the Tokyo subway system in 1995). [Pg.1259]


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See also in sourсe #XX -- [ Pg.17 ]

See also in sourсe #XX -- [ Pg.7 ]

See also in sourсe #XX -- [ Pg.17 ]




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