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Pesticides
Published in David J. George, Poisons, 2017
In terms of toxicity, the most important insecticides are organophosphates and carbamates. These agents act by blocking the action of the enzyme that regulates the amount of acetylcholine available for neurotransmission. Since neurons that utilize acetylcholine as a neurotransmitter are located throughout the body, the effects of these insecticides are widespread. Principal symptoms of toxicity include abnormal muscle contractions, behavioral disturbances, increased pulmonary secretions, and respiratory depression. A listing of possible symptoms for organophosphate poisoning is provided in Table 24.2.
Neurotoxicity of Pesticides
Published in Ana Maria Osorio, Lynn R. Goldman, Proceedings from the Medical Workshop on Pesticide-Related Illnesses from the International Conference on Pesticide Exposure and Health, 2017
Matthew C. Keifer, Jordan Firestone
Persistent central nervous system effects have also been documented in subjects who have suffered an acute organophosphate poisoning.8-13 One investigator has suggested that intoxication with N-methyl carbamates can produce similar decrements of neurobehavioral function.9 The cognitive changes in these cases have been documented through the use of sensitive neurobehavioral testing, revealing subtle changes in brain function. Some studies have also suggested that similar, persistent neurological changes may result from repeated exposure to organophosphates at levels below the threshold for acute intoxication.14-16 However, this finding has been inconsistent.17,18
Paper 4 Answers
Published in James Day, Amy Thomson, Tamsin McAllister, Nawal Bahal, Get Through, 2014
James Day, Amy Thomson, Tamsin McAllister, Nawal Bahal
Treatment of organophosphate poisoning involves atropine, anticonvulsants and oximes. Atropine is given in boluses or as an infusion until the full antimuscarinic effect has been achieved (pulse >90, dilated pupils, red dry skin). Atropine has no effect on the muscular symptoms as these are mediated by the nictonic receptors. Oximes (e.g. pralidoxime) act by reactivating acetylcholinesterase, detoxifying the unbound organophosphate agent through an endogenous anticholinergic effect.
Adrenaline is effective in reversing the inadequate heart rate response in atropine treated organophosphorus and carbamate poisoning
Published in Clinical Toxicology, 2021
Abhishek Samprathi, Binila Chacko, Shilpa Reynal D’sa, Grace Rebekah, C. Vignesh Kumar, Mohammad Sadiq, Punitha Victor, John Prasad, Jonathan Arul Jeevan Jayakaran, John Victor Peter
There are case reports [9–11] and one small case series on high dose atropine therapy in patients with OP poisoning [12]. In one report of Malathion poisoning published in 1990, the patient required 3369 mg of atropine [9]. In response to this communication, the authors [16], in a letter, highlighted other reports of high dose atropine therapy ranging from 3.9 g to over 19 g. They attributed the requirement of high dose atropine to severe poisoning and inadequate dosing of pralidoxime. In a more recent retrospective study of 25 patients with organophosphate poisoning [12], high dose atropine therapy (cumulative atropine dose ranging from 4.01 to 11.6 g) was required in three patients (12%) who also received pralidoxime. The median requirement of atropine in the current study of <1 g over the first five days is much lower than the doses reported in the case reports. The use of adrenaline in our study mitigated the low HR and enabled the use of lower doses of atropine when compared to the other reports.
Black widow spider bite in Johannesburg
Published in Southern African Journal of Infectious Diseases, 2018
Teressa Sumy Thomas, Alan Kemp, Kim Pieton Roberg
Laboratory and imaging investigations are of little assistance in making a diagnosis, but should be done to exclude differential diagnoses. Mimics of black widow envenomation may include scorpion and snake bites, an acute abdomen, myocardial infarction, alcohol withdrawal, organophosphate poisoning and tetanus. Most of these differentials may be suggested on patient history and a detailed account of events leading up to the current symptoms should be taken. Should the patient clearly report an incident he/she thinks to be a bite, scorpion and snake bites should be considered. Features in keeping with latrodectism that may suggest a snake bite include necrosis and severe swelling at the bite site (cytotoxic spider bite) or neurological symptoms such as visual disturbances, muscle weakness, dysphagia and ptosis. These neurological manifestations may also occur with scorpion bites.2 Should abdominal pain be the prominent symptom, causes of an acute abdomen (appendicitis, cholecystitis, renal colic, pancreatitis and perforated peptic ulcer) should be sought with the necessary blood workup and imaging. In a patient who is sweaty and anxious, a myocardial infarct or alchohol withdrawal may be present. Organophosphate poisoning is very common in certain areas of South Africa and should be excluded if cholinergic symptoms predominate. Tetanus and rabies should be considered if symptoms of muscles spasms, sweating and fever occur several days to weeks after a bite or injury.1,4,5
Polyphenol-Rich Fraction of Parquetina nigrescens Mitigates Dichlorvos-Induced Cardiorenal Dysfunction Through Reduction in Cardiac Nitrotyrosine and Renal p38 Expressions in Wistar Rats
Published in Journal of Dietary Supplements, 2018
Ademola A. Oyagbemi, Temidayo O. Omobowale, Grace O. Ochigbo, Ebunoluwa R. Asenuga, Olufunke Eunice Ola-Davies, Temitayo O. Ajibade, Adebowale B. Saba, Adeolu A. Adedapo
Dichlorvos is known to cause acute and chronic neurotoxicity in humans and animals by its cholinesterase-inhibiting ability (Binukumar & Gill, 2010). This inhibition results in acetylcholine accumulation at synapses and, consequently, excessive parasympathetic activation, which results in the observed signs of salivation, lacrimation, diarrhea, vomiting, and so forth (Colovic et al., 2013). Oxidative stress forms part of the foundation for the mechanism of toxicity by dichlorvos through the generation of reactive oxygen species, which may result in lipid peroxidation and destruction of other macromolecules in the body (Sharma and Singh, 2012). Over the years, the management of organophosphate poisoning has utilized the inclusion of antioxidants in the amelioration of the toxic effects in animals with considerable success (Owoeye et al., 2014).