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Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
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In cases of acute poisoning, the primary objective is to prevent further absorption of the toxic substance into the body. Immediate interventions using various decontamination techniques targeting the gastrointestinal (GI) tract can achieve this. Decontamination is crucial to prevent poison from entering the systemic circulation, which involves washing affected areas with water and mild soap and removing contaminated clothing. Once external decontamination is done, attention must be turned to...
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Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
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Toxidromes are specific patterns of symptoms resulting from toxic substance exposure. They help in the identification and treatment of poisoning. The symptoms of each toxidrome group indicate poisoning by a certain class of chemicals or drugs.1. Sympathomimetic: Stimulates the sympathetic nervous system. Symptoms include agitation, increased heart rate (HR), blood pressure (BP), respiratory rate (RR), temperature, and pupil size. Drugs like cocaine and amphetamines, along with tremors and...
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Glycemic Status in Organophosphorus Poisoning.

S Panda1, R Nanda2, M Mangaraj3

  • 1Department of Biochemistry and Medicine, SCB Medical College, Cuttack, Odisha, India.

Journal of Nepal Health Research Council
|March 24, 2016
PubMed
Summary

Organophosphorus poisoning causes hyperglycemia, linked to oxidative stress and atropine dose. Monitoring blood glucose may help assess poisoning severity.

Keywords:
Atropine; hyperglycemia; organophosphorus; oxidative stress; random plasma glucose.

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Area of Science:

  • Toxicology
  • Endocrinology
  • Clinical Chemistry

Background:

  • Organophosphorus (OP) poisoning presents with cholinergic symptoms and metabolic disturbances, notably hyperglycemia.
  • OP compounds inhibit acetylcholinesterase and induce oxidative stress, contributing to hyperglycemia.
  • Understanding glycemic changes in OP poisoning is crucial for patient management.

Purpose of the Study:

  • To evaluate the glycemic status in patients with organophosphorus poisoning.
  • To investigate the association between hyperglycemia and factors like oxidative stress and atropine dosage in OP poisoning.
  • To explore the potential of glycemic status as a severity marker for OP poisoning.

Main Methods:

  • A prospective study involving 102 adult patients with a history of OP poisoning.
  • Patients were classified into mild, moderate, and severe grades using the Peradeniya Organophosphorus Poisoning Scale.
  • Biochemical parameters, including serum malondialdehyde (MDA) and cholinesterase levels, were measured.

Main Results:

  • Hyperglycemia and glycosuria were prevalent, with 57% of hyperglycemia cases in the severe group.
  • Elevated random plasma glucose (RPG), serum MDA, and atropine dose correlated with increased poisoning severity.
  • A significant decrease in plasma glucose from admission to discharge was observed across all severity groups.

Conclusions:

  • Transient hyperglycemia in OP poisoning shows a significant positive association with elevated serum MDA and atropine dosage.
  • Glycemic status at admission may serve as an indicator for assessing the severity of organophosphorus poisoning.