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Related Concept Videos

Prevention of Further Absorption of Poison01:14

Prevention of Further Absorption of Poison

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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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Antidotes are medicinal substances used to counteract the harmful effects of toxins or drugs in the body. They function in various ways, each uniquely designed to combat specific toxic compounds.
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An example of an antidote is atropine, which counteracts the detrimental effects of cholinesterase inhibitors. It achieves this by deactivating muscarinic receptors,...
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Aldehydes and Ketones with HCN: Cyanohydrin Formation Overview01:32

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Cyanohydrins are compounds that contain –CN and –OH groups on the same carbon atom. They are formed by the nucleophilic addition of the cyanide ions to the carbonyl group. Cyanide ions are highly basic and nucleophilic and can be generated from HCN under aqueous conditions. However, since HCN is a weak acid, the number of cyanide ions generated is very small. Hence, a small amount of base or KCN/NaCN is added to HCN to increase the concentration of the cyanide ions in the reaction...
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Cyanohydrins are formed when cyanide nucleophiles and carbonyl compounds like aldehydes and ketones react. A strong base, the cyanide ion, catalyzes cyanohydrin formation. The ions are generated from HCN under aqueous conditions. Once the cyanide ions are generated, the first step involves the nucleophilic attack of the cyanide ions on the electrophilic carbonyl carbon. This attack shifts the π electrons from the C=O to the oxygen atom forming the alkoxide ion intermediate. The alkoxide anion...
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Anticholinesterase Agents: Poisoning and Treatment01:26

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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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Depolarizing Blockers: Pharmocokinetics01:19

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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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Intra-cardiac Side-Firing Light Catheter for Monitoring Cellular Metabolism using Transmural Absorbance Spectroscopy of Perfused Mammalian Hearts
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An Unusual Acute Cyanide Intoxication.

Gholamali Dorooshi1, Amin Dorostkar2, Alireza Rahimi3

  • 1Department of Clinical Toxicology, Isfahan Clinical Toxicology Research Center, Khorshid Hospital, Isfahan, Iran.

Advanced Biomedical Research
|October 19, 2020
PubMed
Summary

Cyanide salt ingestion is rare but highly lethal, causing severe central nervous system and cardiovascular symptoms. This case highlights delayed diagnosis and nonspecific symptoms in fatal cyanide poisoning.

Keywords:
Cyanidespoisoningsuicidesymptom

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Area of Science:

  • Toxicology
  • Emergency Medicine
  • Forensic Pathology

Background:

  • Cyanide poisoning, though rare, is highly lethal, with significant toxicity from oral ingestion.
  • Lethal oral doses of cyanide salts are approximately 200 mg, and blood concentrations over 3 mg/L can be fatal.
  • Symptoms predominantly affect the central nervous and cardiovascular systems.

Observation:

  • A 43-year-old male goldsmith ingested cyanide salt, presenting with confusion, cardiac arrhythmias, hyperkalemia, leukocytosis, metabolic acidosis, and fluctuating blood pressure.
  • Initial diagnosis was delayed due to nonspecific symptoms.
  • The patient received intensive supportive care but died on the third day from cardiac arrest.

Findings:

  • Autopsy revealed hemorrhagic gastritis and a characteristic cherry-red discoloration of chest muscles.
  • Forensic toxicology confirmed the presence of cyanide in blood and tissues.
  • The case demonstrates that cyanide poisoning can manifest with prolonged, nonspecific symptoms.

Implications:

  • This case underscores the importance of considering cyanide poisoning in patients with unexplained metabolic acidosis and cardiovascular compromise.
  • Early recognition and prompt treatment are critical for improving outcomes in cyanide toxicity.
  • Forensic analysis is crucial for confirming cyanide poisoning in fatalities.