Toxicology of Carbon Monoxide, Organophosphates, and Psychotropes

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Poisoning by Carbon Monoxide (CO), Organophosphates, and Psychotropes — Revision Sheet

1. 📌 Essentials

  • CO poisoning results from inhalation of incomplete combustion gases, hypoxia via hemoglobin binding.
  • Carboxyhem (HbCO) levels >15% indicate intoxication; >50% often fatal.
  • Organophosphates irreversibly inhibit acetylcholinesterase, leading to cholinergic crisis.
  • Cholinesterase activity (pseudo and true) helps confirm organophosphate poisoning.
  • Psychotropic overdose affects CNS, cardiovascular, and respiratory systems; antidotes include flumazenil and naloxone.
  • Treatment for CO: high-flow oxygen and hyperbaric oxygen; for organophosphates: atropine + pralidoxime.
  • CO affinity for hemoglobin is 200-250x that of O2; half-life reduces from 320 min in air to 23 min with hyperbaric oxygen.
  • Organophosphates cause muscarinic, nicotinic, and central symptoms.
  • Psychotropes include sedatives, stimulants, neuroleptics, antidepressants, lithium.
  • Early diagnosis and treatment are critical for prognosis.

2. 🧩 Key Structures & Components

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Practice quiz preview

1. What is the primary mechanism by which carbon monoxide (CO) causes toxicity in the human body?

2. Which of the following clinical signs is most characteristic of organophosphate poisoning?

3. In the management of psychotropic overdose, which antidote is specifically used to reverse benzodiazepine effects?

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Flashcard preview

CO — binding to hemoglobin?

Reversibly binds, displacing oxygen

CO toxicity — mechanism?

HbCO formation causes hypoxia and mitochondrial inhibition

Organophosphates — action?

Inhibit cholinesterases, causing cholinergic crisis

CO poisoning — primary cause?

Inhalation of incomplete combustion gases.

HbCO levels indicating intoxication?

Above 15%; >50% often fatal.

Organophosphates — mechanism?

Irreversibly inhibit acetylcholinesterase.

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