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Organophosphate Poisoning: Atropine Antidote

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Antidotes for organophosphate exposure

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Cambodia

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Organophosphate Poisoning: Atropine Antidote
 

Organophosphate Poisoning: Atropine AntidoteOnline version

Antidotes for organophosphate exposure

by HODGES TANIA MAXINE
1

Question 1 (KROK 2021)An unconscious 42-year-old agricultural worker is rushed to the emergency department after accidentally inhaling a high volume of an organophosphate insecticide. The patient presents with profuse sweating, hypersalivation, generalized muscle fasciculations, and severe bradycardia. Which of the following medications must be administered immediately as a specific muscarinic antidote?

2

Question 2 (KROK 2019)A 62-year-old female patient with a history of open-angle glaucoma arrives at an ophthalmology clinic. To manage her elevated intraocular pressure, the physician prescribes a topical solution of Pilocarpine. Which of the following structural and physiological changes will occur in the patient's eye following the administration of this drug?

3

Question 3 (KROK 2022)A 55-year-old male with a history of severe bronchial asthma and chronic peptic ulcer disease presents with severe dry mouth (xerostomia) following radiation therapy. The attending physician considers prescribing Pilocarpine to stimulate salivary gland secretions but ultimately decides it is strictly contraindicated due to the patient's respiratory history. What lethal complication is the physician actively avoiding?

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Organophosphate poisoning locks acetylcholinesterase, keeping acetylcholine at dangerously high toxic thresholds. This shifts body performance toward a severe "rest-and-digest" overload. Atropine is a direct competitive muscarinic receptor antagonist, blocking this excess activation to stabilize cardiac frequency and respiratory secretional output.

Pilocarpine acts directly as an M-cholinomimetic agonist. Stimulating ocular M3 receptors contracts the pupillary sphincter muscle (Miosis). It also pulls the ciliary muscle body inward, tensioning the scleral spur to physically pull open the trabecular meshwork channels and lower intraocular pressures.

While Pilocarpine stimulates salivary flow, it triggers cross-activation across systemic tissue pathways. On smooth muscle lines in respiratory structures, M3 receptor activation drives strict bronchoconstriction and elevates airway fluid secretion. For patients with a past history of structural respiratory disease (such as bronchial asthma), this initiates catastrophic bronchospasm.

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