Question:
In organophosphate (OP) poisoning, which drug reverses the inhibited activity of acetylcholinesterase (AChE)?
In organophosphate (OP) poisoning, which drug reverses the inhibited activity of acetylcholinesterase (AChE)?
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Think of the oxime that cleaves the OP-enzyme bond, not the muscarinic blocker.
Updated On: Jun 25, 2026
- Atropine
- Pralidoxime
- Flumazenil
- Naloxone
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The Correct Option is B
Solution and Explanation
Step 1: Understand OP toxicity. Organophosphates inhibit acetylcholinesterase (AChE) by phosphorylating its active (esteratic) site. This stops breakdown of acetylcholine, causing accumulation at muscarinic, nicotinic and CNS synapses (SLUDGE/DUMBELS features).
Step 2: Identify the drug that reactivates the enzyme. Pralidoxime (2-PAM) is an oxime that binds the phosphorus atom on the inhibited enzyme and cleaves the OP-enzyme bond, thereby reactivating AChE - especially restoring neuromuscular (nicotinic) function. It must be given early, before "aging" (irreversible dealkylation) of the enzyme occurs.
Step 3: Why the others are wrong. Atropine is the physiological antidote that blocks muscarinic receptors to counter secretions/bradycardia, but it does not reactivate AChE. Flumazenil reverses benzodiazepines (GABA-A). Naloxone reverses opioids (mu receptor).
Key fact: Only Pralidoxime reactivates the phosphorylated acetylcholinesterase enzyme in OP poisoning.
Step 2: Identify the drug that reactivates the enzyme. Pralidoxime (2-PAM) is an oxime that binds the phosphorus atom on the inhibited enzyme and cleaves the OP-enzyme bond, thereby reactivating AChE - especially restoring neuromuscular (nicotinic) function. It must be given early, before "aging" (irreversible dealkylation) of the enzyme occurs.
Step 3: Why the others are wrong. Atropine is the physiological antidote that blocks muscarinic receptors to counter secretions/bradycardia, but it does not reactivate AChE. Flumazenil reverses benzodiazepines (GABA-A). Naloxone reverses opioids (mu receptor).
Key fact: Only Pralidoxime reactivates the phosphorylated acetylcholinesterase enzyme in OP poisoning.
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