& x20;An infant ingests a pesticide. Which drug reverses the acetylcholinesterase block? - INI-CET EXAM -2026

INI-CET EXAM -2026

Pharmacology

Medium

Appeared in: INI-CET EXAM -2026

Explanation

Organophosphate pesticides cause toxicity by forming a strong, often irreversible, bond with the acetylcholinesterase (AChE) enzyme, inactivating it.
This inactivation leads to an accumulation of the neurotransmitter acetylcholine in synapses, causing overstimulation of muscarinic and nicotinic receptors.
Pralidoxime (PAM) is a cholinesterase reactivator (an oxime). Its primary mechanism is to break the bond between the organophosphate and the AChE enzyme.
By regenerating active AChE, pralidoxime directly reverses the cause of the neuromuscular and some central nervous system effects of the poisoning.
It is most effective when given soon after exposure, before the enzyme-inhibitor complex 'ages' and becomes permanently irreversible.

Option B: Atropine does not reverse the acetylcholinesterase block. It is a competitive antagonist at muscarinic acetylcholine receptors, meaning it only blocks the effects of the excess acetylcholine at these sites.
Option C: Flumazenil is an antidote for benzodiazepine overdose, not pesticide poisoning.
Option D: Naloxone is an antidote for opioid overdose, not pesticide poisoning.

Clinical Relevance

Nursing practice connection: Use the key finding related to Antidotes for Organophosphate Poisoning to guide bedside assessment, documentation, and the next nursing action.
In clinical practice, atropine and pralidoxime are used together to manage organophosphate poisoning. Atropine is given first and repeated until muscarinic symptoms (like secretions) are controlled, while pralidoxime is started to reverse the underlying enzyme inhibition.
Nurses must recognize the distinct roles of these two antidotes. Atropine provides rapid symptomatic relief, while pralidoxime addresses the root cause and is crucial for preventing delayed complications like the 'intermediate syndrome' (muscle weakness).
What if? If the ingested pesticide was a carbamate instead of an organophosphate, pralidoxime is generally not recommended. Carbamates also inhibit acetylcholinesterase, but the bond is reversible and short-lived, so treatment is primarily supportive with atropine if needed.

How to Approach the Question

First, identify the core of the question: it asks about reversing the acetylcholinesterase block caused by a pesticide.
Recognize that common pesticides are organophosphates, which are known acetylcholinesterase inhibitors.
Recall the pharmacology of antidotes. The question is asking for the drug that fixes the enzyme, not just one that blocks the symptoms.
Evaluate the options: Atropine blocks receptors (symptom control), Flumazenil is for benzodiazepines, and Naloxone is for opioids.
Identify Pralidoxime as the specific cholinesterase reactivator, which directly matches the mechanism described in the question ('reverses the acetylcholinesterase block').
Therefore, select Pralidoxime as the most precise answer to the question asked.

Concept Tested & Keywords

Concept Tested: Antidotes for Organophosphate Poisoning
Stem keywords: infant, pesticide, acetylcholinesterase block
Lead-in keywords: reverses
Clinical cues: The question asks for the drug that 'reverses the block', pointing to the underlying enzymatic mechanism, not just symptom management.

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