Mastering Medical
USMLE Step 1 · Pharmacology

Cholinergic excess vs Anticholinergic toxicity

How to tell Cholinergic excess and Anticholinergic toxicity apart when a board question makes them look alike.

Fastest separator

Cholinergic excess: wet toxidrome with miosis (SLUDGE-M); anticholinergic toxicity: dry toxidrome with mydriasis and ileus.

Side by side

Cholinergic excessAnticholinergic toxicity
Key clue

Wet toxidrome: miosis, salivation, lacrimation, urination, diarrhea, bronchorrhea, bradycardia, plus fasciculations/weakness from nicotinic excess.

Dry toxidrome: mydriasis, hot flushed dry skin, delirium, urinary retention, and decreased bowel sounds.

Mechanism

Cholinesterase inhibition or muscarinic/nicotinic agonism increases acetylcholine signaling.

Antimuscarinic drugs block acetylcholine at muscarinic receptors.

Labs and tests

Organophosphate exposure, low cholinesterase activity, secretions, and fasciculations point cholinergic.

Diphenhydramine/scopolamine/TCAs, dry axillae, urinary retention, and ileus point anticholinergic.

The trap

Agitation, tachycardia, and fever can overlap with sympathomimetic toxicity, so skin moisture and bowel sounds matter.

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The repair move

In toxidromes, check secretions before memorized slogans: wet versus dry usually unlocks the answer.

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Core

A farm worker has salivation, lacrimation, urination, diarrhea, bronchorrhea, bradycardia, miosis, fasciculations, and weakness after pesticide exposure. Which toxidrome best fits?

Show answer and explanation

Answer: A. Cholinergic excess from cholinesterase inhibition. Cholinesterase inhibition causes excess acetylcholine at muscarinic and nicotinic receptors: wet secretions plus weakness/fasciculations.

Why the other choices are tempting

  • B. Anticholinergic toxicity is hot, dry, flushed, delirious, mydriatic, and urinary-retentive.
  • C. Sympathomimetic toxicity has diaphoresis and mydriasis but not bronchorrhea/miosis.
  • D. Opioid toxicity causes miosis and respiratory depression but not wet cholinergic secretions/fasciculations.
  • E. Serotonin toxicity causes hyperreflexia and clonus rather than muscarinic secretions.

Flashcards

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What is the fastest separator for Cholinergic excess vs Anticholinergic toxicity?

Cholinergic excess: wet toxidrome with miosis (SLUDGE-M); anticholinergic toxicity: dry toxidrome with mydriasis and ileus.

What clue should make you choose Cholinergic excess?

Wet toxidrome: miosis, salivation, lacrimation, urination, diarrhea, bronchorrhea, bradycardia, plus fasciculations/weakness from nicotinic excess.

Quick answers

What is the fastest way to tell Cholinergic excess from Anticholinergic toxicity?

Cholinergic excess: wet toxidrome with miosis (SLUDGE-M); anticholinergic toxicity: dry toxidrome with mydriasis and ileus.

What is the key clue for Cholinergic excess?

Wet toxidrome: miosis, salivation, lacrimation, urination, diarrhea, bronchorrhea, bradycardia, plus fasciculations/weakness from nicotinic excess.

What is the key clue for Anticholinergic toxicity?

Dry toxidrome: mydriasis, hot flushed dry skin, delirium, urinary retention, and decreased bowel sounds.

What is the common trap with Cholinergic excess vs Anticholinergic toxicity?

Agitation, tachycardia, and fever can overlap with sympathomimetic toxicity, so skin moisture and bowel sounds matter.