GI Antispasmodics

The gut wall is smooth muscle whose contraction (motility) is driven by the parasympathetic nervous system through acetylcholine acting on muscarinic receptors. In irritable bowel syndrome (IBS) and functional bowel disorders, that muscle can go into painful spasm and cramping. The antispasmodics relieve it by doing the obvious thing: blocking those muscarinic receptors so the muscle relaxes and hypermotility settles.

That makes these drugs anticholinergics (antimuscarinics) — the same pharmacology as atropine in the Autonomic Anticholinergics class, just aimed at the gut. They are used PRN for cramping, not as a cure, and they treat the *symptom* of spasm rather than the underlying disorder.

Because muscarinic receptors are everywhere, blocking them in the gut also blocks them body-wide — producing the classic anticholinergic toxidrome, memorized as "can’t see, can’t spit, can’t pee, can’t poop" (and "hot as a hare, mad as a hatter"): blurred vision, dry mouth, urinary retention, constipation, plus tachycardia, flushing, and — especially in the elderly — confusion. That confusion risk makes them Beers-criteria drugs to avoid in older adults.

The same effects define the contraindications: they are dangerous in narrow-angle glaucoma (can precipitate an acute attack), urinary retention/BPH, GI obstruction or paralytic ileus (they further slow the gut), and myasthenia gravis (they oppose cholinergic transmission). This directly mirrors the atropine story in the Autonomic system.