Gastrointestinal motility

The enteric nervous system

• Myenteric (Auerbach's) plexus: between the longitudinal and circular muscle layers; controls motility.
• Submucosal (Meissner's) plexus: in the submucosa; controls secretion and local blood flow.
• The enteric system works without external nerves, but the parasympathetic supply (vagus, pelvic nerves) generally increases motility and secretion, and the sympathetic supply reduces them and contracts sphincters.
• Excitatory enteric transmitters: acetylcholine and substance P. Inhibitory: nitric oxide and VIP, which relax sphincters and produce receptive relaxation.
• Hirschsprung disease: failure of neural crest cells to migrate leaves an aganglionic distal segment that cannot relax; the bowel above dilates and the rectoanal inhibitory reflex is absent.
• Achalasia: loss of inhibitory (NO, VIP) neurons in the oesophageal myenteric plexus; the lower oesophageal sphincter fails to relax and peristalsis is lost; barium swallow shows a dilated oesophagus with a "bird's beak". Chagas disease gives a similar picture.

Slow waves and spikes

Interstitial cells of Cajal are the pacemakers. They generate slow waves (basic electrical rhythm): about 3/min in the stomach, 12/min in the duodenum, 8–9/min in the ileum. Slow waves alone do not cause contraction; contraction occurs when action potentials (spikes) fire on top of a slow wave, which acetylcholine and stretch promote and noradrenaline opposes. The slow-wave frequency therefore sets the maximum contraction rate of each segment.

Swallowing

• The upper third of the oesophagus is skeletal muscle, the lower third smooth muscle.
• LOS tone is increased by gastrin, acetylcholine and α-adrenergic action, and reduced by progesterone (heartburn of pregnancy), nitrates, calcium-channel blockers, chocolate, fat, alcohol, caffeine and smoking.

The stomach and gastric emptying

• Receptive relaxation: the fundus and body relax when food is swallowed (vagal NO and VIP), so the stomach accepts a meal without a rise in pressure. Lost after vagotomy, causing early satiety.
• Mixing: peristaltic waves sweep from the body to the antrum and grind food against a closed pylorus (retropulsion), reducing it to particles under about 2 mm.
• Emptying is controlled by the duodenum through neural (enterogastric reflex) and hormonal feedback, so chyme enters only as fast as it can be neutralised and digested.

• Liquids empty faster than solids; carbohydrate faster than protein; protein faster than fat.
• CCK slows the stomach but increases intestinal motility and contracts the gallbladder; gastrin increases gastric motility. Motilin increases both gastric and intestinal motility.
• Diabetic autonomic neuropathy causes gastroparesis; metoclopramide and domperidone (D2 blockade) and erythromycin (a motilin receptor agonist) speed emptying.

Dumping syndrome after gastric surgery

After gastrectomy or pyloroplasty, the reservoir and pyloric control are lost, so food enters the small bowel too fast.

• Managed with small dry meals, avoiding simple sugars, separating fluids from solids and lying down after meals.

Small intestine

• Segmentation contractions mix chyme with secretions; peristalsis moves it on (law of the intestine: contraction above, relaxation below a bolus).
• Migrating motor complex (MMC): bursts of strong contraction every 90–120 minutes during fasting, sweeping debris and bacteria from the stomach to the ileum. It is driven by motilin and abolished by eating. Its loss favours small bowel bacterial overgrowth.
• Ileocaecal valve: relaxes when the ileum is distended or after a meal (gastroileal reflex) and closes when the caecum is distended.
• Intestinal obstruction causes visible peristalsis, loud high-pitched (tinkling) bowel sounds and colicky pain as the bowel works against the block; later it fatigues and falls silent.

Large intestine and defecation

• Haustral contractions mix contents slowly for water absorption; mass movements a few times a day push contents towards the rectum, often after meals (gastrocolic reflex, mediated by stretch of the stomach, gastrin and CCK).
• Rectal distension causes reflex relaxation of the internal anal sphincter (smooth muscle, involuntary) and the urge to defecate.
• The external anal sphincter and puborectalis are skeletal muscle supplied by the pudendal nerve (S2–S4) and can delay defecation voluntarily.
• Defecation is a spinal reflex integrated in the sacral cord (S2–S4): pelvic parasympathetic nerves contract the rectum and sigmoid, the internal sphincter relaxes, and higher centres permit relaxation of puborectalis and the external sphincter, helped by a Valsalva effort.
• Spinal cord injury: a lesion above the sacral segments (for example T6) cuts voluntary control but leaves the sacral reflex arc intact, so digital rectal stimulation triggers reliable reflex emptying. A lesion of the conus or cauda equina destroys the arc: the bowel is flaccid and needs manual evacuation.

Remember Fat slows the stomach; fasting starts the MMC; the sacral cord empties the rectum.

Vomiting

Coordinated by the vomiting centre (nucleus tractus solitarius and nearby reticular formation) in the medulla, which receives input from:

• the chemoreceptor trigger zone (area postrema, outside the blood–brain barrier): drugs, toxins, uraemia; receptors D2, 5-HT3, NK1
• vagal afferents from the gut (5-HT3; serotonin released from damaged enterochromaffin cells by chemotherapy)
• the vestibular system (motion sickness; H1 and M1 receptors)
• the cortex and limbic system (smells, anticipatory vomiting)

Acid–base effects of vomiting and diarrhoea

• Prolonged vomiting of gastric contents (classically pyloric stenosis in a 3–8-week-old boy with projectile, non-bilious vomiting and an olive-shaped mass) loses HCl, producing hypochloraemic, hypokalaemic metabolic alkalosis.
• Volume loss activates aldosterone, which reabsorbs sodium in exchange for K⁺ and H⁺, worsening hypokalaemia and maintaining the alkalosis; once K⁺ is very low, the kidney excretes H⁺ and the urine is acid (paradoxical aciduria). Treat with 0.9% saline plus potassium before pyloromyotomy.
• Diarrhoea loses bicarbonate-rich fluid, causing normal anion gap (hyperchloraemic) metabolic acidosis with hypokalaemia.

Exam trap Vomiting gives alkalosis, but diarrhoea gives acidosis: do not mix them up when both are present in the stem.

How FCPS asks about this

• Plexus controlling motility versus secretion: myenteric (Auerbach's) for motility, submucosal (Meissner's) for secretion.
• Hormone that delays gastric emptying: CCK (fat in duodenum); secretin also slows it. Gastrin and motilin speed it.
• Hormone that slows the stomach but increases intestinal motility: CCK.
• Housekeeping contractions between meals: migrating motor complex driven by motilin; erythromycin mimics motilin.
• Early dumping: hyperosmolar chyme pulls fluid into the gut within 30 minutes of a meal.
• Pyloric stenosis or prolonged vomiting: hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria.
• Why digital stimulation works after T6 cord injury: intact sacral (S2–S4) defecation reflex arc.