Nine litres presented, two hundred millilitres lost
across a surface the size of a tennis court.

1. Two kinds of contraction, two jobs. Segmental contractions mix and expose chyme to the brush border; propulsive contractions move it along. Segmentation predominates in the fed state.
2. The migrating motor complex is a fasting phenomenon. Every 90 minutes, four phases, triggered by motilin, sweeping residue and bacteria distally. Feeding abolishes it.
3. The pancreas secretes two things from two cells. Acinar cells make the enzymes and proenzymes; ductal cells make the bicarbonate that keeps them from being denatured. Cholecystokinin drives the first, secretin the second.
4. Two macronutrients go to the portal vein and one does not. Monosaccharides and amino acids leave the enterocyte into the capillary; fat is re-esterified, packaged as chylomicrons and leaves in the lacteal to the thoracic duct.
5. 9000 mL in, 200 mL out. Only 2000 mL of the input is drunk. Ninety-eight per cent of what is presented is reabsorbed, most of it in the jejunum.
6. The colon is a reclaimer, not a digester. It absorbs water and electrolytes, ferments residue to short-chain fatty acids that feed the colonocyte, and moves contents by giant migrating complexes six to ten times a day.

Two consequences follow. First, erythromycin is a motilin agonist, which is why it is used as a prokinetic in the critically ill rather than as an antibiotic in that setting. Second, anything that abolishes the complex — continuous enteral feeding, an ileus, opioids — removes the mechanism that keeps the small intestine relatively sterile, and small-intestinal bacterial overgrowth follows. The healthy small intestine carries fewer than about 100,000 organisms per millilitre against the colon’s enormous population, and it is motility rather than immunity that maintains that difference.

About 1500 mL of pancreatic juice is produced daily and drains into the duodenum. The endocrine pancreas — the islets, which are only 1 to 2 per cent of the mass — belongs to a different syllabus objective and is not taught here.

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On the left, a single intestinal villus in section, with a crypt of Lieberkuhn at its base, a capillary network in red and blue, and a central lacteal in green running its length. On the right, an enlarged enterocyte with its brush border of microvilli at the top and a capillary and a lacteal beneath. Three columns of pathway are drawn across it. In the carbohydrate column, disaccharides are cleaved at the brush border to glucose, galactose and fructose; glucose and galactose cross the apical membrane on SGLT1 coupled to sodium, fructose crosses on GLUT5 by facilitated diffusion, and all three leave through GLUT2 in the basolateral membrane into the capillary, labelled to the portal vein. In the protein column, proteins are broken to amino acids and to di- and tripeptides; amino acids cross on a sodium-coupled carrier and peptides on PepT1 coupled to hydrogen, and both leave basolaterally to the same capillary. In the fat column, a mixed micelle delivers fatty acids and monoglycerides which diffuse in, are re-esterified in the smooth endoplasmic reticulum, packaged into chylomicrons, and released into the lacteal, labelled to the lymphatic and thoracic duct.

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1. In the mouth, salivary alpha-amylase begins the breakdown of starch. It works optimally at the pH of saliva and manages up to about three-quarters of the starch before gastric acid denatures it — protected for longer inside a food bolus than at its surface.
2. In the duodenum, pancreatic alpha-amylase continues it, producing disaccharides and short oligosaccharides. Neither amylase can touch cellulose, which is why it passes through unchanged.
3. At the brush border, specific integral membrane enzymes — sucrase, maltase, lactase — hydrolyse the disaccharides to monosaccharides. Only monosaccharides can be absorbed. Lactose intolerance is a deficiency at exactly this step.
4. Into the enterocyte. Glucose and galactose enter only by secondary active transport on SGLT1, coupled to sodium, whose gradient is maintained by the basolateral Na⁺/K⁺ ATPase. Fructose enters by facilitated diffusion on GLUT5, using no energy at all. Pentoses enter by simple diffusion.
5. Out of the enterocyte. All of them leave through GLUT2 in the basolateral membrane by facilitated diffusion, into the capillary and thence the portal vein.

1. In the stomach, pepsin — activated from pepsinogen by acid — cleaves dietary protein to shorter polypeptides. Useful but not essential; the pancreatic enzymes can do the whole job alone.
2. In the duodenum, trypsin and chymotrypsin cleave those polypeptides progressively, producing dipeptides and tripeptides rather than single amino acids.
3. At the brush border, peptidases cleave some of those to single amino acids.
4. Into the enterocyte, by two routes. Single amino acids cross on sodium-coupled carriers, of which there are separate ones for neutral, basic and acidic amino acids. Di- and tripeptides cross on PepT1, coupled to hydrogen rather than sodium.
5. Inside the enterocyte, the absorbed peptides are hydrolysed to amino acids by cytosolic peptidases, and everything leaves basolaterally by facilitated diffusion into the portal blood.

Both carbohydrate and protein products are osmotically active, so their absorption drags water with them across the epithelium. That is the second mechanism, after the sodium-glucose cotransporter, by which absorbing nutrients absorbs water — and it is why the fluid balance in section 07 depends on the digestion in sections 04 to 06 having worked.

1. Emulsification. Triglyceride is insoluble and aggregates into large droplets. Bile salts, which are amphipathic, coat those droplets and break them into progressively smaller ones. This does not digest anything; it multiplies the surface area on which lipase can act.
2. Hydrolysis. Pancreatic lipase acts only at a droplet surface, hydrolysing each triglyceride to two free fatty acids and one 2-monoglyceride. Gastric and lingual lipase have already made a modest start.
3. Micelle formation. The products combine with bile salts into mixed micelles, which ferry them across the unstirred layer to the brush border. Without micelles the products simply cannot reach the membrane.
4. Absorption. At the enterocyte the lipid contents diffuse passively across the membrane. The bile salts stay in the lumen and travel on to be reabsorbed in the terminal ileum.
5. Reassembly and export. Inside the cell, fatty acids and monoglycerides are re-esterified to triglyceride in the smooth endoplasmic reticulum, packaged with cholesterol, phospholipid and apolipoprotein into chylomicrons, and released into the lacteal — not the capillary. Chylomicrons reach the systemic circulation at the thoracic duct.

Vitamin absorption follows the route its solubility dictates. The fat-soluble vitamins A, D, E and K are absorbed in micelles with dietary lipid, throughout the small intestine. The water-soluble vitamins are absorbed by carrier-mediated transport, mostly in the jejunum, with two site-specific exceptions that matter clinically: iron is absorbed in the duodenum, and vitamin B12 and the bile salts are absorbed in the terminal ileum. A terminal ileal resection therefore produces both vitamin B12 deficiency and bile-salt malabsorption, and the second causes both a diarrhoea and a fat-malabsorption picture.

The ileocaecal valve guards the junction with a simple reciprocal arrangement: distension of the ileum relaxes it and distension of the caecum contracts it, so contents pass forwards and colonic bacteria do not pass back. Its competence is part of what keeps the small intestine relatively sterile, alongside the migrating motor complex and gastric acid.

The sequence is worth carrying because it explains both continence and its failure. Rectal distension stimulates stretch receptors, which produces the rectoanal inhibitory reflex: the internal sphincter relaxes involuntarily, allowing the contents to be sampled by the sensitive anal mucosa, while the external sphincter contracts reflexly to prevent leakage. If the moment is convenient, voluntary relaxation of the external sphincter and puborectalis, with a Valsalva manoeuvre and the squatting posture, straightens the anorectal angle and allows defaecation. If it is not, voluntary contraction of the external sphincter returns the contents to the rectum and the urge subsides until the next mass movement. Relaxation of the internal sphincter is promoted by nitric oxide and vasoactive intestinal peptide, the same non-adrenergic non-cholinergic pair that relaxes every other sphincter in this module.