Learn — Digestive system

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Retroperitoneal structures

Retroperitoneal structures lie behind the parietal peritoneum against the posterior abdominal wall, so they are covered by peritoneum on their anterior surface only and have no mesentery to suspend them. The distinction is not academic: it decides the surgical approach, it explains why pancreatitis and a leaking aortic aneurysm give pain that bores straight through to the back, and it explains why litres of blood can collect there with a soft, unremarkable abdomen and no peritonitis at all.

The mnemonic SAD PUCKER lists them: Suprarenal (adrenal) glands, Aorta and inferior vena cava, Duodenum (second, third and fourth parts), Pancreas (all but the tail), Ureters, Colon (ascending and descending), Kidneys, Oesophagus (its abdominal part) and Rectum (middle and lower thirds).
Primarily retroperitoneal organs developed there and never had a mesentery — the kidneys, ureters, suprarenal glands, aorta and inferior vena cava; secondarily retroperitoneal organs began with a mesentery and were pressed against the posterior wall during rotation of the gut — the duodenum beyond its first part, the pancreas and the ascending and descending colon.
The intraperitoneal contrast to learn alongside it: the stomach, the first part of the duodenum, jejunum, ileum, caecum and appendix, transverse and sigmoid colon, liver, spleen, the tail of the pancreas and the upper third of the rectum.
The kidneys extend from about T12 to L3, the right lying 1 to 2 cm lower than the left because of the liver; each is capped by its suprarenal gland and wrapped in perirenal fat within the renal fascia, and the hilum lies at about the level of the transpyloric plane (L1) roughly 5 cm from the midline.
The pancreas lies transversely across the posterior wall at about L1 to L2, its head cradled in the C of the duodenum and only its tail intraperitoneal in the lienorenal ligament; because it is retroperitoneal, its inflammation gives epigastric pain that bores through to the back and is eased by sitting forward.
The ureters run down on psoas major, cross the pelvic brim at the bifurcation of the common iliac artery and are crossed anteriorly near the bladder by the uterine artery in the woman and the vas deferens in the man — the water-under-the-bridge relation that makes the ureter vulnerable at hysterectomy.
Retroperitoneal bleeding from a leaking abdominal aortic aneurysm, a fractured pelvis or an over-anticoagulated patient can conceal two litres or more with a soft abdomen and no guarding, so the signs to watch are tachycardia, a falling blood pressure, flank or back pain and, late, Grey Turner's bruising in the flank or Cullen's around the umbilicus.
The practical gain of being retroperitoneal is that these organs can be reached without opening the peritoneal cavity — the standard loin approach to the kidney and ureter and percutaneous nephrostomy in the prone position both depend on it.

Motilin

Motilin is a peptide hormone of 22 amino acids secreted by the M cells of the mucosa of the duodenum and upper jejunum, and it is the hormone of the fasting gut rather than of the fed gut. It generates the migrating motor complex, the wave of powerful contraction that sweeps from the stomach through the small intestine roughly every 90 to 120 minutes between meals and clears residue, shed cells and bacteria — the reason it is called the intestinal housekeeper.

Motilin is released cyclically during fasting, about every 90 to 120 minutes, and its secretion is switched off by eating — the exact opposite of gastrin, cholecystokinin, secretin and GIP, which are all released by a meal.
The migrating motor complex runs in four phases, of which phase III is the intense propulsive burst that motilin triggers; the whole cycle is abolished as soon as food arrives and resumes once the stomach is empty again.
Its function is housekeeping — sweeping undigested residue, desquamated epithelium and bacteria distally — so loss of the complex, as in long-standing diabetes or after opioids, permits small intestinal bacterial overgrowth with bloating, diarrhoea and malabsorption.
Erythromycin is a motilin receptor agonist, which is why low-dose erythromycin is used as a prokinetic in diabetic gastroparesis and given before endoscopy in an upper gastrointestinal bleed to clear the stomach of clot; tachyphylaxis develops within days to weeks, so it is a short-term measure.
The other gastrointestinal hormones for contrast: gastrin from the G cells of the antrum increases acid, cholecystokinin from the I cells of the duodenum and jejunum contracts the gallbladder and releases pancreatic enzymes, secretin from the S cells of the duodenum releases bicarbonate-rich pancreatic juice and inhibits gastrin, and GIP inhibits acid and stimulates insulin.
The clinical face of failed gastric motility is gastroparesis: early satiety, bloating, nausea and vomiting of food eaten many hours before, with a succussion splash; the commonest causes are long-standing diabetes with autonomic neuropathy, previous vagotomy, and drugs such as opioids and anticholinergics.
Management follows the physiology — small, frequent, low-fat and low-fibre meals, liquids in preference to solids, sitting upright for an hour after eating, gentle walking after meals, and tight glycaemic control, because hyperglycaemia itself slows gastric emptying further.
Motilin also explains the hunger contractions and the rumbling (borborygmi) that patients notice when the stomach has been empty for a few hours, which is a useful reassurance to be able to give.

Intrinsic factor of Castle

Intrinsic factor is a glycoprotein secreted by the parietal (oxyntic) cells of the body and fundus of the stomach — the same cells that secrete hydrochloric acid — and it is the only carrier by which vitamin B12 can be absorbed. It binds B12 in the small intestine and the complex is taken up by specific receptors in the terminal ileum, so anything that destroys the parietal cells or removes the terminal ileum causes B12 deficiency no matter how much B12 the diet contains.

Intrinsic factor is the only indispensable gastric secretion: a person can live without acid and pepsin, but not without intrinsic factor, because untreated B12 deficiency causes irreversible damage to the spinal cord.
The journey of B12: it is released from food protein by acid and pepsin, bound first by salivary haptocorrin, transferred to intrinsic factor in the duodenum when pancreatic proteases digest the haptocorrin, and finally absorbed as the intrinsic factor complex in the terminal ileum, a step that needs calcium and a near-neutral pH.
The liver stores 2 to 5 mg of B12, enough for 3 to 5 years, so deficiency after gastrectomy or ileal resection appears years later rather than weeks later; folate stores by contrast last only 3 to 4 months, which is why folate deficiency appears much faster.
Pernicious anaemia is autoimmune destruction of the parietal cells, with antibodies against the parietal cell and against intrinsic factor itself; it produces achlorhydria, a megaloblastic macrocytic anaemia with a mean corpuscular volume above 100 fL and hypersegmented neutrophils, glossitis with a beefy red sore tongue, and a raised long-term risk of gastric carcinoma.
The neurological signature of B12 deficiency is subacute combined degeneration of the cord — symmetrical loss of vibration and joint position sense, unsteadiness worse in the dark, brisk knee jerks with absent ankle jerks and extensor plantars — and it can appear before, or without, any anaemia at all.
Giving folic acid alone to a B12-deficient patient corrects the blood picture but allows the neurological disease to advance, so B12 is always measured and replaced first; this is one of the most frequently tested traps in the subject.
Causes of failure: total or partial gastrectomy and bariatric surgery, pernicious anaemia, long-term proton pump inhibitors and metformin, ileal resection or Crohn's disease of the terminal ileum, fish tapeworm and blind-loop bacterial overgrowth, and a strict vegan diet — the last matters in India, because B12 occurs only in animal foods and fortified products.
Treatment when intrinsic factor or the ileum is lost is parenteral, not oral: an intramuscular loading course of hydroxocobalamin 1000 micrograms followed by maintenance every 2 to 3 months, lifelong when the cause is permanent, with the reticulocyte count rising within about 3 to 5 days as proof it is working.
The Schilling test, which used radiolabelled B12 given with and without intrinsic factor to separate a gastric from an ileal cause, is now historical but still appears in examination papers.

HCl secretion

Hydrochloric acid is secreted by the parietal (oxyntic) cells in the body and fundus of the stomach, which pump hydrogen ions into the lumen against a concentration gradient of the order of a million to one and give gastric juice a pH of about 1 to 2. That acid kills swallowed organisms, converts pepsinogen into pepsin, frees vitamin B12 and iron from food and helps their absorption; the enzyme that does the pumping, the hydrogen-potassium ATPase, is the single target that makes proton pump inhibitors the most effective acid-suppressing drugs.

The parietal cell carries three stimulatory receptors that act together: gastrin from the antral G cells on CCK-B receptors, histamine from the enterochromaffin-like cells on H2 receptors, and acetylcholine from the vagus on M3 receptors — histamine is the final common amplifier, which is why an H2 blocker damps the response to all three.
The pump is the hydrogen-potassium ATPase on the apical canalicular membrane, exchanging one hydrogen ion out for one potassium ion in; for every hydrogen ion secreted a bicarbonate ion enters the blood at the basal surface, which is the alkaline tide seen after a meal.
Secretion runs in three phases: the cephalic phase supplies about 30% and is purely vagal, triggered by the sight, smell, taste and thought of food; the gastric phase supplies about 60% through distension and peptides releasing gastrin; and the intestinal phase supplies about 10% and is largely inhibitory.
Inhibition is as important as stimulation: an antral pH below about 3 stops gastrin release directly and through somatostatin from the D cells, and fat, acid and hyperosmolar chyme in the duodenum release secretin, cholecystokinin and GIP, which slow gastric emptying and reduce acid output.
The mucosa defends itself with a mucus and bicarbonate layer, rapid epithelial renewal and prostaglandin-maintained mucosal blood flow; NSAIDs and aspirin remove that defence by blocking prostaglandin synthesis, and Helicobacter pylori is the other main cause of peptic ulceration.
Proton pump inhibitors such as omeprazole and pantoprazole irreversibly inactivate the pump itself and must be given 30 to 60 minutes before food, because they can only reach pumps that are actively secreting; H2 blockers such as famotidine compete at the histamine receptor and are weaker, and antacids only neutralise acid already secreted.
Zollinger-Ellison syndrome is a gastrin-secreting tumour, usually in the pancreas or duodenum, producing massive acid output with multiple ulcers in unusual sites and diarrhoea with steatorrhoea because the acid inactivates pancreatic enzymes.
Long-term acid suppression has consequences the nurse counsels about: reduced absorption of vitamin B12, iron, calcium and magnesium, a higher risk of Clostridioides difficile and other enteric infection, and rebound acid hypersecretion if the drug is stopped abruptly.
Persistent vomiting or continuous nasogastric aspiration loses hydrogen and chloride and produces a hypochloraemic, hypokalaemic metabolic alkalosis — the classic biochemistry of pyloric stenosis, and the reason aspirate volume is measured and replaced rather than simply discarded.

Mineral absorption sites

Absorption in the gut is regionally specialised: the small intestine, about 6 metres long and folded into circular folds, villi and microvilli that give an absorptive surface of roughly 200 to 250 square metres, takes up almost everything, but each nutrient has its own preferred segment. Knowing which segment absorbs what is what lets a nurse predict the exact deficiency a resection or a disease will cause — an ileal resection means vitamin B12 and bile salts, a gastric operation means iron, B12 and calcium.

Duodenum and upper jejunum: iron in the ferrous form, helped by gastric acid and vitamin C; calcium, actively and dependent on vitamin D; magnesium, phosphate and copper; and the fat-soluble vitamins A, D, E and K along with fat, which needs bile salts and pancreatic lipase.
Jejunum: the bulk of the carbohydrate, protein, water-soluble vitamins and folate, folate being absorbed proximally — which is why coeliac disease, a proximal small bowel disease, causes iron and folate deficiency first.
Terminal ileum and nowhere else: vitamin B12 bound to intrinsic factor, and the bile salts of the enterohepatic circulation, of which about 95% are reclaimed there and returned to the liver in the portal blood.
Colon: water, sodium under the influence of aldosterone, and short-chain fatty acids produced by bacterial fermentation, along with vitamin K and some B vitamins made by colonic bacteria; of roughly 9 litres presented to the gut each day, about 1.5 litres reaches the colon and only 100 to 200 mL is lost in the stool.
Iron absorption is regulated at the enterocyte by hepcidin and only about 5 to 10% of dietary iron is taken up; acid, vitamin C and haem iron from meat increase it, while phytates, the tannins in tea, milk and calcium, antacids and proton pump inhibitors reduce it — which is why the iron tablet is given between meals with citrus juice and never with tea, milk or the calcium tablet.
Calcium absorption is active, saturable and vitamin D dependent in the duodenum and upper jejunum and passive further down; parathyroid hormone raises it indirectly by activating vitamin D in the kidney, and absorption falls with age, with oestrogen loss and with long-term steroids.
Practically nothing of nutritional value is absorbed in the stomach — only alcohol, water and some lipid-soluble drugs such as aspirin — so gastric surgery causes deficiency by removing acid and intrinsic factor and by speeding transit, not by removing absorptive surface.
Predictable consequences: terminal ileal resection or Crohn's disease gives B12 deficiency with bile-salt diarrhoea and fat malabsorption; gastrectomy gives iron, B12, calcium and vitamin D deficiency with dumping; coeliac disease gives iron, folate and fat-soluble vitamin deficiency; pancreatic insufficiency gives fat and fat-soluble vitamin loss with a normal mucosa.
Sodium-linked co-transport is the principle behind oral rehydration solution — glucose and sodium are absorbed together by the SGLT1 carrier in the small intestine and water follows by osmosis — which is why ORS keeps working in cholera even while secretion is torrential.

GI enzymes

The digestive enzymes are the hydrolases that break the three macronutrients into absorbable units — starch to monosaccharides, protein to amino acids and small peptides, and triglyceride to fatty acids and monoglycerides — and each is secreted at a named site with its own optimum pH. A nurse is examined on which gland makes which enzyme and on what happens when one is missing, because pancreatic failure, lactase deficiency and loss of intrinsic factor each produce a recognisable clinical picture.

Saliva contains salivary amylase (ptyalin), which begins starch digestion at an optimum pH of about 6.8, and lingual lipase; amylase is inactivated once it meets gastric acid.
The stomach secretes pepsinogen from chief cells, which hydrochloric acid from parietal cells converts to pepsin; pepsin works only in an acid medium with an optimum pH of about 1.8 to 3.5 and is inactive above pH 5.
Parietal cells also secrete intrinsic factor, needed for vitamin B12 absorption in the terminal ileum; without it the patient develops megaloblastic anaemia, which is why gastrectomy demands lifelong parenteral B12.
The pancreas carries the main digestive load: amylase for starch, lipase with colipase for fat, and the proteases trypsin, chymotrypsin, elastase and carboxypeptidase, all secreted as inactive zymogens.
Enterokinase (enteropeptidase) from the duodenal brush border converts trypsinogen to trypsin, and trypsin then activates the remaining zymogens — the safety catch that stops the pancreas digesting itself.
Brush border enzymes finish the work: lactase, sucrase, maltase and isomaltase for disaccharides, and aminopeptidases and dipeptidases for small peptides; lactase is the first to be lost, which is why lactose intolerance is so common in Indian adults.
Bile contains no enzyme at all — bile salts emulsify fat into micelles so that lipase can act on it, and they also carry the fat-soluble vitamins A, D, E and K to the mucosa for absorption.
Two duodenal hormones control pancreatic secretion: secretin, released by acid, calls for a watery bicarbonate-rich juice, and cholecystokinin, released by fat and protein, calls for an enzyme-rich juice and contracts the gallbladder.

Large intestine functions

The large intestine runs about 1.5 metres from the ileocaecal valve to the anus — caecum, ascending, transverse, descending and sigmoid colon, rectum and anal canal — and it secretes no digestive enzyme at all. Its work is the absorption of water and electrolytes, the storage and formation of faeces, and the housing of the bacterial flora that ferment residual carbohydrate and synthesise vitamin K and several B vitamins.

About 1,500 mL of chyme enters the colon each day and only about 100 to 200 mL of water leaves in the stool; the colon can absorb roughly 5 litres a day before it is overwhelmed and diarrhoea results.
Most water is absorbed in the small intestine; the colon performs the final concentration, with the ascending and transverse colon absorbing and the descending and sigmoid colon acting as a store.
Sodium is absorbed actively against a steep gradient under the influence of aldosterone while potassium and bicarbonate are secreted into the lumen, which is why prolonged diarrhoea causes hypokalaemia with a normal anion gap metabolic acidosis.
Colonic bacteria, about 100 billion organisms per gram of stool and mostly anaerobes such as Bacteroides, ferment undigested carbohydrate to short-chain fatty acids; butyrate is the main fuel of the colonocyte, and the gases produced are hydrogen, methane and carbon dioxide.
The flora synthesise vitamin K, biotin, folate and other B vitamins; the vitamin B12 they make is not absorbed, because B12 absorption happens upstream in the terminal ileum.
Goblet cells secrete alkaline mucus for lubrication and mucosal protection, neutralising the acids of bacterial fermentation; there is no enzyme in colonic secretion.
Motility is of three kinds — segmental haustral churning, slow propulsive movements, and one to three mass movements a day, usually after a meal through the gastrocolic reflex, which drive stool into the rectum and produce the urge to defecate.
Defecation is a reflex with the root value S2, S3 and S4: rectal distension relaxes the smooth-muscle internal anal sphincter involuntarily while the skeletal-muscle external sphincter, supplied by the pudendal nerve, remains under voluntary control.

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