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Gastrointestinal Physiology

Usually weeks 15-16 of a medical physiology course, closing the semester

Gastrointestinal physiology is a tube with a brain of its own: the enteric nervous system runs motility and secretion locally, the autonomic nerves and a handful of gut hormones tune it, and every segment is built for one job. Learn it in the order food travels — mouth, esophagus, stomach, small intestine, colon — and at each stop ask the same three questions: how does it move, what does it secrete and what drives that, and what does it absorb. The high-yield outputs are the hormone table (source cell, stimulus, action), the parietal cell and its three stimuli, the transporter that carries each nutrient, the two vitamins with fixed addresses (B12 in the terminal ileum, iron in the duodenum), and the physiology that separates secretory from osmotic diarrhea.

On the PANCE this unit feeds:Gastrointestinal/Nutrition · 8%Hematology · 5%Endocrine · 6%

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AI-authored study notes, not faculty-reviewed and not medical advice. Verify every mechanism against your course materials and faculty; programs differ in emphasis.

High-Yield Pearl

Follow the meal: each segment's motility, secretion, and absorption answer the problem the previous segment handed it — acid is met by secretin's bicarbonate, fat by CCK and bile, and what the ileum fails to reclaim (B12, bile acids) is what its disease costs.

What the exam asks
Mechanisms, curves, and what happens when each one fails.
  • The wall, the enteric nervous system, and autonomic control. From the lumen out: MUCOSA (epithelium, lamina propria, muscularis mucosae), SUBMUCOSA, MUSCULARIS EXTERNA (inner circular and outer longitudinal layers), and serosa or adventitia. The enteric nervous system lives in two plexuses: the SUBMUCOSAL (Meissner) plexus mainly controls secretion, absorption, and local blood flow, while the MYENTERIC (Auerbach) plexus, between the circular and longitudinal layers, mainly controls motility. The ENS can run reflexes with no outside input, but extrinsic nerves modulate it. PARASYMPATHETIC fibers — the vagus to roughly the proximal two-thirds of the colon, pelvic splanchnic nerves (S2–S4) beyond — are mostly excitatory (ACh), though vagal fibers also release VIP and NO to relax sphincters and the proximal stomach. SYMPATHETIC postganglionic fibers from the celiac and mesenteric ganglia release norepinephrine, which inhibits motility and secretion, contracts sphincters, and constricts splanchnic vessels.
  • Slow waves and spike potentials. GI smooth muscle has a resting potential that oscillates rhythmically: SLOW WAVES, generated by the pacemaker INTERSTITIAL CELLS OF CAJAL and spread through gap junctions. Slow waves are not action potentials and by themselves cause little or no contraction; when a wave's plateau depolarizes past threshold, SPIKE POTENTIALS (action potentials carried largely by Ca2+ through L-type channels) fire on the plateau, and the Ca2+ that enters drives contraction. The more spikes, the stronger the contraction. Slow-wave FREQUENCY is intrinsic and sets the MAXIMUM rate of contraction for each segment — about 3/min in the stomach, about 12/min in the duodenum, falling to about 8–9/min in the terminal ileum. ACh and parasympathetic stimulation raise the plateau and add spikes; norepinephrine hyperpolarizes and removes them — neither changes the frequency.
  • Swallowing, the stomach, and gastric emptying. Chewing mixes food with saliva. Swallowing has an ORAL phase (voluntary), a PHARYNGEAL phase (involuntary, coordinated by the medullary swallowing center: the soft palate seals the nasopharynx, the larynx rises and the epiglottis covers it, breathing is briefly inhibited, and the upper esophageal sphincter relaxes), and an ESOPHAGEAL phase: PRIMARY peristalsis follows the swallow, and SECONDARY peristalsis, triggered by distension, clears any bolus left behind. The LOWER ESOPHAGEAL SPHINCTER is tonically contracted and relaxes as the swallow begins, through vagal VIP and NO. The proximal stomach then undergoes RECEPTIVE RELAXATION — a vagovagal, VIP-mediated relaxation that lets it hold a meal with little rise in pressure. The distal stomach (antrum) mixes and grinds with strong peristaltic contractions against a nearly closed pylorus (retropulsion), passing only particles of about 1–2 mm into the duodenum. EMPTYING: liquids empty faster than solids, and isotonic liquids fastest. The duodenum sets the pace so it is never flooded: FAT in the duodenum is the most potent brake (via CCK), ACID slows emptying through the enterogastric reflex and secretin, and HYPERTONIC chyme slows it through duodenal osmoreceptors. The result is that chyme is delivered only as fast as it can be neutralized and digested. Gastric emptying is slowed by vagal damage (as in diabetic autonomic neuropathy) and by opioids and anticholinergics, and sped by motilin agonists such as erythromycin.
  • Small-intestinal and colonic motility; defecation. During a meal the small intestine performs SEGMENTATION (contractions that mix chyme with secretions and bring it to the mucosa without net propulsion) and PERISTALSIS (contraction behind the bolus via ACh and substance P, relaxation ahead of it via VIP and NO — the law of the intestine). Between meals, the MIGRATING MOTOR COMPLEX sweeps from the stomach to the terminal ileum roughly every 90 minutes, driven by MOTILIN; its bursts clear undigested debris and bacteria, and feeding abolishes it. Ileal distension relaxes the ileocecal sphincter, colonic distension contracts it. The colon uses haustral (segmenting) contractions to absorb water and a few daily MASS MOVEMENTS to push contents on; the GASTROCOLIC REFLEX — food entering the stomach increases colonic motility — is why the urge often follows a meal. DEFECATION: rectal distension triggers the RECTOSPHINCTERIC reflex, which relaxes the internal anal sphincter (smooth muscle, involuntary) and creates the urge; the external anal sphincter (skeletal muscle, pudendal nerve) is under voluntary control, so the act can be deferred, and a Valsalva maneuver assists it.
  • GI hormones, paracrines, and neurocrines. GASTRIN — G cells of the gastric antrum (and duodenum); released by small peptides and amino acids, gastric distension, and vagal GRP; inhibited by luminal acid via somatostatin; stimulates H+ secretion (directly and by releasing histamine from ECL cells) and is trophic to the gastric mucosa. CCK — I cells of the duodenum and jejunum; released by fatty acids, monoglycerides, and small peptides; contracts the gallbladder and relaxes the sphincter of Oddi, stimulates pancreatic ENZYME secretion, slows gastric emptying, and signals satiety. SECRETIN — S cells of the duodenum; released by ACID (and fatty acids); stimulates pancreatic and biliary HCO3− and inhibits gastric acid. GIP — K cells of the duodenum and jejunum; released by glucose, fat, and amino acids; stimulates insulin release (an incretin, alongside GLP-1 from L cells). MOTILIN — duodenal cells, released cyclically in FASTING; triggers the migrating motor complex. SOMATOSTATIN — D cells throughout the mucosa; released by luminal acid; inhibits nearly every GI hormone and secretion. Paracrine HISTAMINE comes from ECL cells; neurocrines include ACh, VIP and NO (relaxation and secretion), GRP (gastrin release), and substance P (contraction).
  • Saliva. About 1–1.5 L/day, from the parotid (serous), submandibular (mixed), and sublingual (mostly mucous) glands. ACINAR cells make an isotonic, plasma-like fluid; the DUCTS then reabsorb Na+ and Cl− and secrete K+ and HCO3−, but are relatively water-impermeable, so saliva is HYPOTONIC. Composition is FLOW-DEPENDENT: at high flow the ducts have less time to modify the fluid, so saliva moves toward plasma (more Na+ and Cl−, less K+) yet stays hypotonic, and its HCO3− is highest because secretion itself is stimulated. Both autonomic divisions stimulate salivation (parasympathetic, via CN VII and IX, dominates), so anticholinergics cause dry mouth. Aldosterone acts on the ducts like the collecting duct. Saliva carries α-amylase, lingual lipase, lysozyme, and IgA.
  • Gastric acid — the parietal cell. Parietal cells in the body and fundus secrete HCl and INTRINSIC FACTOR. Inside the cell, CARBONIC ANHYDRASE converts CO2 and water to H+ and HCO3−. The apical H+/K+-ATPase (the proton pump) exchanges H+ for K+ against a gradient of about a millionfold; K+ recycles out through apical K+ channels, and Cl− follows through apical Cl− channels. The HCO3− leaves across the basolateral membrane in exchange for Cl−, so gastric venous blood turns alkaline after a meal — the ALKALINE TIDE. Three stimuli: ACh (vagus, M3 receptor) and GASTRIN (CCK-B receptor) act through Gq → IP3/Ca2+; HISTAMINE from ECL cells acts through H2 → Gs → cAMP. Because they POTENTIATE one another (together they exceed their sum), an H2 blocker blunts the response to ACh and gastrin as well; a proton-pump inhibitor blocks the final common step. Chief cells secrete PEPSINOGEN (cleaved to pepsin below pH about 3, autocatalytically) and gastric lipase; mucous cells secrete mucus and HCO3−; prostaglandins reduce acid and protect the mucosa.
  • Phases and inhibition of acid secretion. CEPHALIC phase (about 30%): sight, smell, taste, and chewing act through the vagus — ACh directly on parietal cells and GRP on G cells (so atropine does not block vagal gastrin release). GASTRIC phase (about 60%): distension triggers vagovagal and local reflexes, and peptides and amino acids release gastrin. INTESTINAL phase (about 10%): protein products in the duodenum add a little. Brakes: when antral pH falls below about 3, D cells release SOMATOSTATIN, which inhibits gastrin release and the parietal cell directly — a negative feedback loop; acid, fat, and hypertonicity in the duodenum release secretin and GIP and trigger neural reflexes that inhibit secretion.
  • Pancreatic secretion. ACINAR cells secrete the enzymes — α-amylase, lipase with colipase, phospholipase A2, cholesterol esterase, and the proteases as inactive ZYMOGENS (trypsinogen, chymotrypsinogen, procarboxypeptidase, proelastase) — stimulated by CCK and ACh (Gq/Ca2+). DUCTAL cells secrete the HCO3−-rich aqueous juice under SECRETIN (cAMP): an apical Cl−/HCO3− exchanger moves HCO3− out while Cl− recycles to the lumen through CFTR. Pancreatic juice is ISOTONIC at every flow rate; as flow rises its HCO3− rises and Cl− falls reciprocally. CCK and secretin potentiate each other. Activation happens only in the duodenum: brush-border ENTEROKINASE (enteropeptidase) converts trypsinogen to TRYPSIN, which activates the other zymogens and more trypsinogen; trypsin inhibitor within the pancreas guards against premature activation.
  • Bile, bilirubin, and the liver. Hepatocytes make the PRIMARY bile acids (cholic and chenodeoxycholic) from cholesterol — the rate-limiting enzyme is 7α-hydroxylase — and CONJUGATE them with glycine or taurine, making them ionized bile salts that stay in the lumen until the ileum. Bile salts are amphipathic: they emulsify fat and form MICELLES that ferry lipid products to the brush border. Gut bacteria deconjugate and dehydroxylate some into SECONDARY bile acids. About 95% are reabsorbed in the TERMINAL ILEUM by Na+-coupled transport and return in portal blood — the ENTEROHEPATIC CIRCULATION — so the small pool cycles several times a day and synthesis replaces only the fraction lost in stool. Between meals the gallbladder concentrates bile; CCK contracts it. Bile also excretes cholesterol, phospholipid, and BILIRUBIN: heme → biliverdin → unconjugated bilirubin (albumin-bound, water-insoluble) → hepatic conjugation with glucuronic acid by UDP-glucuronosyltransferase → secreted into bile → gut bacteria make urobilinogen, some reabsorbed and excreted in urine as urobilin, the rest becoming brown stercobilin. The liver's other metabolic jobs: glycogen storage and gluconeogenesis, VLDL and albumin and clotting-factor synthesis, the urea cycle, drug biotransformation, and storage of vitamin A, B12, and iron.
  • Carbohydrate, protein, and lipid absorption. CARBOHYDRATES: salivary and pancreatic α-amylase cut starch to maltose, maltotriose, and α-limit dextrins; BRUSH-BORDER enzymes (lactase, sucrase-isomaltase, maltase) finish the job, because only MONOSACCHARIDES are absorbed. Glucose and galactose enter by SGLT1 (secondary active, Na+-coupled); fructose enters by GLUT5 (facilitated diffusion); all three exit basolaterally through GLUT2. PROTEINS: pepsin starts digestion, pancreatic proteases do most of it, and brush-border peptidases finish; free amino acids enter by several Na+-coupled carriers, while di- and tripeptides enter faster by the H+-coupled PepT1 and are hydrolyzed inside the cell. LIPIDS: pancreatic lipase (anchored by colipase) makes 2-monoglycerides and free fatty acids, which ride micelles to the brush border and diffuse in; the enterocyte re-esterifies them and packages them with cholesterol, phospholipid, and apoB-48 into CHYLOMICRONS, which exit into LACTEALS and travel in lymph, bypassing the liver. Short- and medium-chain fatty acids go straight to portal blood. Fat-soluble vitamins (A, D, E, K) need micelles.
  • Vitamins, iron, water, and electrolytes. Most water-soluble vitamins use Na+-coupled transport in the upper small intestine. VITAMIN B12 has a fixed route: freed from food by acid and pepsin, bound by haptocorrin (R binder) from saliva, released when pancreatic proteases digest haptocorrin in the duodenum, bound by INTRINSIC FACTOR, and absorbed as the complex in the TERMINAL ILEUM; the liver stores years' worth. IRON is absorbed in the DUODENUM: heme iron directly, non-heme iron after reduction to Fe2+ (helped by vitamin C) via DMT1; it is stored as ferritin or exported by FERROPORTIN onto transferrin, and hepcidin degrades ferroportin. WATER: about 9 L/day enters (about 2 L eaten and drunk, about 7 L of secretions); the small intestine absorbs most, the colon most of the rest, and only about 100–200 mL leaves in stool. Na+ is absorbed with glucose and amino acids and by Na+/H+ exchange in the small intestine and through aldosterone-regulated ENaC channels in the colon, which also SECRETES K+. Crypt cells SECRETE Cl− through apical CFTR (Cl− enters basolaterally on NKCC1), with Na+ and water following; cAMP (cholera toxin, VIP) and cGMP (heat-stable E. coli toxin) hold CFTR open. Colonic bacteria ferment fiber into short-chain fatty acids that fuel colonocytes, and make vitamin K and biotin.
Worth drilling · 44 concepts
Each with the one fact that identifies it. Your course's slides are the authority; use this to check your list against.
  1. 1Myenteric plexus — enteric plexus between circular and longitudinal muscle; mainly controls motility
  2. 2Submucosal plexus — enteric plexus of the submucosa; mainly controls secretion and local blood flow
  3. 3Interstitial cells of Cajal — pacemaker cells that generate slow waves
  4. 4Slow waves — rhythmic subthreshold oscillations that set the maximum contraction frequency
  5. 5Spike potentials — Ca2+-carried action potentials on the slow-wave plateau that trigger contraction
  6. 6Secondary peristalsis — esophageal wave triggered by distension from a bolus left behind
  7. 7Lower esophageal sphincter — tonically closed; relaxes on swallowing via vagal VIP and NO
  8. 8Receptive relaxation — vagovagal, VIP-mediated relaxation of the proximal stomach as food arrives
  9. 9Migrating motor complex — fasting sweep from stomach to ileum about every 90 minutes
  10. 10Motilin — fasting hormone that triggers the migrating motor complex; erythromycin mimics it
  11. 11Segmentation — mixing contractions with no net propulsion
  12. 12Gastrocolic reflex — food entering the stomach increases colonic mass movements
  13. 13Rectosphincteric reflex — rectal distension relaxes the internal anal sphincter
  14. 14External anal sphincter — skeletal muscle on the pudendal nerve that lets defecation be deferred
  15. 15Gastrin — antral G-cell hormone released by peptides, distension, and vagal GRP; raises acid
  16. 16Cholecystokinin — I-cell hormone released by fat and peptides; gallbladder contraction and pancreatic enzymes
  17. 17Secretin — duodenal S-cell hormone released by acid; pancreatic bicarbonate
  18. 18Glucose-dependent insulinotropic peptide — K-cell incretin that amplifies insulin after oral glucose
  19. 19Somatostatin — D-cell brake released by luminal acid; inhibits nearly every GI hormone
  20. 20Gastrin-releasing peptide — vagal neurotransmitter onto G cells; not blocked by atropine
  21. 21Vasoactive intestinal peptide — neurocrine that relaxes sphincters and drives intestinal secretion
  22. 22Enterochromaffin-like cell — releases histamine onto parietal-cell H2 receptors
  23. 23Saliva — hypotonic at every flow rate because the ducts reabsorb NaCl but not water
  24. 24Parietal cell — secretes HCl and intrinsic factor
  25. 25Proton pump — apical H+/K+-ATPase; the final common step of acid secretion
  26. 26Alkaline tide — bicarbonate entering gastric venous blood during acid secretion
  27. 27Potentiation — acid response to combined ACh, gastrin, and histamine exceeds their sum
  28. 28Chief cell — secretes pepsinogen, activated to pepsin below about pH 3
  29. 29Cephalic phase — about 30% of meal-related acid; vagal, triggered by sight, smell, and taste
  30. 30Pancreatic ductal cells — secretin-driven HCO3− secretion that depends on CFTR
  31. 31Enterokinase — duodenal brush-border enzyme that converts trypsinogen to trypsin
  32. 32Enterohepatic circulation — about 95% of bile acids reabsorbed in the terminal ileum
  33. 33Bile salt micelle — carries monoglycerides, fatty acids, and fat-soluble vitamins to the brush border
  34. 34UDP-glucuronosyltransferase — hepatic enzyme that conjugates bilirubin
  35. 35Sucrase-isomaltase — brush-border enzyme that also cleaves α-1,6 bonds of limit dextrins
  36. 36SGLT1 cotransporter — apical Na+-coupled entry of glucose and galactose; the basis of oral rehydration
  37. 37Fructose carrier GLUT5 — apical facilitated diffusion of fructose
  38. 38Basolateral exit transporter GLUT2 — carries all three monosaccharides out of the enterocyte
  39. 39Chylomicron — apoB-48 lipoprotein that leaves the enterocyte through lacteals into lymph
  40. 40Intrinsic factor — parietal-cell protein required for B12 uptake in the terminal ileum
  41. 41Ferroportin — basolateral iron exporter degraded by hepcidin
  42. 42Secretory diarrhea — stool osmotic gap under 50; persists with fasting
  43. 43Osmotic diarrhea — stool osmotic gap over 100; stops with fasting
  44. 44Cholera toxin — locks Gs on, raising cAMP and opening CFTR
Practice it
Active recall over the drill list — flip and claim, match the pairs, produce the answers cold, fill in the diagram, or read the curves like the exam does.

Every concept on the drill list, one card at a time — the name up front, the fact that identifies it on the flip. Claim each card honestly and the deck learns what to lead with next time. Progress lives in this browser only.

What everyone misses
The distinctions that lose points on this material, year after year.
  • Slow waves are not action potentials. The slow wave sets WHEN a contraction can happen, not whether it does; tension appears only when the plateau crosses threshold and spike potentials fire. Neural and hormonal inputs change the plateau height and the number of spikes — and so the force — but not the slow-wave frequency, which is fixed by the interstitial cells of Cajal. 'ACh speeds the stomach's slow waves' is the classic wrong answer.
  • Secretin makes water; CCK makes enzymes. Students swap them. Secretin answers ACID with bicarbonate-rich pancreatic (and biliary) fluid from DUCT cells; CCK answers FAT and PROTEIN with ACINAR enzymes and gallbladder contraction. A vignette about neutralizing duodenal acid is secretin; one about digesting a fatty meal is CCK. The two potentiate each other, but their primary jobs never overlap.
  • Saliva is hypotonic even at maximal flow. At high flow, saliva's Na+ and Cl− rise toward plasma values because the ducts have less time to reabsorb them — but it never becomes isotonic. Pancreatic juice is the opposite: isotonic at every flow rate, with HCO3− and Cl− trading places as flow changes. Don't transfer the saliva rule to the pancreas.
  • Blocking acid raises gastrin. Low antral pH is the main brake on gastrin (via somatostatin). A proton-pump inhibitor, atrophic gastritis, or pernicious anemia removes the acid, so gastrin climbs — high gastrin with LOW acid. Only a gastrinoma gives high gastrin with HIGH acid. Always read the gastrin level alongside the acid output.
  • The stool osmotic gap points the opposite way from intuition. Gap = 290 − 2(stool Na+ + K+). A LARGE gap (over about 100) means an unmeasured solute — lactose, magnesium, PEG, sorbitol — is holding water: OSMOTIC diarrhea, which stops with fasting. A SMALL gap (under about 50) means electrolytes account for the osmolality: SECRETORY diarrhea, which continues through fasting and at night.
  • B12 and iron have different addresses. Iron is absorbed in the DUODENUM, so duodenal disease (celiac) causes iron deficiency. B12 needs intrinsic factor from the STOMACH and is absorbed in the TERMINAL ILEUM, so gastrectomy, pernicious anemia, or ileal resection causes B12 deficiency. Bile acids share the terminal-ileum address, which is why ileal disease also causes fat malabsorption.
  • Chylomicrons skip the portal vein. Long-chain fat leaves the enterocyte as chylomicrons that are too large for capillaries; they enter lacteals and reach the blood through the thoracic duct. Only short- and medium-chain fatty acids — and every water-soluble nutrient — travel in portal blood to the liver first. That is why medium-chain triglyceride oil is used when lymphatic or micelle-dependent absorption fails.
Clinical correlations
Where this unit shows up again — in clinic, on rotations, and on the boards.
  • Achalasia. Loss of inhibitory (VIP/NO) neurons in the esophageal myenteric plexus: the lower esophageal sphincter fails to relax and peristalsis is absent. Dysphagia to BOTH solids and liquids from the start, regurgitation of undigested food, and a dilated esophagus tapering to a 'bird's beak' on barium swallow; manometry is diagnostic. Chagas disease causes the same picture by destroying the plexus.
  • Gastroesophageal reflux disease. Inappropriate transient relaxations or low tone of the lower esophageal sphincter let acid reflux: heartburn worse lying down or after large, fatty meals (fat slows emptying and lowers sphincter tone), chronic cough, and hoarseness. Proton-pump inhibitors block the final step of acid secretion; long-standing reflux can cause Barrett esophagus (intestinal metaplasia).
  • Zollinger-Ellison syndrome. A gastrinoma (duodenum or pancreas, sometimes with MEN1) produces gastrin without feedback: massive acid output, multiple or unusually located ulcers (beyond the duodenal bulb), and diarrhea with steatorrhea because acid inactivates pancreatic lipase. Fasting gastrin is high despite a low gastric pH, and secretin PARADOXICALLY raises gastrin further — the basis of the confirmatory test.
  • Pernicious anemia. Autoimmune destruction of parietal cells (antibodies to parietal cells and intrinsic factor) causes atrophic gastritis, achlorhydria, and reactively high gastrin. Without intrinsic factor, B12 is not absorbed: megaloblastic anemia plus neurologic deficits (subacute combined degeneration). Both methylmalonic acid and homocysteine rise — folate deficiency raises only homocysteine. Oral high-dose or parenteral B12 bypasses the defect.
  • Terminal ileal resection or disease. Removing or inflaming the terminal ileum (as in Crohn disease) breaks two circuits at once: B12–intrinsic factor uptake (megaloblastic anemia) and bile acid reabsorption. Lost bile acids reach the colon and cause a secretory (bile acid) diarrhea; if losses exceed synthesis, micelles fail, producing steatorrhea, fat-soluble vitamin deficiency, cholesterol gallstones, and calcium oxalate kidney stones (unbound oxalate is absorbed in excess).
  • Cholera and oral rehydration. Cholera toxin ADP-ribosylates Gs, locking adenylyl cyclase on; cAMP holds CFTR open and crypt cells pour out Cl− with water — profuse 'rice-water' secretory diarrhea with a small osmotic gap. The toxin spares SGLT1, so an oral rehydration solution containing glucose and Na+ drives Na+ and water absorption and treats most patients without IV fluid.
  • Lactose intolerance. Lactase deficiency (most commonly the normal decline after childhood) leaves lactose unabsorbed: it holds water in the lumen (osmotic diarrhea with a large osmotic gap) and colonic bacteria ferment it into gas and acids — bloating, flatulence, acidic stool. The hydrogen breath test is positive; symptoms stop when lactose is withdrawn.
  • Cystic fibrosis — the gut. Defective CFTR stops Cl− and HCO3− secretion by pancreatic duct cells, so thick secretions plug the ducts and destroy the gland: exocrine pancreatic insufficiency with steatorrhea, fat-soluble vitamin deficiency, and failure to thrive, plus meconium ileus in newborns. The low-HCO3− duodenum also impairs enzyme function and micelle formation; treatment includes pancreatic enzyme replacement with meals.

Frequently asked

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