Gastrointestinal physiology
GI function: regulation, secretion, motility and absorption
The gut is run by its own enteric nervous system, modulated by the vagus and by hormones released from cells in the mucosa. CPSP asks which hormone does what, how swallowing and gastric emptying are controlled, where each nutrient is absorbed, and how these physiological facts explain barium studies, scintigraphy and drugs used during imaging.
Control of motility
- Interstitial cells of Cajal generate slow waves that set the maximum contraction rate (about 3/min in the stomach, 12/min in the duodenum); action potentials on the crests cause contraction.
- Peristalsis: contraction above and relaxation below a bolus, organised by the myenteric plexus.
- Migrating motor complex: a fasting "housekeeper" wave every 90–120 minutes, linked to motilin. Its loss (diabetic autonomic neuropathy) allows small bowel bacterial overgrowth.
- Most bowel gas in ileus is swallowed air.
Swallowing
| Phase | Control | Clinical link |
|---|---|---|
| Oral | Voluntary | Intact after many brainstem strokes |
| Pharyngeal | Involuntary reflex from the medullary swallowing centre; soft palate seals the nasopharynx, larynx rises, epiglottis tilts | Brainstem stroke: choking and aspiration |
| Oesophageal | Primary peristalsis follows the swallow; secondary peristalsis starts at a site of distension by a retained bolus | Seen on barium swallow without a new swallow |
- The fetus swallows amniotic fluid; anencephaly or oesophageal atresia causes polyhydramnios.
Gastric motility and emptying
- Receptive relaxation of the fundus (vagal) lets the stomach accept a meal at low pressure. After truncal vagotomy liquids empty very fast (early fullness, dumping).
- Liquids empty at once; solids show a lag phase of 20–30 minutes while the antrum grinds them to 1–2 mm particles.
- Fat empties slowest. Fat, acid and hyperosmolar chyme in the duodenum slow emptying via CCK, secretin and the enterogastric reflex. Hyperglycaemia also slows emptying (postpone scintigraphy if glucose is high).
- Metoclopramide speeds emptying by D2 blockade in the gut. Hyoscine butylbromide relaxes bowel for CT or MRI without drowsiness because, as a quaternary amine, it cannot cross into the brain.
Colon and defaecation
- Radio-opaque marker study: markers scattered through the colon suggest slow transit; markers clustered in the rectosigmoid suggest an outlet (evacuation) problem.
- Defaecation needs relaxation of puborectalis, which opens the anorectal angle. In dyssynergic defaecation the angle stays acute and a posterior puborectalis impression persists on proctography.
- Gastrografin is hyperosmolar: it draws water into the lumen and can help adhesive obstruction settle.
GI hormones
| Hormone | Cell and site | Stimulus | Main actions |
|---|---|---|---|
| Gastrin | G cells, antrum | Peptides and amino acids, distension, vagal GRP | Acid secretion, mucosal growth; inhibited by acid via somatostatin |
| CCK | I cells, duodenum and jejunum | Fat and protein | Gallbladder contraction, pancreatic enzymes, relaxes sphincter of Oddi, slows emptying |
| Secretin | S cells, duodenum | Acid in the duodenum | Bicarbonate-rich fluid from pancreatic ducts |
| GIP | K cells, duodenum | Glucose, fat | Insulin release |
| Motilin | M cells, duodenum | Fasting | Migrating motor complex |
| Somatostatin | D cells | Acid | Inhibits gastrin and acid |
- Long-term PPIs raise gastrin by removing acid feedback on G cells. Antral H. pylori gastritis reduces D-cell somatostatin, raising gastrin and acid (duodenal ulcer).
- In gastrinoma, secretin causes a paradoxical rise in gastrin.
- Postprandial pain in gallstone disease follows CCK release by a fatty meal. Parenteral nutrition without enteral fat gives no CCK, so gallbladder sludge forms.
- Secretin-enhanced MRCP: secretin distends the pancreatic duct and fills the duodenum with ductal fluid.
Secretion
- Parietal cells secrete acid by the H⁺/K⁺-ATPase, stimulated by histamine (H2), acetylcholine and gastrin, and secrete intrinsic factor. Acid is a barrier to infection (cholera after achlorhydria).
- Gastric mucosa takes up Tc-99m pertechnetate (basis of the Meckel scan); an H2 blocker stops the tracer being secreted into the lumen and blurring the image.
- Saliva is hypotonic because ducts reabsorb Na⁺ and Cl⁻; at high flow there is less time for this, so sodium rises.
Digestion and absorption
| Nutrient | Mechanism | Site |
|---|---|---|
| Glucose, galactose | SGLT1 (secondary active, with Na⁺) | Small bowel |
| Fructose | GLUT5 (facilitated) | Small bowel |
| Protein | Mainly di- and tripeptides (H⁺-coupled), some amino acids | Small bowel |
| Long-chain fat | Micelles (need bile salts); re-formed into chylomicrons, enter lacteals | Jejunum |
| Iron | Ferrous iron via DMT1 after duodenal cytochrome b reduces ferric iron | Duodenum |
| Folate | Active | Jejunum |
| Vitamin B12 | With intrinsic factor | Terminal ileum |
| Bile salts | Active | Terminal ileum |
- Iron: vitamin C keeps iron ferrous and helps absorption; tea tannins bind it. Pregnancy lowers hepcidin, so absorption rises several-fold.
- B12 steps: acid and pepsin release it from food; it binds haptocorrin; pancreatic proteases detach it in the duodenum; it binds intrinsic factor; the complex is absorbed in the terminal ileum. Long-term PPIs impair only the first step (crystalline B12 is absorbed normally). Anti-intrinsic factor antibody is the most specific test for pernicious anaemia.
- Fat-soluble vitamin K needs bile; obstructive jaundice prolongs the INR, corrected by parenteral vitamin K.
- Short bowel with jejunostomy: the jejunum is leaky, so plain water draws sodium into the lumen and increases stoma output; sodium-rich glucose solutions are absorbed by co-transport.
- Proximal jejunal loss causes folate deficiency; ileal loss causes B12 and bile acid problems. SeHCAT retention below about 15% at 7 days shows poor ileal bile acid reabsorption.
- A bleeding ulcer raises urea with normal creatinine because blood protein is digested and absorbed.
- Trypsin cleaves after lysine and arginine.
- After a meal, mesenteric vasodilatation turns the fasting high-resistance SMA Doppler waveform into a low-resistance one with forward diastolic flow.
Remember Gastrin answers protein, CCK answers fat, secretin answers acid.
Exam trap Most iron is absorbed in the duodenum, but B12 and bile salts need the terminal ileum.
Exam trap Liquids leave the stomach first; solids must first be ground down, and fat empties slowest.
Test yourself on this topic
5 of the 47 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
After a swallow, a small bolus stays in the mid-oesophagus once the swallow-induced wave has passed. Without another swallow, a new contraction starts just above the bolus and clears it into the stomach. What is this contraction?
Answer: Secondary peristalsis
Primary peristalsis is triggered by swallowing and travels from the pharynx. Secondary peristalsis is triggered by local distension of the oesophagus by a retained bolus or refluxed material, without a swallow, through intrinsic myenteric reflexes and vagal pathways. It is an important clearing mechanism for reflux. Tertiary contractions are non-propulsive, uncoordinated contractions, often seen in the elderly.
Oesophageal contractions
- Primary: swallow-triggered
- Secondary: triggered by distension
- Tertiary: non-propulsive
- Secondary waves clear reflux
Remember Bolus left behind? Secondary peristalsis cleans up.
Exam trap Tertiary contractions are not a third normal wave; they do not propel.
Why the other options are wrong
- Primary peristalsis Needs a swallow.
- Tertiary contraction Non-propulsive; does not clear the bolus.
- Migrating motor complex A fasting pattern of the stomach and small bowel.
- Receptive relaxation A relaxation of the proximal stomach.
Years after a truncal vagotomy and drainage procedure, a man has early fullness and dumping after meals, and liquids empty from his stomach very rapidly. Loss of which reflex mainly explains the fast liquid emptying?
Answer: Vagal receptive relaxation of the fundus
When food is swallowed, vagovagal reflexes using inhibitory NO and VIP neurons relax the proximal stomach (receptive relaxation and accommodation), so it can hold a meal without a rise in pressure. Liquid emptying depends on the pressure gradient set by fundal tone. After truncal vagotomy, accommodation is lost, fundal pressure rises with each meal and liquids are pushed out rapidly, causing early satiety and dumping. Antral grinding of solids is also impaired, so solids may empty slowly.
Receptive relaxation
- Vagovagal reflex, NO and VIP
- Fundus relaxes to accept food
- Sets liquid emptying rate
- Vagotomy: fast liquids, early satiety
Remember No vagus, no fundal relaxation: liquids rush out.
Exam trap After vagotomy, liquids empty fast while solids may empty slowly.
Why the other options are wrong
- Gastrocolic reflex of the colon A colonic response to eating; not the cause.
- Enterogastric inhibition by secretin Reduces emptying; is not lost by vagotomy.
- Myenteric migrating motor complex A fasting pattern; not responsible for liquid emptying.
- Sympathetic pyloric contraction Not the main control of liquid emptying.
Blood flow in the superior mesenteric artery of a healthy adult rises two- to threefold within an hour of a meal, with high continuous diastolic flow. What explains this change?
Answer: Postprandial mesenteric vasodilatation
In the fasting state the intestinal arterioles are constricted, giving high resistance with little or reversed diastolic flow in the SMA. After a meal, digestion products, gut hormones and local metabolites dilate the intestinal arterioles, lowering resistance so diastolic flow rises and total SMA flow may double or treble. This postprandial hyperaemia explains why patients with mesenteric artery stenosis get pain after meals (intestinal angina). The coeliac artery normally shows low-resistance flow at all times.
SMA Doppler
- Fasting: high resistance
- Fed: low resistance, high diastolic flow
- Gut hyperaemia after meals
- Stenosis: postprandial pain
Remember The gut opens its arterioles after eating.
Exam trap Measuring SMA flow without knowing whether the patient has eaten.
Why the other options are wrong
- Rising systemic blood pressure BP changes little after meals.
- Sympathetic vasoconstriction after meals Arterioles dilate, not constrict.
- Compression of the SMA by the duodenum Not a normal postprandial change.
- Reduced cardiac output after eating Cardiac output rises slightly after meals.
After a mixed meal, liquid starts to leave the stomach at once, but solid food shows a delay of 20–30 minutes before it begins to empty. What causes this lag phase?
Answer: Solids must be ground to about 1–2 mm
Liquids empty from the stomach quickly, mainly by the pressure gradient set up by tone of the proximal stomach. Solids are retained while antral contractions grind them against a closed pylorus (trituration) until particles are about 1–2 mm, small enough to pass. This takes time, causing the lag phase before linear solid emptying. Large indigestible particles are cleared later by the fasting migrating motor complex.
Gastric emptying
- Liquids: fundal tone, no lag
- Solids: antral grinding first
- Particles 1–2 mm pass pylorus
- Then linear solid emptying
Remember Solids wait to be ground; liquids just flow.
Exam trap Fat and hypertonic meals slow emptying further through duodenal feedback.
Why the other options are wrong
- The pylorus stays shut for 30 minutes Liquids pass through it at once.
- Solids enter the fundus first Not the reason for delay.
- Gastrin release is delayed Not the mechanism.
- Liquids block passage of solids Liquids and solids empty independently.
A woman has chronic watery diarrhoea after a right hemicolectomy that included 100 cm of terminal ileum. Which defect most directly causes her diarrhoea?
Answer: Poor ileal bile acid reabsorption
About 95% of bile acids are reabsorbed by the apical sodium-dependent bile acid transporter in the terminal ileum and returned to the liver. After ileal resection, unabsorbed bile acids reach the colon, where they stimulate chloride and water secretion and cause watery diarrhoea. This responds to bile acid sequestrants such as cholestyramine. Retention of less than 15% of a swallowed SeHCAT dose at 7 days confirms bile acid malabsorption.
SeHCAT test
- Synthetic bile acid
- Ileal ASBT reabsorbs ~95%
- Retention < 15% at 7 days: malabsorption
- Colonic bile acids: secretory diarrhoea
Remember Low SeHCAT retention: the ileum is not catching bile acids.
Exam trap Large ileal resections cause fatty diarrhoea too, as the bile acid pool runs low.
Why the other options are wrong
- Bacterial overgrowth in the jejunum Bacteria deconjugate bile acids but this is not what SeHCAT measures.
- Pancreatic lipase deficiency Causes steatorrhoea; not measured by SeHCAT.
- Rapid gastric emptying Not measured by this test.
- Lactase deficiency Not related to bile acid retention.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Gastrointestinal physiology, GI function, regulation and motility
Read next
Drug dose pages
Doses, cautions and practical tips for drugs in this chapter.