Oesophageal and bowel disorders
Oesophagus, stomach and bowel disorders: pathology, physiology and imaging
Gut disorders for FCPS Part 1: oesophageal narrowings, Barrett, motility, gastric secretion and emptying, H. pylori, ulcers, gastric tumours, obstruction, infections, IBD and colorectal cancer. Each is linked to its mechanism and its endoscopic, barium or CT appearance.
Oesophagus
- Normal narrowings measured from the incisor teeth: cricopharyngeus about 15 cm, aortic arch and left main bronchus about 23–27 cm, hiatus about 40 cm. A doxycycline capsule swallowed at bedtime with little water lodges at the arch of the aorta (23 cm) and causes pill oesophagitis.
- Barrett oesophagus: reflux replaces squamous with columnar epithelium (squamocolumnar junction 3 cm or more above the gastro-oesophageal junction); goblet cells confirm intestinal metaplasia. It is the main predisposition to adenocarcinoma of the lower third.
- Squamous cell carcinoma: middle third; smoking, alcohol, hot drinks.
| Motility disorder | Basis | Barium and manometry |
|---|---|---|
| Achalasia | Loss of inhibitory myenteric neurons (NO, VIP) | Dilated (enlarged) oesophagus, smooth bird's beak taper |
| Systemic sclerosis | Smooth muscle atrophy and fibrosis | Aperistalsis with an open, low-pressure sphincter and reflux |
| Oesophagitis | Look | |
| Candida | White plaques | |
| Herpes simplex | Small punched-out ulcers; biopsy the edge | |
| CMV | Large shallow ulcers; biopsy the base | |
| Eosinophilic | Rings and furrows in atopic young men |
- Boerhaave rupture: left posterolateral lower oesophagus. Sliding hiatus hernia: phreno-oesophageal ligament stretches; rolling hernia: fundus beside a normal junction.
Gastric secretion and emptying
- Parietal cells (body and fundus) secrete HCl and intrinsic factor; chief cells pepsinogen; G cells (antrum) gastrin. HCl activates pepsinogen to pepsin, kills ingested organisms and reduces dietary iron to the absorbable ferrous form.
- Prostaglandins (PGE2, PGI2) protect the mucosa: more mucus and bicarbonate, more blood flow, less acid. NSAIDs remove them.
| Hormone | Source | Main gastric effects |
|---|---|---|
| Gastrin | Antral G cells | Increases acid and growth of gastric mucosa (trophic) |
| Secretin | Duodenal S cells (acid) | Pancreatic bicarbonate; inhibits gastric acid and emptying |
| CCK | Duodenal I cells (fat, protein) | Gallbladder contraction, pancreatic enzymes; delays gastric emptying |
| GIP | Duodenal K cells | Insulin release; inhibits acid |
| Motilin | Duodenum (fasting) | Increases gastrointestinal motility (migrating motor complex); erythromycin mimics it |
| Somatostatin | D cells | Inhibits nearly everything |
- Gastric emptying is speeded by distension of the stomach, gastrin, motilin and liquid meals; it is slowed by fat, acid and hyperosmolar chyme in the duodenum (enterogastric reflex, CCK, secretin), sympathetic activity and opioids. Aluminium hydroxide antacids delay emptying and constipate; magnesium salts loosen stools.
Stomach and duodenum
- Helicobacter pylori: antral infection with high acid gives duodenal ulcer (burning epigastric pain eased by food); pangastritis gives atrophy, intestinal metaplasia and intestinal-type cancer, and MALT lymphoma. PPIs suppress the bacterial load and urease activity, giving false-negative breath and stool antigen tests; stop them for 2 weeks before testing.
- MALT lymphoma confined to mucosa and submucosa usually regresses after eradication; the t(11;18) API2–MALT1 fusion makes it resistant.
- Bleeding and perforation: a posterior duodenal ulcer erodes the gastroduodenal artery; a lesser curvature gastric ulcer bleeds from the left gastric artery; a posterior gastric ulcer perforates into the lesser sac and may erode the splenic artery.
| Gastric tumour | Point |
|---|---|
| Intestinal-type adenocarcinoma | Commonest gastric malignancy; follows H. pylori atrophy |
| Diffuse (signet-ring) | Linitis plastica; CDH1 |
| Lymphoma | Thick wall that still distends |
| GIST | Interstitial cells of Cajal; CD117, DOG1 |
| Neuroendocrine type 1 | Pernicious anaemia, gastrin drives ECL hyperplasia |
- Gastric cancer spreads transcoelomically across the peritoneum to the rectovesical pouch (rectal shelf) and ovaries (Krukenberg), and by lymphatics to the left supraclavicular (Virchow) node.
- Gastric antral vascular ectasia (watermelon stomach): parallel red stripes from the pylorus, occult bleeding and iron deficiency; systemic sclerosis and cirrhosis.
- Cushing ulcer after head injury: raised ICP stimulates vagal nuclei, raising acid (deep duodenal or gastric ulcer). Curling ulcer after burns: mucosal ischaemia.
- Zollinger–Ellison: gastrinoma; ulcers beyond the cap and in the jejunum, thick folds, diarrhoea. With hypercalcaemia (parathyroid hyperplasia) and a prolactinoma in the family it is MEN 1 (menin gene, chromosome 11).
- Pyloric stenosis: hypertrophied circular muscle; hypochloraemic alkalosis. Duodenal atresia: double bubble.
Obstruction
- Commonest causes: small bowel adhesions; large bowel colorectal cancer.
- With a competent ileocaecal valve, the caecum perforates because its wide radius gives the highest wall tension (Laplace).
- Strangulation: venous outflow blocks first.
- Gallstone ileus: obstruction, gas in the biliary tree, ectopic stone. Sigmoid volvulus: coffee-bean loop.
- Intussusception: infants, ileocolic, lead point of hypertrophied Peyer patches (adenovirus, HSP); target sign. Adults need a lead point: a smooth intraluminal −100 HU mass is a submucosal lipoma.
- Meckel diverticulum: ectopic gastric mucosa; pertechnetate scan.
Infections of the bowel
| Organism | Clue |
|---|---|
| Yersinia enterocolitica | Fever, diarrhoea, right iliac fossa pain with normal appendix, terminal ileitis and mesenteric adenitis; grows after cold enrichment at 4 °C; reactive arthritis, erythema nodosum |
| CMV colitis | HIV with CD4 below 50; bloody diarrhoea, thick caecum and right colon; owl's-eye intranuclear inclusions in endothelial cells; ganciclovir (foscarnet if UL97 resistance) |
| Giardia | Adhesive disc flattens duodenal villi; no blood |
| Clostridioides difficile | After antibiotics; pseudomembranes |
| Tuberculosis | Ileocaecal strictures, transverse ulcers |
Inflammatory bowel disease
| Feature | Ulcerative colitis | Crohn disease |
|---|---|---|
| Distribution | Rectum upwards, continuous | Mouth to anus, skip lesions, terminal ileum |
| Depth | Mucosa | Transmural: fistulae, strictures |
| Histology | Crypt abscesses | Non-caseating granulomas |
| Perianal disease | Rare | Common (fissures, fistulae, abscess) |
| Barium | Lead-pipe colon, pseudopolyps | Cobblestoning, string sign, fistulae |
| Smoking | Protective | Worsens |
- The main difference: Crohn disease is transmural and patchy with perianal lesions; UC is mucosal and continuous.
Polyps and colorectal cancer
| Polyp | Risk |
|---|---|
| Hyperplastic | Low |
| Tubular adenoma | Lower |
| Villous adenoma | Highest |
| Hamartomatous | Juvenile; Peutz–Jeghers |
- APC, then KRAS, then p53. FAP and Gardner syndrome. Spread to the liver via the portal vein; node status best predicts survival.
Diverticula and appendix
- Colonic diverticula are false and form where vessels pierce the circular muscle; commonest in the sigmoid.
- Appendicitis: lymphoid hyperplasia in children, faecolith in adults.
Metaplasia in the gut
- Metaplasia is one adult epithelium replacing another: squamous to columnar (Barrett), gastric mucosa with goblet cells (intestinal metaplasia), gastric-type epithelium in the gallbladder with chronic cholecystitis.
Remember Barrett is metaplasia leading to adenocarcinoma; squamous cancer comes from the native lining.
Exam trap A thick gastric wall that still distends suggests lymphoma; a thick rigid one suggests diffuse carcinoma.
Exam trap A negative urea breath test on a PPI does not exclude H. pylori.
How FCPS asks about this
- Pill oesophagitis at 23 cm from the incisors: narrowing by the aortic arch.
- Predisposing condition for oesophageal adenocarcinoma: Barrett oesophagus.
- Hormone that delays gastric emptying: CCK (also secretin, GIP); motilin speeds motility.
- Gastrin effects: acid secretion and growth of gastric mucosa.
- Duodenal ulcers, hypercalcaemia and a relative with prolactinoma: MEN 1 (menin).
- Posterior duodenal ulcer bleeding: gastroduodenal artery.
- MALT lymphoma not regressing after eradication: t(11;18).
Test yourself on this topic
5 of the 83 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 55-year-old man has a 9 cm tumour of the greater curve of the stomach removed. It is a spindle cell lesion positive for CD117 and DOG1. Which two features best predict its risk of recurrence?
Answer: Tumour size and mitotic count
Gastrointestinal stromal tumours arise from the interstitial cells of Cajal and carry KIT or PDGFRA mutations. Their behaviour is predicted mainly by tumour size and mitotic count (per 5 mm² or 50 high-power fields), with tumour site as a third factor: gastric tumours behave better than small-bowel ones of the same size. They rarely spread to lymph nodes, so nodal status is not useful, and they metastasise to the liver and peritoneum. KIT staining confirms the diagnosis but its intensity does not predict behaviour.
GIST risk
- From interstitial cells of Cajal
- KIT/PDGFRA mutations
- Risk: size + mitotic count (+ site)
- Rare nodal spread; liver and peritoneum
Remember Big and busy GISTs come back.
Exam trap Lymph node dissection is not routinely needed for GIST because nodal spread is rare.
Why the other options are wrong
- CD117 staining intensity and site Staining confirms the diagnosis but its strength does not predict risk.
- Patient age and sex These do not form part of the risk score.
- Degree of necrosis and nodal status GISTs rarely spread to nodes; necrosis is less important than size and mitoses.
- Serum CEA and tumour depth CEA is a carcinoma marker; GISTs do not secrete it.
A 48-year-old woman has early satiety and weight loss. At endoscopy the stomach is small and rigid, does not distend with air and has lost its rugal folds, although the mucosa looks almost normal. Which finding is most likely on deep biopsy?
Answer: Diffuse infiltration by signet-ring cells
A small, rigid, non-distensible stomach is linitis plastica, the leather-bottle stomach of diffuse-type gastric carcinoma. Discohesive tumour cells, often signet-ring cells with mucin pushing the nucleus aside, infiltrate singly through all layers and provoke dense fibrosis, which makes the wall stiff. The loss of E-cadherin explains why the cells do not form glands or masses. Intestinal-type carcinoma forms glandular masses or ulcers, usually in the antrum.
Linitis plastica
- Rigid, non-distensible stomach
- Folds and peristalsis lost
- Signet-ring cells infiltrate singly
- Dense desmoplasia stiffens the wall
Remember Leather bottle stomach: signet rings in a fibrous wall.
Exam trap Superficial biopsies can miss diffuse carcinoma, because the mucosa may look almost normal; deep or repeated biopsies are needed.
Why the other options are wrong
- Glandular intestinal-type adenocarcinoma Forms polypoid or ulcerated glandular masses rather than a diffuse rigid wall.
- Sheets of atypical lymphoid cells Lymphoma thickens the wall but it usually stays pliable.
- Spindle cells positive for CD117 A GIST forms a focal, often exophytic mass.
- Foveolar hyperplasia with protein loss This is Ménétrier disease, with giant folds, not lost folds.
A 14-year-old girl with patchy hair loss and a habit of chewing her hair has early fullness, vomiting and a firm, mobile epigastric mass. What is the most likely diagnosis?
Answer: Trichobezoar
A trichobezoar is a mass of swallowed hair, usually in young women with trichotillomania and trichophagia. Hair is not digested and its smooth surface is not propelled through the pylorus, so it accumulates, traps food and mucus, and forms a cast of the stomach. It presents with early satiety, vomiting, weight loss and a firm, mobile epigastric mass. Phytobezoars are made of vegetable fibre and occur mainly after gastric surgery or in delayed emptying.
Trichobezoar
- Young woman with hair loss
- Trichotillomania, hair chewing
- Hair forms a cast of the stomach
- Firm, mobile epigastric mass
Remember Hair loss plus an epigastric mass: trichobezoar.
Exam trap A tail of hair extending into the small bowel (Rapunzel syndrome) can cause obstruction further down.
Why the other options are wrong
- Phytobezoar Formed from plant fibre, usually after gastric surgery or with gastroparesis.
- Gastric adenocarcinoma Rare at this age and not linked to hair loss.
- Gastrointestinal stromal tumour A wall tumour, rare in children, not linked to hair chewing.
- Gastric lymphoma Rare at this age and not linked to hair loss.
At colonoscopy, a 4 mm sessile polyp is removed from the rectosigmoid of a 58-year-old man. Histology shows elongated crypts whose upper halves have a saw-tooth (serrated) outline; the crypt bases are narrow and normal, and there is no dysplasia. What is the polyp?
Answer: Hyperplastic polyp
Hyperplastic polyps are the commonest colonic polyps. They are small, usually under 5 mm, and found mainly in the rectosigmoid. Serration is limited to the upper part of the crypts and the crypt bases are normal, reflecting slowed shedding of surface cells. A sessile serrated lesion is usually larger and right-sided, with serration reaching the base and dilated, boot- or L-shaped crypt bases, and it is a precursor of cancer. Adenomas show dysplastic epithelium.
Hyperplastic polyp
- Small, under 5 mm
- Rectosigmoid
- Serration in upper crypt only
- No dysplasia; negligible cancer risk
Remember Serrated at the top only: hyperplastic. Serrated to the bottom: sessile serrated.
Exam trap Large right-sided serrated polyps are not hyperplastic until proven otherwise.
Why the other options are wrong
- Sessile serrated lesion Serration reaches the crypt base, which is dilated and boot-shaped; usually right-sided.
- Tubular adenoma Shows dysplastic, crowded nuclei in tubular glands.
- Juvenile polyp Has cystically dilated glands in inflamed stroma, mainly in children.
- Villous adenoma Has long leaf-like dysplastic fronds.
A 40-year-old renal transplant recipient has severe pain on swallowing. Endoscopy shows several small, discrete, punched-out ulcers in the mid oesophagus on otherwise normal mucosa. Biopsy from an ulcer edge shows multinucleated squamous cells with ground-glass nuclei and moulding. Which organism is responsible?
Answer: Herpes simplex virus
Herpes simplex virus infects squamous epithelium, so the diagnostic changes (multinucleation, nuclear moulding, ground-glass nuclei and Cowdry A inclusions) are found at the edge of the ulcer. It produces small, discrete, punched-out ulcers with normal mucosa in between. Cytomegalovirus infects endothelial cells and fibroblasts in the ulcer base and produces fewer, larger and shallower ulcers. Candida gives white plaques rather than discrete ulcers.
HSV oesophagitis
- Small punched-out ulcers
- Biopsy the ulcer edge (squamous cells)
- Multinucleated cells, ground-glass nuclei
- CMV: large shallow ulcers, biopsy the base
Remember Herpes at the edge, CMV at the base.
Exam trap Taking biopsies only from the ulcer base can miss herpes, whose changes lie in the surrounding squamous epithelium.
Why the other options are wrong
- Cytomegalovirus Gives large shallow ulcers; inclusions are in the ulcer base, not the edge.
- Candida albicans Gives plaques and a shaggy outline, not punched-out ulcers.
- Epstein-Barr virus Causes oral hairy leukoplakia, not ulcerating oesophagitis.
- Human papillomavirus Causes squamous papillomas, not acute ulcers.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Abdominal, renal and reproductive disorders, Oesophagus, stomach and bowel disorders
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