Understanding Your Endoscopy Report
Your endoscopy report describes what the lining looked like, whether any polyps or inflammation were present, and what the biopsies showed. Most findings are benign. Each item has a short explanation, with an optional second line for patients who want more detail.
Gastroscopy Findings
Oesophagus
Reflux oesophagitis: irritation from acid.
Biopsies may show basal cell hyperplasia, papillary elongation or mixed inflammation.
Barrett’s oesophagus: lining changed by long-term reflux when one centimetre or more.
Shows intestinal metaplasia with goblet cells; dysplasia is graded if present.
Eosinophilic oesophagitis: allergic inflammation that affects swallowing.
Shows dense eosinophils, basal zone expansion and surface layering.
Candidiasis: yeast infection; treatable.
Shows fungal hyphae with acute inflammation.
Gastric heterotopia: small patch of stomach-type mucosa; benign.
Shows parietal and chief cells.
Submucosal lesion: deeper lump such as leiomyoma or granular cell tumour.
Shows smooth muscle bundles or S100-positive granular cells depending on type.
Stomach
Gastritis: irritation from acid, medicines, infection or autoimmune causes.
Chronic inflammation, reactive change or atrophy may be seen.
H. pylori: common infection that may cause ulcers; treatable.
Organisms visible on special stains with active gastritis.
Polyps: mostly benign; adenomas are removed.
Histology varies from fundic gland change to dysplasia in adenomas.
Intestinal metaplasia: long-standing inflammation change.
Shows goblet cells and intestinal-type epithelium.
Pancreatic rest: small nest of pancreatic tissue; benign.
Shows acinar cells and ducts.
Submucosal lesion: lipoma, GIST or cyst.
Fat for lipoma; KIT-positive spindle cells for GIST.
Duodenum
Coeliac disease: immune reaction to gluten.
Villous blunting, crypt hyperplasia and raised intraepithelial lymphocytes.
Duodenitis: mild irritation.
Increased inflammatory cells without structural change.
Peptic change: acid-related injury.
Surface erosion or gastric foveolar metaplasia.
Brunner gland hyperplasia: benign enlargement of Brunner glands.
Proliferated mucous glands in submucosa.
Gastric heterotopia: benign stomach-type tissue.
Shows gastric glands with parietal cells.
Pancreatic rest: harmless pancreatic tissue variant.
Acinar tissue and ducts.
Disaccharidase deficiency: low lactase or related enzymes.
Enzyme assays diagnose this; histology often normal.
Giardia: treatable parasite.
Organisms may be seen along the mucosal surface.
Duodenal adenoma / NET: uncommon, removed or monitored.
Adenomas show dysplasia; NETs show chromogranin-positive nests.
Colonoscopy Findings
Diverticulosis: small pockets in bowel wall; common and benign.
Biopsies generally normal unless mild adjacent inflammation exists.
Haemorrhoids: enlarged veins that may bleed.
Biopsies rarely taken; show dilated vessels if sampled.
Ulcerative colitis: continuous inflammation from rectum upwards.
Crypt distortion, basal plasmacytosis and chronic inflammation.
Crohn’s disease: patchy deeper inflammation.
Focal crypt irregularity and granulomas away from ruptured crypts.
Microscopic colitis: watery diarrhoea with normal endoscopic appearance.
Collagen band thickening or increased intraepithelial lymphocytes.
Ischaemic colitis: temporary reduced blood flow to bowel.
Withered crypts and lamina propria hyalinisation.
Infectious colitis: inflammation caused by infection.
Neutrophils with preserved architecture.
Non-specific colitis: mild inflammation without a clear pattern.
No chronic architectural change.
Colonic Polyps
Hyperplastic polyp: very common and low risk.
Serrated surface with normal proliferation.
Sessile serrated lesion: flat serrated polyp.
Distorted crypt bases and serration low in crypts.
Traditional serrated adenoma: less common serrated lesion.
Eosinophilic cytoplasm, slit-like serrations and dysplasia.
Tubular adenoma: common benign adenoma.
Tubular dysplastic glands.
Tubulovillous adenoma: mixed pattern.
Tubular and villous components.
Villous adenoma: higher-risk adenoma.
Long villous projections with dysplasia.
Advanced adenoma: adenoma that is large or has villous features or high-grade dysplasia; still benign. Removal prevents cancer.
Shows complex or high-grade dysplastic change.
Inflammatory polyp: polyp caused by chronic inflammation.
Granulation tissue and chronic inflammatory cells.
Pseudopolyp: healing islands after inflammation; not precancerous.
Reactive but regenerating mucosa.
Mucosal polyp: small raised area of normal lining; benign.
Normal mucosa without dysplasia.
Types of Colitis
(with optional pathology detail)
Ulcerative colitis: continuous inflammation starting in rectum.
Crypt distortion, basal plasmacytosis and chronic architectural change.
Crohn’s disease: patchy deeper inflammation.
Focal inflammation, granulomas away from ruptured crypts and segmental involvement.
Microscopic colitis: chronic watery diarrhoea with normal appearance.
Increased IELs or a thickened collagen plate.
Ischaemic colitis: injury from reduced blood flow.
Withered crypts and hyalinised lamina propria.
Infectious colitis: acute inflammation from infection.
Neutrophils with preserved architecture.
Non-specific colitis: mild inflammation without a defined pattern.
No chronic features; often transient.
How Crohn’s and Ulcerative Colitis Are Distinguished
Biopsies help guide the diagnosis, but endoscopic appearance, symptoms and imaging are equally important. Ulcerative colitis is continuous from the rectum with architectural distortion. Crohn’s disease is patchy, may involve deeper layers, and can show granulomas not related to ruptured crypts. When early, biopsies may be labelled indeterminate colitis.
Small Bowel (DBE) Findings
Coeliac disease: patchy immune reaction to gluten.
Villous blunting and raised IELs.
Crohn’s disease: ulcers or strictures in the small bowel.
Granulomas and focal chronic inflammation.
Ulcers or erosions: from medicines, infection or inflammation.
Acute inflammation or reactive change.
Vascular lesions: angioectasias that may bleed.
Dilated thin-walled vessels.
Polyps: hamartomatous or adenomatous polyps.
Normal elements in hamartomas; dysplasia in adenomas.
Submucosal lesions: lipoma, GIST, NET, cyst.
Spindle cells, fat, neuroendocrine nests or cyst lining.
Infections: occasional parasites.
Organisms or acute inflammation.
Biopsy Results: How to Read Them
Normal mucosa: healthy lining.
No inflammation, distortion or dysplasia.
Mild inflammation: non-specific irritation.
Inflammatory cells without architectural change.
Active inflammation: acute neutrophils in tissue or crypts.
Seen in infections, flares or acute injury.
Chronic inflammation: longer-standing changes.
Crypt distortion, basal plasmacytosis or chronic cell infiltrates.
Increased lymphocytes or eosinophils: immune-type reaction.
Seen in coeliac disease, allergy, infection or irritation.
Architectural distortion: long-term inflammation.
Suggests chronic colitis rather than a short-lived episode.
Negative for dysplasia: no precancerous change identified.
Common reassuring phrase.
Dysplasia: precancerous change.
Low- or high-grade architectural and cytologic changes.
Cancer: abnormal growth invading tissue.
Malignant epithelial proliferation.
Submucosal Lesions (Deeper Lumps)
Lipoma: soft fatty lump; benign.
Mature adipose tissue in submucosa.
Leiomyoma: benign smooth-muscle tumour.
Interlacing smooth muscle bundles.
GIST: deeper-wall tumour; behaviour depends on size.
KIT/DOG1-positive spindle or epithelioid cells.
Pancreatic rest: small area of pancreatic tissue.
Acinar cells, ducts and occasional islets.
Neuroendocrine tumour: usually small and slow growing.
Nests of uniform cells positive for chromogranin or synaptophysin.
Granular cell tumour: rare benign nerve-sheath tumour.
S100-positive granular cytoplasm.
Cystic lesion: duplication or simple cyst.
Epithelial-lined cavity with fluid.