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PH-GI17

Gastrointestinal polyps and polyposis syndromes

What a polyp is and how its tissue decides its future: hyperplastic, serrated, adenomatous, hamartomatous and inflammatory polyps, which can become cancer and why, and the inherited syndromes such as FAP, Lynch and Peutz–Jeghers.

By the end, you can

  • Define a polyp and classify gastrointestinal polyps by the tissue they are made of.
  • Explain how conventional adenomas and serrated lesions arise from crypt cells and how each can progress to cancer.
  • Relate the size, architecture and grade of dysplasia of a polyp to its risk of malignancy.
  • Describe the genes, polyps and other features of the main polyposis and hereditary colorectal cancer syndromes.
  • Explain the complications of polyps: bleeding, intussusception, fluid loss and cancer.
  • Recognise the classic appearances, classifications (polyp types, adenoma architecture and dysplasia, Haggitt levels, syndromes) and tests of polyps, and explain how polypectomy, endoscopic resection, prophylactic colectomy and aspirin act on the route to cancer.

What it is

A polyp is any mass that projects from a mucosal surface into the lumen: the word describes a shape, not a cause. Polyps may be neoplastic (adenomas and some serrated lesions, which can become cancer), hamartomatous (a disorganised overgrowth of the tissue’s own elements), hyperplastic or inflammatory, or a tumour beneath the mucosa, such as a lipoma, pushing it up. A polyposis syndrome is a condition, usually inherited, with many polyps.

5 types to tell apart
Conventional adenoma
Dysplastic glands, by definition, from loss of APC: tubular, tubulovillous or villous, with low- or high-grade dysplasia. The commonest precursor of colorectal cancer.
Serrated lesions
Crypts with a saw-toothed outline: hyperplastic polyps (small, usually left-sided, harmless), sessile serrated lesions (right-sided, can progress; formerly sessile serrated adenoma or polyp) and the rare traditional serrated adenoma.
Hamartomatous polyps
Juvenile polyps (dilated glands in an inflamed stroma) and Peutz–Jeghers polyps (branching smooth muscle). A single one is usually harmless; the syndromes carry raised cancer risk.
Inflammatory polyps (pseudopolyps)
Islands of surviving, regenerating mucosa left between ulcers in inflammatory bowel disease; not neoplastic.
Gastric polyps
Fundic gland polyps (common, linked to long-term acid suppression and to FAP), hyperplastic polyps on chronic gastritis, and gastric adenomas.

US spelling: tumour → tumor.

Normal function

Crypts: cells made at the base, shed at the surface

The colonic mucosa is a sheet of straight . Stem cells at each crypt base divide under Wnt signalling; their daughters move upwards, stop dividing as they leave the base, mature into absorptive and and are shed from the surface within about a week. The number of cells stays constant because production and shedding balance.

The mucosa rests on the thin , with the beneath. A polyp forms when this balance tips: more cells are made than are lost (adenomas), or cells linger instead of being shed (serrated polyps), or the mucosa and its supporting tissue overgrow together (hamartomas).

Polyps are described by shape as well as tissue: pedunculated polyps hang on a stalk of submucosa covered by mucosa, sessile polyps sit on a broad base, and flat lesions barely rise above the surface.

Point to it on the model