Colorectal polyps ✅

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🧪 Normal epithelium → dysplasia → adenoma → adenocarcinoma
This is the classic adenoma–carcinoma sequence, which explains how some adenomatous colorectal polyps can progress to cancer over time. 🇬🇧 In UK practice, polyps are important because management depends on histology, size, number, dysplasia, and completeness of excision.

📖 About

• Colorectal polyps are mucosal lesions projecting into the bowel lumen.
• The key clinical issue is distinguishing premalignant polyps from lesions with little or no malignant potential.
• Polyps are frequently detected during bowel cancer screening and colonoscopy.

🧬 Premalignant / Neoplastic Polyps

• The main conventional premalignant lesions are adenomas.
• Adenomas may be tubular, tubulovillous, or villous.
• Risk of malignancy rises with increasing size, villous architecture, and high-grade dysplasia.
• The classic molecular sequence involves mutations such as APC, KRAS, and later TP53.

⚠️ Adenomatous Polyps – Features Associated with Higher Risk

• Larger size (especially ≥10 mm, and higher again with larger lesions).
• Villous or tubulovillous histology.
• High-grade dysplasia.
• Multiple premalignant polyps.
• Incomplete excision or uncertainty about complete removal.
• Management is usually complete endoscopic removal followed by risk-based surveillance where indicated.

🧬 Serrated Lesions

• Hyperplastic polyps are usually small distal lesions with little malignant potential.
• However, the serrated pathway is important because some serrated lesions, especially sessile serrated lesions and traditional serrated adenomas, can be premalignant.
• For exam safety: not all lesions that appear “hyperplastic” should be assumed biologically harmless.

🧬 Genetic Syndromes with Adenomatous Polyps

• Familial Adenomatous Polyposis (FAP): autosomal dominant APC-associated syndrome with numerous adenomas and very high colorectal cancer risk if untreated.
• Gardner syndrome: phenotypic variant of FAP with extracolonic features such as osteomas, epidermoid cysts, and desmoid tumours.
• Turcot syndrome: polyposis syndrome associated with CNS tumours.

🟢 Other Colorectal Polyps

• Hyperplastic polyps: usually small, often distal, and usually low risk.
• Inflammatory pseudopolyps: associated with inflammatory bowel disease; reflect repeated mucosal injury and healing.
• Hamartomatous polyps: disorganised overgrowth of native tissue, for example juvenile polyps.

🧬 Hamartomatous Polyp Syndromes

• Peutz–Jeghers syndrome: mucocutaneous pigmentation with hamartomatous polyps and increased cancer risk.
• Juvenile polyposis syndrome: multiple hamartomatous polyps with increased GI cancer risk.
• Cronkhite–Canada syndrome: rare, non-hereditary, with diarrhoea, weight loss, nail changes, alopecia, and hyperpigmentation.

📊 Comparative Table of Colorectal Polyps

🔍 Surveillance / UK Practice

• All polyps removed at colonoscopy should be retrieved where possible for histology.
• Need for repeat colonoscopy depends on number, size, histology, dysplasia, and completeness of excision.
• Higher-risk premalignant findings may need surveillance colonoscopy, commonly a one-off 3-year examination in selected patients.
• Lower-risk findings may return to routine bowel screening rather than automatic colonoscopic surveillance.

📚 Teaching Commentary

🩺 Not all polyps are dangerous. The biggest exam distinction is between premalignant adenomas / serrated lesions and clearly benign processes such as many small distal hyperplastic polyps or inflammatory pseudopolyps.

• Villous = villainous still works as a memory aid.
• Size, number, dysplasia, and histology drive risk.
• Serrated lesions matter because they are an important alternative route to colorectal cancer.

💡 UK screening note: in England, FIT bowel cancer screening is offered every 2 years to people aged 50 to 74.