| Download the amazing global Makindo app: Android | Apple | |
|---|---|
| MEDICAL DISCLAIMER: Educational use only. Not for diagnosis or management. See below for full disclaimer. |
Colorectal polyps
🧪 Normal Epithelium → Dysplastic Epithelium → Adenoma → Adenocarcinoma
This is the classic adenoma–carcinoma sequence, explaining how benign colorectal polyps can transform into cancer.
📖 About
- Colorectal polyps = protuberances of colorectal mucosa into the lumen.
- Importance lies in distinguishing polyps with malignant potential vs benign types.
- Polyps are frequently detected during bowel cancer screening (e.g. FIT + colonoscopy in the UK NHS programme).
🧬 Neoplastic Polyps
- Primarily adenomas, with potential progression to adenocarcinoma.
- At autopsy, around 30% of adults are found to have adenomatous polyps.
- Most arise beyond the splenic flexure, especially in the rectosigmoid colon.
- Concern is the adenoma–carcinoma sequence, driven by mutations (APC → KRAS → p53).
⚠️ Adenomatous Polyps – Malignancy Risk Factors
- Histological dysplasia: ↑ mitoses, pleomorphism, loss of polarity.
- Size: Risk increases with size, especially >2 cm.
- Villous adenomas: Highest malignant risk (villous = villainous).
- Tubulovillous/tubular adenomas: Lower but significant risk.
- Carcinoma in situ: Severe dysplasia confined to mucosa.
- Invasive carcinoma: When malignant cells breach muscularis mucosa.
- 👉 Adenomatous polyps should be completely removed. Colonoscopy follow-up is recommended to detect additional lesions.
🧬 Genetic Syndromes with Adenomatous Polyps
- Familial Adenomatous Polyposis (FAP): AD mutation in APC gene → hundreds–thousands of colorectal adenomas; near-100% risk of CRC by 40 yrs without colectomy.
- Turcot’s Syndrome: FAP + CNS tumours (glioblastoma, medulloblastoma).
- Gardner’s Syndrome: FAP + extra features (osteomas, epidermoid cysts, desmoid tumours).
🟢 Non-Neoplastic Polyps (No Malignant Potential)
- Metaplastic/Hyperplastic Polyps: Common in rectum, small (2–5 mm), flat, no dysplasia. Do not progress to malignancy.
- Inflammatory Pseudopolyps: Seen in IBD (UC, Crohn’s). Reflect mucosal regeneration after ulceration.
- Hamartomatous Polyps: Disorganised normal tissue, e.g. juvenile polyps (common in children, may bleed/prolapse, easily resected).
🧬 Genetic Syndromes with Hamartomatous Polyps
- Peutz-Jeghers Syndrome: AD. Polyps in small bowel/colon + mucocutaneous pigmentation (lips, gums). Risks: intussusception, bleeding, ↑ cancer risk.
- Cronkhite–Canada Syndrome: Non-hereditary. Features = alopecia, nail atrophy, skin hyperpigmentation, watery diarrhoea. Rare but exam-favourite.
📊 Comparative Table of Colorectal Polyps
| Type | Histology | Risk of Malignancy | Key Associations |
|---|---|---|---|
| Adenomatous (Neoplastic) | Tubular, Tubulovillous, Villous | Yes – esp. villous, >2 cm, dysplastic | Adenoma–carcinoma sequence |
| Hyperplastic | Metaplastic epithelium | No | Common in rectum, small & flat |
| Inflammatory | Granulation tissue | No | Seen in UC/CD pseudopolyps |
| Hamartomatous | Disorganised normal tissue | Mostly no, but ↑ cancer risk in syndromes | Peutz-Jeghers, Juvenile polyps |
📚 Teaching Commentary
🩺 Remember: not all polyps are dangerous. Adenomas matter because they can follow the adenoma–carcinoma pathway.
- Villous = villainous → high cancer risk.
- Size matters: >2 cm = higher malignant potential.
- Screening saves lives: NHS Bowel Cancer Screening Programme (FIT age 60–74 in England) identifies polyps before malignant change.
💡 Exam tip: “Mucocutaneous pigmentation + intussusception” → think Peutz-Jeghers. “Multiple polyps in a teenager” → think FAP (APC gene).