Makindo Medical Notes

🧪 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).