Clinical Pathology · MU Sofia

84. Benign tumors and carcinoma of the colon. Etiology & pathogenesis. Microscopic & gross pathomorphology. Role of fibrocolonoscopy in early diagnostics.

Covers polyps of the colon, sorting them into inflammatory, hamartomatous, hyperplastic and adenomatous types, then moves to adenocarcinoma and its genetic pathways such as APC loss and microsatellite instability. It includes an AK-53 mnemonic for the adenoma-carcinoma sequence and a section on familial syndromes including familial adenomatous polyposis and Lynch syndrome.

Inside: 1 section · 1 labelled picture · 13 flashcards · 3 min

Topic 84 of 138 in the MU Sofia syllabus for Clinical Pathology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 463 words (3 min of reading), with 13 flashcards.

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  1. Benign tumors and carcinoma of the colon. Etiology & pathogenesis. Microscopic & gross pathomorphology. Role of fibro colonoscopy in early diagnostics

Benign tumors and carcinoma of the colon. Etiology & pathogenesis. Microscopic & gross pathomorphology. Role of fibro colonoscopy in early diagnostics

Polyps are common in the colon, those without stalks are sessile polyps, those with stalks are known as pedunculated polyps. Polyps can be neoplastic or non-neoplastic. The most common neoplastic polyp is adenoma, which can progress to cancer. Let’s look at the classifications below:

  • Inflammatory
  • Part of solitary rectal ulcer syndrome
  • Purely inflammatory lesion
  • Clinical triad of rectal bleeding, mucus discharge and inflammatory lesion on anterior rectal wall
  • Hamartomatous polyps
  • Occur sporadically, comprised of genetic and acquired syndromes
  • Hamartomas are disorganized tumour like growths composed of mature cells
  • Types;
  • Juvenile polyps - most common form of Hamartomatous polyp. Usually in rectum. Most manifest with rectal bleeding.
  • Peutz-Jeghers syndrome - AD disorder defined by many GI hamartomatous polyps and mucocutaneous hyperpigmentation that increases malignancy risk.
  • Hyperplastic polyps
  • Epithelial proliferations, common in 60s and 70s
  • Thought to be a delayed shedding of surface epithelial cells causing a pile up
  • No malignant potential
  • Most commonly found in the left colon (rectosigmoid), usually <5mm diameter
  • Contain mature goblet cells and absorptive cells
  • Adenomas
  • Most common type of neoplastic polyp
  • Are a precancerous lesion to adenocarcinomas
  • Characterised by presence of epithelial dysplasia
  • Common age 50+ (colorectal screening occurs at this age)
  • Typical finding is pedunculated or sessile polyp 0.3-10 cm in diameter with velvet or raspberry texture due to abnormal epithelial growth. Epithelial dysplasia is the most important histological finding.
  • Can be classified as tubular, tubulovillous or villous based on architecture
  • Adenocarcinomas
  • Most common malignancy of the GI tract, more than 130,000 new cases/year with 55,000 deaths.
  • Genetic involvement which causes increased WNT signalling and microsatellite instability (associated with defects in DNA mismatch repair)
  • Loss of APC gene function which regulates beta catenin of the WNT pathway
  • Adenocarcinomas can be found throughout the colon, proximal colon tumours often grow as polypoid exophytic masses, while distal colon tumours tend to form ‘napkin ring’ constrictions and luminal narrowing (think apple core sign).
  • Most tumours are composed of tall columnar cells, resembling dysplastic epithelium from adenomas. Some may be mucin producing
  • Anemia and blood in feces are two of the big indicators. Depth of invasion and presence of metastasis are two big indicators for prognosis

Mnemonic: “AK-53” for the adenoma–carcinoma sequence – APC loss (normal mucosa → adenoma), then KRAS activation (adenoma grows), then TP53 loss (carcinoma). The second pathway, microsatellite instability, comes from defective DNA mismatch repair (MLH1, MSH2 – Lynch syndrome).

Familial neoplastic syndromes

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