Colon cancer screening

Type

Clinical features

Pathogenesis of colon cancer

• Incidence of CRC increases between ages of 40-44
• Typically starts as progression from small polyps  enlarging to dysplasia and adenoma

• Can also develop from non-polypoid adenomas
• Progression from adenoma to carcinoma can take 10 years

Risk factors

• Genetic
  • • African American patients
    • Cystic fibrosis
    • Family history of Lynch syndrome, familial adenomatous polyposis, or Peutz-Jeghers syndrome
    • First degree relatives with CRC or advanced polyp
    • Hereditary non-polyposis colorectal cancer
    • Personal history of adenomatous ployps
    • Personal history of IBD (Crohn disease, ulcerative colitis)
• Environmental/acquired

• • Diet high in red meat and fat
  • History of childhood abdominal radiation
  • Increasing age
  • Obesity
  • Tobacco use

Rationale of screening tests

• Screen high risk population for primary CRC prevention
• Screen patients at average risk
• Follow-up of abnormal initial abnormal test results

Types of polyps

• Inflammatory polyps
  • • Non-neoplastic projections of mucosa into the lumen
    • Occur in response to local or diffuse inflammation
    • Do not usually progress to CRC but can have surrounding dysplasia
  • Hamartous polyps (normal tissue growing in disorganized manner)
• Juvenile polyps

• • • • Contain lamina propria and dilated cystic glands
• Peutz-Jeghers polyps

• • • • Glandular epithelium srrounded by smooth muscle cells
• Sessile serrated lesions
• Hyperplastic polyps

• • • • Associated with low risk to CRC progression
• Sessile serrated polyps (SSP)

• • • • Smooth surface, flat, sessile, and can have dysplasia
• Adenomatous polyps

• • Can be pedunculated, flat, sessile, or depressed
  • Advanced adenoma defined as > 10 mm in size or with dysplasia 
  • Histolgically classified as tubular, villous, or tubulovillous