Adenomatous polyps

High malignant potential
- Tubular adenoma: < 5%
- Tubulovillous adenoma: ∼ 20%
- Villous adenoma: ∼ 50%

Mnemonic

Villous adenomas are villains because they have the highest malignant potential.

Hyperplastic polyps

Most common type of nonneoplastic polyp among those with low malignant potential
Histology: hyperplasia of normal cellular components with a sawtooth/serrated pattern of crypt epithelium
- No dysplasia, see Cellular adaptations

Genetics: Autosomal Dominant mutation of the APC tumor suppressor gene on chromosome 5.
Pathophysiology: Development of 100s-1000s of colorectal adenomatous polyps.
Cancer Risk: 100% risk of colorectal cancer (CRC) by age 40-50 if untreated.
Variants:
- Gardner Syndrome: FAP + Osteomas, Desmoid tumors, and Congenital Hypertrophy of Retinal Pigment Epithelium (CHRPE).
- Turcot Syndrome: FAP + Medulloblastoma (CNS tumor).
Management:
- Dx: Colonoscopy showing massive polyposis; confirmed with APC gene testing.
- Tx: Prophylactic colectomy.
- Surveillance: Upper endoscopy for duodenal polyps.

Inheritance: Autosomal Dominant.
Gene: STK11 (tumor suppressor).
Key Features:
- Mucocutaneous hyperpigmentation: Blue-gray macules on lips, perioral area, buccal mucosa.
- Hamartomatous GI polyps: Most common in the small intestine. t
  - These are benign overgrowths of normal tissue, not precancerous adenomas. But can cause obstruction and intussusception.
Histology: Arborizing smooth muscle within polyps.
Major Complication: Intussusception (presenting as colicky abdominal pain).
Cancer Risks: ↑ risk of GI (colorectal, pancreatic), breast, and gynecologic/testicular cancers.

Tip

Mucocutaneous lentigines is specific to PJS, not other gastric cancers. Don’t mix with Leser-Trélat sign.