🫁 Intestinal Polyps - Robbins Notes (6 Marks Flowchart)

MASTER FLOWCHART

                    INTESTINAL POLYPS
                          |
          ________________|________________
          |                               |
   NON-NEOPLASTIC                    NEOPLASTIC
  (No/Low malignant potential)     (Malignant potential)
          |                               |
    ______|______                   ______|______
    |      |    |                   |            |
Hyper- Inflam- Hamar-           ADENOMA    Sessile Serrated
plastic matory  tomatous                      Polyp (SSP)

BLOCK 1 - NON-NEOPLASTIC POLYPS

1. HYPERPLASTIC POLYPS

Definition: Benign epithelial proliferation
        |
        ↓
Pathogenesis: ↓ epithelial cell turnover → delayed shedding
              → "piling up" of goblet + absorptive cells
        |
        ↓
Location: LEFT colon (sigmoid + rectum)
        |
        ↓
Size: < 5 mm | Sessile | Smooth | Nodular
        |
        ↓
Histology: Serrated surface (saw-tooth pattern)
           - Serration in UPPER 1/3 of crypt
           - Mature goblet + absorptive cells
        |
        ↓
KEY POINT: NO malignant potential
           BUT must distinguish from SSP (which has malignant potential)

2. INFLAMMATORY POLYPS

Cause: Repeated cycles of INJURY → HEALING
        |
        ↓
Best Example: Solitary Rectal Ulcer Syndrome
        |
        ↓
Clinical Triad:
   1. Rectal bleeding
   2. Mucus discharge
   3. Inflammatory lesion of anterior rectal wall
        |
        ↓
Mechanism: Impaired anorectal sphincter relaxation
           → sharp angle → recurrent abrasion
           → mucosal prolapse → polyp
        |
        ↓
Also seen in: IBD (Crohn's, UC) as "pseudopolyps"
        |
        ↓
Malignant potential: NONE (purely reactive)

3. HAMARTOMATOUS POLYPS

Definition: Disorganized but normal tissue components
            → Occur SPORADICALLY or as GENETIC SYNDROMES
        |
        ↓
    ____|____
    |        |
JUVENILE    PEUTZ-JEGHERS
 POLYPS      SYNDROME

Age: Children (< 5 yrs) | Also young adults
Type: Usually SPORADIC (single)
Location: RECTUM most common
        |
        ↓
Morphology:
  • Smooth, spherical, pedunculated
  • Large (up to 3 cm)
  • Histology: Cystically dilated glands
               + abundant lamina propria
               + inflammation
        |
        ↓
Clinical: Rectal bleeding, intussusception
        |
        ↓
Malignant potential:
  • Single sporadic: NONE
  • Juvenile Polyposis Syndrome (>5 polyps): ↑ RISK

Genetics: AD | STK11/LKB1 gene mutation (Chr 19)
        |
        ↓
KEY Features (remember as PJS triad):
   1. Multiple hamartomatous polyps (GI tract - small intestine most)
   2. Mucocutaneous pigmentation (lips, oral mucosa, genitalia)
   3. ↑ Cancer risk (GI + extra-GI: breast, ovary, pancreas, testis)
        |
        ↓
Morphology:
  • Large, pedunculated, lobulated
  • Arborizing smooth muscle bundles in lamina propria
    (this DISTINGUISHES it from juvenile polyps)
        |
        ↓
Malignant potential: YES - ↑ risk (GI + extra-GI cancers)

BLOCK 2 - NEOPLASTIC POLYPS

4. ADENOMAS (Most Important!)

Definition: Benign epithelial NEOPLASM → PRECURSOR to colorectal cancer
            Hallmark = EPITHELIAL DYSPLASIA
        |
        ↓
Epidemiology: ~30% of Western adults by age 60
              Colon cancer surveillance → colonoscopy from age 45
        |
        ↓
Morphology:
  • Size: 0.3 - 10 cm
  • Appearance: Velvety / raspberry surface
  • Pedunculated (with fibromuscular stalk) OR Sessile
        |
        ↓
Histology (hallmarks of dysplasia):
  • Nuclear hyperchromasia
  • Nuclear elongation + stratification
  • Prominent nucleoli
  • Eosinophilic cytoplasm
  • Reduced goblet cells
        |
        ↓
Types by architecture:
  _______________|________________
  |              |               |
TUBULAR       VILLOUS       TUBULOVILLOUS
(75%)          (10%)           (15%)
  |              |               |
Pedunculated   Sessile/large   Mixed
Low risk       HIGHEST risk    Intermediate
                > 4 cm

Normal mucosa
      ↓ (APC mutation - 1st hit)
Small adenoma
      ↓ (KRAS mutation)
Large adenoma
      ↓ (TP53, SMAD4 mutations)
Carcinoma in situ
      ↓
Invasive adenocarcinoma

• Size > 2 cm
• Villous architecture
• Severe dysplasia
• Multiple polyps

5. SESSILE SERRATED POLYPS (SSP)

KEY DISTINCTION from Hyperplastic polyps:
  • Share serrated architecture → look similar
  • BUT: SSP has MALIGNANT POTENTIAL
  • No cytologic dysplasia (unlike adenomas)
  • Serration extends to BASE of crypt (not just upper 1/3)
  • Leads to CIMP pathway cancers (methylation-driven)

BLOCK 3 - FAMILIAL POLYPOSIS SYNDROMES

                FAMILIAL SYNDROMES
                       |
          _____________|_____________
          |                         |
         FAP                      HNPCC
  (Familial Adenomatous        (Lynch Syndrome)
      Polyposis)

FAP vs HNPCC Quick Comparison:

BLOCK 4 - QUICK MEMORY TABLE (All Polyps)

BLOCK 5 - CLINICAL PEARLS (6-Mark Exam Points)

1. Pedunculated = has a stalk | Sessile = broad base, no stalk

2. Hyperplastic ≠ SSP
   (Both serrated, but SSP = malignant; serration at crypt BASE)

3. Adenoma hallmark = DYSPLASIA (nuclear hyperchromasia, stratification)

4. Villous adenoma = highest malignant potential + electrolyte-losing
   (secretory diarrhea → hypokalemia)

5. APC mutation = "gatekeeper" of colon cancer
   (FAP + sporadic adenoma-carcinoma sequence)

6. PJS = STK11/LKB1 mutation + arborizing smooth muscle in stalk
   (distinguishes from juvenile polyp which has NO smooth muscle)

7. Most polyps → START SESSILE → grow → BECOME PEDUNCULATED