Colon Polyps

Question 1

Architecture

Answer 1

Sessile (no stalk) vs Peduncular (with stalk)

Tubular (longer time before follow up) vs Villous (stringent follow up, i.e more likely to be dysplastic)

Question 2

NON NEOPLASTIC

Inlammatory

Answer 2

Due to muscosal prolapse (common in rectum), cycles of injury and healing
Pres: with bleeding
Diagnx: colonoscopy + biopsy

Question 3

NON NEOPLASTIC
Hamartomatous Polyps
(def and types)

Answer 3

hamartoma = “tumor like” overgrowth of tissue normally present
Juvenile (sporadic or syndromic)
Peutz-Jeghers (syndromic)
Other: Cowden, Cronkhite-Canada

Question 4

NON NEOPLASTIC
Hamartomatous Polyps
(locations, considerations)

Answer 4

Various locations
May portend GI carcinoma (40% risk) and extra-GI symptoms
Need to consider familial screening/genetic counseling

Question 5

NON NEOPLASTIC
Hamartomatous Polyps (diagnx)

Answer 5

Benign features on path but SYNDROMIC JUVENILE POLYPS OFTEN HAVE FOCI OF DYSPLASIA

Question 6

NON NEOPLASTIC

Hyperplastic (info/pres)

Answer 6

90% Left colon and rectum, small size, increases with ge
smooth SESSILE nodular lesions, flat base
Need path to determine if hyperplastic or adenomatous

Question 7

NON NEOPLASTIC

Hyperplastic (diagnx)

Answer 7

delayed maturation with overgrowth of superficial epithelium SERRATED ARCHITECTURE
NO DYSPLASIA
NOT “sessile serrated polyp/adenoma”

Question 8

Sessile serrated polyp/adenoma

Answer 8

Pre-malignant
More common on RIGHT
DYSPLASTIC epithelium
LARGER than hyperplastic
Can progress to adenocarcinoma
MMR defect (microsatellite instablity)

Question 9

Adenomas

Answer 9

Variable size and location through colon
50% of western adults by age 50
Cytogenic dysplasia --> adenocarcinoma
SIZE MATTERS (for malignancy risk)
Villous more often contain foci of invasion than tubular

Question 10

Colon Cancer

Protective and Risk Factors

Answer 10

Risks: age obesity, EtOH, smoking, FAP/HNPCC, long standing UC
Protective: (only moderate) high activity, high fiber

Question 11

Colon Cancer

Genetics

Answer 11

Sporadic (65-85%): APC/WNT pathway defect (APC gene, chromosome 5)
FAP (

Question 12

Colon Cancer

Genetic Pathways

Answer 12

APC/beta-catenin: mutated APC can’t destroy b-c–> b-c to nucleus to promote txn/cell growth
Microsatellite instability: (defects in mismatch repair proteins: MMR)
(also epigenetics, methylation of CPG islands)

Question 13

Colon Cancer

pres/sx

Answer 13

Early: nonspecific: fatigue, weight loss, anemia
Advanced: bowel habit changes, narrowing of still, cramping, blood loss (anemia–>Fe defic), unexplained weight loss
important for TMN staging: depth of invasion, lymph node metastasis, distant metastasis (COMMONLY LIVER)

Question 14

Colon Cancer

diagnx

Answer 14

Visualization and biopsy (colonoscopy and barium enema)
Blood in stool (ulcer bleeding)
DNA/mutation detection in stool

Question 15

Colon Cancer

treat

Answer 15

Surgery, radiofrequency ablation, cryosurgery, chemo, radiation, targeted tx (eg. mono Abs, angiogenesis inhibitors)