5. GI Polyps and Colorectal CA

Question 1

LO1: Sessile vs. pedunculated

Answer 1

Sessile -flat no stalk

pedunculated- have a stalk

Question 2

LO1: Tubular vs. villous

Answer 2

Tubular-have tubules, more glandular

Villous - finger-like

Question 3

LO1: serrated vs. conventional

Answer 3

serrated-saw-like

conventional-round

Question 4

LO1: neoplastic vs. non-neoplastic (3)

Answer 4

neoplastic-CA
non-neoplastic-not CA
1) inflammatory polyps
2) Hamartomatous polyps
-Juvenile
-Peutz-Jeghers
3) Hyperplastic polyps

Question 5

LO3: hyperplastic polyps, malignancy, where, shape (3)

Answer 5

1) not pre-malignant
2) left sided
3) star shaped crypts

Question 6

LO3: sessile serrated polyps (3)

Answer 6

1) alternate pathway to carcinoma
2) microsatellite instability
3) CpG island methylation

Question 7

LO4: neoplastic polyps basics (adenomas), size, population, where, risk factor
(4)

Answer 7

1) variable size
2) 50% of western adults
3) Throughout colon
4) Size is most important for risk of malignancy

Question 8

LO4: Cytologic dysplasia (3)

Answer 8

1) Low grade to high grade
2) high grade=carcinoma in situ
3) HG dysplasia increases malignancy risk in polyp, but not in colon overall

Question 9

LO4: Increased malignancy risk

Answer 9

Size of polyps is most important correlary to malignancy

Question 10

LO5: 4 main pathways associated w. colon CA

Answer 10

1) WNT/APC/Beta-catenin -adenoma->carcinoma pathway
2) KRAS-MAP kinase
3) KRAS-PI3 Kinase
4) Microsatellite instability -defects in MMR

Question 11

LO6: Risk factors for colorectal carcinoma (6)

Answer 11

1) advanced age
2) Obesity
3) FAP/HNCC
4) Long lasting UC
5) ETOH abuse
6) smoking

Question 12

LO7: FAP basis, genetics, malignancy risk, feature (5)

Answer 12

1) AD in APC gene
2) APC part of WNT signaling
3) 100% to adenocarcinomas
4) WNT shut off when cell reaches crypt top, mutation allows to remain on
5) Many adenomatous polyps in colon

Question 13

LO7: HNPCC basis, name, inheritance, histo, where, risk of CRC (7)

Answer 13

1) Hereditary non-polyposis colorectal CA
2) Lynch syndrome
3) AD mutation in DNA MMR genes
4) Lack of repair -> microsatellite instability
5) Sessile-serrated polyps
6) Rt sided
7) 80% risk of CRC

Question 14

LO8: Colorectal CA presentations (2)

Answer 14

1) Early colon carcinoma

2) Advanced CRC

Question 15

LO8: Colorectal CA Dx (4)

Answer 15

1) visual -colonoscopy (best) +/- biopsy
2) Barium enema
3) Occult blood stool +
4) stool tumor cell/mutation detection

Question 16

LO9: Histo of invasive colorectal CA (3)

Answer 16

1) Dysplastic epithelial cell beyond lamina propria
2) <1 cm =low risk
3) > 4 cm = high risk

Question 17

L10: Prognostic features of colorectal carcinoma and staging, TNM, Stages III and IV, where does it met (6)

Answer 17

1) T-tumor-size and degree of invasiveness
2) N-lymph nodes-# involved
3) M-metastasis- 0 or 1
4) Stage III-LN involvement
5) Stage IV - distant mets
6) almost always mets to liver

Question 18

KRAS mutation and relationship to EGFR inhibitors, what’s K-RAS, % to malignancy, EGFR-I (4)

Answer 18

1) K-RAS- key signal downsream of EGFR TK receptor
2) Activating K-RAS mutation - 50-60% of CRC
3) EGFR inhibitor - cetuximab, gefitinib
4) EGFR inhibitors only effective in wild type tumors

Question 19

LO8: Early colon carcinoma presentation (2)

Answer 19

1) asymptomatic
2) non-specific
- fatigue, wt loss, anemia

Question 20

LO8: Advanced CRC presentation (4)

Answer 20

1) change in bowel habits, constipation
2) anemia, blood from rectum or in stool
3) cramping, abd pn
4) unexplained wt loss

Question 21

LO2: Hamartomatous polyps and syndromes

Answer 21

1) Peut-Jeghers syndrome - mucocutaneous pigmented lesion. Increased risk of thyroid, breast, lung, pancreas, gonads, and bladder CA
2) Juvenile polyps - risk of GI CA. Pulmonary AVM, digital clubbing