L10- GIT Pathology V (cancer) Flashcards
(40 cards)
In the SI, (benign/malignant) tumors are more common. Although it is the longest segment, it is only responsible for (2)% of GIT tumors.
1- benign
2- 3-6%
list the types of GIT polyps
Non-Neoplastic
- Inflammatory: IBD, granulation tissue
- Non-Inflammatory: hyperplastic, hamartomatous, pseudo-polyps
Neoplastic:
- benign
- malignant
Juvenile Polyp = (1):
- common in (2) age group
- (3) part of GIT affected
1- *Hamartomatous polyp, Retention polyp
2- children <5, but adults also affected
3- rectum
Juvenile Polyp:
- (1) most common form / syndrome with (high/low) risk for malignancy
- rarely (3) a (4) inherited disease with (high/low) risk for malignancy
- (6) is another associated syndrome
(Hamartomatous polyp)
1- Sporadic SINGLE polyp
2- no malignant potential
3- juvenile polyposis syndrome
4- AD
5- high
6- Cowden and Bannayan-Ruvacalba-Riley syndromes (PTEN mutations)
Juvenile Polyp:
- (1) size
- (with/with-out) stalk
- On histology: (3) is expanded, (4) and (5) are abundant,
(Hamartomatous polyp)
1- 1-3 cm, lobulated
2- with stalk
3- expanded lamina propria
4- cystically dilated glands
5- inflammatory cells (neutrophils)
PJ polyp:
- inherited in (1) fashion
- (single/multiple) polyps in (2) part of the GIT
- (4) is the critical other clinical feature
(Peutz Jegher Polyp- hamartomatous polyp)
1- AD
2- multiple
3- entire GIT
4- hyperpigmentation (melantotic pigmentation) in mucocutaneous areas: lips, peri-oral areas, face, genitalia, palms
PJ Syndrome:
- (1) forms
- (2) is the major GIT issue, surrounded by (3)
- high risk to develop (4)
(Peutz Jegher polyp)
1- sporadic, syndromic forms
2- arborizing SM network between glands
3- lined with non-dysplastic epithelium rich in goblet cells
4- cancer of: pancreas, breast, lung, ovary, uterus
PJ Polyp:
- polyp will overlie (1- include composition) which are cutting through (2)
- complex (3) architecture along with (1) distinguish it from a (4) polyp
1- stroma of smooth muscle bundles
2- lamina propria
3- glandular
4- juvenile polyp
Adenoma:
- mostly found in (1)
- (2) forms
- (3) appearing nuclei
- (4) location in GIT wall
- usually (high/low) grade dysplasia
1- colon (90%)
2- flat (sessile), pedunulated
3- tall, hyperchromatic, crowded
4- confined to pre-existing crypts, no invasion
5- low (some are high => premalignant)
Adenoma pathogenesis:
- (1) type mutations
- (2) is an alternate or contributing genetic change
1- APC initially, p53 last (adeno-carcinoma sequence)
2- loss of DNA mismatch repair proteins: MSI
Conventional adenoma refers to (1). (2) is the other type.
1- polyp via APC pathway
2- sessile (flat) via MSIs
Sessile adenomas become dysplastic via (1) process and get their name from (2) appearance. Its classifications are (3).
1- MSI (microsatellite instabilities from loss of DNA mismatch repair)
2- saw-tooth (serrated)
3:
- sessile serrated polyps w/o dysplasia
- sessile serrated adenoma w/ dysplasia
- traditional serrated adenoma w/ dysplasia
Adenoma architecture types
[Note- all are precursors for carcinomas]
Tubular
Villous (pure villous)
Tubulovillous (>20% villous)
list the characteristics (by ranking) of adenomas that indicate in chance of malignancy
1) (by far) polyp size, >10mm/1cm => 40% chance of malignancy
2) dysplasia severity
3) villous > tubulovillous > tubular
4) (number) 3 or more adenomas
tubular adenoma histology
- smooth surface, rounded glands
- active inflammation occasionally
- crypt dilation and rupture
villous adenoma histology
long, slender projections (appear like SI villi)
sessile serrated adenoma histology
- lined with goblet cells
- no features of dysplasia
- neoplastic extensions into crypts –> lateral growth
Colonic Adenomas:
- (1) classic Sxs
- (2) and (3) are possible complications
1- asymptomatic
2- anemia, occult blood loss due to polyp trauma, obstruction, stalk twisting, prolapse
3- intussusception (rarely) in polyps with slender, long stalks
FAP:
- (1) genetic defect
- affects (2) part of GIT
- (3) main characteristic, with (4) as another key identifying feature
- (5) Tx
(familial adenomatous polyposis)
1- APC gene, 5q21
2- colorectum (sometimes SI, stomach)
3- 500-2500 adenomas (termed attenuated if <100)
4- unicrypt adenoma + fundic gland polyp in stomach
5- colectomy to prevent cancer
describe the associated FAP syndromes
(familial adenomatous polyposis)
Garder Syndrome: tubular adenomas with osteomas, desmoid tumors, epidermal cysts
Turcot Syndrome: tubular adenomas with CNS gliomas
Colorectal Carcinomas:
- more common in (younger/older) individuals, where the other needs one of the following predispositions for development, (2)
- (3) other risk factors
1- elderly
2- UC (40%), polyposis syndromes, HNPCC (Lynch syndrome)
3- obesity, low fiber diet, high animal fat diet, low antioxidant intake
list the symptoms of Colon Adenocarcinomas
-mostly asymptomatic
R-sided features (proximal colon): fatigue, weakness, IDA (chronic blood loss) [non-obstructive, several years]
L-sided features (distal colon): altered bowel habits (obstructive- napkin ring constriction]`
Colon Adenocarcinoma diagnosis:
- (1) gold standard
- (2) alternate
- (3) serum marker
1- colonoscopy
2- fecal immunohistochemistry (FIT, colo-guard)
3- carcinoembryonic antigen (CEA)
describe chromosomal instability pathway for colon cancer
(85-90% cases)
- adeno-carcinoma sequence
- APC gene mutations
- FAP, Gardner, Turcot
