L10- GIT Pathology V (cancer) Flashcards Preview

DERS (GIT) > L10- GIT Pathology V (cancer) > Flashcards

Flashcards in L10- GIT Pathology V (cancer) Deck (40):

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

-Inflammatory: IBD, granulation tissue
-Non-Inflammatory: hyperplastic, hamartomatous, pseudo-polyps



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


-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)

-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]

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


-(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


describe the MSI pathway for colon cancer

(microsatellite instability, 10-15% cases)
-arises from adenoma or other lesions (SSA)
-defect in DNA repair mechanism: MLH1, MSH2, MSH6, PMS2)

-85% sporadic, 15% familial (HNPCC/Lynch)


Sporadic MSI cancers:
-(1) main acquired genetic factor
-(2) histology characteristics with inc in (3) cells

1- hypermethylation of MLH1 promoter: loss of MLH1, PMS2

2- mucinous + poorly differentiated histology
3- inc lymphocytes


Colorectal adenocarcinoma:
-usually (solitary/multiple), it will be the other in (2) situations
-(3) distal / L colon tumor features
-(4) proximal / R colon tumor features

1- solitary
2- UC, FAP (multiple)

3- annular, encircling napkin ring constrictions

4- polypoidal, non-obstructive, presents with non-specific anemia (Fe deficiency, weight loss)


Colon adenocarinoma:
-invades (1) layers of the wall
-10-15% tumors are termed (2) based on what they produce

-spread to (3) is more frequent than (4) spread that also occurs

-(5) general prognosis

1- mucosa, submucosa (possibly beyond)
2- mucinous, colloid (excess mucin)

3- regional LNs
4- *liver, peritoneum, lung, bones

5- no metastasis 97% survival, w/ metastasis 4%


list the locations neuroendocrine tumors can occur in the GIT

Esophagus- rare
Stomach- 3 settings
SI, Appendix- most common


describe esophageal and rectal carcinoids

Esophageal are rare to occur

Rectal are usually small and benign


describe the types of stomach carcinomas

Type I: autoimmune gastritis
-glandular atrophy, achlorhydria
-hypergastrinemia => enterochromograffin cell-like (ECL) hyperplasia

Type II: Gastrinoma (Zollinger-Ellison syndrome):
-MEN1 syndrome, hypergastrinemia

Type III: sporadic
-more aggressive and multiple sites


describe carcinoid tumors in the SI / appendix

(most common site in GIT)
-often small, occult primary tumors
-mestastizes widely => carcinoid syndrome when LIVER is involved


Carcinoid Syndrome:
-(1) Sxs
-(2) special test
-(3) unique complication

1- wheezing, flushing, diarrhea (via 5-HT / serotonin release)

2- 5-HIAA urine test

3- R heart fibrosis (because liver and lungs breakdown serotonin, it never reaches L heart)


GI Neuroendocrine Tumors:
-tumor cells are embedded in (1)
-it can be seen on histology spreading to (2)
-high magnification has (3) appearance

1- dense fibrous material
2- mucosal lymphatic channels
3- 'salt-n-pepper' appearance: chromatin with fine, course clumps


GI Lymphomas:
-(1) primary tumor
-(2) secondary tumor

1- arises from MALT (mucosal associated lymphoid tissue) = extranodal lymphomas (NO liver, spleen, bone marrow involvment at Dx)

2- arises due to systemic involvement of GIT from nodal lymphomas (Hodgkin's lymphomas)


GI Lymphomas:
-list the sites involved

(Note- most common site for extranodal lymphomas)

Stomach, 50%
SI, 37%


list the types of Primary GI Lymphomas

low-grade NHL (B-cell)
-Mantle cell (lymphomatous polyposis)
-Follicular Lymphoma

Diffuse large B-cell lymphoma

Burkitt lymphoma

Note- many, many T-cell lymphomas


primary GI lymphomas are often seen in ______ patients

-congenital immunodeficiency
-IBD associated
-MTX therapy


-(1) main associated disease
-(2) age and gender demographics
-(3) earliest / hallmark feature
-(4) Sxs

1- H. pylori infection (chronic gastritis)
2- adult men (~60, 1.6:1 M:F)

3- lympho-epithelial lesions (lymphocytes effacing gastric pit epithelium)

4- dyspepsia 80% / abdominal pain, n/v, weight loss 45%


GI Lymphoma:
-(1) Tx
-(2) general prognosis
-(3) typical growth progression
-(4) are agents used for high stage / unresponsive cases

1- H. pylori eradication via antibiotics

2- 70-90% remission, 10% relapse (90% 5Y survival, 65-75% 10Y)

3- slow, remains localized

4- chemotherapy: Rituximab (anti-CD-20 agent)