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

L10- GIT Pathology V (cancer) Flashcards

1
Q

In the SI, (benign/malignant) tumors are more common. Although it is the longest segment, it is only responsible for (2)% of GIT tumors.

A

1- benign

2- 3-6%

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2
Q

list the types of GIT polyps

A

Non-Neoplastic

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

Neoplastic:

  • benign
  • malignant
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3
Q

Juvenile Polyp = (1):

  • common in (2) age group
  • (3) part of GIT affected
A

1- *Hamartomatous polyp, Retention polyp

2- children <5, but adults also affected

3- rectum

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4
Q

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
A

(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)

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5
Q

Juvenile Polyp:

  • (1) size
  • (with/with-out) stalk
  • On histology: (3) is expanded, (4) and (5) are abundant,
A

(Hamartomatous polyp)
1- 1-3 cm, lobulated
2- with stalk

3- expanded lamina propria
4- cystically dilated glands
5- inflammatory cells (neutrophils)

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6
Q

PJ polyp:

  • inherited in (1) fashion
  • (single/multiple) polyps in (2) part of the GIT
  • (4) is the critical other clinical feature
A

(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

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7
Q

PJ Syndrome:

  • (1) forms
  • (2) is the major GIT issue, surrounded by (3)
  • high risk to develop (4)
A

(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

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8
Q

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
A

1- stroma of smooth muscle bundles
2- lamina propria
3- glandular
4- juvenile polyp

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9
Q

Adenoma:

  • mostly found in (1)
  • (2) forms
  • (3) appearing nuclei
  • (4) location in GIT wall
  • usually (high/low) grade dysplasia
A

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)

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10
Q

Adenoma pathogenesis:

  • (1) type mutations
  • (2) is an alternate or contributing genetic change
A

1- APC initially, p53 last (adeno-carcinoma sequence)

2- loss of DNA mismatch repair proteins: MSI

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11
Q

Conventional adenoma refers to (1). (2) is the other type.

A

1- polyp via APC pathway

2- sessile (flat) via MSIs

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12
Q

Sessile adenomas become dysplastic via (1) process and get their name from (2) appearance. Its classifications are (3).

A

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
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13
Q

Adenoma architecture types

A

[Note- all are precursors for carcinomas]
Tubular

Villous (pure villous)

Tubulovillous (>20% villous)

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14
Q

list the characteristics (by ranking) of adenomas that indicate in chance of malignancy

A

1) (by far) polyp size, >10mm/1cm => 40% chance of malignancy

2) dysplasia severity
3) villous > tubulovillous > tubular
4) (number) 3 or more adenomas

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15
Q

tubular adenoma histology

A
  • smooth surface, rounded glands
  • active inflammation occasionally
  • crypt dilation and rupture
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16
Q

villous adenoma histology

A

long, slender projections (appear like SI villi)

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17
Q

sessile serrated adenoma histology

A
  • lined with goblet cells
  • no features of dysplasia
  • neoplastic extensions into crypts –> lateral growth
18
Q

Colonic Adenomas:

  • (1) classic Sxs
  • (2) and (3) are possible complications
A

1- asymptomatic

2- anemia, occult blood loss due to polyp trauma, obstruction, stalk twisting, prolapse

3- intussusception (rarely) in polyps with slender, long stalks

19
Q

FAP:

  • (1) genetic defect
  • affects (2) part of GIT
  • (3) main characteristic, with (4) as another key identifying feature
  • (5) Tx
A

(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

20
Q

describe the associated FAP syndromes

A

(familial adenomatous polyposis)
Garder Syndrome: tubular adenomas with osteomas, desmoid tumors, epidermal cysts

Turcot Syndrome: tubular adenomas with CNS gliomas

21
Q

Colorectal Carcinomas:

  • more common in (younger/older) individuals, where the other needs one of the following predispositions for development, (2)
  • (3) other risk factors
A

1- elderly

2- UC (40%), polyposis syndromes, HNPCC (Lynch syndrome)

3- obesity, low fiber diet, high animal fat diet, low antioxidant intake

22
Q

list the symptoms of Colon Adenocarcinomas

A

-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]`

23
Q

Colon Adenocarcinoma diagnosis:

  • (1) gold standard
  • (2) alternate
  • (3) serum marker
A

1- colonoscopy

2- fecal immunohistochemistry (FIT, colo-guard)

3- carcinoembryonic antigen (CEA)

24
Q

describe chromosomal instability pathway for colon cancer

A

(85-90% cases)

  • adeno-carcinoma sequence
  • APC gene mutations
  • FAP, Gardner, Turcot
25
Q

describe the MSI pathway for colon cancer

A

(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)

26
Q

Sporadic MSI cancers:

  • (1) main acquired genetic factor
  • (2) histology characteristics with inc in (3) cells
A

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

2- mucinous + poorly differentiated histology
3- inc lymphocytes

27
Q

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
A

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)

28
Q

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
A

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%

29
Q

list the locations neuroendocrine tumors can occur in the GIT

A

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

30
Q

describe esophageal and rectal carcinoids

A

Esophageal are rare to occur

Rectal are usually small and benign

31
Q

describe the types of stomach carcinomas

A

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

32
Q

describe carcinoid tumors in the SI / appendix

A

(most common site in GIT)

  • often small, occult primary tumors
  • mestastizes widely => carcinoid syndrome when LIVER is involved
33
Q

Carcinoid Syndrome:

  • (1) Sxs
  • (2) special test
  • (3) unique complication
A

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)

34
Q

GI Neuroendocrine Tumors:

  • tumor cells are embedded in (1)
  • it can be seen on histology spreading to (2)
  • high magnification has (3) appearance
A

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

35
Q

GI Lymphomas:

  • (1) primary tumor
  • (2) secondary tumor
A

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)

36
Q

GI Lymphomas:

-list the sites involved

A

(Note- most common site for extranodal lymphomas)

Stomach, 50%
SI, 37%
Colon/Rectum

37
Q

list the types of Primary GI Lymphomas

A

low-grade NHL (B-cell)

  • MALToma
  • Mantle cell (lymphomatous polyposis)
  • Follicular Lymphoma
  • CLL/SLL

Diffuse large B-cell lymphoma

Burkitt lymphoma

Note- many, many T-cell lymphomas

38
Q

primary GI lymphomas are often seen in ______ patients

A
  • post-transplant
  • AIDS
  • congenital immunodeficiency
  • IBD associated
  • MTX therapy
39
Q

MALToma:

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

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%

40
Q

GI Lymphoma:

  • (1) Tx
  • (2) general prognosis
  • (3) typical growth progression
  • (4) are agents used for high stage / unresponsive cases
A

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)

DERS (GIT) (21 decks)

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