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CV > EsoGastroNeo > Flashcards

EsoGastroNeo Flashcards

1
Q

Describe the steps in the normal progression of cancer in a stepwise fashion

A

Hyperplasia > Metaplasia > Dysplasia > Neoplasia

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2
Q

increase in the number of cells

A

Hyperplasia

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3
Q

displacement of cells in tissue (wrong location, but normal cells)

A

Metaplasia

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4
Q

increase in the number of cells with abnormal changes (e.g. abnormal shape, increased nuclear size, N/C ratio, increased mitotic activity and lack of differentiation features

A

Dysplasia:

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5
Q

increase in the number of cells with or without a tendency to invade the basement membrane

A

Neoplasia

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6
Q

Barret’s Esophagus is caused by which plastic changes in squamous mucosa?

A

Intestinal metaplasia within the squamous mucosa

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7
Q

Barrett’s esophagus has a high risk for progression to _

A

esophageal adenocarcinoma

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8
Q

The risk of dysplasia in Barrett’s esophagus is proportional to what?

A

□ The risk of dysplasia is proportional to the length of Barrett’s
Long segment of Barrette’s ≥ 3cm +++
Short segment of Barrette’s

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9
Q

Most cases of Esophageal Adenocarcinoma arise from what?

A

Barrett’s

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10
Q

Of the esophageal cancers…

a. which is the most common worldwide
b. which is on the rise in the US?
c. list some other rare esophageal cancers (6)

A

a. Squamous cell carcinoma
b. Adenocarcinoma
c.
Unusual adenocarcinoma
Undifferentiated carcinoma
Carcinoid
Melanoma
Lymphoma
Sarcoma

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11
Q

○ Risk Factors for esophageal adenocarcinoma (8)

A 
Barrett's +++ ↑ 
 Obesity +++ ↑
 Caucasian men +++
 Tobacco ↑
 Radiation ↑
 H. pylori infection (some serotypes) ↓
 Geographic variations (Highest in the US, UK, Canada, Australia, Netherlands and Brazil; Lowest in east Asia)
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12
Q

Describe two general genomic alterations accounting for the development of esophageal adeno

A

Loss of function mutations (in tumor suppressor genes, e.g. p53)
Gain of function mutations (e.g. in EGFR, HER2, etc.)

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13
Q

What is the tx of early stage esophageal adenocarcinoma?

A

esophagectomy

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14
Q

Esophageal Adenocarcinoma (molecular abnormalities)

a. Loss of function mutations in which tumor suppressor genes account for most cases (2)
b. gain of function mutations occur through amplification of which genes? (4)

A

a. p53 (It is also mutated in more than 50% of all cancers (so non-specific); p16 (CDKN2A)
b. EGFR (most imp); HER2 (ERBB2); MET; Cyclin D1 and Cyclin E

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15
Q

List some common risk factors for esophageal squamous cell carcinoma (8)

A 
○ Risk Factors
			§ Caustic ingestion
			§ Achalasia
			§ Bulimia
			§ Tylosis 
			§ Plummer-Vinson syndrome
			§ External-beam radiation
			§ Esophageal diverticula
			§ Hot beverages
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16
Q

Demographics of Esophageal squamous cell carcinoma (ESCC)

a. what age?
b. location?
c. race?

A

a. Older males x 4 (> 45)
b. Underdeveloped and rural areas/countries
c. African Americans x 8 more than whites

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17
Q

Hperkeratosis of the palms of the hands and soles of the feet; risk factors for ESCC

A

Tylosis

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18
Q

Describe the following molecular changes associated with ESCC…

a. TSG loss (3)
b. Gain of function mutations (2)

A

a. p53; E-cadherin; NOTCH1
b. Amplification of the transcription factor SOX2;
Amplification of cyclin D1 (causes progression through cell cycle)

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19
Q

What is the typical location of an esophageal adenocarcinoma? What about an esophageal SCC?

A

AC: distal esophagus
SCC: middle portion (middle third)

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20
Q

Which esophageal neoplasm is insidious in nature (patients may describe having sx for years)?

A

ESCC

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21
Q

List 4 complications that may arise from ESCC

A

Weight loss
Bleeding
Iron deficiency anemia (from bleeding)
Infection

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22
Q

Most important diagnostic tool for esophageal adenocarcinoma and SCC

A

Endoscopy

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23
Q

What is the tx for early stage ESCC?

A

□ Combined chemotherapy and radiation therapy followed or not by esophagectomy

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24
Q

What is the tx for advanced stage ESCC or AC?

A

□ Combined chemotherapy and radiation therapy
□ Chemotherapy alone
□ Palliative care

25
Q

List the different types of gastric tumors (8)

A 
Gastric Polyps
Gastric Adenocarcinoma
Primary Gastric Lymphoma (GGIST,  (MALT))
Stromal Tumors (GIST)
Carcinoid Tumors
Squamous Cell Carcinomas
Small-Cell
Metastatic Spread
26
Q

List three types of gastric polyps

A

Inflammatory and Hyperplastic Polyps
Fundic Gland Polyps
Gastric Adenomas

27
Q

Which type of gastric polyp is the most common (75%) and associated with H. pylori?

A

Inflammatory and Hyperplastic Polyps

28
Q

Which type of gastric polyp is associated with familial adenomatous polyposis (FAP)?

A

Fundic Gland polyps

29
Q

Carcinoma may be present in up to 30% of which type of gastric polyps?

A

gastric adenomas

30
Q

The risk of dysplasia in gastric adenomas (polyps) increases with _

A

size

31
Q

Gastric AC is

a. more common in which gender?
b. which age?
c. race?

A

a. M
b. 60-75
c. 2 x more likely in AA than white

32
Q

Which type of gastric adenocarcinoma (GAC)…

a. are composed of infiltrating gastric mucous cells that infrequently form masses or ulcers
b. are characterized by cohesive cells that form gland-like masses and are often preceded by intestinal metaplasia

A

a. Diffuse-Type Adenocarcinoma

b. Intestinal-type

33
Q

Most common form of gastric cancer

A

Gastric Adenocarcinoma

34
Q

What are the major risk factors for GAC? (4)

A

§ Diet: high intake of salts, nitrates, and smoked or pickled foods
§ Occupational exposure: coal mining and processing of nickel, rubber, and timber
§ Cigarette smoking
§ Helicobacter pylori infection (2.8-fold increase in the relative risk of the disease)

35
Q

Which mutation occurs in the majority of gastric cancers?

A

p53

36
Q

Describe 1 common mutation seen with GAC AND describe 2 other mutations that are seen with GAC

A
  • P53 Mutations (both)
  • E-Cadherin (CDH1) mutation (in hereditary and sporadic, diffuse types)
  • Wnt Signaling mutations (sporadic intestinal types)
37
Q

Which mutation has been linked to a hereditary form of the intestinal-type of adenocarcinomas with (70-80% penetrance) as well as lobular carcinomas of the breast and sporadic diffuse gastric cancers

A

E-cadherin

38
Q

In GACs other than hereditary intestinal forms and sporadic, diffuse forms, how is E-cadherin silenced?

A

hypermethylation

39
Q

What type of mutations are seen in the sporadic intestinal type of GAC and may be gain or loss of function? And list an important gain of function mutation for this type

A

Wnt Pathway mutations; gain of function of beta-catenin (drives cell proliferation)

40
Q

List 4 mechanisms of metastatic spread of gastric cancer

A

§ by direct extension (lesser and greater omentum, liver and diaphragm, spleen, pancreas, transverse colon)
§ regional and distant nodal metastases
§ hematogenous metastases (liver, lungs, bone, brain)
§ peritoneal metastases

41
Q

What is the most important tool for work up (diagnosis) of gastric tumors?

A

EGD with biopsy

42
Q

better than CT for assessment of depth of tumor invasion, including invasion of nearby organs and perigastric regional LN

A

EUS (endoscopic US)

43
Q

List 4 components/possibilities in the tx of gastric cancer

A

§ Gastrectomy (partial or total) with lymphadenectomy
§ Endoscopic mucosal resection (EMR) can be performed in nonulcerated superficial (T1 N0) lesions
§ Radiation therapy (standard)
§ Chemotherapy

44
Q

This gastric cancer is a form of extra-nodal marginal zone B-cell lymphoma; 5% of all primary gastric malignancies

A

Primary Gastric Lymphoma (MALT)

45
Q

MALT cancers are most commonly found where?

A

stomach; at sites of inflammation; usually at tissues devoid of organized lymphoid tissue

46
Q

Primary Gastric Lymphoma (MALT) is associated with which risk factor?

A

H. pylori

47
Q

Primary Gastric Lymphoma (MALT)….

a. list three common translocations
b. all these result in activation of _
c. what does this (b.) do?

A

a.
□ t(11;18)(q21;q21)
□ t(1;14)(p22;q32)
□ t(14;18)(q32;q21)

b. All translocations result in activation of NF-κB
c. Promotes B-cell growth and survival

48
Q

Describe the tx for primary gastric lymphoma (MALT)

A

§ eradication of the H. Pylori infection with a combination of antibiotics and proton pump inhibitor □ Amoxicillin + Clarithromycin + Omeprazole

§ Chemotherapy: with transformation to more aggressive lymphomas

49
Q

Carcinoid tumors of the stomach may be associated with which 5 things?

A 
§ Endocrine cell hyperplasia
 § Autoimmune chronic atrophic gastritis
 § MEN-1
 § Zollinger-Ellison syndrome (ZES)
 § PPI Use (Intense desmoplastic reaction in small bowel carcinoid)
50
Q

The symptoms of carcinoid tumors (of the stomach)…

a. depend on what?
b. Small Intestine tumors can lead to _
c. Duodenum tumors lead to _
d. Ileal tumors can cause what?

A

a. hormone production and location
b. obstruction
c. oversecretion of gastrin (can cause ZES)
d. Carcinoid syndrome (

51
Q

Symptoms of carcinoid syndrome are usually indicative of metastatic disease to which organ? and why?

A

The liver inactivates hormones, so if you have signs of hormone overproduction (e.g. carcinoid syndrome), you known met to liver

52
Q

Tx of carcinoid tumors of the stomach

A
  • Surgery

- Somatostatin analouges (Octreotride) for carcinoid syndrome

53
Q

The most common mesenchymal tumor of the abdomen (>50% in the stomach); Arises from the interstitial cell of Cajal (pacemaker cells)

A

Gastric Gastrointestinal Stromal Tumor (GGIST)

54
Q

GIST arise from what cell type?

A

interstitial cell of Cajal (pacemaker cells)

55
Q

Symptoms of GIST…

a. Large gastric masses cause damage by
b. Ulcerations may be present in which there is _ which can lead to _

A

a. mass effects

b. bleeding; anemia

56
Q

Describe the carney triad; and give the common age group

A

young females

  • Gastric GIST
  • Paraganglioma
  • Pulmonary chondroma
57
Q

Describe two gain of function mutations seen with GGIST; Germline mutations in the same genes are seen in _

A
  • KIT 75-80%
  • PDGFRA 8% (more common in the stomach)

These two mutations are mutually exclusive

Germ line mutations in the same genes are seen in familial GISTs

58
Q

Treatment of GIST…

a. surgical
b. if metastatic

A

a. complete resection

b. imatinib (tyrosine kinase inhib) ONLY if KIT or PDGFRA are mutated

CV (2 decks)

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