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GIR Test 4 > B5.071 - GI Tubal Cancers > Flashcards

B5.071 - GI Tubal Cancers Flashcards

1
Q

types of cancers in the esophagus

A

adenocarcinoma

squamous carcinoma

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2
Q

describe adenocarcinoma in the esophagus

A

distal esophagus

arises from Barretts

more common than squamous

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3
Q

describe squamous cancer of esophagus

A

middle/upper esophagus

not assoicated with barretts

more common world wide

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4
Q

describe barretts esophagus

A

replacement with columnar epithelium and goblet cells

resonse to repeated injury of reflux (10% of pts with GERD)

may develop dysplasia

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5
Q

what is a precursor lesion to adenocarcinoma

A

barretts esophagus

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6
Q
A

normal gastroesophageal junction

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7
Q
A

barretts esophagus

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8
Q
A

histo of barretts esophagus

note transition between esophageal squamous mucosa (L) and barrett metaplasia with abundant metplastic goblet cells

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9
Q
A

dysplasia in barretts esophagus

abrupt transition from barrett metaplasia to low grade dysplasia

note nuclear stratification and hyperchromasia

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10
Q
A

barrett

architectural irregularities, including gland within glad or “cribiform” profiles in high grade dysplasia

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11
Q

what do you do for barretts esophagus (goblet cells, no dysplasia)

A

surveillance biopsies

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12
Q

what do you do for barretts with low grade dysplasia

A

increased surveillance

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13
Q

what do you do for barretts with high grade dysplasia

A

surveillance if single focus

laser ablation, endoscopic resection

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14
Q

risk factors for esophageal adenocarcinoma

A

GERD, obesity, tobacco, alcohol, radiation

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15
Q

protective factors for esophageal adenocarcinoma

A

diets rich in fruits/veggies

H. pylori infx (causes atrophy of stomach, decreased acid secretion)

M>F 7:1

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16
Q

presentation of esophageal adenocarcinoma

A

long standing GERD
odynophagia or dysphagia

weight loss, vomiting. hematemesis

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17
Q

location of esophageal adenocarcinoma

A

distal 1/3 of esophagus

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18
Q

gross appearance of esoph. adenocarcinoma

A

flat/slightly raised lesion early to large, ulcerated mass later

often barretts mucosa around mass

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19
Q

microscopic appearance of esph. adenocarcinoma

A

gland formation, mucin production

may have slight ring formation

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20
Q
A

esophageal adenocarcinoma

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21
Q
A

esophageal adenoarcinoma

glands organized into back to back glands and mucin production

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22
Q
A

signet ring carcinoma

esoph adenocarcinoma

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23
Q

molecular alterations in esoph adenocarcinoma

A

start in barretts

early: p53, p16, APC inactivation
later: ERBB2/HER2

HER2 can be targeted by trastuzumab

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24
Q

treatment for esophageal adenocarcinoma

A

chemo/radiation

surgical resection (esophagectomy)

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25
Q

prognosis for esophageal adenocarcinoma

A

early has good prognosis (80% at 5 years)

late - less than 25% survivial at 5 years

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26
Q

risk factors for esoph squamous cell carcinoma

A

smoking, alcohol, esophageal injury, achalasia, frequent consumption of very hot beverages, radiation, lower SES

more common in iran, china, brazil, SA

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27
Q

precursor lesion for squamousc cell carcinoma of esophagus

A

squamous dysplasia, plaque like thickening

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28
Q

location and clinical presentation of squamous cell carcinoma of esophagus

A

mid esophagus or upper

dysphagia, odynophagia, obstruction

weight loss

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29
Q

gross appearance of esoph squamous cell carcinoma

A

mass like lesion, may protrude into lumen, ulcerate

may infiltrate and cause diffsue thickening

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30
Q

microscopic appearance of esoph squamou cell carcinoma

A

dysplastic/atypical squamous epithelium invading into submucosa or deeper

variably sized nests of tumor cells with epithelioid cells, ample eisinophilic cytoplasm, keratinization

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31
Q
A

low grade squamous dysplasia characterized by proliferation of neoplastic cells involving about 1/3 - 1/2 of thickness of epithelium

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32
Q
A

high grade dysplasia

dysplastic cells extend to surface of the epithelium and are associated with significant loss of surface maturation

squamous cell carcinoma of esophagus

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33
Q
A

esoph. squamous cell carcinoma

dysplastic cells with increased nucelus to cytoplasm ration

marked hyperchromatic nuclei, significant los of polarity and overlapping of cells and nuclei

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34
Q
A

esoph. squamous cell carcinoma

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35
Q
A

esoph. squamous cell carcinoma

well differentiated, with keratin production

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36
Q
A

esph. squamous cell carcinoma

poorly differentiated, keratin production

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37
Q

treatment for esoph. squamous cell carcinoma

A

chemo/radiation

surgery

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38
Q

prognosis for esoph. squamous cell carcinoma

A

early - 75%

late - 20%

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39
Q

types of cancer in the stomach

A

adenocarcinoma (most common)

lymphoma (H. plyori)

neuroendocrine (MEN1)

gastrointestinal stromal tumor (GIST)

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40
Q

risk factors for stomach adenocarcinoma

A

chronic gastritis (incluidng H. pylori)

inherited disorders (FAP, hereditary diffuse gastric cx)

more common in japan, chle, costa rica, eastern europe

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41
Q

presentation of stomach adenocarcinoma and prescursor lesion

A

often asymptomatic, vague sx

dyspepsia, dysphagia, nausea

metastatis often present at time of dx

precursor lesion

intestinal metaplaisa, gastric adenoma/dysplasia

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42
Q

intestinal type stomach adenocarcinoma features

A

gross: mass lesion, often ulcerated
micro: intiltrating atypical glands with mucin production

associated with intestinal metaplasia, FAP, H. pylori

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43
Q

diffuse type stomach adenocarcinoma features

A

gross: diffues thickening (linitis platsica)
micro: sheets of cells sometimes signet ring

associated with hereditary gastric cx

mutations in CDH1 (e-cadherin)

pts also have lobular breast cx

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44
Q
A

intestinal type stomach adenocarcinoma

45
Q
A

intestinal type adenocarcinoma

note: infiltrating glands with various degrees of differentiation

46
Q
A

diffuse type stomach adenocarcinoma

47
Q
A

diffuse type stomach adenocarcinoma

note - prominent intracytoplasmic mucin dorplet with enlarged, eccentrically located, flattened nucleus

48
Q

molecular alterations of stomach adenocarcinoma

A

mutation of TP53

may displat MSI

ERBB2 (HER2) in intestinal type

CDH1 lost in most diffuse type cancers

49
Q

treatment of stomach adenocarcinoma

A

resection

chemo

trastuzumab in HER2 overexpression

50
Q

lymphomas

A

extranodal lymphomas can occur anywhere

GI tract is common site (including stomach)

primary gastric lymphomas are 5% of gastiric malignancy

most are marginal zone B cell lymphoma (MALTomas, mucosa associated lymphoid tissue)

51
Q

risk factors for lymphoma

A

chronic inflammation, H. pylori (eradication of H pylori can resolve lymphoma in early stage)

52
Q

presentation/sx of stomach lymphoma

A

dyspepsia, epigastric pain, hematemesis, melena

53
Q

gross and microscopic appearance of stomach lymphoma

A

gross - thickening of wall of stomach, nodular mucosa

micro - diffuse sheets of lymphocytes, infiltrate the glandular epithelium, comprised of B lymphocytes (+CD20)

54
Q
A

MALT lymphoma

55
Q
A

MALT lymphoma

lymphoepithelial lesions with neoplastic lymphocytes surrounding and infiltrating gastric glands

56
Q

tx of stomach lymphoma

A

treat h pylori

chemo

57
Q

risk factors for carcinoid tumor

A

MEN-1, AMAG

58
Q

what is AMAG

A

antibodies to parietal cells

59
Q

presentation of carcinoid tumor

A

if functional - zollinger ellison syndrome

carcinoid syndrome - cutaneous flushing, bronchospasm, sweating, abdominal pain, diarrhea

60
Q

gross/histo of neuroendocrine tumors

A

gross - mass like lesion or nodule

histo - similar to pancreatic NE tumor, nests, trabeculae (cords), solid

cells are uniform, moderate cytoplasm, stippled or salt and pepper chromatin

61
Q
A

neuroendocrine tumor

62
Q
A

neuroendocrine tumor

63
Q

treatment of neuroendocrine tumor and prognosis

A

resection

prognosis - good cured after resection, sporadic may be more aggresseive

64
Q

what is considered a sporadic NE tumor

A

not associated with AMAG or MEN-1

65
Q

what is GIST

A

most common mesenchymal tumor of the abdomen

more than 1/2 arise in stomach

arise from interstitial cells of cajal within muscularis propria

66
Q

risk factor for GIST

A

NF1

67
Q

presentation of GIST

A

asymptomatic

sx due to mass effect when large, may ulcerate causing bleeding

68
Q

molecular features of GIST

A

most have activating mutation in KIT gene

some have activating mutation in PDGFRA

treatment with imatinib only works in tumors with mutations in these genes

69
Q

gross appearance of GIST

A

`solid, well circumscribed mass with pink-tan fleshy cut surfaces in the wall of the stomach

centered on muscularis propria, but may extend to involve mucosa

70
Q

micro appearance of GIST

A

spindled cells more common, epithelioid also possible

immunohistochemical stains for KIT and DOG1 usually positive

71
Q
A

GIST

72
Q
A

GIST

73
Q
A

GIST

note spindle cell type, typical prominent perinuclear vacuoles

74
Q
A

GIST

epithelioid type, arranged in broad sheets with occasional multinucelated cells

75
Q

treatment of GIST

A

resection

imatinib for unresectable, metastatic or recurrent that has KIT or PDGFRA mutations

76
Q

prognosis for GIST

A

depends on location, size and mitotic activity of GIST

77
Q

features of colon adenocarcinoma

A

3rd most common

behind prostate and lung in men

behind lung and breast in women

78
Q

presentation of colon adenocarcinoma

A

no signs/sx early

advanced on left side - change in bowel habits abdominal distention, hematochezia (if ulcerates)

right side - fatigue, weight loss, anemia

79
Q

risk factors for colon adenocarcinoma

A

physical inactivity

obesity

red meat/smoking/alcohol

high veggies decreases risk

80
Q

surveillance for colon adenocarcinoma

A

starts at 50, earlier if family hx

precursor lesion - adenomas

screening every 10 years, more if precursor found

81
Q

pathogenesis of colon adenocarcinoma (2 pathways)

A

stepwise collection of multiple mutations

APD/beta catenin pathway

microsattelite instable pathway

82
Q

describe the APC/beat catenin pathway

A

classic adenoma –> carcinoma sequence

precursor lesion often the tubular adenoma

more commonly left sided

83
Q

describe the microsattelite instable pathway in colon adenocarcinoma

A

deficiency in mismatch repair proteins

precursor lesion often the sessile serrate adenoma

do not respond well to traditional chemo

more commonly right sided

84
Q

important mutations in colon adenocarcinoma

A

KRAS

NRAS

BRAF

if mutated, less/no response to anti EGFR therapies like cetuximab

85
Q

important hereditary considerations for colon adenocarcinoma

A

FAP - germline APC considerations

Lynch syndrome (HNPCC, hereditary non polyposis colorectal cancer)

86
Q

describe FAP

A

many polyps which are tubular adenomas

follows traditional APC pathway

often have cancer at early age

87
Q

describe lynch syndrome

A

pts do no have multiple polyps

often cancer at earlier age

follows microsattelite instablle pathway

germline mutations in mismatch repair proteins

88
Q

what is a tubular adenoma

A

precursor to adenocarcinoma via the APC/beta catenin classical pathway

by definition has low grade dysplasia

microscopic shows tubular architecture with lowe grade dysplasia/cytologic atypia

low grade –> high grade –> invasive carcinoma

89
Q

what is sessile serrated adenoma

A

prescursor to adenocarcinoma, via the microsattelite instable pathway

micro shows serrated polyp with widened base

no cytologic atypia –> low garde atypia –> high grade atypia –> carcinoma

lesions without atypia though to have similar chance to progress as tubular adenoma; increased risk with cytologic atypia

90
Q

what is a hyperplastic polyp

A

not considered a precursor to adenocarcinoma

microscopic shows serrated polyp without dilation at the base

91
Q
A

tubular adenoma

smooth surface rounded glands

92
Q
A

villous adenoma with long sleder projections that are reminiscent of small intestinal villi

93
Q
A

dysplastic epithelia cells with increased nuc:cytoplasm ratio hyperchromatic and elongated nuceli and nucelar pseudostrarification

94
Q
A

sessile srrated adenoma lined by goblet cells without cytologic features of dysplaisa

extesnison of neoplastic process to crypts resulting in lateral growth. diff from hyperplastic polyp bc of the widened base

95
Q
A

tubular adenoma in colon

96
Q
A

tubular adenoma colon

97
Q
A

hyperplastic polyp

poly surface with irregular tufting of epithelial cells

98
Q
A

hyperplastic polyp

99
Q
A

hyperplastic polyp

100
Q

gross apearance of colon adenocarcinoma

A

often exophytic mass

may be present as diffues, circumferential thickening

101
Q

micro appearanc of colon adenocarcinoma

A

gland formation, mucin production

invasive islands of atypical glands

often has central necrosis

may have poorly differentiated or signet ring features

102
Q
A

colorectal adenocarcinoma

ulcerted rectal cancer (r)

cancer of sigmoid colon invading thru muscularis propria areas of chalky necrosis are present within colon (L)

103
Q
A

colon adenocarcinoma

some necrotic debris noted

104
Q
A

colon adenocarcinoma

few glands with nests of tumor cells

105
Q
A

colon adenocarcinoma

106
Q

colon adenocarcinoma treatment

A

resection

possible chemo

5-FU for non MSS

cetuximab (anti EGFR) for tumors without KRAS/NRAS/BRAF

107
Q

prognosis of adenocarcinoma of colon

A

based on stage

overall 5 yr is 65%

108
Q
A

GIR Test 4 (8 decks)

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