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GIR Test 4 > B5.071 GI Cancers: Tubal Gut > Flashcards

B5.071 GI Cancers: Tubal Gut Flashcards

1
Q

esophageal cancers

A

adenocarcinoma

squamous cell carcinoma

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2
Q

stomach cancers

A

adenocarcinoma
lymphoma (H.pylori)
neuroendocrine tumor (AMAG)
GIST

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3
Q

colon cancers

A

adenocarcinoma and precursor polyps

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4
Q

general differences between adenocarcinoma and squamous carcinoma in the esophagus

A 
adenocarcinoma:
-distal esophagus
-arises from Barrett's
-more common in US
squamous carcinoma:
-middle or upper esophagus
-NOT associated with Barrett's
-more common worldwide
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5
Q

how does Barrett’s contribute to esophageal adenocarcinoma

A

initiates metaplasia of the squamous epithelium due to repeated injury of reflux
-replacement with columnar epithelium and goblet cells
may develop dysplasia
-low > high > adenocarcinoma

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6
Q

histo appearance of barrett’s

A

transition between esophageal squamous mucosa and metaplasia with abundant metaplastic goblet cells

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7
Q

low grade barrett’s dysplasia

A

nuclear stratification and hyperchromasia

longer nuclei migrating up from base of cell

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8
Q

high grade barrett’s dysplasia

A

architectural irregularities

gland within gland, cribriform structure

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9
Q

treatment of barrett’s with high grade dysplasia

A

surveillance if single focus

laser ablation, endoscopic resection of mucosa

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10
Q

risk factors for esophageal adenocarcinoma

A

GERD
tobacco
alcohol
radiation

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11
Q

protective factors against esophageal adenocarcinoma

A

diets rich in fruits/veggies

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

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12
Q

epidemiology of esophageal adenocarcinoma

A

M:F = 7:1
rapidly increasing incidence in US
>50% of esophageal cancers in US

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13
Q

presentation of esophageal adenocarcinoma

A

long standing GERD
odynophagia or dysphagia
weight loss, vomiting, hematemesis

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14
Q

location of esophageal adenocarcinoma

A

distal 1/3 of esophagus

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15
Q

gross appearance of esophageal adenocarcinoma

A

flat/slightly raise lesion to large, ulcerated mass later

Barrett’s mucosa around mass

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16
Q

histo appearance of esophageal adenocarcinoma

A

gland formation and mucin production

may have signet ring formation

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17
Q

molecular alterations present in esophageal adenocarcinoma

A

start to accumulate in Barrett’s and increase in number until adenocarcinoma

early: p53, APC inactivation
later: amplification of ERBB2/HER2

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18
Q

treatment of esophageal adenocarcinoma

A

if HER2 amplification - trastuzamab
chemo/radiation
surgical resection (esophagectomy)

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19
Q

prognosis of esophageal adenocarcinoma

A

early: 80% survival at 5 years
later: less than 25% survival at 5 years

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20
Q

risk factors for esophageal squamous cell carcinoma

A 
smoking
alcohol
esophageal injury
achalasia
consumption of very hot beverages
lower socioeconomic background
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21
Q

epidemiology of squamous cell carcinoma

A

more common in Iran, China, Hong Kong, Brazil, South Africa

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22
Q

precursor lesions associated with squamous cell carcinoma

A

squamous dysplasia

plaque-like thickening

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23
Q

location of squamous cell carcinoma

A

mid esophagus (50-60%)
distal (30%)
upper (10-20%)

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24
Q

clinical presentation of squamous cell carcinoma

A

dysphagia, odynophagia, obstruction
weight loss
no heartburn usually

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25
Q

gross presentation of squamous cell carcinoma

A

mass like lesion, may protrude into lumen and ulcerate

may infiltrate and cause diffuse thickening

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26
Q

histo presentation of squamous cell carcinoma

A

dysplastic/atypical squamous epithelium invading into submucosa or deeper
variable sized nests of tumor cells with epithelioid cells, ample eosinophilic cytoplasm, keratinization (pink pearls)

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27
Q

low grade dysplasia of squamous cell carcinoma

A

proliferation of neoplastic cells involving about 1/3 to 1/2 of the thickness of the epithelium

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28
Q

high grade dysplasia of squamous cell carcinoma

A

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

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29
Q

cellular appearance of dysplasia of squamous cell carcinoma

A 
increased nuclear to cytoplasmic ratio
marked hyperchromatic nuclei
loss of polarity
overlapping
pleomorphic
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30
Q

treatment of squamous cell carcinoma

A

chemotherapy/radiation

surgery

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31
Q

prognosis of squamous cell carcinoma

A

early: 75% at 5 years
late: less than 20% at 5 years

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32
Q

risk factors for stomach adenocarcinoma

A 
chronic gastritis (H.pylori)
inherited disorders (FAP, hereditary diffuse gastric cancer)
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33
Q

epidemiology of stomach adenocarcinoma

A

more common in japan, chile, costa rica, eastern Europe

incidence has been decreasing in US, <2.5% of cancer deaths

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34
Q

presentation of stomach adenocarcinoma

A

often asymptomatic or with vague symptoms similar to chronic gastritis and peptic ulcer disease
-dyspepsia, dysphagia, nausea
weight loss
anorexia
early satiety at later stages
metastasis often present at time of diagnosis

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35
Q

precursor lesions associated with stomach adenocarcinoma

A

intestinal metaplasia

gastric adenoma/dysplasia

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36
Q

2 types of stomach adenocarcinoma

A

intestinal type

diffuse type

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37
Q

gross appearance of intestinal type stomach adenocarcinoma

A

mass lesion, often ulcerated

38
Q

microscopic appearance of intestinal type stomach adenocarcinoma

A

infiltrating atypical glands with mucin production

39
Q

associations with intestinal type stomach adenocarcinoma

A

intestinal metaplasia
FAP
h. pylori

40
Q

gross appearance of diffuse type stomach adenocarcinoma

A

diffuse thickening (linitis plastic)
whole stomach wall involved
loses normal folding pattern, looks shrunken

41
Q

microscopic appearance of diffuse type stomach adenocarcinoma

A

sheets of cells

sometimes signet ring (prominent intracytoplasmic mucin droplet with enlarged eccentrically located, flattened nucleus)

42
Q

associations with diffuse type stomach adenocarcinoma

A

mutations in CDH1 (e-cadherin)

patients also have risk of lobular breast cancer

43
Q

molecular alterations in stomach adenocarcinoma

A

TP53 in 40% of all
may display microsatellite instability (MSI)
ERBB2 (HER2) in intestinal type
CDH1 lost in most diffuse type

44
Q

treatment of stomach adenocarcinoma

A

resection

chemo (trastusamab for HER2)

45
Q

prognosis of stomach adenocarcinoma

A

early: 90% 5 year survival

late/advanced: 20% 5 year survival

46
Q

characterize the occurrence of stomach lymphoma

A 
extranodal lymphomas can occur anywhere
GI tract is a common site
primary gastric lymphomas are 5% of gastric malignancy
-marginal zone B cell lymphoma
-called MALTomas
47
Q

risk factors for stomach lymphoma

A

chronic inflammation

H. pylori infection (eradication resolved lymphoma if at an early stage)

48
Q

presentation/symptoms of stomach lymphoma

A

dyspepsia
epigastric pain
hematemesis
melena

49
Q

gross appearance of stomach lymphoma

A

thickening of wall of stomach

nodular mucosa

50
Q

microscopic appearance of stomach lymphoma

A

diffuse of lymphocytes
lymphocytes infiltrate the glandular epithelium
comprised of B lymphocytes

51
Q

treatment of stomach lymphoma

A

treat H.pylori if present

chemo

52
Q

prognosis of stomach lymphoma

A

90% 5 year survival

53
Q

risk factors for stomach carcinoid tumor

A

MEN-I

autoimmune atrophic gastritis (AMAG)

54
Q

presentation of stomach carcinoid tumor

A

if functional: zollinger-ellison syndrome, acid hypersecretion
carcinoid syndrome in < 10%

55
Q

symptoms of carcinoid syndrome

A 
cutaneous flushing
sweating
bronchospasm
abdominal pain
diarrhea
56
Q

gross appearance of stomach carcinoid tumor

A

mass like lesion or nodule

57
Q

microscopic appearance of stomach carcinoid tumor

A

similar to pancreatic NET
many patterns of growth: nests, trabeculae (cords), solid
cells are uniform, moderate cytoplasm, stippled, or salt and pepper chromatin

58
Q

treatment of stomach carcinoid tumor

A

resection

59
Q

prognosis of stomach carcinoid tumor

A 
generally good (especially when associated with AMAG), considered cured after resection
sporadic tumors may be more aggressive
60
Q

characterize a gastrointestinal stromal tumor (GIST)

A

most common mesenchymal tumor of the abdomen, more than half in the stomach
arise from interstitial cells of Cajal within the muscularis propria

61
Q

risk factors for GIST

A

NF1

62
Q

presentation of GIST

A

asymptomatic when small

symptoms due to mass effects when large, may ulcerate causing bleeding

63
Q

molecular characteristics of GIST

A

most (75-80%) have activation mutations in KIT gene
some (8%) have activating mutations in PDGFRA
treatment with imatinib works in tumors with mutations in these genes

64
Q

gross appearance of GIST

A

solid, well circumscribed mass with pink-tan fleshy cute surface in the wall of the stomach
centered on muscularis propria, but may extend to involve mucosa

65
Q

microscopic appearance of GIST

A

spindled cells more common, but epithelioid also possible
prominent perinuclear vacuoles (artifact of fixation)
immunohistochemical stains for KIT and DOG1 usually positive

66
Q

treatment of GIST

A

resection

imatinib for unresectable, metastatic, or recurrent GISTs with KIT of PDGFRA mutations

67
Q

prognosis of GIST

A

depends on location, size, and mitotic activity

bigger and more mitotic activity = worse prognosis

68
Q

epidemiology of colon adenocarcinoma

A

3rd most common cancer in US

2nd leading cause of cancer deaths in US

69
Q

presentation of colon adenocarcinoma

A

no signs/symptoms early
advanced left sided carcinomas may present with change in bowel habits, abdominal distention, hematochezia
advanced right sided carcinomas: fatigue, weight loss, anemia

70
Q

risk factors for colon adenocarcinoma

A 
fam fistory
inactivity
IBD
obesity
red meat
smoking
alcohol
71
Q

protective factors against colon adenocarcinoma

A

high veggie consumption
oral contraceptive use
estrogen replacement
multivitamin w folic acid

72
Q

prevention of colon adenocarcinoma

A

surveillance important for prevention
start at age 50; earlier if positive family history
every 10 years, more often if precursor lesions found

73
Q

2 pathways for molecular pathogenesis of colon adenocarcinoma

A

APC/ beta catenin pathway

MSI pathway

74
Q

APC/beta catenin pathway

A

classic adenoma > carcinoma sequence
precursor lesion often the tubular adenoma
more commonly left sided

75
Q

MSI pathways

A

deficiency in mismatch repair proteins
precursor lesions often the sessile serrated adenoma
do not respond as well to traditional chemo
more commonly right sided

76
Q

important mutations in colon adenocarcinoma

A

KRAS, NRAS, and BRAF

if mutated, less/no response to anti-EGFR therapies

77
Q

familial adenosis polyposis

A

germline APC mutation
many polyps which are tubular adenomas
follows traditional APC pathways
often have cancer at early age

78
Q

lynch syndrome/HNPCC (hereditary non-polyposis colorectal cancer)

A

patients do NOT have multiple polyps
cancer at an early age
follow MSI pathway (germline mutations in mismatch repair proteins)

79
Q

types of colon polyps

A

tubular adenoma
sessile serrated adenoma
hyperplastic polyp

80
Q

tubular adenoma

A

precursor to adenocarcinoma via APC/beta catenin pathway
low grade dysplasia
microscopic shows tubular architecture with low grade dysplasia/cytologic atypia

81
Q

sessile serrated adenoma

A

precursor to adenocarcinoma via MSA pathway
microscopic shows serrated polyp with widened base
lesions without atypia thought to have similar chance to progress as tubular adenoma; increased risk with cytologic atypia

82
Q

hyperplastic polyp

A

not a precursor to adenocarcinoma

serrated polyp without dilation at the base

83
Q

histo of tubular adenoma

A

smooth surface
rounded glands
active inflammation occasionally present in adenomas causing crypt dilation and rupture

84
Q

histo of villous adenoma

A

long, slender projections that are reminiscent of small intestinal villi

85
Q

histo of dysplastic epithelial cells

A

increased N:C ratio
hyperchromatic
elongated nuclei
nuclear pseudo stratification

86
Q

histo of sessile serrated adenoma

A

goblet cells without features of dysplasia

extension of the neoplastic process to the crypts, resulting in lateral growth

87
Q

histo of hyperplastic polyp

A

irregular tufting of epithelial cells due to epithelial overcrowding
serrated architecture when crypts are cut in cross section

88
Q

gross appearance of colon adenocarcinoma

A

exophytic mass

diffuse, circumferential thickening

89
Q

microscopic appearance of colon adenocarcinoma

A

gland formation, mucin production
invasive islands of atypical glands
central necrosis
may be poorly differentiated or have signet ring features

90
Q

treatment of colon adenocarcinoma

A

resection
possible chemo:
5-FU for non MSI tumors
cetuximab (anti-EGFR) for tumors without KRAS, NRAS, or BRAF

91
Q

prognosis of colon adenocarcinoma

A

based on stage

overall 5 year survival (65%)

GIR Test 4 (20 decks)

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