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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
gross presentation of squamous cell carcinoma
mass like lesion, may protrude into lumen and ulcerate | may infiltrate and cause diffuse thickening
26
histo presentation of squamous cell carcinoma
dysplastic/atypical squamous epithelium invading into submucosa or deeper variable sized nests of tumor cells with epithelioid cells, ample eosinophilic cytoplasm, keratinization (pink pearls)
27
low grade dysplasia of squamous cell carcinoma
proliferation of neoplastic cells involving about 1/3 to 1/2 of the thickness of the epithelium
28
high grade dysplasia of squamous cell carcinoma
dysplastic cells extend to the surface of the epithelium and are associated with significant loss of surface maturation
29
cellular appearance of dysplasia of squamous cell carcinoma
``` increased nuclear to cytoplasmic ratio marked hyperchromatic nuclei loss of polarity overlapping pleomorphic ```
30
treatment of squamous cell carcinoma
chemotherapy/radiation | surgery
31
prognosis of squamous cell carcinoma
early: 75% at 5 years late: less than 20% at 5 years
32
risk factors for stomach adenocarcinoma
``` chronic gastritis (H.pylori) inherited disorders (FAP, hereditary diffuse gastric cancer) ```
33
epidemiology of stomach adenocarcinoma
more common in japan, chile, costa rica, eastern Europe | incidence has been decreasing in US, <2.5% of cancer deaths
34
presentation of stomach adenocarcinoma
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
35
precursor lesions associated with stomach adenocarcinoma
intestinal metaplasia | gastric adenoma/dysplasia
36
2 types of stomach adenocarcinoma
intestinal type | diffuse type
37
gross appearance of intestinal type stomach adenocarcinoma
mass lesion, often ulcerated
38
microscopic appearance of intestinal type stomach adenocarcinoma
infiltrating atypical glands with mucin production
39
associations with intestinal type stomach adenocarcinoma
intestinal metaplasia FAP h. pylori
40
gross appearance of diffuse type stomach adenocarcinoma
diffuse thickening (linitis plastic) whole stomach wall involved loses normal folding pattern, looks shrunken
41
microscopic appearance of diffuse type stomach adenocarcinoma
sheets of cells | sometimes signet ring (prominent intracytoplasmic mucin droplet with enlarged eccentrically located, flattened nucleus)
42
associations with diffuse type stomach adenocarcinoma
mutations in CDH1 (e-cadherin) | patients also have risk of lobular breast cancer
43
molecular alterations in stomach adenocarcinoma
TP53 in 40% of all may display microsatellite instability (MSI) ERBB2 (HER2) in intestinal type CDH1 lost in most diffuse type
44
treatment of stomach adenocarcinoma
resection | chemo (trastusamab for HER2)
45
prognosis of stomach adenocarcinoma
early: 90% 5 year survival | late/advanced: 20% 5 year survival
46
characterize the occurrence of stomach lymphoma
``` 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
risk factors for stomach lymphoma
chronic inflammation | H. pylori infection (eradication resolved lymphoma if at an early stage)
48
presentation/symptoms of stomach lymphoma
dyspepsia epigastric pain hematemesis melena
49
gross appearance of stomach lymphoma
thickening of wall of stomach | nodular mucosa
50
microscopic appearance of stomach lymphoma
diffuse of lymphocytes lymphocytes infiltrate the glandular epithelium comprised of B lymphocytes
51
treatment of stomach lymphoma
treat H.pylori if present | chemo
52
prognosis of stomach lymphoma
90% 5 year survival
53
risk factors for stomach carcinoid tumor
MEN-I | autoimmune atrophic gastritis (AMAG)
54
presentation of stomach carcinoid tumor
if functional: zollinger-ellison syndrome, acid hypersecretion carcinoid syndrome in < 10%
55
symptoms of carcinoid syndrome
``` cutaneous flushing sweating bronchospasm abdominal pain diarrhea ```
56
gross appearance of stomach carcinoid tumor
mass like lesion or nodule
57
microscopic appearance of stomach carcinoid tumor
similar to pancreatic NET many patterns of growth: nests, trabeculae (cords), solid cells are uniform, moderate cytoplasm, stippled, or salt and pepper chromatin
58
treatment of stomach carcinoid tumor
resection
59
prognosis of stomach carcinoid tumor
``` generally good (especially when associated with AMAG), considered cured after resection sporadic tumors may be more aggressive ```
60
characterize a gastrointestinal stromal tumor (GIST)
most common mesenchymal tumor of the abdomen, more than half in the stomach arise from interstitial cells of Cajal within the muscularis propria
61
risk factors for GIST
NF1
62
presentation of GIST
asymptomatic when small | symptoms due to mass effects when large, may ulcerate causing bleeding
63
molecular characteristics of GIST
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
gross appearance of GIST
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
microscopic appearance of GIST
spindled cells more common, but epithelioid also possible prominent perinuclear vacuoles (artifact of fixation) immunohistochemical stains for KIT and DOG1 usually positive
66
treatment of GIST
resection | imatinib for unresectable, metastatic, or recurrent GISTs with KIT of PDGFRA mutations
67
prognosis of GIST
depends on location, size, and mitotic activity | bigger and more mitotic activity = worse prognosis
68
epidemiology of colon adenocarcinoma
3rd most common cancer in US | 2nd leading cause of cancer deaths in US
69
presentation of colon adenocarcinoma
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
risk factors for colon adenocarcinoma
``` fam fistory inactivity IBD obesity red meat smoking alcohol ```
71
protective factors against colon adenocarcinoma
high veggie consumption oral contraceptive use estrogen replacement multivitamin w folic acid
72
prevention of colon adenocarcinoma
surveillance important for prevention start at age 50; earlier if positive family history every 10 years, more often if precursor lesions found
73
2 pathways for molecular pathogenesis of colon adenocarcinoma
APC/ beta catenin pathway | MSI pathway
74
APC/beta catenin pathway
classic adenoma > carcinoma sequence precursor lesion often the tubular adenoma more commonly left sided
75
MSI pathways
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
important mutations in colon adenocarcinoma
KRAS, NRAS, and BRAF | if mutated, less/no response to anti-EGFR therapies
77
familial adenosis polyposis
germline APC mutation many polyps which are tubular adenomas follows traditional APC pathways often have cancer at early age
78
lynch syndrome/HNPCC (hereditary non-polyposis colorectal cancer)
patients do NOT have multiple polyps cancer at an early age follow MSI pathway (germline mutations in mismatch repair proteins)
79
types of colon polyps
tubular adenoma sessile serrated adenoma hyperplastic polyp
80
tubular adenoma
precursor to adenocarcinoma via APC/beta catenin pathway low grade dysplasia microscopic shows tubular architecture with low grade dysplasia/cytologic atypia
81
sessile serrated adenoma
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
hyperplastic polyp
not a precursor to adenocarcinoma | serrated polyp without dilation at the base
83
histo of tubular adenoma
smooth surface rounded glands active inflammation occasionally present in adenomas causing crypt dilation and rupture
84
histo of villous adenoma
long, slender projections that are reminiscent of small intestinal villi
85
histo of dysplastic epithelial cells
increased N:C ratio hyperchromatic elongated nuclei nuclear pseudo stratification
86
histo of sessile serrated adenoma
goblet cells without features of dysplasia | extension of the neoplastic process to the crypts, resulting in lateral growth
87
histo of hyperplastic polyp
irregular tufting of epithelial cells due to epithelial overcrowding serrated architecture when crypts are cut in cross section
88
gross appearance of colon adenocarcinoma
exophytic mass | diffuse, circumferential thickening
89
microscopic appearance of colon adenocarcinoma
gland formation, mucin production invasive islands of atypical glands central necrosis may be poorly differentiated or have signet ring features
90
treatment of colon adenocarcinoma
resection possible chemo: 5-FU for non MSI tumors cetuximab (anti-EGFR) for tumors without KRAS, NRAS, or BRAF
91
prognosis of colon adenocarcinoma
based on stage | overall 5 year survival (65%)

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