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Gastrointes 3 > 012215 neoplasms sm and large intes > Flashcards

012215 neoplasms sm and large intes Flashcards

1
Q

prevalence of neoplasms in sm intes

A

low

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2
Q

most common neoplasm in sm intes

A

adenoma (near ampulla)

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3
Q

risk factors for sm intes adenocarcinoma

A

Crohn’s dis
adenomas
celiac dis
familial polyposis syndrome

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4
Q

tx for GIST

A

imatinib (85% have c-kit mutations)

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5
Q

immunohistochemical markers for GIST

A

CD117 (c-kit)
DOG1 (specific marker)
CD34

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6
Q

mutations in GIST

A

c-kit (80%)
PDGFRA (5-10%)

both are tyrosine kinase receptors–gain of fxn

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7
Q

most common non-epithelial (soft tissue) tumor in GI tract

A

GIST

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8
Q

sm intes neoplasms

A

adenoma (most common)
carcinoid and adenocarcinoma
mesenchymal tumors (rare)-lipoma, GIST, lymphoma

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9
Q

polyp

A

epithelium derived tumor mass which protrudes into gut lumen

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10
Q

two types of polyps-shape wise

A

pedunculated

sessile

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11
Q

in terms of malignant potential, what are the two types of polyps

A

non-neoplastic polyp (abnormal mucosal maturation, inflam, distorted architecture)–no malignant potential

neoplastic polyp-due to prolferation and dysplasia (adenomas). precursor of carcinoma

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12
Q

types of non-neoplastic poyps

A

hamartomatous
inflammatory
lymphoid

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13
Q

hamartoma

A

mature, histologically normal elements from the site growing in disorganized manner

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14
Q

chriostomas

A

haphazard tissue in wrong location (as opposed to hamartoma)

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15
Q

junvenile polyps

A

hamartomatous polyp

abundant cystically dilated glands usually w inflam

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16
Q

juvenile polyposis syndrome

A

multiple juvenile polyps
autosomal dominant mutations
increased risk of adenomas, colon cancer

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17
Q

Peutz Jeghers polyps

A

hamartomatous polyps

no malignant potential

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18
Q

Peutz-Jeghers syndrome

A

mutliple GI polyps–hamartomatous polyps
autosomal dominant
hyperpigmentation/freckles-appearing-mucosal (mouth) and cutaneous (fingers)
increased risk of cancer of pancreas, breast, lung, ovary, uterus

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19
Q

inflammatory polyps

A

regnerating mucosa adjacent to ulceration (severe IBD)

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20
Q

lymphoid polyps

A

mucosal bumps caused by intramucosal lymphoid follicles (normal)

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21
Q

types of colon polyps

A

serrated polyps:
hyperplastic polyp (benign)
sessile serrated polyp (malignant potential)

adenomatous polyp/adenoma (precursor to cancer)

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22
Q

serrated lumina

A

serrated polyps

23
Q

sessile serrated tumors

A 
high malignant potential
interval tumors--develop more quickly
BRAF V600E mutations
methylation (tumor suppressor genes shut down)
can have microsatellite instability
horizontal growth
24
Q

how do adenomatous polyps/adenomas arise

A

epithelial proliferative dysplasia

25
Q

epidemiology of adenomatous polyps

A

common-after age 60

26
Q

3 architectural types of adenomas

A

tubular
villous
tubulovillous

27
Q

tubular adenoma morphology

A

tubular glands

small, pedunculated

28
Q

villous adenoma

A

villous projections

large, sessile

29
Q

clinical symptoms of adenomatous polyps

A

asymptomatic or present with rectal bleeding or anemia

30
Q

tx for adenoma

A

complete resection (regardless of whether carcinoma is present)

31
Q

iron defic anemia in older male signifies

A

colon cancer unless proven otherwise

32
Q

almost all colon cancers have mutations in what gene?

A

APC (tumor suppressor gene)

for those without an APC mutation, 50% of them have beta-catenin mutations

33
Q

depth of invasion of colorectal carcinomas

A

TIS (in situ)–within mucosa
T1–submucosa
T2–muscularis propria
T3–serosa

34
Q

staging colon carcinoma

A

stage 0: in situ carcinoma

stage I: T1 or T2, N0,M0
stage II: T3 or T4, N0, M0
stage III: any T, positive nodes, M0 (N1=1-3, N2=4 or more)
stage IV: any T, any N, M1 (distant mestasis)

35
Q

currently the only proven prognostic marker to identify pts with aggressive colon carcinoma

A

TNM staging

36
Q

biomarkers to guide adjuvant therapy–types?

A

prognostic-provide info about pts overall outcome regardless of therapy

predictive-give info about effects of particular therapeutic intervention

37
Q

what is a key target in cancer?

A

EGFR (turns on cell cycle-it’s a transmembrane tysorine kinase receptor)

38
Q

what pathway is activated by EGFR

A

RAS-RAF-MAP kinase

and two others

39
Q

therapeutic options of colorectal carcinoma

A

targeted therapy for metastatic tumors:
bevacizumab
ceubixmab
panitumumab

if targeted therapy is not effective, then do traditional chemo

surgery (if earlier stage, can completely resect out)

40
Q

what mutations result in decreased efficacy of EGFR monocloncal antibody therapy?

A

KRAS

BRAF

41
Q

familial adenomatous polyposis is inherited in what fashion?

A

autosomal dominant

42
Q

mininum of how many polyps present is needed to be familial adenamtous polyposis?

A

100

43
Q

outlook for FAP

A

colon adenocarcinoma occurs in about 100%

so prophylactic colectomy is required

44
Q

what genetic mutation exists in FAP?

A

APC gene

but 25% of FAP pts have no family hx (new mutations)

45
Q

MYH associated polyposis

A

hereditary colorectal cancer syndrome that has phenotypic overlap with FAP

typically 20-100 adenomatous polyps

autosomal recessive inheritance
due to mutation in MYH gene

46
Q

MYH protein’s role

A

DNA repair protein–base excision repair

47
Q

Lynch syndrome/hereditary nonpolyposis colorectal cancer

A

increased risk of colorectal cancer and extraintestinal cancer. RISK FOR SECOND PRIMARY CANCER (endometrial cancer)

ADENOMAS occur earlier than normal population
COLONIC CARCINOMAS are often MULTIPLE and are not necessarily associated with adenomas
GENETIC DEFECT involves DNA mismatch repair genes (microsatelitte instability pathway)

48
Q

what four genes can be defective in Lynch syndrome/hereditary nonpolyposis colorectal cancer

A

MLH1
PMS2
MSH2
MSH6

latter two identify mismatch. first two fix the mismatch

49
Q

how can you clinically analyze mismatch repair of LYnch syndrome?

A

immunohistochemistry staining for the four different gene/proteins

50
Q

microsatellite instability can be used how?

A

microsatelittes are prone to mismatches, so they are sensitive markers of defective mismatch repair fxn

51
Q

how can microsatellite stability predict prognosis?

A

prognosis for high microsatelitte instability is better long term

52
Q

with regards to adjuvant therapy/chemo, should microsatelittle stable or instable pts get it?

A

microsatelittle stability

53
Q

majority of colorectal cancers have what microsatelittle instability phenotype?

A

microsatelittle stable/low instability

Gastrointes 3 (17 decks)

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