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G.I & Nutrition > Other GI Tumors > Flashcards

Other GI Tumors Flashcards

1
Q

What kind of cells make up serosa?

A

mesothelial cells –> if none, it is called an adventitia

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2
Q

Smooth muscle tumors of GI tract

A

leiomyoma and leiomyosarcoma (rare in GI)

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3
Q

Most common mesenchymal tumor of esophagus?

A

leiomyoma –> lower 1/3 of esophagus, often presents with dysphagia

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4
Q

What is the term to describe multiple leiomyomas in the esophagus?

A

esophageal leiomyomatosis

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5
Q

How do leiomyomas appear on colonoscopy?

A

incidental small nodules

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6
Q

How common are leiomyomas in stomach and small intestine?

A

rare

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7
Q

GIST stands for…

A

gastrointestinal stromal tumor

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8
Q

What is the most common mesenchymal tumor of entire GI tract?

A

GIST –> most in stomach/small intestine vs leiomyoma in esophagus and colon

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9
Q

Immunohistochemistry findings in GIST

A

ckit/CD117 + and driven by KIT, PDGRFA/SDH mutations

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10
Q

What cells do GIST tumors derive from/differentiate to?

A

interstitial cells of Cajal

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11
Q

In which GI layers do GIST occur?

A

near the 2 plexi so around MM/submucosa/MP –> will appear submucosal vs epithelial

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12
Q

GIST morphologies

A

spindle cell (ice cream cone), epithelioid (plump, prominent nucleoli)

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13
Q

T/F a large portion of GISTs do not stain with Kit

A

F –> a very small minority: 5% do not stain

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14
Q

c-Kit negative GISTs are more likely to have what morphology and what mutations?

A

epithelioid morphology and PDGFRA mutation

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15
Q

What IHC might be used in c-kit negative cases?

A

dog1

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16
Q

Tx of GIST

A

surgical resection, imatinib (based on mutation), sunitibe malate for those with imatinib resistance

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17
Q

80% of GIST have a mutation in what gene?

A

KIT

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18
Q

5-7% of GIST have a mutation in what gene?

A

PDGFRA

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19
Q

What are wildtype GIST?

A

10-15% without a mutation in either KIT or PDGFRA

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20
Q

What kinds of people have SDH mutations that lead to GIST?

A

pediatric gastric GIST

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21
Q

T/F Imatinib response in GIST depends on the specific mutation you have.

A

T –> e.g. Exon 11 kit is best response and exon 18 PDGFRA is resistant

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22
Q

What is better? gastric or small intestine GIST

A

gastric GISTs do better

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23
Q

3 factors that determine GIST behavior

A

location, size, mitotic count

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24
Q

Benign or malignant? stomach gists

A

20% malignant

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25
Q

Benign or malignant? small intestine gists

A

50% malignant

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26
Q

Benign or malignant? esophagus/colon gists

A

malignant

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27
Q

2 important hereditary associations with GIST

A

NF1, Carney’s triad

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28
Q

What is Carney’s triad?

A

young females with gastric epithelioid GISTs, pulmonary chondroma/hamartomas, paraganglionomas

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29
Q

How can you tell the difference between a neuroendocrine cell and a paneth cell on histology?

A

neuroendocrine cells have granules facing away from lumen

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30
Q

2 types of neuroendocrine tumors

A

well differentiated/carcinoid and poorly differentiated

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31
Q

T/F Well-differentiated NETs are functional

A

F –> some can be functional and secrete hormone and others can be non functional

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32
Q

2 types of poorly differentiated NETs

A

small cell and large cell (more cytoplasm, less common)

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33
Q

Endoscopic view of NET

A

yellow tinged sessile nodules with intact surface +/- erosion

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34
Q

In which GI layer do NETs develop?

A

mucosal/submucosal junction

35
Q

Cytology of NETs

A

salt n pepper nuclear chromatin

36
Q

NET IHC (3) markers

A

synaptophysin, chromogranin, CD56

37
Q

Are functional NETs of the luminal GI tract more or less aggressive than tumors of the pancreas or nonfunctional NETs?

A

more aggressive

38
Q

What is carcinoid syndrome caused by?

A

increased serotonin produced by an NET

39
Q

Carcinoid syndrome clinical findings

A

serotonin –> flushing of skin, diarrhea/cramps, right side heart disease via fibrosis of tricuspid, increased 5-hiaa urine execretion

40
Q

Why does carcinoid syndrome usually imply metastatic disease?

A

when the primary tumor is in the GI tract, serotonin is inactivated in liver by first pass —> carcinoid presents once there are mets to the liver and serotonin can no longer be broken down

41
Q

T/F gastrinomas arise from the duodenum

A

F –> 50% pancreas, 50% duodenum 1st/2nd parts

42
Q

What syndrome is associated with gastrinomas?

A

MEN1 (25%), ZES (peptic ulcers, enlarge rugae, diarrhea)

43
Q

T/F gastrinomas are usually indolent

A

F –> 70% metastasize aggressively –> also, no first pass metabolism since degraded in kidney –> therefore, can have a funcitonal tumor without a met

44
Q

Dx of gastrinoma

A

increase in serum gastrin

45
Q

Most common site for extranodal lymphomas

A

GI tract (stomach > small intestine/colon)

46
Q

Predisposing factors for extranodal lymphomas

A

Hpylori, celiac disease, IBD, immunodeficiency

47
Q

3 groups of low grade B cell lymphomas

A

marginal zone/MALT, follicular, mantle cell

48
Q

2 groups of high grade B cell lymphomas

A

diffuse large B-cell, Burkitt

49
Q

T cell lymphoma of GI tract

A

enteropathy type T-cell lymphoma

50
Q

B cell migration path

A

bone marrow –> naive cells of the mantle zone –> germinal center –> paracortex or marginal zone or die

51
Q

Most common lymphoma in stomach?

A

MALT

52
Q

Most common lymphoma in small bowel?

A

follicular

53
Q

Most common lymphoma in colon?

A

mantle zone

54
Q

Most common association with MALT lymphoma?

A

Hpylori

55
Q

How aggressive is MALT lymphoma?

A

indolent –> 5 year survival = 90 5, 75% respond to hpylori eradication via antibiotics

56
Q

3 features of MALT lymphomas that do not respond to Hpylori eradication?

A

t(11:18) API2-MALT1, transformation to DLBCL, spread byeond stomach

  • can try surgery, radiation, chemo
57
Q

Most important MALT lymphoma translocation

A

t(11:18) API2-MALT1 aka the one that persists after Hpylori is treated

58
Q

MALT lymphoma histology

A

intact germinal center, expanded marginal zone, lymphoepithelial lesion, monocytoid halo around cell

59
Q

2 presentations of follicular lymphoma

A

mass (duodenum, favorable), 50% as lymphomatous polyposis (polyps)

60
Q

Diff Dx of lymphomatous polyposis

A

reactive lymphoid hyperplasia (HIV/immunodeficiency), Mantle zone lymphoma of colon, follicular lymphoma (50% of them present like this, usually in small bowel)

61
Q

Most common translocation in follicular lymphoma?

A

t(14:18) BCL2

62
Q

Function of BCL2

A

prevents cells from undergoing apoptosis

63
Q

How do you distinguish follicular lymphoma from follicular hyperplasia?

A

BCL2+ vs BCL2-

64
Q

Can you dx lymphoma based on BCL2?

A

no –> it is normally expressed in non-germinal center cells…but if it’s in germinal center, it’s neoplastic

65
Q

How does mantle cell lymphoma present?

A

colonic lymphomatous polyposis

66
Q

Mantle cell lymphoma prognosis

A

terrible –> it’s very aggressive

67
Q

Histologic appearance of mantle cell lymphoma

A

colon with vaguely nodular lymphoid aggregate with monomorphic cells/round, slightly celfted

68
Q

Main translocation in mantle cell lymphoma?

A

t(11,14) cyclin d1/BCL1-Ig

69
Q

What is cyclin d1?

A

promoter of cell cycle progression overexpressed in mantle cell lymphoma

70
Q

Dx of mantle cell lymphoma?

A

IHC of NUCLEAR cyclin D1

71
Q

Most common lymphoma of the whole GI tract?

A

DLBCL

72
Q

DLBCL prognosis

A

bad –> very aggressive

73
Q

DLBCL morphology

A

large lymphocytes with a high proliferation rate

74
Q

Burkitt lymphoma derives what cells?

A

germinal center B cells

75
Q

Morphology of Burkitt

A

starry sky due to tingible body macrophages in a sea of medium lymphocytes

76
Q

Burkitt prognosis

A

high grade/aggressive

77
Q

Most common translocation in Burkitt?

A

t(8:14) c-myc-IgH (80% of cases)

78
Q

What kind of Burkitt presents in abdomen?

A

non-endemic sporadic variant –> adult abdomens (5% EBV+)

79
Q

What lymphoma has a high association with celiac disease?

A

enteropathy type T cell –> jejunum and ileum

80
Q

What condition often precedes enteropathy type t cell lymphoma?

A

refractory sprue

81
Q

Prognosis of enteropathy type t cell lymphoma?

A

aggressive –> median survival of 3 months

82
Q

Histologic presentation of enteropathy type t cell lymphoma

A

variable sized lymphocytes (some are intraepithelial) with mixed inflammatory background

83
Q

Dx of enteropathy type t cell lymphoma

A

cellular atypia, aberrant tcell antigen expression (loss of CD8), clonality

G.I & Nutrition (43 decks)

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