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Bloc E - GI & Metabolism > Feb23 M1,2-Pathology GI-neoplasia > Flashcards

Feb23 M1,2-Pathology GI-neoplasia Flashcards

1
Q

2 cancers in GI tract in general

A

carcinomas (malignant epithelial neoplasm)
1. adenoCA (CA with glandular differentiation)
2. squamous cell CA (SCC): CA with squamous cell differentiation
(and neuroendocrine CA also possible)

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2
Q

charact of adenoCA glandular diff

A
  • prod of glands

- prod of mucous IC or EC (epith cells surround the space of mucous prod)

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3
Q

charact of adenoCA (malignant features)

A
  • architecture (irregular shape, infiltrating pattern)
  • cytology (high NC ratio, prominent nucleoli, large cells w irregular size and shape, irregular nuclei)
  • necrosis
  • frequent mitoses
  • desmoplastic stroma
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4
Q

desmoplasia def (cancer feature)

A

promoted formation of CT between tumor cells (has fibroblasts producing collagen + vessels feeding)

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5
Q

SCC differentiation charact

A
  • keratinocyte-like cells (polygonal, pavement-like, eosinophilic
  • intercellular bridges
  • keratinization
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6
Q

SS malignant features

A
  • architecture: 1. in situ: tumor above BM, normal architecture, malignant cytology 2. invasive SCC: irregulary shaped sheets of cells, infiltrating pattern
  • cytology (irregular nucleus and cells, prominent nucleoli, high NC)
  • necrosis
  • mitoses
  • desmoplastic stroma
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7
Q

invasive SCC charact + stroma diff with adenoCA

A

polygonal cells invading desmoplastic stroma (exact same look as adenoCA stroma). focal keratin formation

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8
Q

invasive SCC cells charact

A
  • intercellular borders
  • desmosomal junction
  • keratinization
  • intercell bridges
  • cytological atypia
  • prominent nucleoli
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9
Q

precursor lesions of adenoCA

A
  1. intestinal metaplasia followed by dysplasia of glandular mucosa = stomach or esophagus
  2. adenoma (stomach or bowel)
  3. dysplasia in chronic inflam bowel disease (bowel)
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10
Q

precursor lesions of SCC

A

SCC in situ

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11
Q

intestinal metaplasia def and dysplasia

A
  • metaplasia = in stomach or esophagys: epith replaced by glandular epith with goblet cells
  • dysplasia = when cells have features of adenoCA (cyto)
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12
Q

adenoma charact

A

-nuclear enlargement
-nuclear stratification
-lack of maturation
looks dark bc lot nuclei
gland like

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13
Q

SCC in situ charact

A
  • no maturation, large nuclei, high NC ratio, atypia

- LP is clean

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14
Q

2 tumors of esophagus and most common

A
  • adenoCA (most common bc devs out of intestinal metaplasia. BE with intestinal metaplasia and goblet cells)
  • SCC
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15
Q

low-grade dysplasia in Barrett esophagus charact

A
  • normal architecture
  • atypica
  • lack of maturation
  • nuclei enlargement and stratification
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16
Q

high-grade dysplasia in BE

A
  • dysplastic glandular mucosa with bridges under the glands
  • absence of maturation of glandular mucosa
  • large atypical, crowded, stratified nuclei
  • complex architecture
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17
Q

esophageal adenoCA charact and symptoms

A
  • usually out of BE so distal esophagus

- symptoms: GERD symptoms, pain, weight loss, anemia

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18
Q

why anemia in esophageal adenoCA and usual causes of anemia

A
  • usual cause = loss through bleeding (menses, GI = NUMBER ONE CONCERN if see Fe deficiency anemia, ..). diet cause is very unusual
  • GI may be ulcer but consider cancer in older people
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19
Q

most likely site of GI bleeding if GI bleeding is happening

A

colon

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20
Q

esophageal adenoCA macro charact

A
  • stricture of GE junction
  • very irregular BE with foci of dysplasia or small CA
  • ulceration
  • necrotic center of the tumor
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21
Q

micro charac of esophageal adenoCA

A

-many glands of various sizes infiltrating the stroma

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22
Q

how degree of differentiation is determined in esophageal adenoCA

A

amount of glands formed
few glands = poor differentiation.
with glands prod, also mucous prod (intra and extra cellular, exported in surrounding stroma)

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23
Q

esophageal SCC causes

A
  • smoking
  • alcohol
  • carcinogens in food
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24
Q

esophageal SCC clinically

A
  • asymptomatic if small
  • dysphagia (tumor causes stricture), chest pain, weight loss
  • DX BY ENDOSCOPY
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25
Q

esophageal SCC charact

A
  • NO BE (mucosa around it is normal)
  • squamous epith
  • tumor may protrude in lumen, show ulceration, stricture
  • usually in distal esophagus
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26
Q

most common cancers depending on esophagus part

A 
upper = SCC
middle = SCC
lower = adenoCA
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27
Q

esophagus SCC in situ charact

A
  • above BM
  • features of malignancy
  • squamous epith pattern
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28
Q

esophagus invasive SCC

A
  • very irregular bottom
  • infiltrates stroma underneath (below BM)
  • some necrosis, some differentiation
  • polygonal cells with focal keratin formation
  • desmoplastic stroma
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29
Q

esophageal SCC specific charact

A
  • pavement like cells
  • cyto atypia
  • keratinization
  • intercellular bridges
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30
Q

2 cancers in the stomach

A

adenoCA (intestinal type or diffuse type (signet ring cell)) and lymphoma

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31
Q

2 types of adenoCA

A
  • intestinal metaplasia

- organ specific type (stomach = signet ring cell type)

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32
Q

risk factors for gastric adenoCA

A
  • H pylori infection
  • diet rich in smoked salted food and nitrites and poor in fruits and vegetables
  • smoking
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33
Q

clinical features of gastric adenoCA

A
  • asymptomatic
  • H pylori infection symptoms
  • advanced = epigastric pain, ANEMIA
  • stenosis symptoms, only if in pylorus
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34
Q

macro and micro charact of intestinal type gastric adenoCA

A
  • macro: grossly forms a mass, sometimes ulcerated with ELEVATED borders. wall thickening. may have hemorrhage, necrosis
  • micro: glands infiltrating stroma
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35
Q

macro and micro charact of diffuse type gastric adenoCA

A

macro:
- infiltrates stomach, no obvious mass
- thickened wall, gastric folds thickened bc of tumor infiltration
micro: no glands, single cells, sometimes signet ring cells morphology infiltrate stroma

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36
Q

precursor lesions of intestinal type gastric adenoCA

A
  • low and high grade dysplasia (in setting of intestinal metaplasia due to H pylori or to autoimmune gastritis)
  • gastric adenoma
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37
Q

gastric mucosa with low-grade dysplasia charact

A

increased NC ratio, lack of maturation, ..

38
Q

gastric mucosa with high-grade dysplasia charact

A

increased complexity

39
Q

diffuse gastric adenoCA macro charact

A
  • thickening
  • thickened folds
  • effacement of folds
  • possible ulcers
40
Q

signet ring cell CA of the stomach microscopy

A
  • signet ring cell: round cells with mucus accum in cytoplasm pushing nucleus on the side + nuclei infiltrate
  • no glands formation except some glands (a bit)
41
Q

complication of signet ring cell gastric adenoCA

A

metastasis to lymph nodes

42
Q

possible tumor mix in the stomach

A

mixed intestinal and signet ring cell tyepe adenoCA

43
Q

why gastric and esophagus cancer can present with anemia

A

bc the tumors bleed. eventually bone marrow runs out of Fe reserve and intake is insufficient to compensate on the loss

44
Q

2 cancers in the colon

A

adenoCA and adenoma (before adenoCA is the polyp that you have to detect early before becomes adenoCA)

45
Q

colonic adenoma on histo

A
  • nuclear enlargement
  • nuclear stratification
  • lack of maturation
    note: still check anemia
46
Q

note on sessile villous adenoma of the rectum

A

have to check on microscopy to make sure there’s no cancer

47
Q

villous adenoma charact on histo

A

finger-like projections with fibro-vascular cores lined by adenomatous epithelium

48
Q

3 types of colorectal adenomas that can dev into colon cancer

A
  • villous
  • tubular villous
  • tubular
49
Q

colonic adenoCA macro features

A
  • many polyps
  • ulcerated tumor possibly, ulcerated mass
  • elevated borders
  • regular center
50
Q

features of a section of colonic adenoCA

A
  • invasion in tunica muscularis: this replaces the submucosa

- possible lymph node metastasis

51
Q

microscopy of colonic adenoCA

A
  • irregular glands infiltrating the stroma
  • desmoplastic stroma
  • necrotic debris with glands
52
Q

possible complication of colonic adenoCA

A

capillary invasion (vascular invasion)

53
Q

(IMPORTANT) 2 pathways of colonic adenoCA formation

A

-chromosomal instability (85%)
-microsatellite instability (15%)
NOTE: both types have hereditary conditions associated

54
Q

chromosomal instab pathway charact

A
  • structural and numeric chromosomal alterations
  • microsat stable
  • MUTATIONS: APC, K-ras, p53
55
Q

microsat instability pathway charact

A
  • diploid
  • microsat instab
  • dysfct of MMR proteins (MSH2, MLH1, MSH6, PMS2)
  • peculiar tumor histology (mucinous differentiation, poorly differentiated tumors)
  • BETTER prognosis
56
Q

hereditary conditions associated with chromosomal instab and microsat instab pathways

A
  • chrom. instab: FAP (familial adenomatous polyposis)

- microsat instab: hereditary nonpolyposis CRC (HNPCC) = Lynch syndrome

57
Q

FAP charact

A
  • many polyps
  • distal colon
  • 1 hit in lifetime is sufficient, is a dominant condition. odd for 2nd hit on APC is high.
  • 100% penetrance
58
Q

HNPCC (Lynch) charact

A
  • autosomal dominant
  • MMR genes mutations
  • rare polyps (BUT have more polyps than general population)
  • proximal colon
  • high penetrance but not 100%
59
Q

carcinoid (neuroendocrine) tumor def

A

well differentiated neoplasm arising in mucosal neuroendocrine cells

60
Q

carcinoid tumor clinical charact

A
  • incidental finding on endoscopy
  • carcinoid syndrome (flushing, teleangiectasias, cyanosis, bronchoconstriction, edema, hyperperistalsis, pulmonary and tricuspid valvular disease)
61
Q

carcinoid tumor charact and location

A
  • esophagus to rectum
  • tiny polyp-like to large tumors
  • firm and beige, tan homogenous surface
  • grow very slowly
  • produce endocrine mediators
  • can still metastasize
62
Q

significant of carcinoid syndrome in carcinoid tumor

A

sign of BAD prognosis:

  • if not metastasis, liver inactivates the mediators
  • so syndrome = metastasized
63
Q

carcinoid tumor types IN THE STOMACH

A
  1. in background of atrophic gastritis
  2. Zollinger-Ellison syndrome
  3. sporadic
64
Q

atrophic gastritis pathophgy

A

lot of gastrin prod to increase acid release and no response so even more gastrin produced

65
Q

ZE syndrome pathophgy

A

tumor producing gastrin. covered in pancreatic and biliary tree material

66
Q

atrophic gastritis carcinoid tumor of the stomach and ZE syndrome carcinoid tumor of the stomach: thing in common

A

hypergastrinemic state

67
Q

carcinoid tumors of the stomach: prognosis

A
  • type 1 (in atrophic gastritis): good prognosis

- type 2 (in ZE): stomach is good prognosis but bc pancreatic tumor causing carcinoid is also there, bad prognosis

68
Q

carcinoid tumors on microscopy (same for 3 gastric types, lung carcinoid, etc.)

A
  • solid sheets separated by thick collagen

- sometimes gland like or tubular structures form or may grow in ribbons or pseudoglandular or cords

69
Q

carcinoid tumor cytology

A
  • rounded or oval nuclei
  • speckled chromatin
  • small cytoplasm
  • can’t see nucleoli (inconspicuous)
70
Q

possible complication of carcinoid tumor

A

lymph node metastasis

71
Q

carcinoid tumor special stain

A

chromogranin or synaptophysin immunostain (neuroendocrine markers: synaptophysin and chromogranin)

72
Q

gastrointestinal stromal tumors (GIST) def

A

tumors arising from ICC (pacemaker cells of peristalsis)

73
Q

GIST clinically

A
  • no symptoms

- symptoms related to bleeding or compression of adjacent structures

74
Q

GIST usual cause

A

gain of fct mutations of either c-KIT or PDGFRA (platelet-derived growth factor receptor A) which is a TM R for tyrosine kinase activity involved in cell prolif and apoptosis

75
Q

GIST macro features

A
  • nodular masses protruding in lumen, covered by stretched mucosa
  • erosion, ulceration of mucosa possible
  • beige and rubbery type
76
Q

GIST vs adenoCA of stomach difference

A

adenoCA of stomach: mucosa not stretched bc cancer starts in mucosa
GIST: stretches mucosa: possibly diminishing blood supply

77
Q

GIST on microscopy

A
  • intersecting bundles of SPINDLE cells

- if epithelioid GIST = polygonal cells

78
Q

staining of GIST

A

immunostain for c-KIT (CD117)

79
Q

lymphomas in the stomach def

A

stomach is primary site or lymphoma arising there from somewhere else

80
Q

most frequent lymphomas in the stomach

A
  • marginal zone lymphoma of the MALT

- diffuse large B-cell lymphoma

81
Q

how is it possible to have marginal zone lymphoma of MALT in stomach if there is NO MALT in the stomach

A

MALT arises in the stomach in the setting of H pylori infection and active gastritis

82
Q

MALT lymphoma of stomach charact

A
  • low grade B cell lymphoma
  • assoc with H pylori infection (may regress if removed)
  • macro = small mucosal lesions, thickening of folds. DOESN’T form masses
83
Q

stomach MALT lymphoma microscopy

A
  • infiltration of small lymphoid cells in mucosa

- partial replacement of glands (lymphoepithelial lesions)

84
Q

MALT lymphoma of stomach: how to check for B cells

A

stain for CD20 (a B cell is CD20+)

85
Q

(IMPORTANT) main feature of stomach MALT lymphoma

A

on cytokeratin stain, lymphoepithelial lesions (infiltrating lymphocytes in mucosa replace glands)

86
Q

MALT lymphoma prognosis

A

is a mild cancer. good prognosis

87
Q

diffuse large B cell lymphoma o the stomach (DLBCL) def

A
  • high grade B cell lymphoma
  • de novo or in setting of MALT lymphoma
  • endoscopy (macro): large soft mass, sometimes ulcerated
88
Q

DLBCL stomach microscopy (all in the name)

A
  • diffuse proliferation
  • LARGE cells (MALT lymphoma, cells are smaller)
  • CD20+ (B cells)
  • neoplastic (lymphoma)
89
Q

DLBCL stomach: why the tumor is soft

A

no stromal reaction to the tumor, no desmoplasia

90
Q

management of gastric CA vs lymphoma

A

gastric CA = gastrectomy

lymphoma = chemotherapy (no gastrectomy)

Bloc E - GI & Metabolism (58 decks)

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