Copy Stomach Workshop

7/29/2019 Copy Stomach Workshop

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STOMACH

DR. AISHAAKBAR


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BLOOD SUPPLY:

a. The left gastric arteryb. Right gastric artery

c. Right gastro-epiploic artery

d. Left gastro-epiploic arterye. Short gastric arteries

The corresponding veins draininto portal system. The lymphaticdrainage of the stomachcorresponding its blood supply.


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Case45yr old lady took salicylates for 3wks and

developed epigastric pain


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ACUTE GASTRITIS

Inflammation of gastric mucosa

Caused byingestion of strong acids or alkalies, NSAIDs,cancer chemotherapy, irradiation, alcohol, uremia, severe stress

& shock states

Proposed mechanisms: acid production with surfacebicarbonate buffer

Morphology: Mucosal edema, hyperemia, PML infiltration,erosions (not deeper than muscularis mucosa) & hemorrhages


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CASE48yr old male presented with 3yr history

of heart burn, temporarily relieved byantacids.


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CHRONIC GASTRITISChronic mucosal inflammation, leading to mucosal atrophy,

intestinal metaplasia & dysplasia.

1)Chronic superficial gastritis -decrease cytoplasmic mucin ,nuclear and nucleolar enlargement some increase in foveolarmitosis.

2)Chronic atrophic gastritis

Gastric atrophy. thining of mucosa without inflammation.


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Clinically:Mild abdominal discomfort, nausea, vomiting; hypochlorhydria,hypergastrinemia & rarely overt pernicious anemiaLong-term risk of cancer is 2-4%

Two types of metaplastic changes:Pyloric metaplasia -fundic type glands---mucus sec.glands

Intestinal metaplasia


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Pathogenesis:

Immune gastritis Type A gastritis Non immune gastritis Type B gastritis

Autoimmunity (>10%): Antibodies to parietal cells cause parietal cell destruction

Chronic infection by Helicobacter pylori (90%): Elaboration of ureaseproduces ammonia that buffers gastric acid, protecting organism from acid

Other diseases associated with H. pyloriInfectionPeptic ulcer disease

Gastric carcinomaGastric lymphoma


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ANTRAL MUCOSA WITH CHRONICACTIVE GASTRITIS


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SYDNEY SYSTEM2 from fundic mucosa2 from antral mucosa1 from incissura

These should be labelled, assessed and recordedseparately

Special stains are required forH-Pylori. Giemsa/ Warthin starryMucin. PAS- neutral mucin

Alcian blue- intestinal mucin


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Revised system in 19941. Antral- jejunal biopsies to be reported

separately

2. Gastritis to be classified intoAcuteChronicSpecial form

3. Contains gradable non gradable entities

non gradable granulomas, eosinophils,intraepithelial lymphocytes, mucin depletion,foveolar hypertrophy, surface erosions, lymphoid

follicles


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Gradable entities

H-Pylori

Normal not seenMild..... OccasionalModerate significantMarked almost masses of H-Pylori

Chronic inflammationNormal. 2-5/ hpf (40x10)MildModerate

marked . ( to be graded away from thefollicles)


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Neutrophils (Activity)

Normal.. Not seen

Mild few

Moderate.. Significant number

Marked.. Pit abscesses(recommended term is Active Gastritis or Active

Chronic Gastritis)


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Atrophy

Mild

ModerateSevere(Thickness of glandular part/ thickness of

mucosa difficult in endoscopic bopsies as

muscularis mucosae presence is essential)

Intestinal metaplasia

Complete (intestinal)

Incomplete (large intestinal)

Etiology (if known), topography (cardia,antrum), morphology all variables


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EXAMPLE

Stomach, endoscopic biopsy:

Active Chronic Gastritis, Antral,

H-Pylori marked

Chronic inflammation marked

Activity. moderate

Atrophy. moderate

Intestinal metaplasia.. incomplete


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Other types of gastritisAcute infectious non bacterial gastroenteritis

Hemorrhagic gastritis

Collagenous gastritisLymphocytic gastritis

Allergic gastroenteritis

Diffuse eosinophilic gastritroentritis

Granulomatous gastritis


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GUESS THE LESION


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Hyperplastic polyp75% of allCauses:

Hypochlorhydria

Dec pepsinogen

HypergastrenmiaChronic gastritis

Grossly: Small sessile,multiple,smooth contours

L/M: elongation, tortous dilated gastric foveolae

with mostly pyloric glands in deeper portion.Foamymacrophages

Malignant transformation is accompanied by

increased proliferative activity and P53ex ression.


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Hyperplastic polyp

]


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AdenomasAntral

Sessile or pedunculated

L/M: dystrophic glands with pseudostratifiedepithelium, nuclear abnormalities, increasemitosis

Gastric type

Intestinal type

Mixed(hyperplastic and adenomatous)


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Fundic gland polypCauses:Sporadic

ZollingerEllison syndrome

proton pump inhibitors

familial adenomatous polyposisGrossly : Multiple, small, polypoidal mass infundus or body

L/M: microcysts lined by fundic epithelium,including oxyphilic cells; the overlying foveolaeare usually shortened.There is also an increasein the smooth muscle content, often in apericystic distribution


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CASEPatient presented with: Epigastric pain 1-3 hours

after meals & worse at night; nausea; vomiting;belching & occult blood in the stools


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ULCERS

Ulcer- a breach in mucosa & extends thru muscularis mucosae into submucosa ordeeper

1) Acute Gastric Ulcers:

acute erosive gastritis = erosions ABOVE the muscularis mucosa

Caused by Severe stress (= Stress Ulcers)

Shock, extensive burns (Curlings ulcers)

Severe head injuries (Cushings ulcers)

NSAIDs.


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2) CHRONIC GARSTRIC ULCER:Ratio of duodenal : gastric = 4 : 1

Age-50 years

Morphology:Surrounding mucosa shows chronic gastritis & radial convergence of rugal folds

towards the ulcer niche (unlike malignant ulcer)Active, well devepled ch.peptic ulcer show 4 distinct layers:

Surface coat of purulent exudate,bacteria,necrotic debris

Fibrinoid necrosis

Granulation tissue

Fibrosis replacing muscle wall extend into subserosa


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CASE

A 40 year old female, presented with epigastricpain and malena

ENDOSCOPIC FINDINGS

Multiple ulcers in small intestine and stomach


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HYPERTROPHICGASTROPATHY

Characterized by Giant enlargement of the gastric rugal foldsCaused by hyperplasia of epithelial cells ( not due to inflammation )risk of cancer

Includes 3 variantsZollinger - Ellison SyndromeCaused by Gastrinoma of Pancreas secreting gastrin elevated serum

gastrin levelsmultiple peptic ulcerations in stomach, duodenum, jejunumHypertrophic rugal folds & Parietal cell hyperplasia and hypertrophy

excess gastric acid productionFundic glands may be cystically dilated-reminiscent of fundic gland

polyps.


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HYPERTROPHIC

GASTROPATHYMenetriers diseaseHyperplasia of surface mucous cells (foveolar hyperplasia) glandular atrophyexcessive loss of proteins in gastric secretion (protein-losing Gastropathy)

Hypersecretory GastropathyHyperplasia of parietal and chief cellsSecondary to excessive gastrin stimulation.


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Regenerative hyperplasiaoccurs most often in areas of mucosal injury

Simple hyperplasia, the cells are immature, with

basophilic cytoplasm, hyperchromatic nuclei, and reduced orabsent mucus secretion.

Uniform in size and shape, with basally or centrally locatednuclei arranged in a row

pseudostratification is slight or absent.

Maturation and differentiation toward the surface arepresent

Glandular dilation and some degree of intraglandularpapillary growth.

Atypicalhyperplasia >pseudostratification andcompression and less maturation and differentiation

inflammatory reaction, sometimes intense, and focal

erosive changes are common.


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Dysplasia

Increased cell proliferation accompanied byabnormalities in cell size, configuration, andorientation.

Mucus secretion is reduced or absent

increase in the nucleocytoplasmic ratio,

loss of nuclear polarity, and pseudostratification. Mitoses arenumerous, and some of them are atypical

Architectural derangement of the glands, cellular crowding,intraluminal folding, and glandular budding and branching.


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Reporting of gastric biopsies

Negative for dysplasiaIndefinite for dysplasia

Low grade dysplasia

High grade dysplasia

Intramucosal carcinoma

Invasive carcinoma


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Intestinal (adenomatous, type 1),

gastric (foveolar, type 2)

combined (hybrid) subtypes,

low-grade and high-grade

High-grade dysplasia is regarded assynonymous with carcinoma in situ (CIS) andmust be distinguished from intramucosal

carcinoma, in which the process has brokenthrough the basement membrane


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CASEA 60 year old male

presented with weightloss and malena.


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CARCINOMA

Age: > 50yr

Etiology:

chronic atrophic gastritis with intestinal metaplasia andpreceded by dysplasia, CIS and superficial Ca

Hypochlorhydria85-90%H.pylori

Gastric polyps, Menetriers disease

Peptic gastric ulcer and gastric stump

Radio and chemotherapy for other maligancies

as r c ancer


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as r c ancer Dietary/Lifestyle Factors

Carl-McGrath S, et al. Cancer Therapy


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Sequence of events:

Increasing risk

NormalChronicgastritis

Mucosal

atrophy

Intestinal

metaplasia

Intestinal-type

carcinoma

Dysplasia


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CLASSIFICATIONBormann, 1926Type I (polypoid)Type II (fungating)Type III (ulcerated)Type IV (infiltrative)

Stout, 1953FungatingPenetrating

SpreadingSuperficial spreadingLinitis plasticaNo special type

Lauren 1965IntestinalDiffuse

Ming, 1977ExpandingInfiltrative

Japanese society for gastriccancer, 1981PapillaryTubularPoorly differentiatedMucinousSignet ring


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CLASSIFICATIONWHO, 2000AdenocarcinomaIntestinal

DiffusePapillary adenocarcinomaTubular adenocarcinomaMucinous adenocarcinomaSignet ring adenocarcinoma

Adenosquamous carcinomaSquamous cell carcinomaSmall cell carcinomaUndifferentiated carcinomaothers


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CARCINOMA

GROSS:Fungating, flat, ulcerating or deeply invasive tumor

growing through wall of stomach

Fleshy, fibrous or gelatinous

Site:Fundic Casubmucosal invasion likely than pyloric CaMulticentricity6%

Adjacent non neoplastic mucosa thickened

L/M: 1 of 4 cell types: foveolar, mucopeptide, intestinalcolumnar or goblet cells


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CARCINOMA TYPES

1. INTESTINAL TYPE:

. Arise from metaplastic epithelium

. Maybe extremely well differentiated, D/D: intestinalmetaplasia

. Mucin is variable, calcification, metaplastic ossification

.Neutrophil or histiocytic infiltrate in stroma

. Poorly differentiatedsolid pattern


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2.DIFFUSE TYPE: (linitis plastica, signet ring Ca)

young prepyloric area pyloric obstruction submucosal fibrosis, mucosal ulceration, muscle

hypertrophy

L/M: diffuse pattern of growthTransmural or intramucosalGland formation rare, individual tumor cellsmostly

Intracytoplasmic mucinsignet ring appearanceExtracellular mucin pools

Presence of signet ring cellstumor categorized assignet ring Ca rather than mucinous adenocarcinoma


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MUC1 for the intestinal type,

MUC5AC for the diffuse type,

MUC2 for the mucinous type

MUC5B for the unclassified type

Reactivity of gastric adenocarcinoma cells forkeratin, epithelial membrane antigen, and CEA

is the rule


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The keratins present are usually of the simpleepithelial type (low molecular weight), butsometimes those seen in normal squamousepithelia (such as CK13 and 16) are alsodetected.

CK7/CK20 expression patterns of gastric cavary

In some cases (particularly of the diffusetype) there is coexpression of keratin andvimentin.

Markers indicative of specific gastric

astr c ancer tag ng


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astr c ancer tag ngSystemsTNM: most important clinical prognostic factor

http://www.hopkins-i.orhttp://www.medscape.com/viewarticle/54


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OTHER TYPES

ADENOSQUAMOUS ANDSQUAMOUS CELL CA:


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OTHER TYPESPARIETAL GLAND

(ONCOCYTIC) CA:

Glandular or solid patternAbundant oncocytic

cytoplasmPTAH and Luxol fast

blue+E/M: abundant

mitochondria,tubulovesicles,intracellular canaliculi andintercellular lumina

LYMPHOEPITHELIOMALIKE CA:Resembles homonymous

tumor in resp tractEBV related

SARCOMATOID CA:Epithelialglands+

sarcoma like spindle cellsHeterologousbone andskeletal muscleNeuroendocrine cells


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Prognostic factorsAge

Tumor stage/lymph node involvement

Location in the stomach

Tumor margins/surgical margins/type ofsurgery

Tumor size

Microscopic type/gradingInflammatory reaction

Perineural invasion

DNA ploidy/p53/c-ERB2

EBV expression

NEUROENDOCRINE


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NEUROENDOCRINE

DIFFERENTIATION1. Well differentiated neuroendocrine tumors

(carcinoid):. Well differentiated, slow growing -Neuroendocrine cellsof gastric mucosa

. Grossly,: gastric WDNETs are small,sharply outlined, and covered by aflattened mucosa..

. May resemble gastric polyps.

. L/M: predominant pattern of growth maybe microglandular, trabecular, or insular


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Carcinoid

NEUROENDOCRINE


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NEUROENDOCRINE

DIFFERENTIATION2. Atypical carcinoid/ neuroendocrine carcinoma/large cell neuroendocrine ca. Tumors with obvious morphological features ofneuroendocrine differentiation but obvious atypia. Trabaculae, rosettes, insulae; dense core secretorygranules, NSE+

. Atypiainvasiveness, necrosis, mitosis

3. Small cell carcinoma:. Analogous to pulmonary counterpart

. Aggressive behavior

4. Otherwise typical adenocarcinoma of diffuse orintestinal type having cells with argyrophilia orneuroendocrine differentiation


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SPREADOF

TUMOR


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CASE63 yr old male presented with abdominal mass

grossly exophytic type

Markers: c-Kit +ve

CD34 veActin-ve


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GASTRO INTESTINAL


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STROMAL TUMOR (GIST)

Most common mesenchymal tumors of the GIT. Arelationship to the interstitial cells of Cajal (ICCs) hasbeen proposed, and expressionof CD117

GISTs are most common in the stomach

(70%),small intestine (20%), colon ,rectum (5%)

esophagus (


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Smooth muscle

differentiationSmaCaldesmon/myosin- frequently

Could arise from muscularis propria,mucosaor vessel.

Spindle tumor cells with acidophilic fibrillarycytoplasm and the presence of cytoplasmicvacuoles at both ends of the nucleus shouldsuggest smooth muscle differentiation

An epithelioid appearance is also more likelyto be associated with evidence of smoothmuscle differentiation- round to polygonalcells with a central nucleus and a usuallyabundant acido hilic or clear c to lasm


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Neural differentiationNeural filaments

Chromogranin

Synaptophysin

Neuron specific enolase+ve

Leu 7S-10

composed of spindle (but sometimesepithelioid) cells growing in the form of

fascicles, palisades, and whorls.Deposition of amorphous eosinophilic

extracellular collections of abnormal collagen(immunoreactive for type VI) referred to as

skenoid fibers is generally associated with


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TUMOR PARAMETERSPERCENT OF PATIENTS WITH PROGRESSIVE DISEASE DURING

LONG-TERM FOLLOW-UP AND CHARACTERIZATION OF RISK (INPARENTHESES) FOR METASTASIS

Group Tumor size Mitotic rate Gastric GISTsJejunal and ilealGISTs

Duodenal GISTs Rectal GISTs

1 =2 cm =5/50-HPFs 0% (none) 0% (none) 0% (none) 0% (none)

2 >2 cm to =5 cm=5/50-HPFs 1.9% (very low) 4.3% (low) 8.3% (low) 8.5% (low)

3a>5 cm to =10cm

=5/50-HPFs 3.6% (low) 24% (moderate)

34% (high)[b] 57% (high)[b]

3b >10 cm =5/50-HPFs 12% (moderate)52% (high)

4 =2 cm >5/50 HPFs 0%[a] 50%[a] [c] 54% (high)

5 >2 cm to =5 cm>5/50 HPFs 16% (moderate)73% (high) 50% (high) 52% (high)

6a>5 cm to =10cm

>5/50 HPFs 55% (high) 85% (high)

86% (high) 71% (high)[b]

6b >10 cm >5/50 HPFs 86% (high) 90% (high)

Rates of metastases or tumor-related death in GISTs grouped by tumorlocation, tumor size and mitotic rate


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DifferentialsSFT

Fibromatosis

Inflammatory fibroid polyp

Glomus tumor

Schwanomma

Leiomyoma/sarcoma

Malignant lymphoma/ca


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CASEA 40 year old male presented with dyspepsia

and epigastric pain.


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MALTOMAExtranodal marginal zone lymphoma of

mucosa-associated lymphoid tissue-3rd mostcommon non-Hodgkin lymphoma subtype

68% of all non-Hodgkin lymphomas in the

West.

clinically indolent, typically chronic, requiringlong-term clinical surveillance and, often,

repeated biopsies.

H pylori is critical for lymphomagenesis andalso creates a microenvironment favouring the

growth of neoplastic B cells, probably through

Grading system indicating the degree of certainty of the diagnosis


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g y g g y gof MALT-type lymphoma

Grade 0 (Normal)Scattered plasma cells in lamina propria. Nolymphoid follicles.

Grade 1 (Chronic active gastritis)Small clusters of lymphocytes in laminapropria. No lymphoid follicles. Nolymphoepithelial lesions.

Grade 2 (Chronic active gastritis with floridlymphoid follicle formation)

Prominent lymphoid follicles with surroundingmantle zone and plasma cells. Nolymphoepithelial lesions.

Grade 3 (Suspicious lymphoid infiltrate inlamina propria, probably reactive)

Lymphoid follicles surrounded by smalllymphocytes that infiltrate diffusely in laminapropria and occasionally into epithelium.

Grade 4 (Suspicious lymphoid infiltrate inlamina propria, probably lymphoma)

Lymphoid follicles surrounded by centrocyte-like cells that infiltrate diffusely in laminapropria and into epithelium in small groups.

Grade 5 (Low-grade B-cell lymphoma of MALT)Presence of dense diffuse infiltrate ofcentrocyte-like cells in lamina propria with

prominent lymphoepithelial lesions


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LARGE CELLLYMPHOMA


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LARGE CELLLYMPHOMAheterogeneous category

transformed MALT lymphomas

75%de novo lymphomas

A high proportion of large cell lymphomas ofthe stomach express BCL6 (in contrast to low-grade lymphomas), whether they are thoughtto be related to MALT lymphoma or not

EBV+


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large lobulated (sometimes polypoid) mass.Superficial or deep ulceration is common

Gastric large B-cell lymphoma are composedof cells resembling large noncleaved cells(centroblasts) but with a slightly more

abundant cytoplasm, sometimes resulting in aplasmablastic or immunoblastic appearance

D/D-Undifferentiation carcinoma

lack of continuity between epithelium andtumor cells

lack of suggestion of an acinar pattern

preservation of muscularis mucosae fibers


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THANKYOU

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