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Pathology of the Pathology of the Stomach Stomach

Pathology of the Stomach. Objectives and aim To learn the congenital disorders of the stomach To learn the congenital disorders of the stomach To learn

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Page 1: Pathology of the Stomach. Objectives and aim To learn the congenital disorders of the stomach To learn the congenital disorders of the stomach To learn

Pathology of the Pathology of the StomachStomach

Page 2: Pathology of the Stomach. Objectives and aim To learn the congenital disorders of the stomach To learn the congenital disorders of the stomach To learn

Objectives and aimObjectives and aim

To learn the congenital disorders To learn the congenital disorders of the stomachof the stomach

To learn the inflammatory To learn the inflammatory diseases of the stomachdiseases of the stomach

To learn the tumors of the To learn the tumors of the stomachstomach

Page 3: Pathology of the Stomach. Objectives and aim To learn the congenital disorders of the stomach To learn the congenital disorders of the stomach To learn

Congenital gastric anomaliesCongenital gastric anomalies Inflammatory disordersInflammatory disorders TumorsTumors

Page 4: Pathology of the Stomach. Objectives and aim To learn the congenital disorders of the stomach To learn the congenital disorders of the stomach To learn

Congenital gastric anomaliesCongenital gastric anomalies Pyloric StenosisPyloric Stenosis

– Young infant (1 in 300 to 900 live births); Young infant (1 in 300 to 900 live births); M/F=3/1M/F=3/1 Projectile vomiting in second to third week of lifeProjectile vomiting in second to third week of life Visible peristalic contractions seen on abdominal Visible peristalic contractions seen on abdominal

examinationexamination Dehydration and wastingDehydration and wasting

– Muscular hypertrophy of pyloric smooth Muscular hypertrophy of pyloric smooth muscle wallmuscle wall..

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Diaphragmatic HerniasDiaphragmatic Hernias– Rare; Acute respiratory problem in Rare; Acute respiratory problem in

newbornnewborn– Diaphragmatic defectDiaphragmatic defectherniationherniation into into

thoraxthorax Gastric heterotopiaGastric heterotopia

– Uncommon; asymptomaticUncommon; asymptomatic– Nidus of gastric Nidus of gastric

mucosamucosaesophagus/small intestineesophagus/small intestine

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Page 7: Pathology of the Stomach. Objectives and aim To learn the congenital disorders of the stomach To learn the congenital disorders of the stomach To learn

Inflammatory disordersInflammatory disorders–Gastritis

Acute gastritisChronic gastritis

–Gastric ulcerationsAcute gastric ulcerPeptic ulcer

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GastritisGastritis Acute gastritisAcute gastritis

AAcute mucosal inflammatory cute mucosal inflammatory process, usually of a transient process, usually of a transient naturenature

may be accompanied by may be accompanied by hemorrhage into the mucosahemorrhage into the mucosa

in severe erosive form of the in severe erosive form of the disease is an important cause of disease is an important cause of acute gastrointestinal bleedingacute gastrointestinal bleeding..

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Acute gastritis is frequently associated with:Acute gastritis is frequently associated with:

NNonsteroidal anti-inflammatory drugs, particularly aspirinonsteroidal anti-inflammatory drugs, particularly aspirin Excessive alcohol consumptionExcessive alcohol consumption Heavy smokingHeavy smoking Treatment with cancer chemotherapeutic drugsTreatment with cancer chemotherapeutic drugs UremiaUremia Systemic infections (e.g., salmonellosis)Systemic infections (e.g., salmonellosis) Severe stress (e.g., trauma, burns, surgery)Severe stress (e.g., trauma, burns, surgery) Ischemia and shockIschemia and shock Suicidal attempts, as with acids and alkaliSuicidal attempts, as with acids and alkali Gastric irradiationGastric irradiation Mechanical trauma (e.g., nasogastric intubation)Mechanical trauma (e.g., nasogastric intubation) Following distal gastrectomyFollowing distal gastrectomy (with reflux of bilious (with reflux of bilious

material)material)

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Morphology of the Acute gastritisMorphology of the Acute gastritis

MMild formild form EEdema and slight hyperemiadema and slight hyperemia in the in the

lamina proprialamina propria,, The surface epithelium is intact,The surface epithelium is intact, SScattered neutrophils are present cattered neutrophils are present

among mucosal epithelial cells. among mucosal epithelial cells. The presence of neutrophils above The presence of neutrophils above

the basement membrane signifies the basement membrane signifies active inflammationactive inflammation of of Helicobacter Helicobacter pyloripylori

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Severe formSevere form EErosion and hemorrhage rosion and hemorrhage (acute erosive (acute erosive

gastritis)gastritis) AAccompanied by ccompanied by mucosal edema, mucosal edema,

inflammatory infiltrate (neutrophils, few inflammatory infiltrate (neutrophils, few lymphocytes), regenerative proliferation of lymphocytes), regenerative proliferation of epithelial cells.epithelial cells.

Healing within days (complete restitution). Healing within days (complete restitution). Hemorrhage may occur independently, Hemorrhage may occur independently,

generating punctate dark spots in an generating punctate dark spots in an otherwise hyperemic mucosa, or in otherwise hyperemic mucosa, or in association with erosion.association with erosion.

Concurrent erosion and hemorrhage Concurrent erosion and hemorrhage acute erosive hemorrhagic gastritiacute erosive hemorrhagic gastritiss

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Chronic gastritisChronic gastritis CChronic mucosal inflammatory changes hronic mucosal inflammatory changes

leading eventually to mucosal atrophy leading eventually to mucosal atrophy and epithelial metaplasia,and epithelial metaplasia,– The major etiologic association of chronic The major etiologic association of chronic

gastritis gastritis isis chronic infection by chronic infection by Helicobacter pyloriHelicobacter pylori :: Highest infection rates Highest infection rates H.pyloriH.pylori (enzymes+toxins) + neutrophilic (enzymes+toxins) + neutrophilic

chemicalschemicals gastritis gastritis

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EtiologyEtiology Chronic infectionChronic infection ( (Helicobacter pyloriHelicobacter pylori)) IImmunologicmmunologic ( (associated with pernicious anemiaassociated with pernicious anemia)) ToxicToxic ( (alcohol and alcohol and tobacco)tobacco) PostsurgicalPostsurgical ( (especially following antrectomy and especially following antrectomy and

gastroenterostomy with reflux of bilious duodenal gastroenterostomy with reflux of bilious duodenal secretionssecretions))

Motor and mechanical, Motor and mechanical, ((obstructionobstruction, , gastric atonygastric atony)) RadiationRadiation Granulomatous conditions (e.g., Crohn’s disease)Granulomatous conditions (e.g., Crohn’s disease) GGraft-versus-host disease, raft-versus-host disease, AAmyloidosis, myloidosis, UUremiaremia

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MorphologyMorphology– AAn inflammatory infiltrate within the n inflammatory infiltrate within the

lamina proprialamina propria: : LymphocytesLymphocytes,, PPlasma cellslasma cells, , occasionally neutrophils.occasionally neutrophils.

– In the early stagesIn the early stages:: ththee infiltrate is usually limited to the infiltrate is usually limited to the

upper third of the gastric mucosa upper third of the gastric mucosa (chronic superficial gastritis)(chronic superficial gastritis),,

H.pyloriH.pylori within the mucus layer. within the mucus layer.

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– In severe formsIn severe forms::– TThe inflammatory infiltrate involves the full he inflammatory infiltrate involves the full

thickness of the mucosa.thickness of the mucosa.– Intestinal Intestinal MetaplasiaMetaplasia:: Metaplastic columnar Metaplastic columnar

absorptive cells and mucous goblet cells of absorptive cells and mucous goblet cells of intestinal phenotype (primarily small intestinal phenotype (primarily small intestine) may partially replace portions of intestine) may partially replace portions of the gastric mucosathe gastric mucosa dysplasia dysplasia ca. ca.

– Lymphoid Lymphoid tissue:tissue: H.pyloriH.pylori induced induced lymphoid lymphoid aggregates, some with germinal aggregates, some with germinal centerscenters gastric lymphoma. gastric lymphoma.

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ComplicationsComplications

• Peptic ulcerPeptic ulcer• DysplasDysplasia ia in situin situ carcinoma carcinoma• Gastric carcinomaGastric carcinoma

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Gastric ulcerationsGastric ulcerationsAcute gastric ulcer Acute gastric ulcer (st(stress ress

ulcersulcers)) Focal, acutely developing gastric mucosal Focal, acutely developing gastric mucosal

defects may appear following severe defects may appear following severe stress.stress.

GenerallyGenerally multiple lesionsmultiple lesions.. ErosionErosion ((acute erosive gastritisacute erosive gastritis)) or or ulcerationulceration

inin– shock shock – extensive burnsextensive burns (Curling ulcers) (Curling ulcers) – sepsissepsis– severe trauma severe trauma – intracranial conditionintracranial conditionss (e.g., trauma, brain (e.g., trauma, brain

surgerysurgery; Curling ulcers); Curling ulcers)– ppharmaceutical agents, harmaceutical agents, ((NSAIDsNSAIDs).).

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– LLess than 1 cm in diameter, ess than 1 cm in diameter, – circular and small, circular and small, – tthe ulcer base is frequently stained a dark he ulcer base is frequently stained a dark

brown by the acid digestion of extruded blood. brown by the acid digestion of extruded blood. – anywhere in the stomachanywhere in the stomach ( (contrast to chronic contrast to chronic

peptic ulcerspeptic ulcersduodenum/lesser duodenum/lesser curvaturecurvature)). . MicroscopicallyMicroscopically::

– acute stress ulcers are abrupt lesions, acute stress ulcers are abrupt lesions, – with essentially unremarkable adjacent with essentially unremarkable adjacent

mucosamucosa,, – erosion or ulcer.erosion or ulcer.

Morphology of Acute Gastric Ulcers

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Acute (Erosive) Acute (Erosive) GastritisGastritis

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Peptic ulcerPeptic ulcer CChronic, hronic, MMost often solitary, ost often solitary, Any portion of the GI tract Any portion of the GI tract exposed to the exposed to the

aggressive action of acid-peptic juices.aggressive action of acid-peptic juices. RRemittingemitting//relapsing lesionsrelapsing lesions,, most often diagnosed in middle-aged to most often diagnosed in middle-aged to

older adults,older adults, may first become evident in young adult may first become evident in young adult

lifelife..

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Predispositions...Predispositions...

alcoholic cirrhosis, alcoholic cirrhosis, chronic obstructive pulmonary chronic obstructive pulmonary

disease, disease, chronic renal failure, chronic renal failure, hyperparathyroidism. hyperparathyroidism.

– iin the last two conditions, we should note n the last two conditions, we should note that that hypercalcemia,hypercalcemia, whatever its cause, whatever its cause, stimulates gastrin production and stimulates gastrin production and therefore acid secretion. therefore acid secretion.

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EtiologyEtiology

H.pyloriH.pylori PPatients chronically using NSAIDs, atients chronically using NSAIDs,

including aspirinincluding aspirin.. Cigarette smoking impairs healing Cigarette smoking impairs healing

and favors recurrenceand favors recurrence.. AAlcoholic cirrhosislcoholic cirrhosis.. Corticosteroids. Corticosteroids. PPsychologicsychological al stresstresss..

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Normal

Increased Attack Hyperacidity

Weak defense Helicobacter pylori, stress, drugs, smoking

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PathogenesisPathogenesis Gastric acid and pepsin.Gastric acid and pepsin. H.pyloriH.pylori (70-90% duodenal; 70% gastric).(70-90% duodenal; 70% gastric). H.pyloriH.pylori cytokines (IL-1, IL-6, IL-8, TNF)cytokines (IL-1, IL-6, IL-8, TNF) neutrophil neutrophil

activation.activation. H.pyloriH.pylori urease urease toxic compounds toxic compounds Rebound Rebound

acid production.acid production. H.pyloriH.pylori phospholipase phospholipase damage epithelial cells. damage epithelial cells. H.pyloriH.pylori protease, phospholipase protease, phospholipase breakdown of breakdown of

gastric mucus.gastric mucus. H.pyloriH.pylori enhances gastric acid enhances gastric acid impairs duodenal impairs duodenal

bicarbonate production.bicarbonate production. H.pyloriH.pylori immunogenic proteins immunogenic proteins activated T & B activated T & B

cells cells form follicles. form follicles.

Page 29: Pathology of the Stomach. Objectives and aim To learn the congenital disorders of the stomach To learn the congenital disorders of the stomach To learn

H.pyloriH.pylori related disordersrelated disorders

H. pyloriH. pylori can be transmitted from can be transmitted from person to person through close contactperson to person through close contact: : – Chronic gastritis – 90%Chronic gastritis – 90%– Peptic ulcer disease – 95-100%Peptic ulcer disease – 95-100%– Gastric carcinoma – 70%Gastric carcinoma – 70%– Gastric lymphomaGastric lymphoma– Reflux OesophagitisReflux Oesophagitis– Non ulcer dyspepsiaNon ulcer dyspepsia

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Zollinger-Ellison Zollinger-Ellison syndromesyndrome– CCarcinoid tumorsarcinoid tumors– Excess gastrin secretion Excess gastrin secretion

((Pancreatic Islet cell tumorPancreatic Islet cell tumor))

– Excess gastric acid productionExcess gastric acid production – Multiple peptic ulcerations Multiple peptic ulcerations

(stomach, dudenum, jejenum)(stomach, dudenum, jejenum)

Page 32: Pathology of the Stomach. Objectives and aim To learn the congenital disorders of the stomach To learn the congenital disorders of the stomach To learn

MorphologyMorphology At least 98% of peptic ulcers are located in the At least 98% of peptic ulcers are located in the

first portion of the duodenum or in the stomachfirst portion of the duodenum or in the stomach ((along the along the lesser curvaturelesser curvature).).– Most duodenal ulcers occur in the first portion of the Most duodenal ulcers occur in the first portion of the

duodenum, generally within a few centimeters of the duodenum, generally within a few centimeters of the pyloric ring. pyloric ring.

– The The anterior wall of the duodenumanterior wall of the duodenum is more often is more often affected than the posterior wall. affected than the posterior wall.

– Gastric ulcers are predominantly located along the Gastric ulcers are predominantly located along the lesser curvaturelesser curvature..

MMore than 50% of peptic ulcers have a diameter ore than 50% of peptic ulcers have a diameter less than 2 cm, less than 2 cm,

10% of benign ulcers are greater than 4 cm.10% of benign ulcers are greater than 4 cm.

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The classic peptic ulcer is a round-to-oval, sharply The classic peptic ulcer is a round-to-oval, sharply punched-out defect with relatively straight walls.punched-out defect with relatively straight walls.

The margins are usually level with the The margins are usually level with the surrounding mucosa or only slightly elevatedsurrounding mucosa or only slightly elevated..

Heaping-up of these margins is rare in the benign Heaping-up of these margins is rare in the benign ulcer but is characteristic of the malignant lesion. ulcer but is characteristic of the malignant lesion.

The depth of these ulcers varies The depth of these ulcers varies ::– superficial lesions involving only the mucosa and superficial lesions involving only the mucosa and

muscularis mucosa muscularis mucosa – deeply excavated ulcers having their bases on the deeply excavated ulcers having their bases on the

tunica tunica muscularismuscularis..

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The base of a peptic ulcer is smooth and The base of a peptic ulcer is smooth and clean to inspection, owing to peptic digestion clean to inspection, owing to peptic digestion of any exudate. of any exudate.

At times, thrombosed or patent blood At times, thrombosed or patent blood vessels (the source of life-threatening vessels (the source of life-threatening hemorrhage) are evident in the base of the hemorrhage) are evident in the base of the ulcer. ulcer.

Scarring may involve the entire thickness of Scarring may involve the entire thickness of the stomachthe stomach..

The gastric mucosa surrounding a gastric The gastric mucosa surrounding a gastric ulcer is somewhat edematous and reddened, ulcer is somewhat edematous and reddened, owing to the almost invariable gastritis.owing to the almost invariable gastritis.

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Kissing ulcers Kissing ulcers (face-to-face ulcers)(face-to-face ulcers) When the entire wall is When the entire wall is

penetrated, the base of the ulcer penetrated, the base of the ulcer may be formed by adherent may be formed by adherent – pancreas, pancreas, – omental fat, omental fat, – liver. liver.

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Page 41: Pathology of the Stomach. Objectives and aim To learn the congenital disorders of the stomach To learn the congenital disorders of the stomach To learn

The histologic appearance varies from active The histologic appearance varies from active necrosis, to chronic inflammation and scarring, to necrosis, to chronic inflammation and scarring, to healing. healing.

In active ulcers with ongoing necrosis, four zones In active ulcers with ongoing necrosis, four zones are demonstrable: are demonstrable: – (1) The base and margins have a superficial thin layer (1) The base and margins have a superficial thin layer

of necrotic fibrinoid debris not visible to the naked eye; of necrotic fibrinoid debris not visible to the naked eye; – (2) beneath this layer is the zone of a nonspecific (2) beneath this layer is the zone of a nonspecific

inflammatory infiltrate, with neutrophils predominating; inflammatory infiltrate, with neutrophils predominating; – (3) in the deeper layers, especially in the base of the (3) in the deeper layers, especially in the base of the

ulcer, there is active granulation tissue infiltrated with ulcer, there is active granulation tissue infiltrated with mononuclear leukocytes; and mononuclear leukocytes; and

– (4) the granulation tissue rests on a more solid fibrous (4) the granulation tissue rests on a more solid fibrous or collagenous scaror collagenous scar..

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ComplicationsComplications

PerforationPerforation ( (into the peritoneal cavityinto the peritoneal cavity))– Penetration (Penetration (pancreas, omental fat, liverpancreas, omental fat, liver))

BleedingBleeding (frank hemorrhage; anemia) (frank hemorrhage; anemia) Gastric cancersGastric cancers FibrosisFibrosis and stenosis and stenosis (s (stricture tricture and/or and/or

obstructionobstruction))..

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Summary...peptic ulcusSummary...peptic ulcus

90% ulcers in first portion of duodenum or 90% ulcers in first portion of duodenum or lesser curvature of stomach(4:1).lesser curvature of stomach(4:1).

80 to 90% cases single ulcer. 80 to 90% cases single ulcer. RoundRound-s-small ulcers with sharply punched mall ulcers with sharply punched

out edgesout edges.. Microscopy: 4 zones. Microscopy: 4 zones.

– Superficial necrotic layer.Superficial necrotic layer.– Inflammatory cells zone.Inflammatory cells zone.– Granulation tissue zone Granulation tissue zone – Collagenous scar layer.Collagenous scar layer.

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Pyloric StenosisPyloric Stenosis

Acquired type.- Long term complication of gastritis or peptic ulcer disease involving the pylorus.- May also be secondary to carcinoma of the pylorus, head of the pancreas, or gastric lymphoma producing functional obstruction- Same symptoms as congenital stenosis.

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TUMORS of the STOMACHTUMORS of the STOMACH

Benign tumorsBenign tumors– EpithelialEpithelial

Gastric PolypsGastric Polyps

– MMesenchymal esenchymal lipomas,lipomas, leiomyoma,leiomyoma, neurofibromasneurofibromas

Malignant tumorsMalignant tumors– CCarcinoma (90 to arcinoma (90 to

95%). 95%). – LLymphomas (4%), ymphomas (4%), – CCarcinoids (3%), arcinoids (3%), – MMalignant spindle cell alignant spindle cell

tumors (2%).tumors (2%).

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Gastric PolypsGastric Polyps NoNodule or mass that projects above the dule or mass that projects above the

level of the surrounding mucosa.level of the surrounding mucosa.– hyperplastic naturehyperplastic nature (80-85%) (80-85%)– fundic gland polyps (10%)fundic gland polyps (10%)– adenomatous polyps (5%)adenomatous polyps (5%)

Histologically, these polyps exhibit a Histologically, these polyps exhibit a mixture of mixture of – hyperplastic pyloric-type glandular tissue,hyperplastic pyloric-type glandular tissue,– edematous lamina propriaedematous lamina propria,,– inflammatory cells. inflammatory cells.

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Gastric CGastric Carcinomaarcinoma

MMost important and the most common (90 to ost important and the most common (90 to 95%)95%)

Risk factors:Risk factors:– DietDiet

Nitrites derived from nitrates (food, drinking water, Nitrites derived from nitrates (food, drinking water, preservatives preservatives nitrosamines&nitrosamides) nitrosamines&nitrosamides)

Smoked foods & pickled vegetablesSmoked foods & pickled vegetables Excessive saltExcessive salt Decreased intake of fresh vegs&fruits (less antioxidants)Decreased intake of fresh vegs&fruits (less antioxidants)

– Chronic gastritis with intestinal metaplasiaChronic gastritis with intestinal metaplasia Infection with Infection with H.pyloriH.pylori Pernicious anemiaPernicious anemia

– Altered anatomyAltered anatomy After subtotal distal gastrectomyAfter subtotal distal gastrectomy

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MorphologyMorphology

The three macroscopic growth patterns The three macroscopic growth patterns of gastric carcinomaof gastric carcinoma::

(1)(1) Vegetan Vegetan ((EExophyticxophytic)):: with protrusion with protrusion of a tumor mass into the lumenof a tumor mass into the lumen..

((22)) Ulcerating (Ulcerovegetan; Ulcerating (Ulcerovegetan; EExcavatedxcavated):): when a shallow or deeply when a shallow or deeply erosive crater is presenterosive crater is present..

(3) Diffuse (Infiltrative; F(3) Diffuse (Infiltrative; Flat or lat or depresseddepressed):): in which no tumor mass is in which no tumor mass is visibly obviousvisibly obvious..

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Vegetan (Exophytic; Fungating)

Ulcerating

Diffuse

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ExcavatedExcavated (ulcerating) (ulcerating) cancers may cancers may closely mimic, in size and appearance, closely mimic, in size and appearance, chronic peptic ulcers. chronic peptic ulcers.

AA broad region of the gastric wall or broad region of the gastric wall or the entire stomach is extensively the entire stomach is extensively infiltrated by malignancy, creating a infiltrated by malignancy, creating a rigid, thickened “leather bottle,” rigid, thickened “leather bottle,” termed termed linitis plasticalinitis plastica. .

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Linitis plasticaLinitis plastica

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The histologic types of gastric cancerThe histologic types of gastric cancer:: IIntestinal typentestinal type

– neoplastic intestinal glands resembling those of neoplastic intestinal glands resembling those of colonic adenocarcinoma,colonic adenocarcinoma,

– the the neoplastic cells often contain apical mucin neoplastic cells often contain apical mucin vacuoles, vacuoles,

– abundant mucin may be present in gland lumina. abundant mucin may be present in gland lumina. DDiffuse typeiffuse type

– gastric-type mucous cells, gastric-type mucous cells, – do not form glands do not form glands – ““infiltrative” growth pattern. infiltrative” growth pattern. – mucin formation expands the malignant cells and mucin formation expands the malignant cells and

pushes the nucleus to the periphery, creating a pushes the nucleus to the periphery, creating a “signet-ring”“signet-ring” conformation conformation..

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EExcessive mucin production xcessive mucin production large mucinous large mucinous lakes lakes dissect tissue planes dissect tissue planes

Infiltrative tumors Infiltrative tumors desmoplastic reaction desmoplastic reaction fibrosis creates local rigidity of the wall.fibrosis creates local rigidity of the wall.

GGastric carcinomas astric carcinomas penetrate the wall to involve the serosa penetrate the wall to involve the serosa spread to regional and distant lymph nodes spread to regional and distant lymph nodes Virchow’s nodeVirchow’s node:: gastric carcinomas may gastric carcinomas may

metastasize to the supraclavicular sentinel metastasize to the supraclavicular sentinel (Virchow’s) node (Virchow’s) node (( first clinical manifestation first clinical manifestation of an occult neoplasmof an occult neoplasm))

Krukenberg tumorKrukenberg tumor:: metastatic metastatic adenocarcinoma to the ovaries (from adenocarcinoma to the ovaries (from stomach, pancreas, and even gallbladder)stomach, pancreas, and even gallbladder)..

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Spreading...

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LYMPHOMALYMPHOMA

Extra-nodal lymphomas can arise in any Extra-nodal lymphomas can arise in any tissue, most commonly in the GI tract, tissue, most commonly in the GI tract, particularly the stomach. particularly the stomach.

Nearly 5% of all gastric malignancies are Nearly 5% of all gastric malignancies are primary lymphomas, the most common primary lymphomas, the most common of which are indolent extra-nodal of which are indolent extra-nodal marginal zone B-cell lymphomas. marginal zone B-cell lymphomas.

In the gut these tumors are often In the gut these tumors are often referred to as lymphomas of referred to as lymphomas of mucosa-mucosa-associated lymphoid tissue (MALT)associated lymphoid tissue (MALT), or , or MALTomasMALTomas..

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LYMPHOMALYMPHOMA

Extra-nodal marginal zone B-cell Extra-nodal marginal zone B-cell lymphomas usually arise at sites of lymphomas usually arise at sites of chronic inflammation. chronic inflammation.

They can originate in the GI tract at They can originate in the GI tract at sites of preexisting MALT, such as the sites of preexisting MALT, such as the Peyer's patches of the small intestine, Peyer's patches of the small intestine, but more commonly arise within but more commonly arise within tissues that are normally devoid of tissues that are normally devoid of organized lymphoid tissue. organized lymphoid tissue.

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LYMHOMALYMHOMA

The most common cause of "pro-The most common cause of "pro-lymphomatous" inflammation in the lymphomatous" inflammation in the stomach is chronic stomach is chronic H. pyloriH. pylori infection, infection, which is found in association with most which is found in association with most cases of gastric MALToma.cases of gastric MALToma.

MALTomas can transform into more MALTomas can transform into more aggressive tumors that are aggressive tumors that are histologically identical to diffuse large histologically identical to diffuse large B-cell lymphomas. B-cell lymphomas.

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GASTROINTESTINAL GASTROINTESTINAL STROMAL TUMORSTROMAL TUMOR A wide variety of mesenchymal A wide variety of mesenchymal

neoplasms may arise in the neoplasms may arise in the stomach.stomach.

GI stromal tumor (GIST)GI stromal tumor (GIST) is the is the most common mesenchymal most common mesenchymal tumor of the abdomen, and more tumor of the abdomen, and more than half of these tumors occur in than half of these tumors occur in the stomach. the stomach.

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GISTGIST

Symptoms of GISTs at presentation Symptoms of GISTs at presentation may be related to mass effects. may be related to mass effects. Mucosal ulceration can cause blood Mucosal ulceration can cause blood loss, and approximately half of loss, and approximately half of individuals with GIST present with individuals with GIST present with anemia or related symptoms. GISTs anemia or related symptoms. GISTs may also be discovered as an incidental may also be discovered as an incidental finding during radiologic imaging, finding during radiologic imaging, endoscopy, or abdominal surgery endoscopy, or abdominal surgery performed for other reasons. Complete performed for other reasons. Complete surgical resection is the primary surgical resection is the primary treatment for localized gastric GIST.. treatment for localized gastric GIST..

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GISTGIST

The prognosis correlates with tumor The prognosis correlates with tumor size, mitotic index, and location, size, mitotic index, and location, with with gastric GISTs being somewhat less gastric GISTs being somewhat less aggressive than those arising in the aggressive than those arising in the small intestinesmall intestine. Recurrence or . Recurrence or metastasis is rare for gastric GISTs metastasis is rare for gastric GISTs under 5 cm but common for under 5 cm but common for mitotically active tumors larger than mitotically active tumors larger than 10 cm10 cm

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