3.the Stomach

8/3/2019 3.the Stomach

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The Stomach


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The normal gastric mucosa

Cardia mainlymucus-secretingcellsFundus (body) acid producingparietal cells,pepsin producingchief cellsPylorus hormone(gastrin) production


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Congenital disorders

Hiatus herniaDiaphragmatic hernia (through a non-physiological defect)Congenital pyloric stenosis. Maleinfants with hypertrophy of pyloricsmooth muscle leading to projectilevomiting


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Gastritis

Acute gastritis often due to chemicalinjury (alcohol drugs)Chronic gastritis:

Helicobacter pylori infectionChemical damage (bile reflux, drugs)

Autoimmune (associated with vitaminB12 malabsorption (pernicious anaemia)


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Acute gastritis

Drugs (non-steroidalanti-inflammatorydrugs NSAID), alcoholcause acute erosion(loss of mucosasuperficial tomuscularis mucosae).Can result in severehaemorrhageAcute Helicobacter infection has aprominent neutrophilinfiltrate


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Chronic gastritis ABC

A autoimmuneB bacterial ( helicobacter )C - chemical


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Autoimmune chronic gastritis

Autoantibodies to gastric parietal cellsHypochlorhydria/achlorhydriaLoss of gastric intrinsic factor leads tomalabsorption of vitamin B12 withmacrocytic,megaloblastic anaemia


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Morphology of chronic gastritis

Chronic inflammatorycell infiltrationMucosal atrophyIntestinal (goblet cell)metaplasia

Seen in Helicobacter and autoimmune gastritis (not chemical)


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Helicobacter pylori

Adapted to live inassociation withsurface epitheliumbeneath mucus barrierCauses cell damageand inflammatory cellinfiltrationIn most countries themajority of adults areinfected


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Helicobacter gastritis

Acute inflammationmediated bycomplement andcytokinesPolymorphismsinfiltrate epitheliumand may be partlyresponsible for itsdestructionAn immune responseis also initiated(antibodies may bedetected in serum)


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Helicobacter gastritis

2 patterns of infectionDiffuse involvement of body and antrum(pan gastritis associated withdiminishing acid output)Infection confined to antrum (antralgastritis, associate with increased acidoutput)


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Chemical gastritis

Commonly seen withbile reflux (toxic tocells)Prominent hyperplasticresponse(inflammatory cellsscanty)

With time intestinalmetaplasia


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Consequences of gastritis

Peptic ulcer disease ( Helicobacter )Adenocarcinoma (all types)

The African enigma are complicationsof H.pylori infection less frequent in

Africans?Case not yet resolved


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Peptic ulcer disease

A surface breach of mucosal lining of GItract occurring as a result of acid and pepsin attackSites:

Duodenum (DU)Stomach (GU)

OesophagusGastro-enterostomy stomaRelated to ectopic gastric mucosa (e.g. inMeckels diverticulum)


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Acute peptic ulcer

Like acute erosion but breachingmuscularis mucosaeSpecific examples

Curlings ulcer (following severe burns) Cushings ulcer (following head injury)


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Chronic peptic ulcer

Complex epidemiologyDU most common in Europe, GU in

JapanIncidence of DU declining, GU stable


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Pathogenesis

In normalacid/pepsin attackis balanced bymucosal defencesIncreased attack byhyperacidity

Weakenedmucosal defence the major factor ( H.pylori related)


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Acid production

Tends to be high in DU patients. Antralgastritis causes increased gastrin

production and acid secretionAcid stimulates development of gastricmetaplasia in the duodenumHelicobacter organisms colonise themetaplastic epithelium and causeinflammatory damage leading to ulceration


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Acid in GU

Pan gastritis diminishes acid secretionOngoing gastritis and epithelialdamage is the main causal factor forulceration


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Helicobacter factors inpathogenesis

Some strains are more pathogenic thanothers. The Cag A (cytotoxic) antigen is one

important virulence factorHuman variability also plays a part (e.g.individuals who produce high levels of IL-1 b in inflammation get pan gastritis and GU,lower levels associated with antral gastritisand DU)


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Morphology of peptic ulcers

Clean, non-elevated edge

Granulation tissuebase (floor)Underlying fibrosis


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Gastric neoplasms

Polyps are common but usually notneoplastic (hyperplastic polyps.

Hamartomas, ectopic pancreas)Adenomas occur but are rare


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Carcinoma of the stomach

The second most common fatal malignancy in the world

(after lung cancer)Commonest in Far East (Japan)Incidence decliningHigh mortality unless disease detectedearly


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Pathology

Vast majority areadenocarcinomasArise on backgroundof chronic gastritis,intestinal metaplasia,dysplasiaMost cases advancedat presentation


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Macroscopic Pathology

Gross typesPolypoid

UlcerativeInfiltrative (extremeis linitis plastica leather bottlestomach)


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Microscopy

Intestinal type(forms glands likecancers of colonand oesophagus)Diffuse type dissociated tumourcells oftencontaining amucinous blob signet ring cells


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Spread of gastric carcinoma

Local infiltration (through wall of stomach toperitoneum, pancreas etc)

Lymphatic local and regional lymph nodesBlood liver, lungsTranscoelomic (across peritoneal cavity).Often involves ovaries (esp. signet ringcancer) Krukenberg tumour.


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Less common gastricneoplasms

LymphomaGastrointestinal stromal tumour (GIST)Neuroendocrine (carcinoid) tumours


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Gastric lymphoma

Malignantneoplasm of

mucosa associatedlymphoid tissue(MALT)A (usually) lowgrade B-cell(marginal cell)lymphoma


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Gastric lymphoma (maltoma)

Neoplastic cellsinfiltrate theepithelium(lymphoepitheliallesions)Strongly associatedwith H. pylori andcan be cured byeliminatinginfection.


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Gastrointestinal stromaltumours (GIST)

Mesenchymal neoplasmsDerived from interstitial cells of Cajal

(pacemaker cells controllingperistalsis)Overexpress c-kit oncogene

Used as diagnostic aid on tissueA target for therapy with tyrosine kinaseinhibitor imatinib (also used in CML)


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GIST-spindle cell neoplasm ofGI tract


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GIST

Larger tumours with high mitotic ratetend to behave malignantly

Stomach is commonest site


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Neuroendocrine tumours

Carcinoids are tumours of residentneuroendocrine cells in gastric glands

Usually seen in context of chronicatrophic gastritis (driven by gastrin)Clinical behaviour variable

3.the Stomach

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