3.the Stomach
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Transcript of 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