2 8.1.1 ESOPHAGITIS reflux esophagitis Definition: esophageal irritation and inflammation due to reflux of gastric secretions into the esophagusPathologic changes:Eosinophiles, with or without neutrophils, in the epithelial layerBasal zone hyperplasiaElongation of lamina propria papillaeIntraepithelial neutrophils are markers of more severe injuryPresentation: heartburn and reguritationComplications: bleeding, stricture, bronchospasm and asthma,barrett esophagus
3 2.Barret esophagusDefinition: metaplasia of the squamous eosphageal mucosa to a more protective columnar type because of chronic exposure to gastric secretionsCause: gastroesophageal reflux diseaseGross: irregular gastroesophageal junction with tongues of red granular mucosa extending up into the esophagusIncreased risk of dysplasia and esophageal adenocarcinoma
4 Esophageal carcinoma Squamous cell carcinoma Adenocarcinoma EpidemiologyThe most common type of esophageal cancerMales>females; age usually>50Risk factorsHeavy smoking and alchol useAchalasiaPlummer-vinson syndromeTylosisPrior lye ingestionPresentationOften asymptomatic until late in the courseProgressive dysphagiaWeight loss and anorexiaBleedingHoarseness or cough (advanced cancers)Diagnosis: endoscopy and biopsyTreatment: surgeryPrognosis: poorAdenocarcinomaArises in the distal esophagusAssociated with Barrett esophagus and dysplasiaPrognosis: poor
9 acute gastritisDefinition: acute inflammation, erosion, and hemorrhage of the gastric mucosa due to a breakdown of the mucosal barrier and acid-induced injuryEtiology: chronic aspirin or NSAID use/ Alcohol use/ Smoking/ Postsurgery/ Burns/ Ischemia/ Stress/ Uremia/ ChemotherapyPresentation Epigastric abdominal pain Gastric hemorrhage, hematemesis, and melena
14 2. chronic gastritis—chronic mucosal inflammatory changes leading eventually to mucosal atrophy and epithelial metaplasia.PathogenesisHP chronic infectionchronic irritationautoimmunereflex of bilious duodenal secretion
23 Intestinal metaplasia replacement of gastric epithelium with absorptive and goblet cells of intestinal-typeVariable gland loss and mucosal atrophy, lymphocyte and plasma cell infiltration in the lamina propria.
25 Fundic type (type A) Antral type （type B) Autoimmune atrophic gastritisrareInvolve the body and fundusAutoantibodies to parietal cells / intrinsic factorLoss of parietal cellsDecreased acid secretionIncreased serum secretion ( G cell hyperplasia)Pernicious anemia (megaloblastic anemia due to lack of intrinsic factor and B12 malabsorption)Helicobactor pylori gastritisCommonHelicobactor pyloriCurved, gram negative rodsUrease producingRisk of infection increase with ageAssociated with chronic gastritis (type B)Associated with duodenal / gastric peptic ulcersAssociated with gastric carcinomaGross: loss of rugal folds in the body and fundusMicro:mucosal atrophy with loss of glands and parietalcellsChronic lymphoplasmacytic inflammationIntestinal metaplasiafoci of acute inflammationChronic inflammation with lymphoid folliculesIncreased risk of gastric carcinoma
26 8.1.3 peptic ulcerUlcer: defects in the mucosa that penetrate at least into the submucosa, and often into the muscularis propria or deeperDefinition: ulcers of the distal stomach and proximal duodenum caused by gastric secretion (hydrochloric acid and pepsin) and impaired mucosal defensesDiagnosis: endoscopy ±biopsyTreatment:acid suppression (H2 blocker, proton pump inhibitor)eradication of H. pyloriComplications:hemorrhage: 1/3，common, hematemesis, melena, shockiron deficiency anemiapenetration into adjacent organs: 5%, acute diffuse peritonitis , local peritonitisperforation (X-ray: free air under the diaphragm)pyloric obstruction : 2- 3%gastric ulcer: 1%; duodenal ulcer: no
27 2)Pathogenesis of peptic ulcer Increased damageDamaging factorsHPNSAIDssmokingalcoholgas. acidityDuo-gast.refluxPeptic acidpepsinhemorrhagep.stenosisNormal mucosaPeptic ulcerhealingImpaired defensesDefensive factorsischeriashockDelayedgastric emptyMalignant t.Surface mucus secr.HCO- into mucusMucosal blood flowEpithelia regeneraPGEpithelial barrierperforation2)Pathogenesis of peptic ulcerNSAIDs：非类固醇类抗炎药
39 Duodenal ulcer common Location: anterior wall of the proximal duodenum Classic presentation: burning epigastric pain 1-3 hours after eating, which is relived by foodPeptic ulcer of the dudenum. The ulcer is small with a sharply punched-out appearance. Unlike cancerous ulcers, the margins are not elevated. The ulcer base shows a small amount of blood but is otherwise clean.
42 8.2.1 Gastric carcinoma Epidemiology: Japan/ Chile/ Columbia Risk factors:dietary factors: smoked fish and meats/ pickled vegetablesHP infectionchronic atrophic gastritissmokingprior subtotal gastrectomypresentationoften asymptomatic until late in the courseweight loss and anorexiaepigastric abdominal pain mimicking a peptic ulcerearly satietyoccult bleeding and iron deficiency anemiaLocation: lesser curvature of the antrum
44 GrossLarge (>2cm), irregular ulcerHeaped-up margins and a necrotic ulcer baseMay also occur as a flat or polypoid massMetastasisVirchow (sentinel) node: left supraclavicular lymph nodeKrukenberg tumor: spread to the ovaryDiagnosis: endoscopy and biopsyTreatment: gastrectomyPrognosis: poor; over all 5-year survival 20%
45 Intestinal typemicro: gland-forming adenocarcinomaDiffuse typediffuse infiltration of stomach by poorly differentiated tumor cellssignet-ring cells: nucleus is displaced to the periphery by intracellular mucinlinitis plastica: thickened “leather bottle”-like stomach
47 pathologic change (1) early gastric car. (shallow spread car.） concept confined to the mucosa and submucosa, regardless of the size of area, or absence of perigastric lymph node metastasis
48 protruded type (typeⅠ) >2 times thickness gastric mucosa, polypoid 图9-10 早期胃癌各型模式图2）gross typesprotruded type (typeⅠ)>2 times thickness gastricmucosa, polypoidsuperficial type (type Ⅱ)superficial elevated type（Ⅱa）< 2 times thicknesssuperficial flat type （Ⅱb）superficial depressed （ Ⅱc）depth within mucosaexcavated type (type Ⅲ)common, ulcer早期胃癌各型模式图
54 (2) advanced gastric carcinoma concept：extended below the submucosa into the muscular wall and has perhaps spread more widelygross① polypoid or fungating type② ulceration type：erosive crater, D>2.5cm③ infiltrating type:（Linitis plastica）
64 ulceration type (the ulcer is large with irregular, heaped-up margins ulceration type (the ulcer is large with irregular, heaped-up margins. There is extensive excavation of the gastric mucosa with a necrotic gray area in the ddepest portion.
66 infiltrating type (a broad region of the gastric wall, or the entire stomach, is extensively infiltrated by maglinancy. The rigid and thickened stomach is termed a leather bottle stomach, or linitis plastica.)
67 Gastric adenocarcinoma (gland formation by malignant cells, which are invading the muscular wall of the stomach.)