最新:消化统疾病3课件文档资料.ppt

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1、,Composition,Digestive tube 消化管,Mouth 口腔 Pharynx 咽 Esophagus 食管 Stomach 胃 Small intestine小肠 Large intestine大肠 Anus 肛门,Duodenum 十二指肠,Jejunum 空肠,Ileum 回肠,Digestive glands 消化腺,Superior digestive tube 上消化道,Inferior digestive tube 下消化道,Major salivary glands 大唾液腺Liver 肝Pancreas 胰,Main Function:ingestion,d

2、igestion,absorption,egestion,非肿瘤性疾病食管炎胃炎:慢性胃炎消化性溃疡阑尾炎非特异性肠炎肝脏疾病:病毒性肝炎,肝硬化胆道疾病:胆囊炎,胆石症胰腺疾病:胰腺炎,肿瘤性疾病食管癌胃癌结直肠癌(大肠癌)原发性肝癌胰腺癌,Normal esophageal mucosa,Squamous esophagus,Glandular stomach,Squamous Epithelium,Lamina Propria,Lamina Muscularis,Normal esophageal squamous mucosa,Stratum spinosum;Stratum luci

3、dum;Stratum corneum;Stratum granulosum,Stratum basle,Normal GE junction,Esophagitis,Esophagitis is the inflammation of esophageal mucosa which can be divided into acute and chronic inflammations.They can be caused by some factors as follows:Reflux Infection(viral,fungal,bacterial)Gastric intubationI

4、ntake of corrosive or irritant substances(alkali,acid)Others(over hot or rigid foods,severe smoking,etc),Reflux Esophagitis,Esophageal irritation and inflammation due to reflux of gastric contents into the esophagus.GrossMucosal rednessErosions and/or ulcerationMicroscopicElongation of lamina propri

5、a papillaeBasal zone hyperplasiaEosinophils,+/-other inflammatory cells,Linear erosionsTypical appearance of refluxesophagitis,Reflux esophagitis.Note papilae elongation and basallayer hyperplasia.,Eosinophils in refluxesophagitis,Reflux esophagitis,PresentationHeartburn;,regurgitation of a sour bra

6、sh,rarely chest painThe severity of symptoms is not related closely to the anatomic findingsSequelaeBarretts esophagus,Replacement of the esophageal normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells.It is a complication of long-standing gastroesophag

7、eal reflux,Barretts Esophagus,Barretts esophagus-pathology,GrossIrregular band of dark pink,velvety mucosa extending upward from the gastroesophageal junction as tongues of mucosaMay be very patchy or focalHistologyMetaplastic columnar epithelium with goblet cells,Barretts esophagus,Normal whiteSqua

8、mousmucosa,Pink abnormalGlandularmucosa,Barretts esophagusNote goblet cell metaplasia,Barretts esophagus with dysplasia.Note lack of mucin,nuclear hyperchromasia,and variation in size and shape.,Note nuclear variation,prominent nucleoli,increased mitoses.,High power view of dysplasia in Barretts eso

9、phagus.,Barretts esophagus-sequelae,UlcerationBleedingStrictureAdenocarcinoma:30-to 40-fold greater risk of developing AC than normal populations,Squamous mucosa,Carcinoma arising in Barrettsesophagus,Anatomy of Stomach,Cardia,Fundus,Antrum,Pylorus,body,Lesser curvature,greater curvature,Bulb,Normal

10、 gastric antrum;it contains only mucus glands,and no specialized parietal or chief cells.,Stomach-normal histology,Parietal cells:in fundus and body,make HCl(hydrochloric acid)Chief cells:in fundus and body,make pepsinogenMucous cells:all over,make mucusG cells:in antrum,produce gastrin,Gastritis,In

11、flammation of the gastric mucosa,the majority of which are chronic gastritis but some distinct forms of acute gastritis are sometimes encounteredThis diagnosis is often both overused and missed.,Chronic Gastritis,Defined as the presence of chronic mucosal inflammatory changes leading eventually to m

12、ucosal atrophy and epithelial metaplasiaOften asymptomatic,but probably present in over 50%of older adults,Chronic Gastritis,Chronic superficial gastritis,Chronic atrophic gastritis,A type:an autoimmune gastritis,can lead to pernicious anemia due to the deficiency of intrinsic factor which is caused

13、 by losing large amounts of parietal cells,B type:mainly affects antrum,No atrophy and epithelial metaplasia,Chronic Gastritis Etiologies,Helicobacter pylori,H.pyloriBile refluxOthers,including smoking,alcohol,radiation,uremiaAutoimmune reaction,This photo taken with a high powered electron microsco

14、pe shows the tiny H.pylori bacteria(pink)attacking the gastric cells which line the inside of the stomach.This bacteria was discovered by Dr.Barry Marshall and Robin Warren in Australia in 1982.,Chronic superficial gastritis,Chronic superficial gastritis,Grossly:(on gastroscopy examination)frequentl

15、y affects the antrumCongestion and edema in mucosa,deep red colour.Erosive and hemorrhagic in the superficial layer.,Histologically:infiltration of lymphocytes and plasma cells within the upper third of the gastric mucosa.Lamina propria mucosa gland is normal.Tiny foci hemorrhagic erosions may appea

16、r.,Chronic superficial gastritis,Chronic superficial gastritis,Chronic superficial gastritis,Chronic superficial gastritis,Chronic Atrophic Gastritis,Chronic Gastritis-Pathology,Gross:The mucosal folds are flattened,and mucosa layer become thin and grey-white.So submucosal vessels can be seen throug

17、h the thinned mucosa,Chronic atrophic gastritis,Chronic Gastritis-Pathology,HistologyInfiltration of lymphocytes and plasma cells all over the gastric mucosa,accompanied by gathering lymphocytesMucosal epithelium and lamina propria mucosa glands are atrophyMetaplasia:Intestinal metaplasia and pseudo

18、pyloric metaplasia,Intestinal metaplasia gastric mucosa is displaced by intestinal mucosapseudopyloric metaplasia The parietal cells and principal cells of the gastric corpus glands and fundic glands are displaced by mucous cells which resemble those of the pyloric glands,Chronic atrophic gastritis,

19、Neutrophilic infiltration of gastric glands and increasedchronic inflammatory cells in the lamina propria are seen in chronic gastritis secondary to Helicobacter pylori.,Chronic atrophic gastritis,Intestinal metaplasia,Dysplasia(mild),Dysplasia(moderate),Dysplasia(severe),Chronic Gastritis-Clinical,

20、May be asymptomaticEpigastric discomfort,anorexia,nausea,vomitingComplications:Peptic ulcersIncrease the risk of gastric carcinoma,about five-fold higherHP infection can induce gastric lymphoma,Hypertrophic gastritis/gastropathyMenetrier diseaseHypertrophic hypersevretory gastropathyZollinger-Elliso

21、n syndromeSpecific forms of gastritisGastritis verrucosaEosinophilic gastrtisothers,Peptic Ulcers,Definition:Ulcer:a breach in the mucosa of the alimentary tract that extends through the muscularis mucosae into the submucosa,or deeperErosion:only a breach in the superficial mucosa,Peptic Ulcers,Pept

22、ic ulcers are chronic,usually solitary,lesions that mainly occur in the stomach and duodenum where exposed to acid-pepsin juicesOver 98%are in the first portion of duodenum or stomach,DU:GU is about 4:1Remitting and relapsing lesions,H.pylori:present in 70%of gastric ulcers and 70%-90%duodenal ulcer

23、sNSAIDS:the major cause of peptic ulcers which have no H.pylori infectionOthers:smoking,alcoholic cirrhosis,renal failure,increased calcium,psychological stressGenetic of racial influences appear to play little or no roleZollinger-Ellison syndrome:caused by gastrinoma,Etiology,Morphology,GrossLocati

24、on:usually in the first portion of duodenum,especially the anterior or posterior walls,or lesser curvature of the stomach Defects in the mucosa that penetrate into the submucosa,often into the muscularis propria or deeper,Round,sharply punched-out craters,generally no more than 2 cm in diameterMargi

25、ns are perpendicular,flat and regularSurrounding mucosal folds may radiate like wheel spokesThe bottom usually appears clean owing to peptic digestion of the exudate and necrotic tissue,Chronic peptic ulcer.Note that it is solitary,with clean,Punched-out craters and smooth edges.,Chronic peptic ulce

26、r,Microscope:A classical ulcer bottom can be distinguished four zones,from luminal surface to the outer:First exudation Second necrotic layerThird granulation tissueFourth fibrous,collagenous scar,Clinical Symptoms,Epigastric gnawing,burning,boring painPain appears 1 to 3 hours after meals during da

27、y and can be relieved by alkalis or food,worse at night Nausea,vomiting,bloating,belching,and weight loss,Results and Complications,Healing:fibrous scarringHemorrhage:10%35%,chiefPerforation:5%,fewer but more severe,cause peritonitis which can lead to deathPyloric obstruction or stenosisMalignant transformation:less than 1%,Perforation,Deseases of Small and large intestines,1.Appendicitis2.Crohn Disease3.Ulcerative Colitis4.Tumors,

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