【正文】 ate and severe dysplasia is considered to be possible precancerous conditions4 / 24atrophiainflammationmetaplasiaClinical manifestationsymptoms : dyspepsia signs : without。既往無胃病及肝病史。 ⒈可能的診斷是什么？請寫出診斷依據(jù) ⒉確診應選用哪項檢查？ ⒊請寫出治療原則Peptic UlcerContents?Introduction?Atiology and Pathogenesis?Pathology ?Clinical Presentation?Laboratory Evaluation?Diagnosis and Differential Diagnosis?Medical ManagementI. Introduction（1 ）definition of PU? Ulcers are defects in the gastrointestinal mucosa that perate the muscularis mucosae.? Peptic Ulcer ? gastric ulcer, GU, duodenal ulcer, DU ? Low esophagus, Distal duodenum and jejunum, ileum in or near Meckel’s diverticula.（2）Epidemiology⒈ Case rate?A mon disease（10% individuals）?The most mon PU: DU amp。 fallII. Etiology and pathogenesis（I）Causes?Helicobacter Pylori（Hp）?Acid amp。④ Vagal hyperactivity.nonsteroid antiinflammatory drugs, (NSAIDs) NSAIDs mainly cause GU. DU can occur as a result of NSAIDs use but to a lesser degree than GU.⑴ NSAIDs and PU ①Leading to PU Hinder PU healing ②Increasing incidence of plications and recurrence of PU⑵ Pathogenic Mechanisms of NSAIDs①Suppression endogenous Prostaglandin synthesis②Cause decreased mucus and bicarbonate secretion③Diminished mucosal blood flow④Reduced epithelial cell renewalgeic factor① Familial aggregation of PU② HyperpepsinogenemiaⅠ(PGI)③ Individuals with blood group O have an increased risk of PU④ Monozygotic twins⑤ Gene markers（HLABB1BW35）⑥ Linked to some inherited syndromesabnormal motor function ①GU Patient： Abnormalities in pyloric sphincter Decreased gastric emptying②DU Patient： Increased gastric emptying Postpone of migrating motor plex(MMC)6 . stress and psychologic factors⑴ Proof ①Psychologic stress are more frequently developed DU. ②May induce the recurrence and aggravate the symptoms of PU. ③At war time ,more PU⑵ Mechanisms ①Acid secretion increasedVagal mechanisms ②Direct effects on mucosal integrity (? blood flow). other factors① Smoking② Diet：Alcohol、Tea、Coffee、Salt③ Infection of virus： Herpes simplex virus（HSV1） Cytomegalo virusSummaryI、Causes of PU：?Hp：no Hp，no ulcer ?PH：no acid，no ulcer?NSAIDs?geic factor?abnormal motor function?stress and psychologic factors?other factors（II） 、Mucosal Barrier1. Mucus/Bicarbonate Barrier；2. Mucosal barrier；3. Mucosal Blood flow 4. Gastrointestinal hormones： Epidermal growth factor(EGF)， Insulinlike growth factor(IGF1) at al.（III）Pathogenic mechanisms Invasive(Aggressive) Factors ：AcidPeptic, Microanism, HPBile salt,Alcohol, DrugsDefensive Factors ： Mucus/Bicarbonate Barrier,Mucosal Blood flow, Prostaglandin, Epidermal growth factorSummary Pathogenic mechanisms of PUInvasive (Aggressive)Factors↑ Acid PepticDefensive Factors↓ Mucus/Bicarbonate BarrierDU — Invasive Factors↑ GU — Defensive Factors↓III. Pathology1. Location： DU：Anterior wall of duodenal bulb GU：Lesser curvature of gastric antrum, gastric angle2. Number： Single or multiple3. Size amp。 6 / 24?Like DU， Middle night pain and backache；?easily to bleeding。 Shape： Round or oval in shape， Often＜A. Have smooth, regular, rounded edges.B. With a flat,smooth ulcer base often filled with exudate.C. Hyperemia and edema around ulcer.D. Folds radiating to ulcer margin.E. Relatively smaller.3. Stages in EndoscopyA（active stage） Hyperemia, Edema around ulcer。 Tissue regenerate to fill the ulcer crater.S（scar stage） Granulation tissue converts to fibrous tissue. Contraction of the scar. V. Complications1． bleeding The most mon causes of UGIH（50%）⑴ DU: 1520%, GU: 1015%.⑵ Being the initial symptom in 1020% PU patients.⑶From occult blood loss to massive bleeding.(4) Easily to be induced by NSAIDs.(5) 3050% patients will bleed again. 2．Perforation① Acute perforation (Free perforation) Rupture into the peritoneal cavity。 Resulting in persistent and intractable pain.③ Fistula formation Extension into a hollow viscus。 Can remitting after effective treatment. ②Chronic(anic) obstruction: Fibrosis of the ulcer scar。 GCGU 　　 GCAge （40y↓）　 （40y↑）Courses Longer，Episodicity Shorter, progressCharacters Rhythmicity pain， No rhythmicityCondition well Condition poorEffective treatment Difficult treatmentOccult blood Temporary + Continued +Acid test N or↓ ↓↓↓ Xray Crater outside gastric wall Within Endoscopy Small, Smooth,Clear,Flat OppositeVII. Prevention and treatmentAims?Remove causes?Eliminate symptoms?Cure ulcer?Prevent recurrence?Avoid plication（I） General Treatment?A regular life, avoidance of overwork and mental stress。⑵ Antimuscarine drugs?Affect： Block gastric muscarinic receptorsreduce fast and food stimulated acid secretion.?Drugs ： Pirenzipine?Side effects :Block other muscarinic receptors. Delay gastric emptying, GU can not be used.⑶ H2 Receptor antagonists (H2RA) Drugs Intensity Direction Cimetidine 1 400mg bid( 800mg hs ) Ranitidine 410 150mg bid ( 300mg hs )Famotidine 2050 20mg bid ( 40mg hs )Nizatidine 410 150mg bid( 300mg hs ) Course：DU 68 weeks ，GU 812 weeks⑷ Proton pump inhibitor（PPI ） Drugs DirectionOmeprazole 20 mg qdLansoprazole 30 mg qdPantoprazole 40 mg qdRabeprazole 10 mg qd唉索美拉唑 40mg qd2．Enhancing Mucosal Defense Drugs⑴ sucralfate ① Affect：Form