【正文】 omy 5) Gastrojejunostomy 3) Vagotomy amp。 drainage DU DU pyloroplasty HeineckeMikulicz pyloroplasty Finney pyloroplasty Excision pyloroplasty Posterior gastroenterostomy Anterior juxtapyloric gastroenterostomy Pyloric dilation by gastrotomy DU 1) Subtotal gastrectomy 2) Vagotomy amp。 drainage 3) Vagotomy amp。 drainage 3) Vagotomy amp。Diseases of the Stomach and Duodenum Dept. of Gastrointestinal Surgery First Affiliated Hospital Sun Yatsen University Surgical treatment for peptic ulcer “If there is no acid, peptic ulceration cannot occur.” In fact, peptic ulcers may occur anywhere where pepsin and acid occur together . They may occur in the esophagus, the duodenum, the stomach itself, the jejunum after surgical construction of a gastrojejunostomy, or in the Meckel’s diverticulum . Peptic Ulcer Disease Duodenal ulcer(DU) Gastric ulcer(GU) The causes, Clinical features, and prognosis of DU and GU are different. DU and GU ?Etiology ? acid ? Nerval and humoral secretion ? mucosal defences ? mucosal barrier prevent antidromic diffuse ? Pylori infection ? impair mucosal defences PU is caused by an imbalance between secretion of acid and pepsin, and breakdown of mucosal defence. An acid environment and reduced mucosal defences provide ideal circumstances for pepsin to cause mucosal ulceration. Etiology and Pathogenesis DU or overexcitment of vagus nerve number of parietal cells quick gastric emptying GU retention of duodenal juice of parietal cells Etiology and Pathogenesis Overexcitement of vagus nerveDU Breakdown of mucosal defencesGU Helicobactor Pylori infectionBoth Incidence M?F： Men are affected 3 times as often as women. DU ?GU： DU is 10 times more mon than GU in the young pts. But in the older age groups the frequency is about equal. In general terms, the ulcerative process can lead to 4 types of disability: ?Pain: most mon ?Bleeding ?Perforation ?Obstruction Chief cellpepsinogen Cardiac gland area mucous secreting cell Parietal cellacid oxyntic gland area parietal amp。 chief cell pyloric gland area G cell Crowsfoot Latarjet N 90% afferent 10% efferent Duodenal Ulcer Duodenal Ulcer Occurrence A mon disease 10% of the adult population in USA Incidence ↓ since 1955 Complications remain high DU Men:Women = 3:1 DU : GU = 10 :1 (young) = 1 :1 (old) DU Any age group Most mon in 20 45 years old 95% within 2cm from the pylorus 5% postbulbar ulcer DU Physiological Abnormalities ↑numbers of parietal and chief cell ↑parietal cell sensitivity to gastrin ↑gastrin response to meal ↑gastric emptying ↓inhibition of gastrin release to acid DU Clinical Findings Morning Noon Afternoon Evening 2Am Symptoms Epigastric Pain Aching Burning Gnawing Daily Cycle of Pain Some : no GI plains DU Food, milk,or antacid temporary relief Back pain Perating ulcer Nausea Vomiting， belching Tendeness localized epigastric Many no tenderness DU Laboratory Findings 1) Test for occult blood 2) Gastric analysis 3) Serum gastrin Interpretation of the results of gastric analysis Normal DU ZES BAO mM/hr 5 15 MAO mM/hr 30 40 40 DU Serum Gastrin Performed if ZES suspected Readily available Normal basal levels: 50100 pg/ml (Conventional PU) Abnormal 200 pg/ml 1) ZES 2) Retained antrum after BII op. DU Barium meal (upper GI series) Direct sign: Crater Indirect sign: Duodenal deformity Xray: 90% reliable DU DU stomach Duodenal bulb pylorus DU Duodenal bulb stomach pylorus Thickened folds DU Ulcer crater(niche) DU Gastroduodenoscopy: Useful Essentials of Diagnosis ?Epigastric pain relieved by food or antacids ?Epigastric tenderness ?Normal or increased gastric