浙江大学医学院：酒精肝 Peptic Ulcer（PPT讲稿）

浙医一院 Peptic Ulcer Chaohui Yu vch623 asina.co13957161659

Peptic Ulcer Chaohui Yu ych623@sina.com 13957161659

浙医一院 Suggested readings >消化性溃疡,内科学第二版人民卫生出版 社,434-445 >Acid peptic disease, Cecil medcine, 24t edition. 886-895 >Peptic ulcer disease, Lancet, 2009: 374 1449-1461 Helicobacter pylori infection, N Engl J Med2010:363:1597-1604

Suggested readings ➢消化性溃疡,内科学第二版,人民卫生出版 社,434-445 ➢Acid peptic disease, Cecil medcine,24th edition,886-895 ➢Peptic ulcer disease, Lancet, 2009; 374: 1449-1461 ➢Helicobacter pylori infection, N Engl J Med,2010;363;1597-1604

The self-digestion of GI mucosa 浙医 caused by gastric acid and pepsin The rate is 10%/ in population

The self-digestion of GI mucosa caused by gastric acid and pepsin The rate is 10% in population

Why does the ulcer happen? 浙医一院 normal defense Bicarbonate gastric mucosa mucous cells Acid, pepsine H H HCO parietal cell pH 6- Lcus laver G cell ecl cell chief cell ella ce GASTRIC GLAND mucosa

Why does the ulcer happen?- normal defense Acid, pepsine epithelial cell submucosa mucus layer Bicarbonate

Defensive barrier of gastric and duodenal mucosa mucus barrier mucosal barrier physical defense chemical counteraction quick refreshment of epithelial cell abundant circulation of blood HCO, nutrition factor: pgelege intercellular tight junction abundant submucosal blood vessel HCO, counteracts h+

Defensive barrier of gastric and duodenal mucosa mucus barrier physical defense chemical counteraction mucosal barrier quick refreshment of epithelial cell abundant circulation of blood nutrition factor: PGE1,EGF intercellular tight junction abundant submucosal blood vessel HCO3 - counteracts H+

浙医一院 A cid, pepsine Balance in attack d

Balance in attack and defence Acid, pepsine

Mucosal damage 浙医一院 Pathogenesy of pu .Acid and pepsine .Helicobacter pylori NSAIDs .Motility disturbance Stress .Systemic inflammatory disorders . schemia Hypergastrinemic Syndromes .Hyperhistaminic syndromes Anastomotic or marginal Ulceration Alcohol Tobacco

Mucosal damage Pathogenesy of PU •Acid and Pepsine •Helicobacter pylori •NSAIDs •Motility disturbance •Stress •Systemic inflammatory disorders •Ischemia •Hypergastrinemic Syndromes •Hyperhistaminic Syndromes •Anastomotic or marginal Ulceration •Alcohol •Tobacco

浙医一院 Pathogenesy of PU--Acid Pepsine Pepsine Maxim um activity of enzyme%) rely on Acid o no acid no ulcer 60 parietal cell mass parietal sensibility feedback suppression 1 2 3 Gastric fluid pH e vagal tone

Pathogenesy of PU—Acid & Pepsine 0 20 40 60 80 100 Maximum activity of enzyme(%) 1 2 3 Gastric fluid pH 4 2 4 Pepsine rely on Acid no acid,no ulcer parietal cell mass parietal sensibility feedback suppression vagal tone

Pathogenesy ofpu 浙医一院 -Helicobacter pylori Biology abostrychoid,have flegalla, microamount requirement of oxygen urase urea NH3 oVac A cag A Evidence-based medicine high positive rate of HP in PU the eradication of Hp facilitate the healing of PU the eradication of Hp degrades the recurrence of PU

Biology bostrychoid,have flegalla, microamount requirement of oxygen urase: urea NH3 Vac A, Cag A Evidence-based medicine high positive rate of HP in PU the eradication of Hp facilitate the healing of PU the eradication of Hp degrades the recurrence of PU Pathogenesy of PU —Helicobacter Pylori

The Nobel prize in physiology or Medicine 2005 for their discovery of the bacterium Heficobacter pylori and its role in gastritis and peptic ulcer disease Barry J. Marshal 1. Robin warren ①1/2 of the prize ①1/2 of the prize Australia Australia NHMRC Helicobacter pylori Research Laboratory, QEII Perth, Australia Medical Centre: University of Western Australia Nedlands, Australia b,19512005年10月 b.1937

2005年10月