بسم الله الرحمن الرحیم

1. بسم الله الرحمن الرحیم 1

2. H.M.Mozaffari

3. Peptic ulcer disease 3

4. PUD occures most commonly in duodenal bulb(DU) and stomach(GU). It may also occur in esophagus,pyloric channel,duodenal loop,jejunum,meckel’s diverticulum. PUD results when aggressive factors(gastric acid and pepsin)owerwhelm defensive factors involved in mucosal resistance(mucus,bicarbonate,microcirculation,PG )and from effects of H.P. 4

5. Causes and risk factors General : Major role for H.P that colonizes gastric antral mucosa in up to 100% of persons with DU and 80% with GU.also found in normals(increasing prevalence with age) and those of low socioeconomic status.HP always associated with chronic active gastritis,which can progress to atrophic gastritis and cancer Other major cause is NSAIDs. Fewer than 1% are duo to Z-E syn. Other risk factors and associations:smoking,BGO(antigens may bind HP) mastocytosis,hypercalcemia. Unproven :stress,coffee,alcohol. 5

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9. Other associations: CRF COPD Cirrhosis Renal transplant glucocorticoids 9

10. Clinical features DU:burning epigastric pain 90 min to 3 h after meals,often nocturnal,relieved by food. GU:burning epigastric pain made worse by or unrelated to food,anorexia,weight loss in 40%,gfeat individual variation. Similar symptoms may occur in persons without PUD(NUD),less responsive to standard therapy. 10

11. complications Bleeding Obstruction Penetration causing acute pancreatitis Perforation intractability 11

12. diagnosis DU:upper endoscopy or upper GI barium radiography. GU:upper endoscopy preferable to exclude malignancy(brush cytology,>6 biopsies of ulcer margin) Radiographic features suggesting malignancy:ulcer within a mass,folds that don’t radiate from ulcer margin,large ulcer >2.5-3 cm. 12

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16. Detection of HP Rapid urease:sen(80-95%),spec(95-100%) simple,false negative with recent use of PPIs,antibiotics,bismuth. Histology:sen(80-90%),spec(>95%),requires pathology, provides histologic information Serology:sen(>80%),spec(>90%),inexpensive not usefull for early follow-up. Urea breath test:sen(>90%),spec(>90%),rapid simple,usefull for early follow-up,false negative with recent therapy. 16

17. treatment Medical: discontinue NSAIDs Stop smoking Eradication of H.P Acid suppression Rule out malignancy in GU 17

18. H2 blockers Sucralfate Antacids PPIs 18

19. HP eradication Triple therapy: Bismuth+metronidazole+tetracycline Ranitidinebismuth+tetracycline+ clarithromycin or metronidazole Omeprazole+clarithromycin+metronidazole or amoxicillin 19

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21. Quadruple therapy: Omeprazole + Bismuth + Tetracycline + metronidazole 21

22. surgury Indications: Persistent or recurrent bleeding Obstruction Perforation Intactability(first screen for NSAIDs use and gastrinoma) 22

23. Surgical treatmant Vagotomy+antrectomy(billroth I or II) recurrence:1% complication:highest Vagotomy+pyloroplasty recurrence:10% complication:intermediate Parietal cell(superselective)vagotomy recurrence:>19% complication:lowest 23

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27. Complications of surgery Obstructed afferent loop(bilruth II) Bile reflux gastritis Dumping syn.(rapid gastric emptying with abdominal distress+postprandial vasomotor symptoms) Postvagotomy diarrhea Bezoar Gastric remnant carcinoma 27

28. Compliction of ….. Anemia(iron,B12,folate malabsorption) Ostepmalacia and osteoporosis malabsorption 28

29. Erosive gastropathy Causes: NSAIDs Burns Sepsis Trauma Surgery shock Renal failure Resp.failure Liver failure 29

30. Symptoms and signs May be asymptomatic Epigastric discomfort Nausea Hematemesis Melena Diagnosis by endoscopy 30

31. treatment Remove of offending agent Maintenance of o2 and blood volume Prevention of stress ulcer in ill patients: Hourly oral antacids IV H2 antagonists target PH>4 Sucralfate Misoprostol,high dose famotidine,omeprazole, can be used to prevent NSAIDs induced ulcers. 31

32. Chronic gastritis Type A: body predominant,less common, generally asymptomatic,common in elderly. autoimmune machanism may be associated with achlorhydria,pernicious anemia and increased risk of gastric cancer,Ab to parietal cells in>90%. 32

33. Type B: antral predominant caused by H.P. often asymptomatic but may be associated with dyspepsia may also lead to atrophic gastritis and low grade gastric lymphoma 33

34. Other types of gastritis Alcoholic gastropathy Menetrier’s disease Eosinophilic gastritis Granulomatous gastritis Crohn’s disease Sarcoidosis Infections(TB,syphilis,fungi,virus,parasite) Radiation Corrosive gastritis 34

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39. Zollinger-Ellison syn. Consider when : Ulcer disease is severe Refractory to therapy Atypical locations Associated with diarrhea 39

40. Tumors: Usually pancreatic or in the duodenum May be multiple Slowly growing > 60% malignant 25% associated with MEN I(gastrinoma, hyperpara,pituitary neoplasm) 40

41. Diagnosis: Serum gastrin>1000ng/l or rise in gastrin of 200 ng/l following IVsecretin. 41

42. Gastric cancer 42

43. Risk factors Lower socioeconomic groups Smoked foods Heavily salted foods Genetic factors Atrophic gastritis H.P infection Adenomatous gastric polyps 43

44. Pernicious anemia Menetrier’s disease BG A Billroth II gastrectomy Hyperplastic gastric polyps 44

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47. pathology Adenocarcinoma 85%-90% Lymphoma 5-10% Liomyosarcoma (rare) 47

48. Clinical features Progressive upper abdominal discomfprt Weight loss Anorexia Nausea Acute or chronic GIB Dysphagia Vomiting Early satiety 48

49. Abdominal tenderness Pallor Cachexia Mass Hepatomegaly Ascitis Left supraclavicular node Acanthosis nigricans IDA Occult blood 49

50. diagnosis Double contrast radiography Gastroscopy and biopsy 50