Stomach Diseases PUD and a Little More

1. Stomach DiseasesPUD and a Little More ד"ר שאול יערי המכון הגסטרואנטרולוגי הדסה ע"כ

2. על מה נדבר? • Physiology • PUD – • Stomach • Duodenum • Etiologies • Treatment • Misceleneous • Gastritis • Stress related mucosal injury • Menetrier’s disease • Celiac?

3. STOMACH: NORMAL ANATOMY

4. Normal Stomach- endoscopic view

5. Normal Duodenum

6. Structure of Gastric Mucosa Gastric pits

7. GASTRIC GLAND (FUNDUS) Surface cells Parietal cells Mucus neck cells Endocrine cells

8. הקיבה איבר מופלא

9. MUCOSAL INTEGRITY * Pre-epithelial Mechanism: Mucus-Bicarbonate & surface active Phospholipids layer * Epithelial Cell Mechanisms: Tight junctions; Apical cell membrane; Ion pumps; Cell renewal * Post Epithelial Mechanism: Mucosal blood flow

12. Regulation of Acid Secretion

15. לסיכום - פיזיולוגיה • הקיבה איבר מופלא • מנגנוני הגנה פרה, אינטרא ופוסט-אפיתליאלים. • לפרוסטגלנדינים תפקיד חשוב במערך ההגנה על הקיבה. • התאים הפריאטאלים הינם התאים מפרישי החומצה. • הבקרה על הפרשת חומצה מורכבת. • Cephalic, gastric and intestinal stages of digestion • הגירוי החזק ביותר להפרשת חומצה הינו פעולת ההיסטמין על התאים הפריאטלים המופרש בתאי ECL בתגובה לגסטרין.

16. PEPTIC ULCER A Defect in the UGI mucosaEncompasses both gastric and duodenal ulcers. 

17. Duodenal ulcers (DUs) and gastric ulcers (GUs) share many common features in terms of pathogenesis, diagnosis, and treatment, but several factors distinguish them from one another.

18. PEPTIC ULCER- Histology EROSION:Necrotic process extending to the muscularis mucosa ULCER: > 5mm in size process extending deeper to the muscularis mucosa

19. PEPTIC ULCER (histology)

21. PEPTIC ULCER: Endoscopic View INFLAMMATION EROSION ULCER

22. DU and Inflammation ULCER

23. “KISSING” DUODENAL ULCERS

24. http://www.youtube.com/watch?v=K-Ao6kyoaNk • 04:20 • 01:00 • 06:00

25. PEPTIC ULCER DISEASE • Chronic, usually solitary lesions occurring at any GI site exposed to acid & pepsin. • Over 90% occur in the 1st part of duodenum and in the stomach. • 4 million individuals (new cases and recurrences) affected per year. • Lifetime prevalence of PUD in the United States is ~12% in men and 10% in women. • 15,000 deaths per year occur as a consequence of complicated PUD.

26. PUD: PATHOPHYSIOLOGY 1.ACID & PEPSIN SECRETION “No acid no ulcer” Hypersecretory States: Gastrinoma 2.ALTERATIONS IN MUCOSAL INTEGRITY

27. PUD: LOCATION ESOPHAGUS STOMACH DUODENUM “BULB” POST BULBAR

28. DU: EPIDEMIOLOGY • DUs are estimated to occur in 6–15% of the Western population. • The incidence of DUs declined steadily from 1960 to 1980 and has remained stable since then. • The death rates, need for surgery, and physician visits have decreased by >50% over the past 30 years • Before the discovery of HP, the natural history of DUs was typified by frequent recurrences after initial therapy. • Eradication of H. pylori has greatly reduced these recurrence rates.

29. Most often in the first portion of the duodenum (>95%), with ~90% located within 3 cm of the pylorus. They are usually  1 cm in diameter but can occasionally reach 3–6 cm (giant ulcer). Ulcers are sharply demarcated, with depth at times reaching the muscularis propria. DU: PATHOLOGY

30. GU: EPIDEMIOLOGY • GUs tend to occur later in life than duodenal lesions, with a peak incidence reported in the sixth decade. • M>F • Less common than DU. • Same rates at autopsies. • Higher likelihood of GUs being silent and presenting only after a complication develops.

31. In contrast to DUs, GUs can represent a malignancy and should be biopsied upon discovery. Benign GUs are most often found distal to the junction between the antrum and the acid secretory mucosa. Benign GUs associated with H. pylori are also associated with antral gastritis. NSAID-related GUs are not accompanied by chronic active gastritis. GU: PATHOLOGY

32. ENDOSCOPY:Malignant Gastric Ulcer Benign Malignant

33. PUD: CAUSATIVE FACTORS

34. HELICOBACTER PYLORI The Infection discovered to be the etiology of PUD

35. WARREN&MARSHALL פרס נובל לרפואה 2005

36. Discovery of H. Pylori Change in paradigm

37. Epidemiology • The prevalence of H. pylori varies throughout the world. • In developing countries, 80% of the population may be infected by the age of 20. • Prevalence of 20–50% in industrialized countries. • The overall prevalence of H. pylori in the United States is ~30%. • About 10% of Americans <30 years of age are colonized with the bacteria. • The rate of infection with H. pylori in industrialized countries has decreased substantially in recent decades. • Mathematical models suggest that with the present rate of intervention, the organism will be ultimately eliminated from the United States. • Poor socioeconomic status and less education predispose to higher colonization rates. • Transmission of H. pylori occurs from person to person, following an oral-oral or fecal-oral route.

38. Pathogenesis • למען האמת אנחנו לא באמת מבינים. • ובכל זאת...

41. PUD: PATHOPHYSIOLOGY 1.ACID & PEPSIN SECRETION “No acid no ulcer” 2.ALTERATIONS IN MUCOSAL INTEGRITY

43. Pathogenesis • Gastric ulcers - Associated withH. pyloriinduced pangastritis and normal or low gastric acid secretion. • Duodenal Ulcers - • Associated with H. pylori antral infection and increased acid production. • Gastric metaplasia • Decreased duodenal mucosal bicarbonate production. • Data supporting and contradicting each of these interesting theories have been demonstrated.

45. PUD GERD MALT Esophageal CA? Gastric CA Asthma? ITP? Obesity? IDA? Diabetes?

46. HP - את מי לבדוק ובמי לטפל • יש לבדוק רק את מי שיש כוונה לטפל בו/יש לטפל בכל מי שיש לו תשובה חיובית. • כל מי שיש לו מחלה פפטית מוכחת בעבר או בהווה. • MALT Lymphoma • Resectable adenocarcinoma of stomach • דיספפסיה ללא סמני אזהרה. • בכל המצבים יש לודא ארדיקציה.

48. PUD: Therapy For a Bacterial Disease:Eradication of H.Pylori

50. Non steroidal anti-inflammatory drugs (NSAIDs) and the Gastrointestinal tract