Stomach & Doudenum Disease

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Stomach & Doudenum Disease

  1. 1. <ul><li>Disease OF </li></ul><ul><li>Stomach & </li></ul><ul><li>Duodenum </li></ul><ul><li>By Dr. Osman Bukhari </li></ul>
  2. 2. <ul><li>Functions of the stomach </li></ul><ul><li>1- Reservoir of food </li></ul><ul><li>2- Grinding & mixing of food </li></ul><ul><li>3- Digestion </li></ul><ul><li>4- Absorption </li></ul><ul><li>5- Propulsion of contents to duodenum </li></ul><ul><li>6- Defensive </li></ul><ul><li>7-Intrinsic factor </li></ul>
  3. 3. <ul><li>Mucosa </li></ul><ul><li>Surface epithelium with rich blood supply & rapid turnover. It's covered with mucous rich in bicarbonate. </li></ul><ul><li>1-Parietal cells ــــــــ Hcl & intrinsic factor </li></ul><ul><li>2-Chief cells ــــــــ pepsinogen ـــ pepsin in </li></ul><ul><li>the presence of Hcl. </li></ul><ul><li>3-Mucous secreting cells ـــــــ mucous & </li></ul><ul><li>CHO3 </li></ul><ul><li>4- G- cells ــــــ Gastrin---high Hcl </li></ul><ul><li>5- D- cell ــــــــ Somatostatin ــــــ low Hcl </li></ul>
  4. 4. <ul><li>* Parietal cells has receptors for Acetyl choline, Gastrin & Histamine which stimulate release of Hcl. H/K </li></ul><ul><li>A.T.Pase is the final pathway for acid secretion (P.P) </li></ul>
  5. 5. <ul><li>Acute </li></ul><ul><li>Gastritis </li></ul>
  6. 6. <ul><li>Acute Gastritis </li></ul><ul><li>- Inflammatory disease involving superficial epithelium ـــــــ erosion + ulceration </li></ul><ul><li>* Causes </li></ul><ul><li>1-Asprin & NSAID </li></ul><ul><li>2-Alcohol </li></ul><ul><li>3-Bilary reflux </li></ul><ul><li>4-Infection (H.pylori, CMV, Herpes) </li></ul>
  7. 7. <ul><li>5-Sress (Trauma, burns, shock, MOF, Hepatic & renal disease) </li></ul><ul><li>Clinical Feature </li></ul><ul><li>1-Asymptomatic </li></ul><ul><li>2-Dyspepsia </li></ul><ul><li>3-Rarely bleeding or iron deficiency </li></ul><ul><li>aenmia </li></ul>
  8. 8. <ul><li>Diagnosis </li></ul><ul><li>1-Clinical in almost all cases </li></ul><ul><li>2-Gastroscopy if there is bleeding to exclude PU & Ca </li></ul>
  9. 9. <ul><li>Treatment </li></ul><ul><li>1-Stop offending drug </li></ul><ul><li>2-Treat any cause including infection </li></ul><ul><li>3-Symptoms settle in most cases without treatment </li></ul><ul><li>4-Some need anti acid, acid suppression + anti emetic </li></ul>
  10. 10. <ul><li>Chronic </li></ul><ul><li>Gastritis </li></ul>
  11. 11. <ul><li>Chronic Gastritis </li></ul><ul><li>-In chronic active gastritis there is infiltration of lamina propria with lymphocytes & plasma cells leading to atrophic gastritis & gastric atrophy with loss of parietal & chief cells & subsequent metaplasia </li></ul>
  12. 12. <ul><li>Causes </li></ul><ul><li>1-Autoimmune </li></ul><ul><li>2-H. pylori </li></ul><ul><li>3-Drugs & bile </li></ul><ul><li>4-T.b, Crohns, CMV & Sarcoidosis </li></ul><ul><li>5-Idiopathic </li></ul>
  13. 13. <ul><li>Type A Gastritis </li></ul><ul><li>1-It is autoimmune disease with circulating Abs against parietal cells & intrinsic factor </li></ul><ul><li>2-Evidance of organ specific Auto immune disease </li></ul><ul><li>3-Gastric atrophy affecting body & fundus </li></ul><ul><li>4-Pernicious anemia </li></ul><ul><li>5-Increased incidence of Ca </li></ul>
  14. 14. <ul><li>Type B Gastritis </li></ul><ul><li>1-Affects the Antrum </li></ul><ul><li>2-Due to H. Pylori ــــــــ PU </li></ul><ul><li>Clinical feature </li></ul><ul><li>1-Asymptomatic </li></ul><ul><li>2-Dyspepsia </li></ul><ul><li>3-Often associated with PU </li></ul><ul><li>4-Diagnosed by gastroscopy </li></ul>
  15. 15. <ul><li>Helicoloater pylori (H.pylori) </li></ul><ul><li>1-Gram + spiral bacteria </li></ul><ul><li>2-Produces Urease </li></ul><ul><li>3-Found in gastric auntrum & area of gastric metaplasia in the duodenum deep to mucous layer closely adherent to epithelial surface, protected from acid & pepsin digestion by over lying mucous, bicarbonate & by release of ammonia (Urease action) ــــــ high PH </li></ul>
  16. 16. <ul><li>4-Prevalence increases with age & 2/3 are acquired in childhood. </li></ul><ul><li>5-Person to person transmission </li></ul><ul><li>6-Found in 90% of patients with DU & 70% with GU </li></ul><ul><li>Pathogenesis </li></ul><ul><li>1-Increases fasting & postprandial gastrin </li></ul>
  17. 17. <ul><li>2-Increases pepsinogen secretion </li></ul><ul><li>3-Decreases gastric mucosal resistance </li></ul><ul><li>4-Suppresses somatostatin release </li></ul><ul><li>5-Releases tissue damaging cytotoxins </li></ul><ul><li>-Cag – A (Cytotoxin associated gene) </li></ul><ul><li>-Vac – A (Vacillating Cytotoxin) </li></ul>
  18. 18. <ul><li>Clinicopath. features </li></ul><ul><li>1-Though 2/3 of population are infected with H. pylori, only 10 ـــ 15% develop PU & the majority are asymptomatic </li></ul><ul><li>2-Lead to acute gastritis ـــــــ chronic gastritis </li></ul><ul><li>+_PU </li></ul><ul><li>3-Long standing chronic gastritis ـــــــ gastric atrophy & increased risk of metaplasia & the earlier H. pylori acquired , the greater </li></ul>
  19. 19. <ul><li>is risk of Ca </li></ul><ul><li>4-More than 90% of MALT lymphomas have H. pylori & low grade tumours regress with H. pylori eradication </li></ul><ul><li>5-Treat all patients with H. pylori because of associated risk of Ca </li></ul>
  20. 20. <ul><li>Diagnosis </li></ul><ul><li>1-Rapid Urease breath test:- </li></ul><ul><li>Used for screaming & to test for H. pylori eradication following treatment, expensive </li></ul><ul><li>2-Serology:- </li></ul><ul><li>Sensitive, specific & used for epidemiological surveys </li></ul>
  21. 21. <ul><li>3- Endoscpic antral biopsy for </li></ul><ul><li>- Rapid Urease test (CLO) </li></ul><ul><li>- Culture & sensitivity (Gold standard </li></ul><ul><li>investigations) </li></ul><ul><li>-Histological examination </li></ul>
  22. 22. <ul><li>H. pylori eradication therapy </li></ul><ul><li>A) P.P.I based triple therapy with two antibiotic </li></ul><ul><li>1-Omeprazole 20mg bid + Metronidazole 400mg bid + Claithromycin 500mg bid for 7 days, (90% effective) OR </li></ul><ul><li>2-Omeprazole 20mg bid + Metronidazole 400mg bid +Amoxil 1gm bid for 7- 10 days (85- 90% effective) OR </li></ul>
  23. 23. <ul><li>3-Omeprazole 20mg bid + Amoxil 1gm bid + Claithromycin 250mg bid for 7-10 days. (85%) effective </li></ul><ul><li>B) H2 RA based triple therapy </li></ul><ul><li>*Bisthmus is included in some regimens </li></ul>

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