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chronicgastritis

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  • 1. Chronic Gastritis
  • 2. Definition Chronic gastritis is defined as the presence of chronic inflammatory changes in the mucosa leading eventually to mucosal atrophy and epithelial metaplasia.
  • 3. Etiology/types/classification Less than 10% 90%
  • 4. Less common etiologies • radiation injury, • chronic bile reflux, • mechanical injury, and • systemic disease such as Crohn disease, amyloidosis, or graftversus-host disease.
  • 5. Autoimmune gastritis (Body predominant) Type A • The most common cause of Less than 10% atrophic gastritis, • Spares the antrum • Hypergastrinemia
  • 6. Autoimmune gastritis is characterized by: • Antibodies to parietal cells and intrinsic factor • Reduced serum pepsinogen I concentration • Antral endocrine cell hyperplAsiA • Vitamin B12 deficiency • Defective gastric acid secretion (achlorhydria )
  • 7. Pathogenesis Autoimmune gastritis is associated with loss of parietal cells, which are responsible for secretion of gastric acid and intrinsic factor. The absence of acid production stimulates gastrin release, resulting in hypergastrinemia and hyperplAsiA of antral gastrinproducing G cells.
  • 8. • Lack of intrinsic factor disables ileal vitamin B12 absorption, leading to B12 deficiency and a slow-onset megaloblastic pernicious AnemiA ). anemia ( • The reduced serum pepsinogen I concentration results from chief destruction. cell
  • 9. clinicAl feAtures • Chronic gastritis usually causes few or no symptoms; 1.Upper abdominal discomfort 2.Nausea 3.Vomiting 4.symptoms of anemia 5.atrophic glossitis, 6. diarrhea. 7.peripheral neuropathy, spinal cord lesions, and cerebral dysfunction.
  • 10. The median age at diagnosis is 60 years. Slightly more women than men are affected.
  • 11. >90%
  • 12. Epidemiology AssociAted with : Poverty, Household crowding, Llimited education, African-American or MexicanAmerican ethnicity, Residence in rural areas .
  • 13. • the mode of h. pylori trAnsmission is not well defined, but humans are the only known host, making oral-oral, fecaloral, and environmental spread the most likely routes of infection.
  • 14. Pathogenesis • The most import cause is infection by H. pylori. Gastritis develops as a result of the combined influence of • bacterial enzymes and • toxins and release of • noxious chemicals by the recruited neutrophils.
  • 15. • After initial exposure to H.pylori, gastritis may develop in two patterns: • 1. antral- tyPe with high acid production and higher risk for the development of duodenal ulcer, and • 2. Pangastritis with multifocal mucosal atrophy, with low acid secretion and increased risk for carcinoma.
  • 16. Four features are linked to H. pylori virulence: 1. Flagella , which allow the bacteria to be motile in viscous mucus 2.urease , which generates ammonia from endogenous urea and thereby elevates local gastric pH 3.adhesins that enhance their bacterial adherence to surface foveolar cells 4. toxins , such as cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer development by poorly defined mechanisms
  • 17. Autoimmune gastritis
  • 18. Type B Ant Ant Pan Pan Type A
  • 19. Clinical Features/Diagnosis . Histologic identification of the organism, Serologic test for antibodies to H. pylori, Fecal bacterial detection, and The urea breath test based on the generation of ammonia by the bacterial urease.
  • 20. • Gastric biopsy specimens can also be analyzed by • the rapid urease test, • bacterial culture, or • bacterial DNA detection by PCR.
  • 21. treatment • Combinations of antibiotics and proton pump inhibitors. • Individuals with H. pylori gastritis usually improve after treatment, although relapses can occur after incomplete eradication or reinfection. • Prophylactic and therapeutic vaccine development is still at an early stage of development.
  • 22. UNCOMMON FORMS OF GASTRITIS Reactive Gastropathy Eosinophilic gastritis Lymphocytic gastritis
  • 23. Complications of Chronic Gastritis • PEPTIC ULCER DISEASE • MUCOSAL ATROPHY AND INTESTINAL METAPLASIA • DYSPLASIA • GASTRITIS CYSTICA
  • 24. CanCer risk • The long-term risk of gastriC CarCinoma for persons with H. pyloriassociated chronic gastritis is increased about fivefold relative to the normal population. • For autoimmune gastritis, the risk for cancer is in the range of 2% to 4% of affected individuals, which is well above that of the normal population.

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