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Upper GI - Coggle Diagram

- - - - Testing for H. pylori: 1) urease breath test (not reliable of on a PPI):2) stool antigen test (use to see if treatment was successful) 3) serologic test: only indicates exposure and does not indicate current infection. can also be seen on biopsy, histology or culture. * you can have a false negate rate on PPI, thus you should stop 10-14 days prior to testing, antibiotics should be stopped 2-4 weeks prior to testing
      - Treatment: PPI, 2 antibiotics, (triple therapy) quadruple therapy: PPI, 2 antibiotics and bismuth. This is the recommended therapy in practice
      - pathophysiology: transmitted through oral-oral or fecal-oral routes. once in lumen it needs a defense against acid. to survive it releases urease which turns HCL into Co2 and ammonia. This creates and alkaline cloud around the bacteria allowing it to survive in the low pH environment. the H pylori penetrates the thick mucus layer (key to our gastric health it protects our gastric) and attaches to the gastric epithelial cells. it then injects virulence factors (saga, vacA). it does not invade the cells! over time it releases lipase and proteases that slowly degrade the mucus layer. We have no way to asses if a disease is acuete or chronic. the usual site of infection is the Antrum. As H pylori causes the pH to rise antrum is gostantly secreting gastrin cells that will produce more acid, attempting to lower the pH. this exacerbates. the duodenum does not have a thick mucus layer in the stomach (no defense) --> large acid load --> duodenal ulceration.
        mostly causes a pan gastritis which can lead to a MALT. in early stages it can just be treated as an H. Pylori irradiation.