DD H. Pylori
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| what is the shape of H pylori | curved
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| catalase status of H pylori | positive
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| 02 requirements of H pylori | microaerophilic
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| oxidase status of H pylori | positive
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| urease status of H pylori | positive
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| how do you diagnose H pylori | urease breath test and serology
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| what are the virulence factors of H pylori | urease, flagella, adhesins, VacA, CagA, LPS
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| what does Urease do? | protects from gastric acid
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| what does flagella do? | motility
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| what do adhesins do | bind frucose carb on antrum cells
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| what does VacA do? | induces vacule formation and interferes with vesicle trafficking
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| what does CagA do | injected into the host and alters cytoskeleton
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| how does H pylori get CagA | pathogenicity island there are 40 genes
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| what does CagA tripper | IL8
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| what does LPS do? | Lewis group blood ag may cross react and damage H/K atpase
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| what diseases can H pylori cause | active gastritis, chronic superficial gastritis, gastric ulcers, duodenal ulcers, MALT B cell lymphoma, Atrophic Gastritis, Gastric Adenoma, and Nonulcer dyspepsia
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| what is active gastritis | mild asymptomatic antral gastritis with pain cramping, nausea and vomiting that goes away after a month
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| what is chronic superficial gastritis | asymptomatic in ALLLL ind. infected
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| what percent of gastric ulcers are caused by H. Pylori | 70% the rest are caused by NSAIDS
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| what percent of duodenal ulcers are caused by H. Pylori | 100% but there must be gastric metaplasia
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| what is MALT B Cell Lymphoma caused by | chronic immune stimulation
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| what is atrophic gastritis | destruction of acid secreting glands
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| what percent of gastric adenomas are caused by H. pylori | 80-95%
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| what percent of people in developing countries are infected with H pylori | 90%
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| what percent in developed contries are infected with H pylori | 30%
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| how is H pylori spread or determined in children | fecal oral route based on number of siblings and age differences
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| where is H. pylori found | feces, dental plaques, saliva
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| how long is someone infected | life long carriage
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| where can H. pylori colonize | only antral gastric mucosa or gastric metaplasia in the duodenum
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| what is H pylori famous for | most common bacterial infection in the world
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| what happens when there is too much acid | gastric ulcers and gastric metaplasia ulcers
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| how is it that there would be too much acid | increased gastrin with reduced somatostatin
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| what happens when there is too little acid | promotes atrophic gastritis and gastric adenocarcinoma
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| what do you commonly find with normal stomach acid? | Malt B cell lymphoma
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| what is the component of H. Pylori that acts a molecular mimickry | Lewis b
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| what percent of the worlds population is affected | half
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| what percent of those infected have overt disease | 10-15%
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| how long does it take H. pylori to invade | it doesn't
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| what must mutate to go from h.pylori to chronic gastritis | tpr-met
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| what must be lost to go from atrophic gastritis to int. metaplasi | k-ras
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| what must you lose to go from int. metaplasia to dysplasia | p53
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| what must you lose to go from dysplasia to CA | DCC
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| what is the active and chronic mucosal response to H. pylori | IL - 8 secretion
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| what does IL-8 do? | ROS and NO secretion
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| ROS and NO do? | DNA damage
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| how is CagPA1 delivered | Type IV injection
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| people with ? tend to progress to gastric cancer | IL-1 B
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| what can you use to diagnose treatment progress of H. pylori | urease breath test not serology because Abs stick around for months or years
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| when do you test for H.pylori | when you intend to treat (greater than 50 with chronic dyspepsia or warning signs)
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| what percent of those infected with H. pyloric convert to active gastritis | .4%/year
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| what class carcinogen is H pylori | Class I
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| how do you treat H. pylori | PPI, clarithromycin and amoxicillin
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| how do you treat Hpylori that does not respond well | quadruple therapy- bismuth, metronidazole, tetracyclin and PPI
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| how do you treat peptic ulcer disease | H2 block, PPI, eradicate H. pylori, stop ASA/NSAIDS, surgury?
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