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Bact: H. Pylori

DD H. Pylori

what is the shape of H pylori curved
catalase status of H pylori positive
02 requirements of H pylori microaerophilic
oxidase status of H pylori positive
urease status of H pylori positive
how do you diagnose H pylori urease breath test and serology
what are the virulence factors of H pylori urease, flagella, adhesins, VacA, CagA, LPS
what does Urease do? protects from gastric acid
what does flagella do? motility
what do adhesins do bind frucose carb on antrum cells
what does VacA do? induces vacule formation and interferes with vesicle trafficking
what does CagA do injected into the host and alters cytoskeleton
how does H pylori get CagA pathogenicity island there are 40 genes
what does CagA tripper IL8
what does LPS do? Lewis group blood ag may cross react and damage H/K atpase
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
what is active gastritis mild asymptomatic antral gastritis with pain cramping, nausea and vomiting that goes away after a month
what is chronic superficial gastritis asymptomatic in ALLLL ind. infected
what percent of gastric ulcers are caused by H. Pylori 70% the rest are caused by NSAIDS
what percent of duodenal ulcers are caused by H. Pylori 100% but there must be gastric metaplasia
what is MALT B Cell Lymphoma caused by chronic immune stimulation
what is atrophic gastritis destruction of acid secreting glands
what percent of gastric adenomas are caused by H. pylori 80-95%
what percent of people in developing countries are infected with H pylori 90%
what percent in developed contries are infected with H pylori 30%
how is H pylori spread or determined in children fecal oral route based on number of siblings and age differences
where is H. pylori found feces, dental plaques, saliva
how long is someone infected life long carriage
where can H. pylori colonize only antral gastric mucosa or gastric metaplasia in the duodenum
what is H pylori famous for most common bacterial infection in the world
what happens when there is too much acid gastric ulcers and gastric metaplasia ulcers
how is it that there would be too much acid increased gastrin with reduced somatostatin
what happens when there is too little acid promotes atrophic gastritis and gastric adenocarcinoma
what do you commonly find with normal stomach acid? Malt B cell lymphoma
what is the component of H. Pylori that acts a molecular mimickry Lewis b
what percent of the worlds population is affected half
what percent of those infected have overt disease 10-15%
how long does it take H. pylori to invade it doesn't
what must mutate to go from h.pylori to chronic gastritis tpr-met
what must be lost to go from atrophic gastritis to int. metaplasi k-ras
what must you lose to go from int. metaplasia to dysplasia p53
what must you lose to go from dysplasia to CA DCC
what is the active and chronic mucosal response to H. pylori IL - 8 secretion
what does IL-8 do? ROS and NO secretion
ROS and NO do? DNA damage
how is CagPA1 delivered Type IV injection
people with ? tend to progress to gastric cancer IL-1 B
what can you use to diagnose treatment progress of H. pylori urease breath test not serology because Abs stick around for months or years
when do you test for H.pylori when you intend to treat (greater than 50 with chronic dyspepsia or warning signs)
what percent of those infected with H. pyloric convert to active gastritis .4%/year
what class carcinogen is H pylori Class I
how do you treat H. pylori PPI, clarithromycin and amoxicillin
how do you treat Hpylori that does not respond well quadruple therapy- bismuth, metronidazole, tetracyclin and PPI
how do you treat peptic ulcer disease H2 block, PPI, eradicate H. pylori, stop ASA/NSAIDS, surgury?
Created by: jmuame03