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Bact: H. Pylori
DD H. Pylori
| Question | Answer |
|---|---|
| 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
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