H. pylori Flashcards
How is H pylori spread?
mostly unclean water supply, making this often a disease of low SES
oral-oral transmission possible
food refrigeration and proper food preservation helps reduce spread
What conditions are associated with H pylori infection?
inflammatory gastritis, gastric and duodenal ulcers, gastric cancers. But, in most ppl, H pylori resides as a harmless comensal organism.
Acid secretion in the stomach
acid secretion stimulated from parietal cells after food triggers gastrin release form G cells. gastrin simulates parietal cells directly and also stimulates histamine release from the ECL population. Histamine also stimulates gastrin release. ECL cells may also be stimulated by vagal nerve.
Feedback inhibition: gastric acid directly stimulates the somatostatin secreting D cells of the antrum. somatostin inhibits G cells.
How does H pylori affect gastric acid secretion?
inflammatory gastritis of h pylori leads to selective destruction of D cells. loss of feedback inhibition on gastin release from G cells: high levels of basal and meal-stimulated acid release.
Natural hx of duodenal ulcer disease
chronic relapsing/remitting disease that usually occurs in younger people, esp. in countries where H pylori infection occurs at a young age. (ages 20-50 in US; teens in developing nations). duodenal ulcers may present bc infection causes aggressively inflammatory gastritis and hyperacidity, esp. in first 2 decades post-infection.
with treatment, we dramatically decrease the risk of recurrance from 60% in 1 yr to less than 10%. This effect persists for more than 7 yrs
Natural hx of gastric ulcer disease
generally seen in moderately older pts than in duodenal ulcer disease- after 20-30 yrs of infection, the mucosa burns out from chronic damage and the residual tissue is atrophic gastritis. damaged tissue causes ulcers due to decreased mucosal defense. H pylori eradication still helps prevent relapses of gastric ulcer disease
How does gastric adenocarcinoma arise in the context of H pylori infection?
atrophic gastritis (tissue left after 20-30 yrs of h. pylori infection and mucosal burnout) is pro-neoplasm.
serology for H pylori
serologic testing useful for establishing h pylori infection, but doesn’t turn negative for yrs after treatment, so not good at determining success of tx. Additionally, it is important to remember that our job is to diagnose the cause for symptoms (ulcers, cancer, etc.), not just determine who has asymptomatic infection. Don’t treat h. pylori until you know for sure what the underlying pathology is- otherwise you may miss CANCERS.
urea breath test
capsule with labeled urea is ingested by the pt. active h pylori infection will cleave the urea, releasing labeled CO2 to be exhaled. lower sensitivity than serology but better for follow-up to determine if eradication was successful
tx for h pylori infection
drug combinations, usually triple therapies. pepto bismol with tetracycline and metronidazole. give for 2 wks with an acid suppressor (rinitidine).
easier therapy: PPI +clarithromycin and either amoxicillin or metrodnidazole. test for eradication 4 wks after completion of therapy.
What should I know about NSAIDs and risk?
safe drugs: but so widely prescribed that complications are common. account for half of all hemorrhaging ulcers in elderly pts.
mechanisms for NSAID injury
topical, systemic, and re-exposure
who is at high risk of developing NSAID ulcers?
elderly, ppl with prior ulcers, ppl on steroids, high dose NSAIDs, combined aspirin and NSAIDs, coinfection with H pylori
high risk of hemorrhage for pts
on multiple anti-platelet agents
chronic anticoagulation
protective strategies for pts
only use drugs when indicated (ie if you need an analgesic, try tylenol or alternating tylenol and an NSAID), cotherapy with protective drugs: misoprostol or PPIs
