treatment of gastric/duodenal ulcers Flashcards
common symptoms of gastric ulcers
epigastric pain and burning sensation after meals
diagnosis of gastric ulcers+ H pylori
positive carbon-urea breath test, with stool test confirming H pylori
how H pylori causes gastric uclers- which enzyme importance
epithelial cells covered by mucus- parts of this mucus layer dissolved, causing cell death- does this by 1) increasing gastric acid formation through less gastrin/more somatostatin, 2) less defence factors, 3) gastric metaplasia: all this is done via UREASE
treatment of gastric ulcers
antibiotics like amoxicillin/clarithromycin, 2nd like then quinolones, and then bismuth (create less acidicity) if antibiotics then work- THEN PPI’s if antibiotics alone not effective
what urease does
converts urea into NH4CL, which damages epithelial cell- urease also causes inflammation
features of H pylori- type, and location
gram -, usually stays in Gi tract
what exotoxins does H pylori produce
CAGa and VAPa, which can cause tissue inflammation
how Proton pumps works+ cells involved
parietal cells exchange K+ for H+ into stomach- increaase in Ca2+=increased cAMP, more pumps to cell membrane= more H+/acid secretion
how long to use proton pumps
4-12 weeks
if person is negative for carbon-urea breath test/stool antigen test, what is another cause for peptic ulcers, and why
NSAIDS- they reduce mucus production (protective layer), and increase risk of bleeding
treatment of NSAID related peptic ulcers
remove NSAID H2 receptor antagonists eg ranitidine (H2 receptors ie histamine receptors increase acid)
how long to use H2 receptor antagonists
4-8 weeks
how gastric acid regulated- stimulatory vs protective, and what they do+ receptors
ACH from vagus increases Ca2+, gastrin increases Ca2+ via CCK B receptors, histamine increases cAMP, BT prostaglandins (affected by NSAIDS) lower cAMP via EP3 receptors ie protective
