Peptic Ulcer Disease Flashcards
peptic ulcer disease
ulceration of upper GIT
ulcer
open sore on external/internal body surface d/t break in skin or mucous membrane that fails to heal
stomach’s protection against acidity of HCl
stomach secretes mucus that unaffected by HCl acidity
duodenum protection against acidity of HCl
uses pancreatic juice that is released into duodneum and buffers low pH of gastric content and neutralizes acid
when do ulcers occur
when acid affects mucosa (1st layer of tissue) and penetrates into deeper layers
etiology
helicobacter pylori infection
H. pylori adhesion factors
it secretes adhesion factors to invade body and attach to stomach or duodenum wall
how H. pylori survives acidic HCl
- produces urease which converts urea into CO2 + NH2
- water in stomach combines w/ CO2 to produce H2CO3
- H2CO3 dissociates into HCO3- and H+ (volatile acid)
- HCO3- buffers HCl to protect bacteria from harm (micro-niche)
how H. pylori does harm (patho)
- produces inflm mediators that damage stomach/intestinal wall where bacteria attached too
- produces mediators that trigger hypergastrinemia (excess prod of gastrin in blood)
gastrin
hormone that inc HCl secretion
how hypergastrinemia causes harm
- inc gastrin –> inc HCl –> inc acid –> inc urease produced by H. pylori to buffer acid and protect itself
- results in acid eroding stomach/intestinal wall (inflm) whilc bacteria remains unharmed
ulceration occurs where
- most inflm occurs
- acid most impactful (mainly where bacteria attached)
protective factors used by GI T
- buffering in duodenum w/ pancreatic juice
- regeneration of mucosal cells
- mucus protection in stomach
risk factors
- NSAIDs
- irregular HCl and biliary acid
- chronic gastritis
- smoking
- alcohol
- caffeine
- along w/ H. pylori infection
mnfts
- heartburn (acid affects tissue)
- abd cramping/burning on an empty stomach
- N/V (local mnfts)
