B5.032 Prework 1 Gastric Ulcers Flashcards
definition of gastric ulcer
5 mm or greater break in the lining of the stomach that extends into the submucosa on biopsies or has an appreciable depth during upper endoscopy
how does pepsin play a role in causing gastric ulcers
enzyme active at acidic pH
pepsin can digest proteins within ulcer base and grow ulcer
epidemiology of gastric ulcers
0.14-0.19% annual incidence in US
17-22% in China (H.pylori more prevalent)
incidence inclines with improvements in sanitation
major complications of ulcers
GI bleeding (0.02-0.006% incidence)
perforation (0.004-0.014% incidence)
overall:
bleeding in 10% of ulcer, perforation in 1%
why is acid a necessary component of the digestive system?
acid helps with protein digestion by converting pepsinogen to pepsin
promotes absorption of nonheme iron, vitamin B12, and meds such as ketoconazole and thyroxine
prevent bacterial overgrowth
parietal cell
main cell that makes acid
gastrin
main hormone produced by antral G cells to stimulate parietal cells to secrete acid
somatostatin
main inhibitor of acid secretion
vagus nerve/ Ach
main neurotransmitter that regulates acid secretion by modulating the secretion of gastrin, somatostatin and histamine
H+K+ATPase
final common pathway from acid secretion from all stimuli
how is H+ secreted
occurs in exchange for uptake of K+ ions to maintain neutral electric charge inside the cell
K+ in gastric juice exceeds plasma K+ 2-4 fold
main defenses against gastric ulcer
mucus secretion
bicarb secretion
pH gradient across epithelial surface into lumen
mucus secretion as a defense against acid
firm adherent viscous layer that covers the gastric surface
composed of 95% water and 5% cross linked mucin glycoproteins that are produced by MUC genes
prostaglandin secretion promotes mucus secretion
major causes of ulcers
H. pylori
NSAIDs
idiopathic
Zollinger Ellison
discuss H.pylori infections
majority of people have pangastritis involving both antral and fundic mucosa that lowers stomach defenses by reducing mucous protection
minority of patients have an antrum predominant gastritis which results in high gastric acid secretion (major mechanism of duodenal ulcer formation)
clinical presentation of ulcers
epigastric pain
periodicity (every 6-12 weeks)
some older patients may not develop ab pain and present with bleeding or perforation
diagnosis of ulcers
EGD is procedure of choice for uncomplicated
CT scan is the diagnostic modality of choice for perforated ulcers
special considerations about ulcer causes
type A personality is a risk factor
combo of steroids + NSAID increases risk 8 fold
HP proportion declining, but idiopathic is growing (20-30% in US are idiopathic)
treatment of gastric ulcers
mainstay is medical management
types of medical management for gastric ulcers
treat HP or remove offending NSAID agent
antacids only 67% effective
anti secretory agents to reduce acid production
mucosal protective agents
types of anti secretory agents
H2 blockers
proton pump inhibitors
types of mucosal protective agents
sucralfate
pepto bismol
misoprostol
H2 blockers
competitive inhibitors of histamine stimulated acid secretion and markedly suppress acid secretion
PPIs
inhibit H+K+ATPase
final common pathway
“big guns” for acid suppression
pro-drugs and must be activated by acid
sucralfate
ulcer exposes positively charged proteins which can bind to the sulfate anions in sucralfate
covers the surface of the ulcer and prevents further damage
pepto bismol
can form complexes with mucus to coat ulcers
also has activity against HP infection
turns stools black
colonic bacteria convert bismuth salts to bismuth sulfide that turns stool black
misoprostol
PGE analog which can enhance mucosal defense mechanisms and also inhibit gastric secretion through inhibition of histamine stimulated cyclic AMP pathway
refractory gastric ulcers
most heal within 8 weeks
