B5.032 Gastric Ulcers Flashcards
where are G cells
antrum
where are parietal cells
body
why do ulcers form?
levels of acid and pepsin in the stomach overwhelm mucosal defense mechanisms
stimuli > receptors > signal transduction pathways of acid secretion
ACh from gastric enteric neurons > muscarinic M3 receptors > intracellular Ca2+
gastrin from G cells > CCK2 receptors > intracellular Ca2+
histamine from oxyntic ECL cells > H2 receptors > cAMP pathway
main inhibitory mechanism against acid secretion
somatostatin
why does H pylori cause ulcers in stomach but not organs like colon/pancreas?
- strict tropism for the gastric mucosa
- does not invade cells; attaches to receptor expressed on gastric surface like Lewis antigens
- causes inflammation that leads to increased secretion which bacteria uses as nutrients
what is a cag pathogenicity island
expressed by some strains of H. pylori
genes within the island form a special apparatus to transport bacterial products inside the host cell to cause more inflammation
why can H pylori cause gastric ulcers in some but duodenal ulcers in others?
antral gastritis (15%) -decreased somatostatin -increased gastrin -increased acid -duodenal ulcer pangastritis (85%) -decreased acid
how do NSAIDs cause gastric ulcers
decreased mucus production by inhibiting COX1 enzyme with reduced prostaglandin secretion
possibilities when you see a “gastric ulcer” in the stomach
benign gastric ulcer
gastric adenocarcinoma
gastric lymphoma
surgical treatment of ulcers
vagotomy and/or distal gastrectomy
what happens when a tumor produces excess gastrin
the basal and maximal acid outputs will increase because parietal cells will produce more acid
ulcers will develop in unusual locations
zollinger ellison
gastrinoma
tumor produces excess gastrin
increased production of histamine
systemic mastocytosis
mast cells produce excessive histamine to increase gastric acid production
