Path-Gastritis Flashcards
name the 5 sections of the stomach from top to bottom
cardia, fundus, body, antrum, pyloris
rugae of the stomach contain which layers of stomach tissue?
mucosa and submucosa
what type of epithelium is in the stomach?
simple columnar epithelium with gastric pits and glands
gastric pits are also known as?
foveola (together = foveolar compartment)
which portion of the gatric mucosa varies depending on the region of the stomach?
gastric glands (the foveola is the same throughout)
gastric glands of the fundus and body contain?
parietal cells (acid, IF) and chief cells (pepsinogen)
gastric glands of the cardia, antrum, and pyloris contain?
mucous cells and G cells (gastrin)
parietal cells are (higher/lower) than chief cells and appear (pink/blue)
higher; pink (chief cells are purple/blue)
short pits are found in the ____, while long pits are found in the _____
cardia, antrum
G cells are only found in the _____
antrum
h pylori is a gram ____ rod found in the _____ only
negative; layer of mucus adherent to gastric foveolar cells ONLY (not intestinal)
h pylori is located where ____ levels are highest
urea
how has h pylori adapted to the acidic environment of the stomach?
it synthesizes urease, which degrades urea into ammonia causing local pH to rise
pathogenesis of h pylori
proteases degrade mucus barrier (lose protection) + produce ammonia, cytotoxins which directly injure epithelium
what 4 natural histories are possible as a result of epithelial injury from h pylori?
acute gastritis, chronic gastritis, gastric lymphoma/adenoCA, peptic ulcer dz
how to detect h pylori infection (histo)
silver stain (black dots on yellow background)
definition/pathogenesis of acute gastritis
direct/indirect injury -> acute inflammation of mucosa with neutrophils +/- necrosis (erosion) +/- hemorrhage if deep enough
name 4 etiologies of acute gatritis
drugs (NSAIDs, EtOH, Chemo), infection (h pylori), complication of other dz (uremia), mucosal hypoxia=”stress” (shock, trauma, burns, surgery)
name 3 etiologies of chronic gastritis
- h pylori, 2. autoimmune, 2. diet
pathogenesis of chronic gastritis
lymphocytes, plasma cells, macrophages = immune response = epithelial necrosis +/- atrophy of glands (eventually mucosa) +/- cancerous changes (metaplasia?)
gross pathology of chronic gastritis
thin, atrophic gatric wall lacking rugae
if metaplasia occurs in chronic gastritis, what are gastric cells converted to?
intestinal cells with both columnar absorptive cells and goblet cells
autoimmune chronic gastritis has what inheritance pattern, and attacks what cells?
AD; parietal cells
autoimmune chronic gastritis results in what other condition?
pernicious anemia due to decreased intrinsic factor
in peptic ulcer dz, where are ulcers most commonly found (two locations)?
duodenum (proximal), stomach (lesser curvature of antrum, pre-pylorus)
name 3 causes of PUD
H pylori, NSAIDs, gastrinoma (Zollinger-Ellison)
describe the gross pathology of a peptic ulcer
“punched out” or “cookie cutter” excavation with perpendicular sides and flat surface
four characteristic histopathologic zones of a peptic ulcer
fibropurulent exudate, necrotic tissue, granulation tissue, fibrotic tissue/scar
name 3 complications of a peptic ulcer
hemorrhage (common), perforation (usually in duodenum), obstruction (gastric outlet)
what occurs upon perforation of a peptic ulcer?
peritonitis
what is the most common location of a gastrinoma?
pancreas
pathogenesis of Zollinger-Ellison syndrome
gastrinoma leads to increased gastrin secretion, causing parietal cell hyperplasia and increased gastric HCl secretion, which causes severe peptic ulceration (uncomon cause of ulcers)
