Gastric Disease Flashcards
contrast curling ulcer and cushing ulcer
curling: second to burns, loss of fluid causes mucosal hypoxia
cushing: brain trauma causes more CN10 firing and more gastric acid secretion
chronic gastritis etiologies
prolonged H pylori infection
autoimmune
other like diet
pathogenesis of chronic gastritis
lymphs, plasma cells, macros can cause epithelial cell necrosis- sometimes atrophy, metaplasia, cancer
gross patho of chronic gastritis
thin, atrophic gastric wall and atrophy of rugal folds
histopath of chronic gastritis
can have gland and mucosa atrophy
can have intestinal metaplasia- turn into simple columnar epithelium w/ goblet cells- dense pink absorptive cells
pathogenesis of autoimmune chronic gastritis
autoAb to parietal cells cause chronic inflamation
atrophy and less acid production
less intrinsic factor cause less B12 and pernicious anemia
PUD etiologies
H pylori, NSAIDs, increased gastric acid (ZE syndrome)
PG role in ulcer formation
they are defensive, constitutive from COX 1 to help w/ mucus protection
inhibited by NSAIDs
gross path of PUD
usually just one, punched out cookie cutter appearance w/ smooth base and margins
4 zones of active ulcer
from top to bottom: fibrinopurulent exudate necrotic tissue granulation tissue fibrotic tissue/scar
uncomplicated PUD presentation
epigastric pain
can have nausea, bloating, fullness
3 main complications of PUD
hemorrhage (common)
perforation (more common in duodenum)- can cause peritonitis
obstruction- esp in pylorus, gastric outlet obstruction (from edema, scar, hypertrophy)
presentation of complicated PUD
bleeding- melena, hematemesis
perforation- toxic appearance/ shock, peritoneal signs
obstruction- vomiting, succusion splash
management for uncomplicated vs complicated PUD
uncomplicated: mainly medical- PPI, eradicate H pylori, stop NSAIDs and smoking
complicated- scope for bleeding, NG suction and/or surgery for obstruction, surgery for perforation
ZE syndrome
rare disease, gastrinoma in pancreasa secretes gastrin and causes ulcers