Professional Documents
Culture Documents
Ulcer:
o Breach in muscularis mucosa of GI tract
o Erosion is more superficial breach
o Ulcers begin as erosions, but not all erosions progress to ulcers
Peptic ulcer:
o Chronic, usually solitary, due to acid-peptic juices
Causes:
o Mucosal injury due to Helicobacter pylori infection, NSAID use, Zollinger-Ellison
syndrome (multiple peptic ulcerations in stomach, duodenum and jejunum due
to excess gastrin secretion by a tumor), ischemia, bile / pancreatic juice reflux
o Alcohol, smoking, COPD and corticosteroids use may exacerbate peptic ulcer
disease and impair healing
o Hyperacidity present in minority of duodenal ulcers and only rarely in gastric
ulcers
o H. pylori has nearly universal association for duodenal ulcers; present in 65% of
gastric ulcers and 90% of gastric ulcers not related to NSAID use or Zollinger-
Ellison syndrome
Clinical features
Incidence in US of 4 million, 350,000 new cases / year
3,000 deaths per year
Affects 10% of American men, 4% of women (M/F = 3:1 for duodenal ulcers, 1.5-
2:1 for gastric ulcers)
Incidence has decreased recently for duodenal ulcers, not for gastric ulcers
Pathophysiology
H. pylori related ulcers:
o Produces urease (to protect it from acid), protease (breaks down glycoproteins
in gastric mucus), phospholipase (damages epithelial cells, may release
leukotrienes)
o Attracts neutrophils that produce myeloperoxidase (turns HCl into hypochlorous
acid, combines with NH3 to form monochloramine)
o Both hypochlorous acid and monochloramine destroy mammalian cells