Stomach
Ulcers
Peptic ulcer disease

Author: Elliot Weisenberg, M.D. (see Authors page)

Revised: 29 November 2016, last major update August 2012

Copyright: (c) 2003-2016, PathologyOutlines.com, Inc.

PubMed Search: peptic ulcer disease[title]
Cite this page: Peptic ulcer disease. PathologyOutlines.com website. http://www.pathologyoutlines.com/topic/stomachPUD.html. Accessed December 9th, 2016.
Definition / General
  • Ulcer:
    • Breach in muscularis mucosa of GI tract
    • Erosion is more superficial breach
    • Ulcers begin as erosions, but not all erosions progress to ulcers

    Peptic ulcer:
    • Chronic, usually solitary, due to acid-peptic juices

  • Causes:
    • 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
    • Alcohol, smoking, COPD and corticosteroids use may exacerbate peptic ulcer disease and impair healing
    • Hyperacidity present in minority of duodenal ulcers and only rarely in gastric ulcers
    • 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:
    • Produces urease (to protect it from acid), protease (breaks down glycoproteins in gastric mucus), phospholipase (damages epithelial cells, may release leukotrienes)
    • Attracts neutrophils that produce myeloperoxidase (turns HCl into hypochlorous acid, combines with NH3 to form monochloramine)
    • Both hypochlorous acid and monochloramine destroy mammalian cells

  • NSAID related ulcers:
Sites
  • Duodenum, antrum, lesser curvature near incisura most common site in stomach, GE junction, margins of gastrojejunostomy, adjacent to Meckel diverticulum containing ectopic gastric mucosa, lower esophagus
  • 98% in stomach or duodenum
  • Duodenum:stomach 4:1
  • Gastric ulcers on greater curvature or not in antrum are more likely to be related to NSAID use, ulceration may also be caused by tumors, infections (other than H. pylori) especially in immunocompromised patients
Treatment
  • Antibiotics if H. pylori induced promote healing of ulcers and reduce greatly recurrences, proton pump inhibitors, discontinuation of NSAIDS and corticosteroids, smoking cessation
Gross Description
  • 90% < 4 cm, 50% < 2cm, clean base (due to peptic enzymes), surrounded by erythematous mucosa, may see blood vessel in ulcer base
Micro Description
  • Generally associated H. pylori gastritis, may see reactive gastropathy if history of NSAID use
  • Ulcer may be transmural or limited to mucosa and submucosa
Micro Images

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Various images