eMedicine Specialties > Emergency Medicine > Gastrointestinal

Gastritis and Peptic Ulcer Disease

Author: Philip Shayne, MD, Associate Professor, Residency Program Director, Vice Chair for Education, Department of Emergency Medicine, Emory University School of Medicine
Contributor Information and Disclosures

Updated: Aug 21, 2008

Introduction

Background

Gastritis includes a myriad of disorders that involve inflammatory changes in the gastric mucosa, including erosive gastritis caused by Helicobacter pylori bacterial infections, other infectious gastritises, nonsteroidal anti-inflammatory drugs (NSAIDs), noxious irritants, reflux gastritis from exposure to bile and pancreatic fluids, infectious gastritis, and gastric mucosal atrophy.

Peptic ulcer disease (PUD) refers to a discrete mucosal defect in the portions of the gastrointestinal tract (gastric or duodenal) exposed to acid and pepsin secretion. Presentations of gastritis and PUD usually are indistinguishable in the ED, and thus the ED management is generally the same. Emergent complications include hemorrhagic shock and peritonitis secondary to a perforated ulcer. The clinician should be concerned about other life-threatening conditions (eg, acute coronary syndromes and aortic aneurysms), which can mimic the presentation of gastritis.

For more information, see Medscape's Peptic Ulcer Disease Resource Center.

Pathophysiology

The mechanisms of mucosal injury in gastritis and PUD are thought to be mainly caused by H pylori infections, coupled an imbalance of aggressive factors, such as acid production or pepsin, and defensive factors, such as mucus production, bicarbonate, and blood flow.

Erosive gastritis usually is associated with serious illness or with various drugs. Stress, ethanol, bile, and nonsteroidal anti-inflammatory drugs (NSAIDs) disrupt the gastric mucosal barrier, making it vulnerable to normal gastric secretions.

Infection with H pylori, a short, spiral-shaped, microaerophilic gram-negative bacillus, is the leading cause of PUD and is associated with virtually all ulcers not induced by NSAIDs. H pylori colonize the deep layers of the mucosal gel that coats the gastric mucosa and presumably disrupts its protective properties. H pylori is thought to infect virtually all patients with chronic active gastritis. Eradication of H pylori was thought to be the pathway to curing ulcer disease, but that has proven increasingly challenging.

NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal prostaglandins. Many people with known H pylori colonization or who are taking NSAIDs do not suffer from gastritis or PUD, which indicates other important causative factors must be involved.

Frequency

United States

Approximately 10% of Americans eventually develop PUD, and about 10% of patients presenting to the ED with abdominal pain are diagnosed with PUD. Prevalence has decreased in the United States over the last 30 years.

International

Frequency of PUD is decreasing in the developed world but increasing in developing countries.

Mortality/Morbidity

  • Complications of gastritis include PUD and, rarely, extensive bleeding. PUD accounts for more than 50% of all causes of upper gastrointestinal bleeds in the United States.
  • Complications of peptic ulcer disease include bleeding, occasionally massive, and perforation leading to peritonitis and sepsis (rare).
  • The mortality rate is low.

Sex

  • Male-to-female ratio of gastritis is approximately 1:1
  • Male-to-female ratio of PUD is approximately 2:1

Age

  • An estimated 60% of Americans older than 60 years harbor H pylori.
  • Duodenal ulcers usually occur in those aged 25-75 years.
  • Gastric ulcer prevalence peaks in those aged 55-65 years.

Clinical

History

  • Patients typically present with abdominal pain that has the following characteristics:
    • Epigastric to left upper quadrant
    • Frequently described as burning
    • May radiate to the back
    • Usually occurs 1-5 hours after meals
    • May be relieved by food, antacids (duodenal), or vomiting (gastric)
    • Typically follows a daily pattern specific to patient
  • NSAID-induced gastritis or ulcers are usually silent.
  • Sudden onset of symptoms may indicate perforation.
  • Gastritis may present as bleeding, which is more likely in elderly patients.
  • Symptoms consistent with anemia (eg, fatigue, dyspnea) may manifest.

Physical

  • Epigastric tenderness is present and usually mild.
  • Bowel sounds are normal.
  • Signs of peritonitis or GI bleeding may be manifest. Perform a rectal examination and Hemoccult testing.

Causes

  • H pylori (most common cause of ulceration)
  • NSAIDs, aspirin
  • Gastrinoma (Zollinger-Ellison syndrome)
  • Severe stress (eg, trauma, burns), Curling ulcers
  • Alcohol
  • Bile reflux
  • Pancreatic enzyme reflux
  • Radiation
  • Staphylococcus aureus exotoxin
  • Bacterial or viral infection

More on Gastritis and Peptic Ulcer Disease

Overview: Gastritis and Peptic Ulcer Disease
Differential Diagnoses & Workup: Gastritis and Peptic Ulcer Disease
Treatment & Medication: Gastritis and Peptic Ulcer Disease
Follow-up: Gastritis and Peptic Ulcer Disease
Multimedia: Gastritis and Peptic Ulcer Disease
References

References

  1. Friedman LS, Peterson WL. Peptic ulcer and related disorders. In: Fauci AS, Braunwald E, Isselbacheret KJ, et al, eds. Harrison's Principles of Internal Medicine. 14th ed. McGraw-Hill; 1998:1596-1616.

  2. Logan RP, Walker MM. ABC of the upper gastrointestinal tract: Epidemiology and diagnosis of Helicobacter pylori infection. BMJ. Oct 20 2001;323(7318):920-2. [Medline].

  3. McColl KE. Helicobacter pylori-negative ulcer disease. J Gastroenterol. 2000;35 Supple 12:47-50. [Medline].

  4. Moss SF, Sood S. Helicobacter pylori. Curr Opin Infect Dis. Oct 2003;16(5):445-51. [Medline].

  5. Pang SH, Leung WK, Graham DY. Ulcers and gastritis. Endoscopy. Feb 2008;40(2):136-9. [Medline].

  6. Peek RM, Blaser MJ. Pathophysiology of Helicobacter pylori-induced gastritis and peptic ulcer disease. Am J Med. Feb 1997;102(2):200-7. [Medline].

  7. Soll AH. Consensus conference. Medical treatment of peptic ulcer disease. Practice guidelines. Practice Parameters Committee of the American College of Gastroenterology. JAMA. Feb 28 1996;275(8):622-9. [Medline].

  8. Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med. Oct 10 2002;347(15):1175-86. [Medline].

  9. The Medical Letter. Drugs for treatment of peptic ulcers. Med Lett Drugs Ther. Jan 3 1997;39(991):1-4. [Medline].

  10. Yeomans ND. Management of peptic ulcer disease not related to Helicobacter. J Gastroenterol Hepatol. Apr 2002;17(4):488-94. [Medline].

  11. Yuan Y, Padol IT, Hunt RH. Peptic ulcer disease today. Nat Clin Pract Gastroenterol Hepatol. Feb 2006;3(2):80-9. [Medline].

Further Reading

Contributor Information and Disclosures

Author

Philip Shayne, MD, Associate Professor, Residency Program Director, Vice Chair for Education, Department of Emergency Medicine, Emory University School of Medicine
Philip Shayne, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey Glenn Bowman, MD, MS, Consulting Staff, Highfield MRI, Columbus, Ohio
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Eugene Hardin, FAAEM, FACEP, Former Chair and Associate Professor, Department of Emergency Medicine, Charles R Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King, Jr/Drew Medical Center
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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