Gastrointestinal Pathology I Case Studies


CASE 3: Peptic ulcer


Clinical History:

A 55-year-old woman, with a history of epigastric pain relieved by food, complained of episodes of hematemesis that have occurred in the past week. Upper GI endoscopy with biopsies was performed (image 3.1). The specimen shown here is from the subsequent partial gastrectomy (image 3.2). The lesion appears as a cup-shaped ulcer filled with blood clot. The ulcer, which was found to extend almost through the gastric wall, is lined by necrotic debris and acute inflammatory cells overlying a base of granulation tissue and fibrosis (images 3.3 and 3.4) with a large vessel at the base (image 3.5).
  1. What is the diagnosis?

    2. This proved to be a benign chronic peptic ulcer of stomach, despite the large size.

  2. What is the cause of the hematemesis?

    3. There is erosion of the ulcer into the wall and into a large artery, which explains the hematemesis in this patient.

  3. Why should biopsy of such lesions be performed?

    4. Biopsy should be done because it is not possible to tell a benign from a malignant ulcer by appearance alone.

  4. What does the adjacent gastric mucosa show?

    5. The adjacent mucosa shows chronic gastritis, which is usually present in about 75% of gastric ulcers.

  5. What infectious agent can increase the risk for these findings?

    6. Helicobacter pylori is associated with chronic superficial gastritis, and some of these patients develop peptic ulcer disease, and a smaller number of infected persons develop gastric cancer or gastric lymphoma.

  6. What drug therapy could help prevent this condition?

    7. Patients with H. pylori infection should receive eradication treatment. Successful treatment requires that antibiotics be used in combination with acid suppressants or bismuth. Regimens such as amoxicillin and clarithromycin or metronidazole and clarithromycin with the proton pump inhibitor omeprazole have achieved eradication rates of approximately 90% in trials, though lower eradication rates are probably more common. Some H. pylori strains are resistant to clarithromycin or metronidazole, or both.

    Omeprazole suppresses gastric acid secretion by inhibiting the H+/K+ ATPase enzyme system (the "proton pump") at the secretory surface of the parietal cell, blocking the last step in acid formation. Omeprazole is thus characterized as an acid-pump or proton pump inhibitor. This effect is dose-related. After oral administration, omeprazole begins to have an effect within an hour, and the maximal effect of a single dose is achieved within two hours. Inhibition lasts up to 72 hours, despite the less than one hour plasma half-life, because of prolonged binding of the drug to the acid-pump enzyme. Normal acid secretion returns gradually over 3 to 5 days following discontinuation of the drug. The effect of omeprazole on acid secretion achieves a plateau after four days of single daily doses.