Peptic ulcers
Peptic ulcers: Excerpt from Handbook of Diseases
Peptic ulcer is a disruption in the gastric or duodenal mucosa when normal defense mechanisms are overwhelmed or impaired by acid or pepsin. Ulcers are circumscribed lesions that extend through the muscularis mucosa. Ulcers are five times more common on the duodenum.
Duodenal ulcers occur most commonly between ages 30 and 55; gastric ulcers, between ages 55 and 70.
Causes
Researchers recognize three major causes of peptic ulcer disease: infection with Helicobacter pylori, use of nonsteroidal anti-inflammatory drugs (NSAIDs), and pathologic hypersecretory states such as Zollinger-Ellison syndrome.
H. pylori is the cause of the majority of duodenal and gastric ulcers. Following treatment with standard therapies, 70% to 85% of patients have a documented recurrence (by endoscopy) within 1 year.
Other causes include the use of certain drugs, such as salicylates and other NSAIDs, which encourage ulcer formation by inhibiting the secretion of prostaglandins (the substances that suppress ulceration). Certain illnesses — such as pancreatitis, hepatic disease, Crohn’s disease, Zollinger-Ellison syndrome, and preexisting gastritis — are also known causes. Additionally, having a type A personality increases autonomic nervous system effects on the gastric mucosa.
Predisposing factors
Ulcers are more common in smokers and those who regularly use NSAIDs. (Smoking increases the amount ofhydrochloric acid in the stomach; nicotine reduces the bicarbonate content of pancreatic secretions and also decreases the degree of acid neutralization.) Diet and alcohol don’t appear to contribute to the development of peptic ulcer disease. It’s unclear whether emotional stress is a contributing factor.
Signs and symptoms
Symptoms vary with the type of ulcer.
Gastric ulcers
Gastric ulcers are usually signaled by pain that becomes more intense with eating. The pain is usually constant because the gastric mucosa is sensitive to acid secretion. Nausea or anorexia may occur.
Duodenal ulcers
Duodenal ulcers produce epigastric pain that’s gnawing, dull, aching, or “hunger-like.” The pain is relieved by food or antacids and typically recurs 2 to 4 hours later. Weight loss or vomiting is typically a sign of malignancy or gastric outlet obstruction.
CLINICAL TIP: If the pain changes from rhythmic to constant or radiates, ulcer penetration into the pancreas or perforation may have occurred.
Well-localized midepigastric pain (relieved by food), weight gain (because the patient eats to relieve discomfort), and a peculiar sensation of hot water bubbling in the back of the throat are other reported signs.
Exacerbations tend to recur several times a year, then fade into remission. Vomiting and other digestive disturbances are rare.
Complications
Both kinds of ulcers may be asymptomatic or may penetrate the pancreas and cause severe back pain. Other complications of peptic ulcers include perforation, hemorrhage, and pyloric obstruction.
Diagnosis
A patient with dyspepsia may have an upper GI series to help diagnose a peptic ulcer. For a patient with a confirmed gastric ulcer, an upper endoscopy should be performed to help distinguish between benign and malignant disease. An endoscopy should also be performed in a patient with GI bleeding to identify areas of ulceration. In a patient with a history of peptic ulcer disease, H. pylori may be diagnosed with urease breath testing or serologic testing. H. pylori can also be diagnosed by biopsy via upper endoscopy.
Other tests may disclose occult blood in the stools and a decreased hemoglobin level and hematocrit from GI bleeding.
Treatment
H. pylori can be treated with a combination of agents and eradicated with antibiotics. Pharmacologic treatments include antisecretory agents, such as proton pump inhibitors and histamine-2 (H2)-receptor antagonists. Proton pump inhibitors work by binding to hydrogen-potassium adenosine triphosphatase, located at the surface of gastric parital cells to block formation of gastic acid. H2-receptor antagonists inhibit histamine binding to H2 receptors on the gastric parietal cell, which in turn decreases acid secretion. Drug therapy, which protects the mucosa, includes prostaglandin analogs and antacids. Prostaglandin analogs may be given to patients taking NSAIDs to suppress ulceration.
GI bleeding may be treated by giving H2-receptor antagonists I.V. as a continuous infusion. Upper endoscopy is preferred as a diagnostic tool when GI bleeding is present because an injection of epinephrine or saline (to surround the ulcer) can be performed to stop the bleeding during the procedure; cautery may also be used for hemostasis.
Surgery is indicated for perforation of the ulcer, continued bleeding despite medical treatment, and suspected malignancy. Surgical procedures for peptic ulcers and gastric outlet obstruction include:
❑ vagotomy and pyloroplasty: severing one or more branches of the vagus nerve to reduce hydrochloric acid secretion and refashioning the pylorus to create a larger lumen and facilitate gastric emptying
❑ distal subtotal gastrectomy (with or without vagotomy): excising the antrum of the stomach, thereby removing the hormonal stimulus of the parietal cells, followed by anastomosis of the remainder of the stomach to the duodenum or the jejunum.
Special considerations
Management of peptic ulcers requires the administration of medications, a focus on patient education, and appropriate postoperative care.
❑ Administer medications as directed.
❑ Observe the patient for adverse reactions to H2-receptor antagonists and omeprazole (such as dizziness, fatigue, rash, and mild diarrhea).
❑ A patient with a history of cardiac disease or with a sodium-restricted diet should be instructed to take only those antacids that contain low amounts of sodium.
❑ Advise the patient to avoid taking NSAIDs.
❑ Warn the patient to avoid stressful situations, excessive intake of coffee, and ingestion of alcoholic beverages during exacerbations of peptic ulcer disease. Counsel the patient to enroll in a smoking cessation program.
❑ Educate the patient about the potential adverse effects of antibiotic therapy in the treatment of H. pylori, which include nausea, vomiting, and diarrhea.
After gastric surgery:
❑ Maintain patency of the nasogastric (NG) tube. Don’t manipulate the tube. If it isn’t functioning, notify the surgeon.
❑ Monitor intake and output. Record NG tube drainage.
❑ Assess the patient for bowel sounds.
❑ Maintain the patient on nothing-by-mouth status until the NG tube is removed or clamped.
❑ Replace fluids and electrolytes. Assess the patient for signs of dehydration, sodium deficiency, and metabolic alkalosis, which may occur secondary to gastric suction.
❑ Monitor the patient for possible complications: hemorrhage; shock; iron, folate, or vitamin B12 deficiency anemia (from malabsorption or continued blood loss); and dumping syndrome (weakness, nausea, flatulence, diarrhea, distention, and palpitations within 30 minutes after a meal).
❑ To avoid dumping syndrome, advise the patient to sit upright for up to 2 hours after eating, to drink fluids between meals rather than with meals, to avoid eating large amounts of carbohydrates, and to eat four to six small, high-protein, low-carbohydrate meals throughout the day.
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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