Peptic ulcers
Peptic ulcers: Excerpt from Professional Guide to Diseases (Eighth Edition)
Peptic ulcers — circumscribed lesions in the mucosal membrane — can develop in the lower esophagus, stomach, pylorus, duodenum, or jejunum. About 80% of all peptic ulcers are duodenal ulcers, which affect the proximal part of the small intestine.
Gastric ulcers, which affect the stomach mucosa, are most common in middle-aged and elderly men, especially in chronic users of nonsteroidal anti-inflammatory drugs (NSAIDs), alcohol, or tobacco. Duodenal ulcers usually follow a chronic course, with remissions and exacerbations; 5% to 10% of patients develop complications that necessitate surgery.
Causes and incidence
Researchers recognize three major causes of peptic ulcer disease: infection with Helicobacter pylori (formerly known as Campylobacter pylori), use of NSAIDs, and pathologic hypersecretory disorders such as Zollinger-Ellison syndrome. (See How peptic ulcers develop.)
How H. pylori produces an ulcer isn’t clear. Gastric acid, which was considered a primary cause, now appears mainly to contribute to the consequences of infection. Ongoing studies should soon unveil the full mechanism of ulcer formation.
Salicylates and other NSAIDs encourage ulcer formation by inhibiting the secretion of prostaglandins (the substances that suppress ulceration). Certain illnesses, such as pancreatitis, hepatic disease, Crohn’s disease, preexisting gastritis, and Zollinger-Ellison syndrome, are also known causes.
Besides peptic ulcer’s main causes, several predisposing factors are acknowledged. They include blood type (gastric ulcers tend to strike people with type A blood; duodenal ulcers tend to afflict people with type O blood) and other genetic factors. Exposure to irritants, such as alcohol, coffee, and tobacco, may contribute by accelerating gastric acid emptying and promoting mucosal breakdown. Ulceration occurs when the acid secretion exceeds the buffering factors. Physical trauma, emotional stress, and normal aging are additional predisposing conditions.
In the United States, about 1.6 million people acquire peptic ulcers yearly. Males and females are affected equally, and incidence increases with age. A higher percentage of H. pylori infection occurs in people older than age 50.
Signs and symptoms
Heartburn and indigestion usually signal the beginning of a gastric ulcer attack. Eating stretches the gastric wall and may cause or, in some cases, relieve pain and feelings of fullness and distention. Other typical effects include weight loss and repeated episodes of massive GI bleeding.
Duodenal ulcers produce heartburn, 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. Attacks usually occur about 2 hours after meals, whenever the stomach is empty, or after consumption of orange juice, coffee, aspirin, or alcohol. Exacerbations tend to recur several times per year and then fade into remission. Vomiting and other digestive disturbances are rare.
Ulcers may penetrate the pancreas and cause severe back pain. Other complications of peptic ulcers include perforation, hemorrhage, and pyloric obstruction. Ulcers may, on occasion, produce no symptoms.
Diagnosis
CONFIRMING DIAGNOSIS Esophagogastroduodenoscopy confirms the presence of an ulcer and permits cytologic studies and biopsy to rule out H. pylori or cancer.
Diagnosis may be confirmed by the following tests:
❑ Barium swallow or upper GI and small-bowel series may reveal the presence of the ulcer. This is the initial test performed on a patient whose symptoms aren’t severe.
❑ Laboratory analysis may detect occult blood in stools.
❑ Serologic testing may disclose clinical signs of infection such as an elevated white blood cell count.
❑ Carbon 13 (13C) urea breath test results reflect activity of H. pylori.
Treatment
Experts recommend treating the patient with antibiotics to eradicate H. pylori. The patient taking NSAIDs may take a prostaglandin analog (misoprostol) to suppress ulceration (or the patient may take the analog with NSAIDs to prevent ulceration). Histamine-2 (H2) receptor antagonists or proton pump inhibitors may reduce acid secretion. A coating agent or bismuth may be administered to the patient with a duodenal ulcer to protect the lining.
If GI bleeding occurs, emergency treatment begins with passage of a nasogastric (NG) tube to allow for iced saline lavage, possibly containing norepinephrine. Gastroscopy allows visualization of the bleeding site and coagulation by laser or cautery to control bleeding. This type of therapy allows postponement of surgery until the patient’s condition stabilizes. Surgery is indicated for perforation, unresponsiveness to conservative treatment, and suspected malignancy. Surgery for peptic ulcers may 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 rest of the stomach to the duodenum or the jejunum
❑ pyloroplasty: surgical enlargement of the pylorus to provide drainage of gastric secretions.
Special considerations
Management of peptic ulcers requires careful administration of medications, thorough patient teaching, and skillful postoperative care.
❑ Watch for adverse reactions to H2-receptor antagonists and omeprazole (dizziness, fatigue, rash, and mild diarrhea).
❑ Advise any patient who uses antacids, who has a history of cardiac disease, or who follows a sodium-restricted diet to take only those antacids that contain low amounts of sodium.
❑ Warn the patient to avoid NSAIDs because they irritate the gastric mucosa. For the same reason, advise the patient to stop smoking and to avoid stressful situations, excessive intake of coffee, and drinking alcoholic beverages during exacerbations of peptic ulcer disease.
After gastric surgery:
❑ Keep the NG tube patent. If the tube isn’t functioning, don’t reposition it; you might damage the suture line or anastomosis. Notify the surgeon promptly.
❑ Monitor intake and output, including NG tube drainage. Check for bowel sounds, and allow the patient nothing by mouth until peristalsis resumes and 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 (pernicious anemia) due to lack of intrinsic factor causing malabsorption of vitamin B12; and dumping syndrome (a rapid gastric emptying, causing distention of the duodenum or jejunum produced by a bolus of food). Signs and symptoms of dumping syndrome include diaphoresis, weakness, nausea, flatulence, explosive diarrhea, distention, and palpitations within 30 minutes after a meal.
❑ To avoid dumping syndrome, advise the patient to lie down after meals, 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 during the day.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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