Peptic ulcer disease

59 Peptic ulcer disease




Overview/pathophysiology


Peptic ulcers are erosions of the upper gastrointestinal (GI) tract mucosa, potentially extending through the muscularis mucosa and into the muscularis propria. They may occur anywhere the mucosa is exposed to the erosive action of gastric acid and pepsin. Commonly, ulcers are gastric or duodenal, but the esophagus, surgically created stomas, and other areas of the upper GI tract may be affected. Autodigestion of mucosal tissue and ulceration are associated with increased acidity of the stomach juices or increased sensitivity of the mucosal surfaces to erosion. Erosions can penetrate deeply into the mucosal layers and become a chronic problem, or they can be more superficial and manifest as an acute problem resulting from severe physiologic or psychologic trauma, infection, or shock (stress ulceration of the stomach or duodenum). The most common causes of peptic ulcer disease are use of nonsteroidal antiinflammatory drugs (NSAIDs) and infection with Helicobacter pylori (H. pylori). Duodenal and gastric ulcers also can occur in association with high-stress lifestyle, smoking, use of irritating drugs, as well as secondary to other diseases. Ulceration may occur as a part of Zollinger-Ellison syndrome, in which gastrinomas (gastrin-secreting tumors) of the pancreas or other organs develop. Gastric acid hypersecretion and ulceration subsequently occur.


H. pylori, a gram-negative, spiral-shaped bacterium with four to six flagella on one pole, was first isolated from gastric biopsies in 1983. H. pylori can reside below the mucosa of the stomach because it produces the enzyme urease, which hydrolyses urea to ammonia and carbon dioxide, providing a buffering alkaline halo. Infection can go undetected for years because there may be no symptoms until gastric or duodenal ulceration or gastritis occurs. Transmission of H. pylori has been determined to be by fecal-oral and oral-oral routes of transmission. A high duodenal acid load is one of the characteristics of duodenal ulcer disease inasmuch as it reduces concentration of bile acids that normally inhibit growth of H. pylori. Gastric ulcers tend to occur on the lesser curvature of the stomach. Ulcers in both locations are characterized by slow healing leading to metaplasia. In turn, a greater colonization with H. pylori causes slow healing and results in a vicious cycle.


Serious and disabling complications, such as hemorrhage, GI obstruction, perforation, peritonitis, or intractable ulcer pain, are common. With treatment, ulcer healing usually occurs within 4-6 wk (gastric ulcers can take as long as 12-16 wk to heal), but there is potential for recurrence in the same or another site.



Health care setting


Primary care; acute care for complications



Assessment




Signs and symptoms:


Burning, gnawing, dull pain typically 1-3 hr after eating. Discomfort occurs more often between meals and at night. With duodenal ulcer, eating usually alleviates discomfort; with gastric ulcer, pain often worsens after meals. Older adults have less sensory perception in the stomach and may not experience pain as a symptom. In addition, 40% of patients with active ulcers deny abdominal pain. However, on evaluation there may be findings of ulcers, gastritis, and other conditions. Even so, pain symptoms warrant further investigation.


Hematemesis, melena, dizziness, and syncope are associated with an actively bleeding ulcer. Sudden, severe epigastric pain, often radiating to the right shoulder, suggests perforation of an ulcer. Pain described as piercing through to the back suggests penetration of the ulcer into adjacent posterior structures in the abdomen.



Physical assessment:


Tenderness over the involved area of the abdomen. With perforation, there is severe pain (see “Peritonitis” for more information) and rebound tenderness. With penetration, the pain is usually altered by changes in back position (extension or flexion).



History of:


NSAID use; smoking; use of irritating agents such as caffeine, alcohol, corticosteroids, salicylates, reserpine, indomethacin, or phenylbutazone; disorders of the endocrine glands, pancreas, or liver; and hypersecretory conditions, such as Zollinger-Ellison syndrome.



Diagnostic tests




Endoscopy:


Allows visualization of the stomach (gastroscopy), duodenum (duodenoscopy), both stomach and duodenum (gastroduodenoscopy), or the esophagus, stomach, and duodenum (esophagogastroduodenoscopy) via passage of a lighted, fiberoptic, flexible tube. Patient is given nothing by mouth (NPO) for 8-12 hr before the procedure, and written consent is required. Before the test, a sedative is administered to relax the patient, and an opioid analgesic may be given to prevent pain. Local anesthetic may be sprayed into the posterior pharynx to ease passage of the tube. A biopsy may be performed as part of the endoscopy procedure. Biopsied tissue may be sent for histologic examination and for culture and sensitivity to identify H. pylori infection. Postprocedure care involves maintaining NPO status for ½-1 hr; ensuring return of the gag reflex before allowing the patient to eat (if local anesthetic was used); administering throat lozenges or analgesics as prescribed; and monitoring for complications, such as bleeding or perforation (e.g., hematemesis, pain, dyspnea, tachycardia, hypotension).



H. pylori testing:


Serum antigen testing identifies exposure to H. pylori bacteria; this is the least expensive means of identifying H. pylori infection. However, antibody tests remain positive many months after successful therapy and are not reliable for assessing therapy effectiveness. A breath test is available to identify H. pylori infection by detecting carbon dioxide and ammonia as by-products of the action of the bacterium’s urease in the patient’s expired air. Histologic identification of the microorganism and culture are other direct tests for H. pylori. Direct tests and stool antigen testing require discontinuation of all drugs that suppress H. pylori for 2 wk before testing.



Barium swallow:


Uses contrast agent (e.g., barium) to detect abnormalities. Patient should maintain NPO status and not smoke for at least 8 hr before the test. Postprocedure care involves administration of prescribed laxatives and enemas to facilitate passage of the barium and prevent constipation and fecal impaction.

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Jul 18, 2016 | Posted by in NURSING | Comments Off on Peptic ulcer disease

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