Peptic Ulcer Disease
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Robbie Steele is a 49-year-old insurance agent with epigastric pain. For approximately 6 months, Mr. Steele has had vague abdominal distress after meals and at night, and he now uses antacids on a regular basis. However, the antacids are no longer effective. Although he admits to one instance of blood in his stool and occasional nausea, he denies repeated melena, change in bowel habits, or weight loss. He smokes a pack of cigarettes a day, uses aspirin sparingly, and drinks socially. The remainder of his history is negative.
What other important information should be obtained?
The following information should be elicited:
When antacid use was started
Use of other over-the-counter antacids or histamine receptor antagonists
Any vomiting of blood
Diminished ability to eat a whole meal
Mr. Steele has used antacids for 1 to 2 years for epigastric pain as well as for heartburn. He vomited blood once 6 months ago, but his appetite has not been impaired. His weight dropped 10 pounds during the past year. Mr. Steele has an average build with normal vital signs, and other than being nervous, he is not in acute distress. The findings of the head, neck, and chest examinations are normal. The abdominal examination reveals epigastric tenderness with deep palpation. There is no guarding or rebound tenderness, and bowel sounds are present. No mass or groin hernia is present. Findings of rectal examination and hemoccult tests are negative.
What is the first step in assessing a new patient with symptoms such as Mr. Steele’s?
The clinician must determine how sick the patient is. Factors that must be considered include severity of pain and associated symptoms, hemodynamic status, and any indications for immediate surgery. The need for urgent workup for acute symptoms must be determined, and a plan for resuscitation, if needed, must be made.
What is the differential diagnosis for epigastric pain?
Diagnoses include but are not limited to peptic ulcer disease, gastritis, pancreatitis, pancreatic cancer, biliary tract disease, abdominal aortic aneurysm, early appendicitis, gastroenteritis, and ischemic heart disease.
Why is acute myocardial infarction (MI) included in the differential diagnosis of epigastric pain?
Pain from the inferior wall of the left ventricle may be referred to the epigastrium and can be associated with nausea, vomiting, and diaphoresis.
Mr. Steele’s laboratory tests show the following: hemoglobin level, 14.2 g per dL; hematocrit, 41%; white blood cell count, 12,800 per mL; normal blood urea nitrogen, creatinine, amylase, and lipase levels. Liver function is normal. An electrocardiogram (ECG) shows normal sinus rhythm at 82 per minute with no acute changes.
What is the most likely diagnosis according to the laboratory results?
The normal ECG eliminates acute MI. Normal liver function studies suggest there is probably no acute biliary tract disease, although an ultrasound examination is needed if cholecystitis is suspected. Normal amylase and lipase levels rule out pancreatitis and, along with a normal hemoglobin, reduce the likelihood of pancreatic carcinoma. Gastritis, gastroenteritis, and early appendicitis are unlikely but possible according to his history and presentation. The absence of a palpable pulsatile mass on initial examination reduces the possibility of abdominal aortic aneurysm. Peptic ulcer disease is the most likely diagnosis.
How is peptic ulcer disease confirmed?
Upper endoscopy (esophagogastroduodenoscopy) is the next step toward confirming the diagnosis and defining the extent of the disease. This test not only allows ulcers to be seen but also helps rule out other diagnoses such as reflux esophagitis, Barrett’s esophagus, and gastritis. All gastric ulcers must be sampled for biopsy (four-quadrant specimens must be obtained), and if the ulcers appear suspect for malignancy, gastric washings must be obtained for cytologic examination. Gastric ulcers that have not healed as determined by endoscopy after several weeks of treatment must also be aggressively assessed with repeat biopsies. Although cancer of the duodenum is unusual, biopsy of anomalous, nonhealing duodenal ulcers is necessary. Experience in Japan has demonstrated that early diagnosis and treatment of gastric cancer improve survival (1).
What is the incidence of peptic ulcer disease?
What causes peptic ulcer disease?
Historically, excess gastric acid was believed to be the single cause of peptic ulcer disease. It is now estimated, however, that 90% of duodenal ulcers and 80% of gastric ulcers are associated with Helicobacter pylori, the putative causative agent (3). This organism is found in the gastric mucous layer or on the gastric mucosa. Other factors associated with peptic ulcers are cigarette smoking, high alcohol intake, nonsteroidal antiinflammatory drug use, and a stressful lifestyle. Excess gastric acid production continues to accompany peptic ulceration.
Mucosal injury of the stomach (gastric ulceration or stress gastritis) is associated with specific stressors such as major body surface burns (Curling’s ulcer), multiple organ failure, multiple trauma, and head injuries (Cushing’s ulcer) (4).
What is H. pylori and how is H. pylori infection diagnosed?
H. pylori is a spiral flagellated organism found worldwide. In countries such as China, where H. pylori infects more than half the population during early childhood, the rate of gastric cancer, also associated with this organism, is high. H. pylori infection is linked to both duodenal and gastric ulcers and to the lymphoid type of mucosal lymphoma. Approximately two thirds of the world population is infected with H. pylori. In the United States, the organism is most often seen in African Americans, Hispanics, the elderly, and the poor (5). Three tests diagnose H. pylori infection: rapid urease test, serologic antibody measurement, and urea breath test. The organism may also be seen on endoscopic biopsy.
What is the treatment for peptic ulcer disease?
Uncomplicated peptic ulcer disease is treated medically with a number of agents. Triple therapy based on proton pump inhibitors is the most common treatment aimed at eliminating H. pylori (6). Surgical intervention is reserved for recalcitrant cases that progress to complications such as bleeding, obstruction, perforation, and intractability. Before the role of H. pylori in peptic ulcer disease was discovered, primary treatment centered on histamine receptor antagonists such as cimetidine, ranitidine, and famotidine. Proton pump inhibitors have proven to be more potent acid suppression agents than H2 antagonists but are not used for long-term treatment. Five proton pump inhibitors are available: three older drugs—omeprazole, lansoprazole and pantoprazole—and two newer drugs—rabeprazole and esomeprazole. The latter two newer proton pump inhibitors offer more consistent acid inhibition, especially in the elderly patient (7). Sucralfate, an aluminum salt of sulfated sucrose that binds to the ulcer base and promotes healing, is used to treat acute duodenal ulcers. Pain resolution with sucralfate is less prompt than with H2 blockers.
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