peptic ulcer disease


Also found in: Dictionary, Thesaurus, Financial, Acronyms, Encyclopedia, Wikipedia.
Related to peptic ulcer disease: gastritis

peptic ulcer disease

An often painful ulcer/mucosal erosion of 0.5 cm or greater in diameter in an area of upper GI tract which is normally acidic. Up to 90% of peptic ulcers are associated with Helicobacter pylori. Peptic ulcers are usually worsened by drugs (aspirin, other NSAIDs), and occur from the oesophagus to the ligament of Treitz.

Pathogenesis, peptic ulcer
Breakdown of protective mechanisms
• Bicarbonate
• Mucosal blood flow
• Prostaglandins
• Apical surface membrane
• Epithelial regeneration
Ulcerogenic factors
• Gastric acidity
• Peptic enzymes

peptic ulcer disease

See Duodenal ulcer, Gastric ulcer, GERD.

Peptic ulcer disease (PUD)

A stomach disorder marked by corrosion of the stomach lining due to the acid in the digestive juices.
Mentioned in: Indigestion

Peptic Ulcer Disease

DRG Category:326
Mean LOS:15.4 days
Description:SURGICAL: Stomach, Esophageal, and Duodenal Procedure With Major CC
DRG Category:383
Mean LOS:5.6 days
Description:MEDICAL: Uncomplicated Peptic Ulcer With Major CC

Peptic ulcer disease refers to ulcerative disorders in the lower esophagus, upper duodenum, and lower portion of the stomach. Approximately 4 to 5 million people in the United States have peptic ulcers. The types of peptic ulcers are gastric and duodenal, both of which are chronic diseases. The ulcer represents the development of a circumscribed defect in the gastric or duodenal mucosa that is exposed to acid and pepsin secretion. The ulcer may extend through the tissue layers of the muscle and serosa into the abdominal cavity. Stress ulcers, which are caused by a physiological response to major trauma, are clinically distinct from chronic peptic ulcers.

Gastric ulcers are less common than duodenal ulcers and usually occur in the lesser curvature of the stomach within 1 inch of the pylorus. The ulcer formation is caused by an inability of the mucosa to protect itself from damage by acid pepsin in the lumen (which is caused by a breakdown of the defensive factors). Duodenal ulcers occur in the proximal part of the duodenum (95%), are less than 1 cm in diameter, and are round or oval. A higher number of parietal cells in the stomach causes hypersecretion, or rapid emptying of the stomach; this may lead to a larger amount of acid being delivered to the first part of the duodenum and may result in the formation of an ulcer. Hemorrhage and peritonitis can occur if the peptic ulcer erodes through the intestinal wall. Other complications include abdominal or intestinal infarction or erosion of the ulcer into the liver, pancreas, or biliary tract.

Causes

Factors that contribute to the development of peptic ulcers include a genetic predisposition to ulcer formation; poor cell restitution; excessive acid secretion; stress; excessive alcohol intake; smoking; ingestion of aspirin and NSAIDs; and chronic use of drugs such as steroidal, potassium, or iodine compounds. The Helicobacter pylori bacterium, the principal causative agent of type B chronic gastritis, is also thought to be a major cause of peptic ulcers. Associated diseases include hyperparathyroidism, chronic lung disease, and alcoholic cirrhosis.

Genetic considerations

A polymorphism in the interferon-gamma receptor-1 gene (IFNGR1) is associated with an increased likelihood of H. pylori infection. Another susceptibility factor is a variation in the Lewis (b) blood group antigen, an epithelial receptor for H. pylori. Autosomal dominant transmission of elevated serum pepsinogen I (PG I) levels has been seen in families with a history of duodenal ulcer. Peptic ulcer is also seen as a component of other genetic conditions, including Zollinger-Ellison syndrome.

Gender, ethnic/racial, and life span considerations

The incidence of duodenal ulcers is highest in people ages 40 to 50 and is equally common in men and women. Gastric ulcers, which occur most often in people ages 60 to 70, are more common in men. Mortality with gastric ulcer perforation is three times greater than that with duodenal ulcer perforation, partly because of the increased age of the patients. Duodenal ulcers occur in approximately 10% of the population at some time in their lives. More than half of the people who have duodenal ulcers heal spontaneously but have a high incidence of recurrence within 2 years. Hospitalization rates for peptic ulcer disease are highest for people with African American and Asian/Pacific Islander ancestry.

Global health considerations

In developed nations, the incidence of peptic ulcer disease is decreasing with the recognition of the role of H. pylori bacteria in its development. The incidence of peptic ulcer disease in developing nations is increasing depending on the association with H. pylori and NSAID patterns of use.

Assessment

History

Epigastric pain is the major symptom. Assess pain by obtaining a history of the onset, duration, and characteristics in relation to food intake and medications. Patients may describe pain as sharp, burning, or gnawing, or it may be achy and perceived as abdominal pressure. Pain with duodenal ulcer occurs from 90 minutes to 3 hours after eating, is relieved with food or antacids, and may awaken a person at night. It is located to the right of the midline epigastrium with duodenal ulcers and to the left of the midline with gastric ulcers. Gastric ulcer pain is precipitated by food and is not relieved by antacid use to the same extent as duodenal ulcer pain is. Some patients have constant pain or no clear pattern of discomfort. As a result of the pain, weight loss and anorexia may occur with gastric ulcers. Weight gain may result with duodenal ulcers because food relieves the pain.

Question the patient about a family history of ulcer disease; smoking and alcohol habits; presence of other symptoms, such as nausea and vomiting; and changes in stool color, level of energy, appetite, and body weight. Review the patient’s medication profile, both prescribed and over-the-counter (OTC). Ask about the amounts of caffeinated beverages taken daily. Determine the foods that aggravate the symptoms. Assess the patient’s level of stress and coping skills.

Physical examination

On inspection, you may note pale mucous membranes and skin because of anemia from acute or chronic blood loss. Some patients have black or tarry stools. Currant-colored or bright red stools occur only with massive bleeding. During auscultation, you may note that bowel sounds are hyperactive initially but diminish because of a paralytic ileus with ulcer perforation and peritonitis. Palpation in the midline may reveal epigastric tenderness.

Psychosocial

Researchers have not been able to establish a characteristic duodenal ulcer personality. Chronic stress and anxiety, however, are believed to increase gastric secretions and may be factors in exacerbating ulcer recurrence. Assess the patient’s response to the disease and note any unusual stressors that have an effect on the patient’s or significant other’s life.

Diagnostic highlights

TestNormal ResultAbnormality With ConditionExplanation
Barium radiographic studiesNormal gastrointestinal tractPresence of ulcers often as a protrusion on radiographic examinationBarium study highlights presence of ulcer in stomach or duodenum
EsophagogastroduodenoscopyNormal gastrointestinal mucosaPresence of mucosal ulcerations in the stomach or duodenumFlexible endoscopy to allow visualization of mucosa

Other Tests: Serum gastrin levels, hemoglobin, hematocrit, complete blood count; tests for H. pylori: (1) antibody detection (immunoglobulin G) to H. pylori is measured in serum, plasma, urine, or whole blood; (2) urea breath tests detect active H. pylori infection by identifying enzymatic activity of bacterial urease; and (3) fecal antigen testing detects presence of H. pylori antigens in stools.

Primary nursing diagnosis

Diagnosis

Pain (acute) related to inflammation and irritation

Outcomes

Comfort level; Pain control behavior; Pain level; Symptom severity

Interventions

Analgesic administration; Anxiety reduction; Environmental management: Comfort; Pain management; Medication management; Patient-controlled analgesia assistance

Planning and implementation

Collaborative

The treatment of choice for patients with peptic ulcers is generally pharmacologic. Drugs can be used to buffer or inhibit acid secretion that leads to ulceration and causes symptoms. Nutritional therapy is also prescribed. The current treatment is to eliminate foods that cause discomfort and symptoms. There is no evidence that bland or soft diets reduce gastric acid, promote healing, or relieve symptoms. Instruct the patient to avoid alcohol, coffee, and other caffeine-containing beverages. Refer patients with significant weight loss to a dietitian.

Most patients do not require surgery. However, in the event of the primary complications of hemorrhage, perforation, or obstruction, surgery may be necessary. Hemorrhage occurs in 15% of patients with duodenal ulcers and occurs more frequently in patients with NSAID-associated ulcers who have no prior symptoms. Perforation into the peritoneal cavity, which occurs in 6% of patients, happens when the ulcer erodes through the entire thickness of the gastric or duodenal wall. Obstruction occurs in 2% to 4% of patients with duodenal or pyloric ulcers. Treatment begins conservatively with gastric suction and fluid and electrolyte therapy. Pyloroplasty may follow.

The most common surgical interventions required for persons who do not respond to medical treatments are vagotomy with antrectomy, vagotomy with pyloroplasty, and parietal cell vagotomy (also called superselective or proximal gastric vagotomy). Several important complications can occur after surgery. Bile reflux gastritis, which occurs because of a reflux of duodenal contents into the stomach, occurs after a pyloroplasty or when the pylorus is bypassed or removed. Marginal ulcers are those that develop where gastric acids contact the operative site, usually at the site of anastomosis. Acute gastric dilation occurs in the postoperative period when dilation of the stomach causes reflex hypotension, pain, and tachycardia. The symptoms are relieved with vomiting or gastric suction.

Pharmacologic highlights

General Comments: Most duodenal ulcers heal in 4 to 6 weeks, and treatment seldom extends past 8 weeks. Maintenance drug therapy is indicated for at least 1 year for patients with frequent recurrences. Gastric ulcers should heal in 8 to 12 weeks, and more rapidly when acid is completely suppressed with use of a proton pump inhibitor such as omeprazole (Prilosec). If gastric ulcers do not heal with treatment, malignancy is suspected.

Medication or Drug ClassDosageDescriptionRationale
H2 antagonistVaries with drugCimetidine, rantidine, famotidine, nizatidineReduces acid secretion to optimize ulcer healing
Proton pump inhibitorsVaries with drugOmeprazole, esomeprazole, lansoprazole, rabeprazole, pantoprazoleOptimizes ulcer healing by binding to the proton pump of parietal cell and inhibiting secretion of hydrogen ions into gastric lumen
Triple therapies: Antibiotics (for patients with H. pylori bacteria) and proton pump inhibitorOmeprazole (Prilosec), 20 mg PO bid for 14 days with clarithromycin (Biaxin) 500 mg PO bid for 14 days and amoxicillin (Amoxil) 1 g PO bid for 14 daysOther protein pump inhibitors may be used: Lansoprazole (Prevacid); rabeprazole (Aciphex); esomeprazole (Nexium)Antibiotics eradicate H. pylori and protein pump inhibitor reduces acid secretion; triple therapy may also consist of antibiotics and bismuth-based therapy such as Pepto-Bismol

Other Drugs: Antacids (aluminum and magnesium hydroxide), prostaglandins

Independent

Provide information about the cause and contributing factors as they pertain to the individual patient. Explain the relationship of gastric acidity, mucosal damage, and the significance of the symptoms of ulcer formation (pain, bleeding, nausea and vomiting, black stools). Discuss possible complications of peptic ulcer disease as it progresses: hemorrhage, perforation, and obstruction because of repeated ulcerations and scarring. Emphasize the need to adhere to the medication schedule, even when symptoms subside, to ensure complete healing and to prevent recurrence. Encourage the patient to avoid aspirin and other NSAIDs for aches and pains and suggest alternatives, such as acetaminophen (Tylenol). Provide a list of OTC drugs that contain aspirin.

Explore ways to reduce stress and emphasize the importance of emotional and physical rest to reduce gastric secretion. Teach relaxation exercises to use during rest periods that fit into daily routines. Explain why elimination of smoking facilitates healing and reduces recurrence. Provide a list of community agencies that have smoking-cessation programs. Discuss the patient’s concerns openly. Identify attitudes and situations that could interfere with the needed lifestyle changes. Involve the family or significant others in these discussions and plans to gain their support.

Evidence-Based Practice and Health Policy

Derogar, M., Sandblom, G., Lundell, L., Orsini, N., Bottai, M., Lu, Y., & Sadr-Azodi, O. (2013). Discontinuation of low-dose aspirin therapy after peptic ulcer bleeding increases risk of death and acute cardiovascular events. Clinical Gastroenterology and Hepatology, 11(1), 38–42.

  • Discontinuation of low-dose aspirin therapy is often recommended to reduce bleeding risks associated with peptic ulcer disease. However, investigators suggest that discontinuation of aspirin therapy may increase the risk of cardiovascular-related mortality.
  • In a retrospective study among 118 patients treated for peptic ulcer bleeding who were also previously taking low-dose aspirin, aspirin therapy was discontinued in 40%. During the first 6 months of follow-up among patients with cardiovascular comorbidities, 31% of patients who discontinued aspirin therapy experienced an acute cardiovascular event or death compared to 8% of patients who continued aspirin therapy (p < 0.01).
  • Patients who discontinued aspirin therapy were 6.3 times more likely to experience an acute cardiovascular event or death within 6 months compared to patients who continued aspirin therapy (95% CI, 1.3 to 31.1).

Documentation guidelines

  • Physical findings of epigastric or abdominal pain, nausea, vomiting, tarry stools, bleeding, infection, presence of complications (hemorrhage, perforation, obstruction)
  • Response to medication therapy, nutritional therapy, emotional/physical rest
  • Response to surgical interventions

Discharge and home healthcare guidelines

Advise the patient that recurrence is greater than 50% with noncompliance. Reinforce the need to avoid the following: aspirin products and NSAIDs, alcohol intake, caffeine products, and smoking. Review signs and symptoms that should be reported—those that may indicate recurrence or complications, including pain, nausea, vomiting, black tarry stools, fatigue, and frank bleeding. Stress the importance of eating three meals at approximately the same time each day. Put patient in contact with the Helicobacter Foundation (http://www.helico.com).

Postoperatively, tell the patient what to expect if infection occurs so she or he can tell the healthcare provider when the first signs occurred. The symptoms include pain, redness, swelling, and drainage at the incisional site. After a Billroth II surgical procedure, the patient may develop symptoms of the dumping syndrome. Explain the reason and timing of the symptoms that may occur, noting that the episodes will subside in 6 to 12 months. Teach the patient how to control the problems with the following suggestions: (1) Take fluids only between meals and none with meals; (2) eat smaller amounts more frequently in a semirecumbent position; (3) eat a low-carbohydrate diet, concentrating on high-protein and moderate-fat foods; (4) avoid refined sugars (sweets); (5) lie down after meals for 30 minutes; (6) take anticholinergic drugs 30 minutes before meals as prescribed; and (7) reinforce the need to stop smoking to promote healing and prevent recurrence.

References in periodicals archive ?
Hyperdigoxinemia is important in the pathogenesis of cirrhosis liver, ulcerative colitis, irritable bowel syndrome and peptic ulcer disease [2].
2 million of the hospitalizations were for a primary diagnosis of complicated gastric ulcer, duodenal ulcer, or peptic ulcer disease.
Using a combination of antibiotics to eradicate a stomach bacterium may finally offer a cure to the 25 million Americans who at some time in their lives develop peptic ulcer disease.
Also, ibuprofen should not be given to patients with ulcerative colitis, active peptic ulcer disease, or gastritis the drug should be used with caution if there is a history of these disorders.
Sometimes the symptoms accompany a disease such as peptic ulcer disease, gallbladder disease, or gastritis.
Robin Warren for their discovery of Helicobacter pylori and its role in gastritis and peptic ulcer disease has again put infectious diseases on to the front page of newspapers around the world.
A sampling of topics includes persistent diarrhea, upper gastrointestinal bleeding, growth failure, helicobacter pylori and peptic ulcer disease, necrotizing enterocolitis, systemic conditions affecting the liver, and pancreatic function tests.
Three patients had a documented history of upper GI bleeding, 23 had a history of peptic ulcer disease, and 30 were receiving NSAID therapy that was not stopped before stenting.
Systemic follow-up of patients who undergo stomach surgery for peptic ulcer disease is recommended, as early detection is the most important factor contributing to successful treatment.