Drugs Used to Treat Gastroesophageal Reflux and Peptic Ulcer Disease

Objectives

1 Describe the physiology of the stomach.

2 Cite common stomach disorders that require drug therapy.

3 Identify factors that prevent breakdown of the body’s normal defense barriers resulting in ulcer formation.

4 Discuss the drug classifications and actions used to treat stomach disorders.

5 Identify interventions that incorporate pharmacologic and nonpharmacologic treatments for an individual with stomach disorders.

Key Terms

parietal cells () (p. 519)

hydrochloric acid () (p. 519)

gastroesophageal reflux disease (GERD) () (p. 519)

heartburn () (p. 519)

peptic ulcer disease (PUD) () (p. 520)

Helicobacter pylori () (p. 520)

Physiology of the Stomach

http://evolve.elsevier.com/Clayton

As a major part of the gastrointestinal (GI) tract, the stomach has three primary functions: (1) storing food until it can be processed in the lower GI tract; (2) mixing food with gastric secretions until it is a partially digested, semisolid mixture known as chyme; and (3) slowly emptying the stomach at a rate that allows proper digestion and absorption of nutrients and medicine from the small intestine.

Three types of secretory cells line portions of the stomach—chief, parietal, and mucus cells. The chief cells secrete pepsinogen, an inactive enzyme. Parietal cells are stimulated by acetylcholine from cholinergic nerve fibers, gastrin, and histamine to secrete hydrochloric acid, which activates pepsinogen to pepsin and provides the optimal pH for pepsin to start protein digestion. Normal pH in the stomach ranges from 1 to 5, depending on the presence of food and medications. Hydrochloric acid also breaks down muscle fibers and connective tissue ingested as food and kills bacteria that enter the digestive tract through the mouth. The parietal cells also secrete intrinsic factor needed for absorption of vitamin B₁₂. The mucus cells secrete mucus, which coats the stomach wall. The 1-mm-thick coat is alkaline and protects the stomach wall from damage by hydrochloric acid and the digestive enzyme pepsin. It also contributes lubrication for food transport. Small amounts of other enzymes are also secreted in the stomach. Lipases digest fats, and gastric amylase digests carbohydrates. Other digestive enzymes are also carried into the stomach from swallowed saliva.

Prostaglandins play a major role in protecting the stomach walls from injury by stomach acids and enzymes. Prostaglandins are produced by cells lining the stomach and prevent injury by inhibiting gastric acid secretion, maintaining blood flow, and stimulating mucus and bicarbonate production.

Common Stomach Disorders

Gastroesophageal reflux disease (GERD), more commonly referred to as heartburn, acid indigestion, or sour stomach, is a common stomach disorder. Approximately one third of the U.S. population experiences heartburn once each month, and 5% to 7% have heartburn daily. Common symptoms are a burning sensation, bloating, belching, and regurgitation. Other symptoms that are reported less frequently are nausea, a “lump in the throat,” hiccups, and chest pain.

GERD is the reflux of gastric secretions, primarily pepsin and hydrochloric acid, up into the esophagus. Causes of GERD are a weakened lower esophageal sphincter, delayed gastric emptying, hiatal hernia, obesity, overeating, tight-fitting clothing, and increased acid secretion. Acid secretions are increased by smoking, alcohol, carbonated beverages, coffee, and spicy foods.

Most cases of GERD pass quickly with only mild discomfort, but frequent or prolonged bouts of acid reflux cause inflammation, tissue erosion, and ulcerations in the lower esophagus. Anyone who has recurrent or continuous symptoms of reflux, especially if the symptoms interfere with activities, should be referred to a health care provider. These symptoms may also accompany more serious conditions, such as ischemic heart disease, scleroderma, and gastric malignancy.

Clinical Pitfall

Nurses need to be aware that the symptoms of gastroesophageal reflux disease (GERD) may also accompany more serious conditions, such as ischemic heart disease, scleroderma, and gastric malignancy. It is important to do a thorough physical assessment whenever a patient presents with heartburn or acid indigestion and not simply dismiss the symptoms as gastrointestinal in origin.

Peptic ulcer disease (PUD) refers to several stomach disorders that result from an imbalance between acidic stomach contents and the body’s normal defense barriers, causing ulcerations in the GI tract. The most common illnesses are gastric and duodenal ulcers. It is estimated that approximately 10% of all Americans will develop an ulcer at some time in their lives. The incidence in men and women is approximately the same. Race, economic status, and psychological stress do not correlate with the frequency of ulcer disease. Often, the only symptom reported is epigastric pain, described as burning, gnawing, or aching. Patients often report that varying degrees of pain are present for a few weeks and are then gone, only to recur a few weeks later. The pain is most often noted when the stomach is empty, such as at night or between meals, and is relieved by food or antacids. Other symptoms that cause patients to seek medical attention are bloating, nausea, vomiting, and anorexia.

Ulcers appear to be caused by a combination of acid and a breakdown in the body’s defense mechanisms that protect the stomach wall. Proposed mechanisms are oversecretion of hydrochloric acid by excessive numbers of parietal cells, injury to the mucosal barrier such as that resulting from prostaglandin inhibitors (nonsteroidal anti-inflammatory drugs [NSAIDs], including aspirin), and infection of the mucosal wall by Helicobacter pylori. It had been thought that no bacterium could survive in the highly acidic environment of the stomach; however, H. pylori was first isolated from patients with gastritis in 1983. The bacterium seems able to live below the mucus barrier, where it is protected from stomach acid and pepsin. H. pylori is now thought to be associated with as many as 90% of duodenal and 70% of gastric ulcers. The exact mechanism whereby H. pylori contributes to ulcer formation is not known, but several hypotheses are being tested.

Several risk factors increase the likelihood of peptic ulcer disease:

1 There seems to be a genetic predisposition to PUD. Some families have a much greater history of PUD than others.

2 It is a commonly held belief that stress causes ulcers, but no well-controlled studies have supported this.

3 Cigarette smoking increases acid secretion, alters blood flow in the stomach wall, and retards prostaglandin synthesis needed for defense mechanisms.

4 NSAIDs have a twofold effect: they inhibit prostaglandins that protect the mucosa and directly irritate the stomach wall. Once ulcerations have formed, NSAIDs also slow healing.

5 It is commonly thought that certain foods (e.g., spicy foods) and alcohol contribute to ulcer formation. It is true that certain foods increase acid secretion and that alcohol irritates the stomach lining, but results from studies have not corroborated this concept.

Goals of Treatment

The goals of treatment of GERD are to relieve symptoms, decrease the frequency and duration of reflux, heal tissue injury, and prevent recurrence. The most important treatment is a change in lifestyle, which includes losing weight (if significantly over the ideal body weight), reducing or avoiding foods and beverages that increase acid production, reducing or stopping smoking, avoiding alcohol, and consuming smaller meals. Additional therapy includes remaining upright for 2 hours after meals, not eating before bedtime, and avoiding tight clothing over the abdominal area. Lozenges may be used to increase saliva production, and antacids and alginic acid therapy may provide relief for patients who experience infrequent heartburn. If the patient’s symptoms do not improve within 2 to 3 weeks, or if the condition is severe, additional pharmacologic measures should be tried to reduce irritation. About 5% to 10% of patients with GERD require surgery.

The treatment of PUD and GERD is somewhat similar: relieve symptoms, promote healing, and prevent recurrence. Lifestyle changes that eliminate risk factors, such as cigarette smoking and foods (and alcohol) that increase acid secretion, should be initiated. Patients rarely need to be restricted to a bland diet. If NSAIDs are being taken, consideration should be given to switching to acetaminophen if feasible. For decades, ulcer treatment focused on reducing acid secretions (anticholinergic agents, H2 antagonists, gastric acid pump inhibitors), neutralizing acid (antacids), or coating ulcer craters to hasten healing (sucralfate). Major changes in therapy have come about because the U.S. Food and Drug Administration (FDA) has approved antibiotics to eradicate H. pylori. Several large studies are under way to refine the healing and reduce ulcer recurrence rate. Various combinations of antimicrobial agents (e.g., amoxicillin, tetracycline, metronidazole, clarithromycin), bismuth, and antisecretory agents (e.g., H2 antagonists, proton pump inhibitors) are used to eradicate H. pylori. Antibiotics are not recommended for individuals who are asymptomatic with H. pylori because there is concern that resistant strains of bacteria may develop.

Drug Therapy

Actions

• Antacids neutralize gastric acid, thereby causing the gastric contents to be less acidic.

• Coating agents provide a protective covering over the ulcer crater.

• H2 antagonists decrease the volume of hydrochloric acid produced, which increases the gastric pH and thereby results in decreased irritation to the gastric mucosa.

• Proton pump inhibitors block the formation of hydrochloric acid, reducing irritation of the gastric mucosa.

• Prokinetic agents increase the lower esophageal sphincter muscle pressure and peristalsis, hastening emptying of the stomach to reduce reflux.

• Antispasmodic agents reduce the secretion of saliva, hydrochloric acid, pepsin, bile, and other enzymatic fluids necessary for digestion, and decrease GI motility and secretions.

Uses

• Antacids decrease hyperacidity associated with PUD, GERD, gastritis, and hiatal hernia.

• Coating agents provide a protective barrier for the mucosal lining where hydrochloric acid may come into contact with inflamed eroded areas. They are used to treat existing ulcer craters on the gastric mucosa.

• H2 antagonists are used to treat acute gastric and duodenal ulcers and gastroesophageal disease, as well as for maintenance to prevent ulcer recurrence.

• Proton pump inhibitors are used to treat hyperacidity conditions (e.g., GERD, Zollinger-Ellison syndrome) and peptic and gastric ulcer disease.

• Prokinetic agents are used to treat GERD.

• Antispasmodic agents decrease gastric secretions by inhibiting vagal stimulation. They are used in treating GI disorders requiring decreased gastric motility or decreased gastric secretions.

Nursing Implications for Agents Used for Stomach Disorders

Assessment

Nutritional Assessment.

Obtain patient data about current height, weight, and any recent weight gain or loss. Identify the normal pattern of eating, including snacking habits. Use a food guide such as MyPlate (see Figure 47-1) as a guide when asking questions to identify the usual foods eaten by the individual. Ask about any nutritional or cultural restrictions associated with dietary practices. Are there any food allergies (obtain details), or foods that particularly cause gastric distress when eaten? Does the individual take any nutritional supplements? How often and how much fast food is eaten?

Esophagus, Stomach.

Ask patients to describe symptoms. Question in detail what is meant by the terms indigestion, heartburn, upset stomach, nausea, and belching.

Pain, Discomfort

• Ask the patient to describe the onset, duration, location, and characteristics of pain or discomfort. Determine whether there is a relationship between the ingestion of certain types of food or drinks and the onset of pain. Ask specifically about coffee, tea, cola, chocolate, and alcohol intake.

• What has the patient done to relieve the pain or discomfort? Have there been any changes in taste (e.g., bitterness, sourness)? Record pain using a rating scale before and after medications are administered.

Activity, Exercise.

Ask specifically what type of work or activities the individual performs that may increase intra-abdominal pressure (e.g., lifting heavy objects, bending over frequently).

History of Diseases or Disorders

• What other diagnoses have been made for diseases or disorders (e.g., ulcer, gallbladder, liver, jaundice, irritable bowel syndrome)?

• Have there been any changes in bowel elimination or stool color, consistency, or frequency?

Medication History

• What self-medications have been tried?

• What prescribed medications are being taken?

• What is the schedule of medication administration (e.g., how frequently and when are antacids taken)?

Anxiety or Stress Level.

Ask the patient to describe his or her lifestyle. What does the patient think are stressors, and how often do they occur?

Smoking.

What is the frequency of smoking?

Implementation

• Routine orders: Most health care providers order antacids 1 hour before meals, 2 to 3 hours after meals, and at bedtime. As-needed (PRN) medication dosages must be discussed.

• Each type of medication used to treat GERD or PUD may require somewhat different scheduling to avoid drug interactions. When developing the time frames for administration of medications on the medication administration record (MAR), schedule the other prescribed drugs 1 hour before or 2 hours after antacids.

• Changes in diet require careful planning with the patient as well as the person responsible for purchasing and cooking the meals. Schedule teaching sessions appropriately. Not only may some foods need to be altered, but also the number of meals per day may need to be increased with a smaller serving at each meal.

Patient Education and Health Promotion

Nutrition

• Implement prescribed dietary changes: eat small, more frequent meals to support optimal energy requirements and healing; avoid overdistention of the stomach; avoid any seasonings that are intolerable or that aggravate the condition; and avoid coffee, teas, colas, alcoholic beverages (including beer), carbonated beverages, peppermint, spearmint, and citric juices, which may produce discomfort in those with GERD.

• Avoid late-night snacks or meals that could result in increased gastric secretions.

• Observe for foods that aggravate the condition, and eliminate these from the diet. Drink only small amounts of fluid with the meal and drink mostly between meals. Increase protein foods and decrease fats to about 45 g/day or less; use nonfat milk.

Pain, Discomfort.

Keep a written record of the onset, duration, location, and precipitating factors for any pain. Sit upright at the table when eating and do not lie down for at least 2 hours after eating. When a hiatal hernia is present, elevate the head of the bed on 6- to 8-inch blocks to prevent reflux during sleep. Have the patient keep a log of the pain including time of day, any factors that might have precipitated the pain, and degree of pain relief from medications used.

Medications

• Take prescribed medications at recommended times to promote optimal healing. See individual drug monographs for suggested scheduling.

• Avoid NSAIDs and aspirin-containing medicines that irritate the gastric mucosa. Consult the prescriber or pharmacist regarding scheduling of or discontinuation of these medications.

Lifestyle Changes

• Discuss stress and its effects on the person, and implement needed lifestyle changes.

• Encourage a significant reduction or cessation of smoking.

• Implement plans to gain sufficient rest.

Fostering Health Maintenance

• Discuss medication information and how it will benefit the course of treatment to produce an optimal response. Medications used in the treatment of hyperacidity are important measures to alleviate the irritating effects on the mucosal tissue; stress the importance of not discontinuing treatment, and the need for continued medical follow-up.

• Seek cooperation and understanding of the following points so that medication adherence is increased: name of medication, dosage, route and times of administration, and common and serious adverse effects. Stress the need to complete a full course of treatment for H. pylori so that the organisms are indeed killed and not only suppressed; H. pylori can regrow if medications are discontinued too early.

Written Record.

Enlist the patient’s aid in developing and maintaining a written record of monitoring parameters (e.g., a list of foods causing problems, degree of pain relief) (see Patient Self-Assessment form for Agents Affecting the Digestive System on the Evolve Web site at http://evolve.elsevier.com/Clayton). Complete the Premedication Data column for use as a baseline to track response to drug therapy. Ensure that the patient understands how to use the form and instruct the patient to bring the completed form to follow-up visits. During follow-up visits, focus on issues that will foster adherence with the therapeutic interventions prescribed.

Drug Class: Antacids

Actions

Antacids lower the acidity of gastric secretions by buffering the hydrochloric acid (normal pH is 1 to 2) to a lower hydrogen ion concentration. Buffering hydrochloric acid to a pH of 3 to 4 is highly desired because the proteolytic action of pepsin is reduced and the gastric juice loses its corrosive effect.

Uses

Antacid products account for one of the largest sales volumes (more than $1 billion annually) of over-the-counter medication. Antacids are commonly used for heartburn, excessive eating and drinking, and PUD. However, nurses and patients must be aware that not all antacids are alike. They should be used judiciously, particularly by certain types of patients (e.g., those with heart failure, hypertension, renal failure). Long-term self-treatment with antacids may also mask symptoms of serious underlying diseases, such as a bleeding ulcer.

The most effective antacids available are combinations of aluminum hydroxide, magnesium oxide or hydroxide, magnesium trisilicate, and calcium carbonate. All act by neutralizing gastric acid. Combinations of these ingredients must be used because any compound used alone in therapeutic quantities may produce severe systemic adverse effects. Other ingredients found in antacid combination products include simethicone, alginic acid, and bismuth. Simethicone is a defoaming agent that breaks up gas bubbles in the stomach, reducing stomach distention and heartburn. It is effective in patients who have overeaten or who have heartburn, but it is not effective in treating PUD. Alginic acid produces a highly viscous solution of sodium alginate that floats on top of the gastric contents. It may be effective only for the patient being treated for GERD or hiatal hernia and should not be used in the patient with acute gastritis or PUD. Bismuth compounds have little acid-neutralizing capacity and are therefore poor antacids.

The following principles should be considered when antacid therapy is planned:

• For indigestion, antacids should not be administered for more than 2 weeks. If after this time the patient is still experiencing discomfort, a health care provider should be contacted.

• Patients with edema, heart failure, hypertension, renal failure, pregnancy, or salt-restricted diets should use low-sodium antacids, such as Riopan, Maalox, or Mylanta II. Therapy should continue only on the recommendation of a health care provider.

• Antacid tablets should be used only for the patient with occasional indigestion or heartburn. Tablets do not contain enough antacid to be effective in treating PUD.

• A common complaint of patients consuming large quantities of calcium carbonate or aluminum hydroxide is constipation. Excess magnesium results in diarrhea. If a patient experiences these symptoms and still has stomach discomfort, a health care provider should be consulted.

• Effective management of acute ulcer disease requires large volumes of antacids. The selection of an antacid and the quantity to be taken depend on its neutralizing capacity. Any patient with coffee-ground emesis, bloody stools, or recurrent abdominal pain should seek medical attention immediately and not attempt to self-treat the disorder.

• Calcium carbonate and sodium bicarbonate may cause rebound hyperacidity.

• Patients with renal failure should not use large quantities of antacids containing magnesium. The magnesium ions cannot be excreted and may produce hypermagnesemia and toxicity.

• Most antacids have similar ingredients. Selection of an antacid for occasional use should be determined by quantity of each ingredient, cost, taste, and frequency of adverse effects. Patients may need to try more than one product and weigh the advantages and disadvantages of each.

Therapeutic Outcomes

The primary therapeutic outcomes expected from antacid therapy are relief of discomfort, reduced frequency of heartburn, and healing of irritated tissues.

Nursing Implications for Antacids

Premedication Assessment

1 Check renal function test results to ensure that renal function is normal. When renal failure is present, patients should not take large quantities of antacids containing magnesium. Monitor the patient’s renal function tests, including BUN (blood urea nitrogen), creatinine, and serum electrolyte levels, including magnesium and potassium. Magnesium and potassium ions cannot be excreted and may produce hypermagnesemia, hyperkalemia, and toxicity.

2 Check the pattern of bowel elimination for diarrhea or constipation.

3 Record the pattern of gastric pain being experienced; report coffee-ground emesis, bloody stools, or recurrent abdominal pain to the health care provider for prompt attention.

4 If the patient is pregnant or has edema, heart failure, hypertension, or salt restrictions, ensure that a low-sodium antacid has been prescribed.

5 Schedule other prescribed medications to be taken 1 hour before or 2 hours after antacids are to be administered.

Life Span Considerations

Antacids

Those older than 65 years are the most common purchasers of antacid products. Gastrointestinal disorders such as PUD, NSAID-induced ulcers, and GERD occur more often in this age-group. Magnesium-containing antacids are often used as laxatives. Although the primary symptom of ulcer disease in a younger person is usually burning epigastric pain, the symptoms in an older person, if present at all, usually include complaints of vague abdominal discomfort, anorexia, and weight loss.

Availability

See Table 33-1.

• Liquid forms of antacid preparations should be used for treatment of PUD because tablets do not contain enough of the active ingredients to be effective.

• Antacid tablets may be used for occasional episodes of heartburn. They should be well chewed before swallowing for a more rapid onset of action.

Table 33-1

Ingredients of Commonly Used Antacids

PRODUCT	FORM	CALCIUM CARBONATE	ALUMINUM HYDROXIDE	MAGNESIUM OXIDE OR HYDROXIDE	SODIUM BICARBONATE	SIMETHICONE	OTHER INGREDIENTS
Aludrox	Tablet, suspension	—	X	X	—	X	—
Baking soda	Powder	—	—	—	X	—	—
Di-Gel	Tablet, liquid	—	X	X	—	X	—
Gelusil	Tablet	—	X	X	—	X	—
Maalox Maximum Strength	Suspension	—	X	X	—	X	—
Mylanta	Tablet, suspension	—	X	X	—	X	—
Mylanta Extra Strength	Suspension	—	X	X	—	X	—
Mylanta Supreme	Liquid	X	—	X	—	—	—
Phillip’s Milk of Magnesia	Tablet, suspension	—	—	X	—	—	—
Riopan	Suspension	—	—	—	—	—	Magaldrate
Riopan Plus	Tablet, suspension	—	—	—	—	X	Magaldrate
Titralac Plus	Tablet, suspension	X	—	—	—	X	—
Tums	Tablet	X	—	—	—	—	—

< div class='tao-gold-member'>

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Tags: Basic Pharmacology for Nurses

Jul 11, 2016 | Posted by admin in NURSING | Comments Off

Nurse Key

Fastest Nurse Insight Engine

33. Drugs Used to Treat Gastroesophageal Reflux and Peptic Ulcer Disease

Drugs Used to Treat Gastroesophageal Reflux and Peptic Ulcer Disease

Objectives

Key Terms