Gastrointestinal Medications
Objectives
1. Identify common uses for antacids and histamine H2-receptor antagonists.
3. Compare the actions and adverse reactions of the five major classifications of laxatives.
5. Describe indications for disulfiram use and what is meant by “disulfiram reaction.”
Key Terms
antacids (ănt-ĂS-ĭdz, p. 336)
antidiarrheals (ăn-tĭ-dī-ă-RĒ-ălz, p. 340)
antiflatulents (ăn-tĭ-FLĂ-tū-lěnts, p. 347)
digestive enzymes (dī-JĔS-tĭvĔN-zīmz, p. 349)
disulfiram reaction (dī-SŬL-fĭ-răm, p. 350)
emetics (ěm-ĔT-ĭks, p. 347)
histamine H2-receptor antagonists (HĬS-tă-mēn, ăn-TĂG-ō-nĭsts, p. 336)
laxatives (LĂK-să-tĭvz, p. 341)
motility (mō-TĭL-ĭ-tē, p. 340)
Overview
http://evolve.elsevier.com/Edmunds/LPN/
This chapter discusses medications used to treat the many diseases and disorders that affect the gastrointestinal (GI) tract. Many of these drugs are available over the counter (OTC); many others are used, often in combination, to relieve the symptoms of common GI tract problems.
There are three major types of GI medications. The first type includes products designed to help restore or maintain the lining that protects the GI tract. These drugs include antacids, which act to neutralize or reduce the acidity of the gastric contents; histamine H2-receptor antagonists, which reduce gastric acid secretion by limiting the action of histamine at the H2 receptors in the stomach; and proton pump inhibitors, which reduce gastric acid by blocking the proton pump. These medications are described in the first section.
A second type of GI medication affects the general motility, or movement, of the GI tract. These medications include the anticholinergics and antispasmodics, which not only reduce gastric motility but also decrease the amount of acid secreted by the stomach, and the antidiarrheals, which reduce diarrhea by slowing the intestinal peristalsis. These drugs are discussed in the second section.
The third type of GI drugs also affect motility, but their action is primarily in the colon. These are the laxative agents. These preparations promote bowel emptying in a variety of ways. They may increase intestinal bulk, lubricate the intestinal walls, soften the fecal mass by retaining water, or produce increased peristalsis through local tissue irritation or by direct action on the intestine. These drugs are discussed in the third section.
The fourth section presents miscellaneous medications. These preparations include antiflatulents, which are used to reduce gas and bloating; and digestive enzymes, which are used in deficiency states to break down fats, starches, and proteins in the digestive process. (Antiemetic preparations are discussed in Chapter 16, along with antivertigo agents.)
Digestive System 
The digestive system is composed of the mouth, esophagus, stomach, intestines, and accessory structures (Figure 19-1). This system performs the mechanical and chemical process of digestion, absorbs nutrients, and eliminates waste.
Digestion begins in the mouth with chewing and mixing of food with enzyme-rich saliva secreted by salivary glands. The passages and spaces from the mouth to the anus are called the alimentary canal. Here is where the complex compounds created in the mouth are reduced to soluble substances that can be absorbed; the usable food substances are absorbed; and the indigestible and waste material is eliminated. The digestive glands secrete enzymes and other chemicals essential to the breakdown of food substances and their absorption into the bloodstream. The salivary glands, gallbladder, liver, and pancreas are included as accessory glands.
Almost all oral medications use the digestive system as a means to reach target organs or tissues. Many of the side effects, such as diarrhea, nausea, or constipation, are results of the direct action of medications on the alimentary tract itself. Medications, as well as all swallowed materials, are acted on by the digestive tract and are metabolized and excreted.
The digestive tract must work without being destroyed by the strong acid it makes to digest food. Several factors work together to protect the GI tract mucosa from injury. The gastric mucosal barrier resists backward diffusion of hydrogen and thus has the ability to have a high concentration of hydrochloric acid (HCl) within the gastric lumen unless something breaks this barrier. Endogenous prostaglandins (those produced in the GI tract) are thought to protect the cells against agents that would be harmful. Prostaglandins are produced in great numbers in the mucosa of the stomach and duodenum. They are known to produce both mucus and bicarbonate and to maintain mucosal blood flow. Mucus helps protect the mucosa. It is secreted by surface epithelial cells and forms a gel that covers the mucosal surface and physically protects the mucosa from abrasion. It also resists the passage of large molecules such as pepsin. Bicarbonate is produced in small amounts by surface epithelial cells and moves up from the mucosa to create a thin layer of alkalinity between the mucus and the epithelial surface. Other protective factors include mucosal blood flow, epithelial healing or renewal, and epidermal growth factor that is secreted in saliva and by the duodenal mucosa.
There is a lot of variability in the body’s ability to absorb medications from the GI tract over the course of a lifetime. Changes in GI blood flow, amount of surface available, and motility are found in very young and older adult patients. Thus dosages of some medications may need to be changed when the patient is very young or very old.
Antacids, H2-Receptor Antagonists, Proton Pump Inhibitors
Overview
The lining of the stomach is usually strong enough to resist the powerful digestive juices and acids that bathe it. When stress or disease produce excess secretion of gastric acids, or when there is destruction of the protective mucosal lining because of alcohol, chemicals, or disease, gastric distress is produced. If the protective lining is not repaired or the gastric acid level reduced, duodenal, gastric, or peptic ulcers are produced, leading to increased pain and bleeding. Antacid therapy, histamine H2-receptor antagonists, and proton pump inhibitors reduce gastric acidity and promote healing. More than one medication may be used at the same time to help in healing. Two unique medications, sucralfate and misoprostol, are designed to assist in the protection of GI mucosa from the effects of nonsteroidal antiinflammatory drugs (NSAIDs).
Action
Antacids are OTC agents that neutralize HCl and increase gastric pH, thus inhibiting pepsin (a gastric enzyme). Antacids work in a variety of ways. Some antacids cause hydrogen ion absorption (buffering the acid), tightening of the gastric mucosa, and increased tone of the cardiac sphincter. Formation of gas that may be released by burping is another way in which antacids work.
Histamine H2-receptor antagonists are unique, because they promote healing of ulcers and act with antacids to produce more alkaline conditions in the GI tract. Histamine H2-receptor antagonist drugs can bind to the H2 receptor, thereby displacing histamine from receptor binding sites and preventing stimulation of the secretory cells. Thus they block histamine, inhibit the secretion of gastric acid, and are rapidly absorbed; they reach their peak of effectiveness in 45 to 90 minutes.
Another class of drugs that works to heal gastric ulcers is proton pump inhibitors. These drugs irreversibly stop the acid secretory pump embedded within the gastric parietal cell membrane by altering the activity of H+, K+-ATPase, the enzyme inhibiting hydrogen ion transport into the gastric lumen, and thus decrease acid secretion. Because proton pump inhibitors act on the basolateral membrane of the parietal cells, they do not affect gastric emptying, basal or stimulated pepsin output, or secretion of intrinsic factor. These drugs do not seem to affect the level of adenosine triphosphatase (ATPase) of other organ systems.
Uses
Antacids are used with other drugs to treat peptic ulcer disease, gastritis, gastric ulcer, peptic esophagitis, hiatal hernia, gastric hyperacidity, and esophageal reflux.
Histamine H2 blockers are generally considered first-line therapy to relieve symptoms and prevent complications of peptic ulcer disease when used for 6 to 8 weeks. (It is common for the patient to have a relapse after the medication is stopped.) They are also used in the prophylaxis and treatment of peptic esophagitis, benign gastric ulcers, duodenal ulcers, stress ulcers, and Zollinger-Ellison syndrome. The H2 blockers are similar in effectiveness and side effects.
Many peptic ulcers may be caused by Helicobacter pylori. This organism may be controlled and the ulcer healed by use of antibiotics plus products such as ranitidine.
Proton pump inhibitors are used in the short-term treatment of active duodenal ulcers, usually after adequate courses of H2-receptor antagonists have not been successful. Longer therapy is not indicated. Severe erosive esophagitis and poorly responsive gastroesophageal reflux disease (GERD) are indications for these types of medications as well. Long-term treatment with proton pump inhibitors is needed for pathologic hypersecretory conditions.
There are other important drugs that do not fit into these three categories but also assist in the healing of ulcers. Sucralfate is an aluminum salt of sulfated sucrose and a polysaccharide with antipeptic activity. It aids in the healing of ulcers by forming a protective layer at the ulcer site, providing a barrier to hydrogen ion diffusion, but does not alter gastric pH. It also works to stop pepsin’s action and adsorbs bile salts. Misoprostol is a synthetic prostaglandin analogue with both an antisecretory and a mucosal protective action. It is indicated for use in patients who have gastric distress or ulceration secondary to the use of NSAIDs.
Adverse Reactions
Some adverse reactions occur only with a certain category of antacids; others are common to most. Antacids may produce malaise (weakness), anorexia (lack of appetite), bowel obstruction, constipation, diarrhea, frequent burping, thirst, and muscle weakness. In cases of extreme hypermagnesemia, cardiotoxicity with bradyarrhythmia (slow heart beat), asystole (no heart beat), and hypotension may be seen. The most severe reactions include coma, decreased reflexes, and respiratory depression.
With histamine H2-receptor antagonists, side effects are unusual, but the patient may have mild and self-limiting problems such as dizziness, headaches, somnolence, mild and brief diarrhea, some hematologic changes, rash, impotence, mild gynecomastia (enlargement of the breasts in men), muscle pain, and fever. With proton pump inhibitors, reactions include headache, diarrhea, abdominal pain, and nausea. Rare reactions include rash, vomiting, and dizziness.
Drug Interactions
Antacids prevent the absorption of the antibiotic tetracycline. Enteric coatings of various medications dissolve more quickly in the presence of antacids, leaving the upper GI tract more sensitive to irritation. Some antacids have been known to either bind with or alter the absorption rate of digitalis products, anticoagulants, iron, phenothiazines, antiinflammatory agents, antihypertensives, antiarthritic agents, hydantoin, and possibly propranolol. Aluminum-magnesium hydroxide gel may increase absorption of aspirin.
Clinical Pitfall
Cimetidine
Cimetidine inhibits the cytochrome P-450 system and interacts with many other medications. Care should be used when any other medications are taken at the same time as cimetidine.
Antacids may increase the absorption of cimetidine, a histamine antagonist agent. Cimetidine may increase the effects of anticoagulants, hydantoin, beta-adrenergic blocking agents, lidocaine, benzodiazepine derivatives, and theophylline. Decreased white blood cell counts have been reported in cimetidine-treated patients who also received other drugs and treatments known to produce neutropenia. Apnea, confusion, and muscle twitching may be produced when cimetidine is administered with morphine. Serum digoxin levels may be reduced when digoxin and cimetidine are administered together. Cigarette smoking may neutralize the action of cimetidine. Ranitidine does not appear to interact with warfarin-type anticoagulants, theophylline, or diazepam, although it does produce false-positive urine protein tests.
Proton pump inhibitors also inhibit the cytochrome P-450 system and may interfere with the metabolism of other drugs using the P-450 system. They may also increase concentration of oral anticoagulants, diazepam, and phenytoin, making overdosage a possibility.
Nursing Implications and Patient Teaching
n Assessment
Learn everything possible about the patient’s health history, including GI symptoms, the presence of disease (especially renal failure), the presence of allergy, and whether any medications that might cause drug interactions are currently being taken by the patient.
n Diagnosis
In addition to the medical diagnosis, what is the source of the patient’s problem? Does the patient drink too much coffee or alcohol or use cigarettes extensively—all of which are harmful to the gastric mucosa? Is the patient under stress from financial, family, or job-related difficulties? Does the patient experience gastric distress because of other medications (such as NSAIDs) or disease processes? Look beyond the symptoms to find the cause of increased gastric acid production. This may assist the patient in focusing on the true source of the problem.
n Planning
The patient’s fluid intake should be increased, and the patient who is taking antacids that cause constipation, such as those containing calcium or aluminum, should be carefully monitored. These drugs may be alternated with antacids that have cathartic-like actions, such as those containing magnesium.
n Implementation
Antacids are available in several different forms. Liquids or solutions are the preferred choice whenever possible, because they neutralize acid more rapidly. Suspensions, gels, chewable tablets, effervescent tablets, and powders are also available. Tablets should be considered the last alternative, even though they may be the patient’s first choice. The gastric emptying time of the peptic ulcer patient may vary, so it is wise to individualize the antacid schedule. The neutralizing abilities of antacids vary, requiring different quantities of medication, depending on the product. Discuss flavor preferences with the patient. Many patients discontinue antacid therapy because they dislike the flavor. Products come in many flavors, and various drugs may be tried if compliance becomes a problem.
Antacids with a laxative effect should be taken at bedtime to allow adequate rest before the bowel is stimulated.
The sodium content of various antacids must be carefully assessed before giving them to patients who are on restricted sodium intake. These patients include pregnant women and patients with congestive heart failure (CHF) or other cardiac conditions, hypertension (high blood pressure), edema (fluid buildup in the body tissues), or renal failure.
Histamine H2-receptor antagonists may be given via intravenous (IV) or oral (PO) medications. Preparations given PO should be given with meals and at bedtime. IV injections should be diluted and injected over 1 to 2 minutes or given by infusion, and are usually given to patients with hypersecretion of gastric acid or intractable pain from ulcers. These medications should be given for 2 to 6 weeks, until endoscopy tests reveal healing. This drug may mask underlying malignancy.
Lifespan Considerations
Older Adults
Antiulcer Therapies
Modified from McKenry LM, Tessier E, Hogan MA: Mosby’s pharmacology in nursing, ed 22, St Louis, 2006, Mosby.
Table 19-1 presents a summary of antacids and histamine H2-receptor antagonists.
Table 19-1
Antacids, Histamine H2-Receptor Antagonists, and Proton Pump Inhibitors
| GENERIC NAME | TRADE NAME | COMMENTS |
| Antacids | ||
| aluminum carbonate gel | Basaljel | Take between meals and at bedtime, followed by a sip of water if desired. |
| aluminum hydroxide gel | Dialume | Helps delay stomach emptying and binds bile salts. Drug of choice in peptic ulcer disease. Take between meals and at bedtime, followed by a sip of water if desired. |
| calcium carbonate | Tums | Very effective; promotes prolonged and powerful neutralizing effect greater than aluminum hydroxide. Primarily suited for short-term therapy; given in small doses. Constipating effects may be minimized by alternating with doses of a magnesium-containing antacid such as magnesium carbonate. |
| magaldrate | Losopan Riopan |
Combination of magnesium and aluminum hydroxide. Effectiveness depends on GI pH. Give between meals and at bedtime; not to be taken for more than 2 wk. |
| magnesium hydroxide | Milk of Magnesia | Helpful because cathartic effect counteracts constipation of aluminum hydroxide. Osmotic diarrhea may occur when given alone. Take with water up to 4 times daily. |
| magnesium oxide | Mag-Ox Maox Uro-Mag |
Acts more slowly than sodium bicarbonate but has a more prolonged action and increased neutralizing ability. As with other magnesium antacids, osmotic diarrhea may develop, but it may be alleviated if alternated with aluminum or calcium salts. |
| sodium bicarbonate | Bell/ans | Take 1 to 4 times/day. |
| sodium citrate | Citra pH | Take daily. |
| Antacid Combinations | ||
| aluminum hydroxide and magnesium hydroxide | Maalox | Combined to provide a nonconstipating, noncathartic antacid for relief of hyperactivity of peptic ulcer. Suspension may be followed by a sip of water. |
| aluminum hydroxide, magnesium hydroxide, and simethicone | Gelusil | Products use simethicone to reduce gas formation; come in many flavors and a variety of combinations. |
| calcium carbonate | Titralac | Form an insoluble antacid-protective compound for the relief of hyperacidity. Take after meals; tablets can be chewed, swallowed, or allowed to dissolve slowly in the mouth. |
| Histamine H2-Receptor Antagonists | ||
| cimetidine | Tagamet | Widely used in prophylaxis and treatment of ulcers. Has more drug interactions than other preparations and a much wider range of actions than other preparations. Should be taken with antacids. |
| famotidine | Pepcid | Reduce dose in those with decreased renal function. |
| nizatidine | Axid | Give reduced dose for those with decreased renal function. |
| ranitidine | Zantac | Similar in action to cimetidine, but has fewer drug interactions. Headaches are frequent; extrapyramidal symptoms may be noted. Dose should not exceed 150 mg/24 hr if creatinine clearance is below 50 mL/min. |
| Agents to Treat Helicobacter pylori | ||
| bismuth subsalicylate, metronidazole, and tetracycline | Helidac Pylera |
Each dose includes 4 pills: 2 pink chewable 262.4-mg tablets (bismuth subsalicylate); 1 white 250-mg tablet (metronidazole); and 1 pale orange and white 500-mg capsule (tetracycline). Patient should take each dose 4 times daily, with meals and at bedtime, chew and swallow pink tablets, swallow others whole, and drink plenty of water with medication, especially at night. |
| Miscellaneous Products | ||
| misoprostol | Cytotec | Take daily with meals and at bedtime; reduce dose if higher dose cannot be tolerated. Patient should use throughout the course of NSAID therapy. |
| sucralfate | Carafate | Antacids may be prescribed as needed for pain relief, but patient should not take within  hr before or after this medication. |
| Proton Pump Inhibitors | ||
| esomeprazole | Nexium | Take delayed-release capsule 1 hr before eating. |
| lansoprazole | Prevacid  |
Adults: 15 mg once daily before meals for 4 wk. May also use 30 mg with 500 mg clarithromycin and 1 g amoxicillin twice daily for 14 days; or 30 mg with 1 g amoxicillin 3 times daily for 14 days for those intolerant to clarithromycin. |
| omeprazole | Losec  Prilosec |
Adults: 20 mg daily before eating for 4-8 wk. Most ulcers heal within 4 wk, but some require an additional 4 wk. Do not open, chew, or crush capsule. |
| pantoprazole | Protonix | Use delayed-release capsule once daily for 8 wk; also available as an IV infusion. |
| rabeprazole | Aciphex | Use delayed-release tablet every morning for 4-8 wk. |
GI, Gastrointestinal; IV, intravenous; NSAID, nonsteroidal antiinflammatory drug.
n Evaluation
Watch to see if the patient seems to have less GI distress or develops any adverse reactions.
n Patient and Family Teaching
Anticholinergics, Antispasmodics, and Antidiarrheals
Overview
Motility is the spontaneous but unconscious or involuntary movement of food through the GI tract. Much of the discomfort of GI disease is caused by increased intestinal peristalsis (muscle contraction). Abdominal cramping, bloating, and pain may be related either to acute minor illnesses associated with diarrhea and increased gas, or to chronic diseases such as ulcers or colitis. Also, many drugs have both diarrhea and increased bowel motility as common adverse reactions.
The medications used to treat these problems are classified as anticholinergics, antispasmodics, or antidiarrheals. Their actions are somewhat different, although they are often used interchangeably.
Action
The anticholinergic-antispasmodic agents are parasympatholytic drugs (natural and synthetic) that act with antacids in prolonging or continuing the therapeutic benefits of both drug categories. Anticholinergics reduce GI tract spasm and intestinal motility, acid production, and gastric motility and thus reduce the associated pain. Gastric emptying time is slowed, and neutralization is increased. Pancreatic secretions of fluid, electrolytes, and enzymes are also stopped. However, the adverse reactions resulting from the high dosages necessary to obtain these effects make the use of such dosages questionable. GI motility stimulants are also available and are particularly helpful in the elderly patient with GERD because they do not have cholinergic activity.
Antidiarrheals reduce the fluid content of the stool and decrease peristalsis and motility of the intestinal tract. They increase smooth muscle tone and diminish digestive secretions. The bismuth salts absorb toxins and provide a protective coating for the intestinal mucosa.
