Drugs and the Gl system The GI tract is basically a hollow, muscular tube that begins at the mouth and

ends at the anus; it encompasses the pharynx, esophagus, stomach, and the small and large intestines. Its primary functions are to digest and absorb foods and fluids and excrete metabolic waste.

Classes of drugs used to improve GI function include: antiulcer drugs adsorbent, antiflatulent, and digestive drugs antidiarrheal and laxative drugs antiemetic and emetic drugs.

Anti-Ulcer Drugs

A peptic ulcer is a circumscribed lesion in the mucosal membrane, developing in the lower esophagus, stomach, duodenum, or jejunum. The major causes of peptic ulcers include: bacterial infection with Helicobacter pylori the use of nonsteroidal anti-inflammatory drugs (NSAIDs) hypersecretory states such as Zollinger-Ellison syndrome (a condition in which excessive gastric acid secretion causes peptic ulcers) cigarette smoking, which causes hypersecretion and impairs ulcer healing a genetic predisposition, which accounts for 20% to 50% of patients with peptic ulcers.

Antiulcer drugs are formulated to eradicate H. pylori or restore the balance between acid and pepsin secretions and the Gl mucosal defense. These drugs include: systemic antibiotics antacids histamine-2 (H2) receptor antagonists proton pump inhibitors other antiulcer drugs, such as misoprostol and sucralfate.

Systemic antibiotics H. pylori is a gram-negative bacteria that's thought to be a major causative factor in peptic ulcer formation and gastritis (inflammation of the stomach lining). Eradicating the bacteria promotes ulcer healing and decreases recurrence. Successful treatment involves the use of two or more antibiotics in combination with other drugs. Systemic antibiotics used to treat H. pylori include: Amoxicillin Clarithromycin Metronidazole Tetracycline

Pharmacokinetics Systemic antibiotics are variably absorbed from the Gl tract. Food, especially dairy products, decreases the absorption of tetracycline but doesn't significantly delay the absorption of the other antibiotics. All of these antibiotics are distributed widely and are excreted primarily in urine.

Pharmacodynamics (how drugs act) Antibiotics act by treating the H. pylori infection. They're usually combined with an H2-receptor antagonist or a proton pump inhibitor to decrease stomach acid and further promote healing.

Pharmacotherapeutics (how drugs are used) Systemic antibiotics are indicated for H. pylori eradication to reduce the risk of a duodenal ulcer.

Treatment Plan Treatment plans that use at least two antimicrobial drugs and a proton pump inhibitor for 14 days and then continue the proton pump inhibitor for 6 more weeks, help reduce acid in the patient with peptic ulcers.

Drug interactions Tetracycline and metronidazole can interact with many other drugs. For example, tetracycline increases digoxin levels and, when combined with methoxyflurane, increases the risk of nephrotoxicity. Metronidazole and tetracycline increase the risk of bleeding when taken with oral anticoagulants.

Adverse reactions Metronidazole, clarithromycin, and tetracycline commonly cause mild GI disturbances. Clarithromycin and metronidazole may produce abnormal tastes.

Metronidazole may cause a disulfiram-like reaction (nausea, vomiting, headache, cramps, flushing) when combined with alcohol. Discourage concomitant use. Amoxicillin may cause diarrhea.

Nursing process

Assessment Assess the patient's infection before therapy and regularly thereafter. Assess signs and symptoms of the patient's ulcer. Watch for edema, especially in the patient who's also receiving corticosteroids; antibiotics, such as metronidazole, may cause sodium retention. Assess for adverse reactions and drug interactions. Identify risk factors for peptic ulcer disease, such as cigarette smoking, stress, and drug therapy with irritating medications (aspirin, other NSAIDs, corticosteroids, or antineoplastics). Assess the patient's and family's understanding of drug therapy.

Key nursing diagnoses Ineffective health maintenance related to presence of susceptible organisms Risk for deficient fluid volume related to drug-induced adverse Gl reactions Deficient knowledge related to drug therapy

Planning outcome goals The patient's overall health status will improve. Stable vital signs and the patient's urine output will indicate improved fluid volume status. The patient and his family will demonstrate an understanding of drug therapy.

Implementation Administer drugs as appropriate for the patient's condition and diagnosis. Use measures to prevent or minimize peptic ulcer disease and gastric acid-induced esophageal disorders.

Observe the patient for improvement in symptoms.

Evaluation Patient is free from infection. Patient maintains adequate hydration throughout therapy. Patient and his family demonstrate an understanding of drug therapy.

Antacids

Antacids are over-the-counter (OTC) medications used in combination with other drugs to treat peptic ulcers. Types of antacids include: aluminum carbonate gel calcium carbonate magaldrate (aluminum-magnesium complex) magnesium hydroxide and aluminum hydroxide a simethicone.

Pharmacokinetics Antacids work locally in the stomach by neutralizing gastric acid. They don't need to be absorbed to treat peptic ulcers. Antacids are distributed throughout the GI tract and are eliminated primarily in feces.

Pharmacodynamics The acid-neutralizing action of antacids reduces the total amount of acid in the GI tract, allowing peptic ulcers time to heal. Pepsin, a digestive enzyme, acts more effectively when the stomach is highly acidic; therefore, as acidity drops, pepsin action is also reduced.

Pharmacotherapeutics Antacids are primarily prescribed to relieve pain and are used ad-junctively in peptic ulcer disease. Antacids also relieve symptoms of acid indigestion, heartburn, dyspepsia (burning or indigestion), or gastroesophageal reflux disease (GERD), where the contents of the stomach and duodenum flow back into the esophagus.

Antacids may be used to control hyperphosphatemia (elevated blood phosphate levels) in kidney failure. Because calcium binds with phosphate in the Gl tract, calcium carbonate antacids prevent phosphate absorption.

Drug interactions All antacids can interfere with the absorption of oral drugs if given at the same time. Absorption of digoxin, phenytoin, ketoconazole, iron salts, isoniazid, quinolones, and tetracycline may be reduced if taken within 2 hours of antacids. If a patient is taking an antacid in addition to other drugs, separate the drugs' administration times.

Adverse reactions diarrhea constipation electrolyte imbalances aluminum accumulation in serum.

Nursing Process Assessment Assess the patient's condition before therapy and regularly thereafter. Record the number and consistency of stools. Assess the patient for adverse reactions. Monitor the patient receiving long-term, high-dose aluminum carbonate and aluminum hydroxide for fluid and electrolyte imbalance, especially if he's on a sodium-restricted diet. Monitor phosphate levels in the patient receiving aluminum carbonate or aluminum hydroxide. Watch for signs of hypercalcemia in the patient receiving calcium carbonate. Monitor magnesium levels in the patient with mild renal impairment who takes magaldrate.

Key nursing diagnoses Constipation related to adverse effects of antacids containing aluminum Ineffective protection related to drug-induced electrolyte imbalance Deficient knowledge related to drug therapy

Planning outcome goals

The patient's underlying symptoms will improve. Laboratory studies will show normal electrolyte balance. The patient and his family will demonstrate an understanding of antacid therapy.

Implementation Manage constipation with laxatives or stool softeners, or ask the prescriber about switching the patient to a magnesium preparation. If the patient suffers from diarrhea, obtain an order for an an-tidiarrheal, as needed, and ask the prescriber about switching the patient to an antacid containing aluminum. Shake the container of a liquid form well. When giving the drug through a nasogastric (NG) tube, make sure that the tube is patent and placed correctly. After instilling the drug, flush the tube with water to ensure passage to the stomach and to clear the tube.

Evaluation Patient regains a normal bowel pattern. Patient maintains a normal electrolyte balance.

H2-receptor antagonists H2-receptor antagonists are commonly prescribed antiulcer drugs in the United States. Drugs in this category include: o cimetidine o famotidine o nizatidine o ranitidine.

Pharmacokinetics Cimetidine, nizatidine, and ranitidine are absorbed rapidly and completely from the Gl tract. Famotidine isn't completely absorbed. Food and antacids may reduce the absorption of H2-receptor antagonists. H2-receptor antagonists are distributed widely throughout the body, metabolized by the liver, and excreted primarily in urine.

Pharmacodynamics H2-receptor antagonists block histamine from stimulating the acid-secreting parietal cells of the stomach. Acid secretion in the stomach depends on the binding of gastrin, acetylcholine, and histamine to receptors on the parietal cells. If the binding of any one of these substances is blocked, acid secretion is reduced The H2-

receptor antagonists, by binding with H2receptors, block the action of histamine in the stomach and reduce acid secretion. Pharmacotherapeutics H2 receptor antagonists are used therapeutically to: promote healing of duodenal and gastric ulcers provide long-term treatment of pathologic GI hypersecretory conditions such as Zollinger-Ellison syndrome reduce gastric acid production and prevent stress ulcers in severely ill patients and in those with reflux esophagitis or upper GI bleeding.

Drug interactions H2 receptor antagonists may interact with antacids and other drugs: Antacids reduce the absorption of cimetidine, nizatidine, ranitidine, and famotidine. Cimetidine may increase the blood levels of oral anticoagulants, propranolol (and possibly other betaadrenergic blockers), benzodiazepines, tricyclic antidepressants, theophylline, procainamide, quinidine, lidocaine, phenytoin, calcium channel blockers, cyclo-sporine, carbamazepine, and opioid analgesics by reducing their metabolism in the Uver and their subsequent excretion. Cimetidine taken with carmustine increases the risk of bone marrow toxicity. Cimetidine inhibits ethyl alcohol metabolism in the stomach, resulting in higher blood alcohol levels.

Adverse reactions Using H2-receptor antagonists may lead to adverse reactions, especially in elderly patients or in patients with altered hepatic or renal function: Cimetidine and ranitidine may produce headache, dizziness, malaise, muscle pain, nausea, diarrhea or constipation, rashes, itching, loss of sexual desire, gynecomastia (cimetidine), and impotence. Famotidine and nizatidine produce few adverse reactions, with headache being the most common, followed by constipation or diarrhea and rash.

Nursing process These nursing process steps are appropriate for patients undergoing treatment with H2-receptor antagonists.

Assessment

Assess for adverse reactions, especially hypotension and arrhythmias. Periodically monitor laboratory tests, such as complete blood count and renal and hepatic studies.

Key nursing diagnoses Impaired tissue integrity related to the patient's underlying condition Decreased cardiac output related to adverse cardiovascular effects (cimetidine) Deficient knowledge related to drug therapy

Planning outcome goals The patient's tissue integrity will improve as evidenced by a reduction in underlying symptoms. Stable vital signs and the patient's urine output will indicate adequate cardiac output. The patient and his family will demonstrate an understanding of drug therapy.

Implementation Administer a once-daily dose at bedtime to propote compliance. Twice-daily doses should be administered in the morning and evening; multiple doses, with meals and at bedtime. Don't exceed the recommended infusion rates when administering H2-receptor antagonists I.V.; doing so increases the risk of adverse cardiovascular effects. Continuous I.V. infusion may suppress acid secretion more effectively. Administer antacids at least 1 hour before or after H2-receptor antagonists. Antacids can decrease drug absorption. Anticipate dosage adjustments for the patient with renal disease. Avoid stopping the drug abruptly.

Evaluation Patient experiences decrease in or relief from upper Gl symptoms with drug therapy. Patient maintains a normal heart rhythm. Patient and his family demonstrate an understanding of drug therapy.

Proton Pump Inhibitors Proton pump inhibitors disrupt chemical binding in stomach cells to reduce acid production, lessening irritation and allowing peptic ulcers to better heal. They include:

esomeprazole lansoprazole omeprazole pantoprazole rabeprazole

Pharmacokinetics

Proton pump inhibitors are given orally in enteric-coated formulas to bypass the stomach because they're highly unstable in acid. They dissolve in the small intestine and are rapidly absorbed. These drugs are highly protein bound and extensively metab olized by the liver to inactive compounds and then eliminatedin urine.

Pharmacodynamics Proton pump inhibitors block the last step in gastric acid secretion by combining with hydrogen, potassium, and adenosine triphosphate in the parietal cells of the stomach.

Pharmacotherapeutics Proton pump inhibitors are indicated for: short-term treatment of active gastric ulcers active duodenal ulcers erosive esophagitis symptomatic GERD that isn't responsive to other therapies active peptic ulcers associated with H. pylori infection (in combination with antibiotics) long-term treatment of hypersecretory states such as Zollinger-Ellison syndrome.

Drug interactions Proton pump inhibitors may interfere with the metabolism of diazepam, phenytoin, and warfarin, causing increased half-lives and elevated plasma concentrations of these drugs. Proton pump inhibitors may also interfere with the absorption of drugs that depend on gastric pH for absorption, such as ketoconazole, digoxin, ampicillin, and iron salts.

Adverse reactions Adverse reactions to proton pump inhibitors include: abdominal pain diarrhea nausea and vomiting.

Nursing process These nursing process steps are appropriate for patients undergo ing treatment with proton pump inhibitors.

Assessment Assess the patient's condition before therapy and regularly thereafter. Assess the patient for adverse reactions and drug interactions. Monitor the patient's hydration status if adverse GI reactions occur. Assess the patient's and family's knowledge of drug therapy

Key nursing diagnoses Impaired tissue integrity related to upper gastric disorder Risk for deficient fluid volume related to drug-induced adverse reactions Deficient knowledge related to drug therapy

Planning outcome goals The patient's tissue integrity will improve as evidenced by a reduction in presenting symptoms. Adequate fluid volume, as evidenced by the patient's vital signs and urine output, will be maintained The patient and his family will demonstrate an understanding of drug therapy.

Implementation Administer the drug 30minutes before meals. Dosage adjustments aren't needed for patients with renal or hepatic impairment Tell the patient to swallow capsules whole and not to open or crush them.

Evaluation Patient responds well to therapy. Patient maintains adequate hydration throughout therapy. Patient and his family demonstrate an understanding of drug therapy.

Other antiulcer drugs Research on the usefulness of other drugs in treating peptic ulcer disease continues. Two other antiulcer drugs currently in use are: misoprostol (a synthetic prostaglandin) sucralfate

Pharmacokinetics Each of these drugs has slightly different pharmacokinetic properties. After an oral dose, misoprostol is absorbed extensively and rapidly. It's metabolized to misoprostol acid, which is clinically active, meaning it can produce a pharmacologic effect. Misoprostol acid is highly protein bound and is excreted primarily in urine. Sucralfate is minimally absorbed from the GI tract. It's excreted in feces.

Pharmacodynamics Misoprostol protects against peptic ulcers caused by NSAIDs by reducing the secretion ofgastric acid and by boosting the production of gastric mucus, a natural defense against peptic ulcers. Sucralfate works locally in the stomach, rapidly reacting with hydrochloric acid to form a thick, pastelike substance that adheres to the gastric mucosa and, especially, to ulcers. By binding to the ulcer site, sucralfate actually protects the ulcer from the damaging effects of acid and pepsin to promote healing. This binding usually lasts for 6 hours.

Pharmacotherapeutics
Misoprostol prevents peptic ulcers caused by NSAIDs in patients at high risk for complications resulting from gastric ulcers. Sucralfate is used for short-term treatment (up to 8 weeks) of duodenal or gastric ulcers and preventionof recurrent ulcers or stress ulcers

Drug interactions Misoprostol and sucralfate may interact withother drugs: Antacids may bindwithmisoprostolor decrease its absorption. However, this effect doesn't appear to be clinically significant. Cimetidine, digoxin, norfloxacin, phenytoin, fluoroquinolones, ranitidine, tetracycline, and theophylline decrease the absorption of sucralfate. Antacids may reduce the binding of sucralfate to the gastric and duodenal mucosa, reducing its effectiveness.

Adverse reactions Adverse reactions to misoprostol include: diarrhea (common and usually dose-related) abdominal pain gas indigestion nausea and vomiting spontaneous abortion (womenof childbearing age shouldn't become pregnant while takingmisoprostol).

Adverse reactions to sucralfate include: constipation nausea and vomiting metallic taste.

Nursing process These nursing process steps are appropriate for patients undergoing treatment withthe antiulcer drugs misoprostol and sucralfate. Assessment Assess the patient's condition before therapy and regularly thereafter. Assess for adverse reactions and drug interactions. If the patient is taking misoprostoland is female, the drugcan cause danger to the fetus if pregnancy occurs; discuss contraceptive methods or alternative treatment. Monitor the patient's hydration status if adverse Gl reactions occur. Assess the patient's and family's understanding of drug therapy.

Key nursing diagnoses Impairedtissue integrity related to upper gastric disorder

Risk for deficient fluid volume related to drug-induced adverse Gl reactions Deficient knowledge related to drug therapy

Planning outcome goals The patient's tissue integrity will improve as evidenced by a reductionin presenting symptoms. Adequate fluidvolume will be maintained as evidenced by stable vital signs and urine output. The patient and his family will demonstrate an understandingof drug therapy.

Implementation Administer sucralfate 1 hour before meals and at bedtime. Administer misoprostol with food. Tell the patient to continue the prescribed regimen at home to ensure complete healing. Pain and ulcerative symptoms may subside withinthe first few weeks of therapy. Urge the patient to avoid cigarette smoking because it may increase gastric acid secretion and worsen disease. Tell the patient to avoid alcohol, chocolate, spicy foods, or anything that irritates his stomach. I Elevate the head of the bed for comfort. Tell the patient to avoid large meals within2 hours before bedtime. In women, start misoprostol therapy onthe secondor third day of the next normal menses to ensure that the patient isn't pregnant.

Evaluation Patient responds well to therapy. Patient maintains adequate hydrationthroughout therapy. Patient and his family demonstrate an understandingof drugtherapy.