Chapter 36. Drugs Used to Treat Gastrointestinal Disorders

The various components of the gastrointestinal (GI) tract serve several functions, including digestive, excretory, endocrine, and exocrine. Control of these functions requires neuronal activity from both local and higher centers.

The GI system has a complex collection of highly organized neurons called the enteric nervous system(ENS) located in the intestinal walls (Figure 36–1). The ENS may be considered a third division of the autonomic nervous system, and includes the myenteric plexus and the submucosal plexus. These neuronal networks receive preganglionic fibers from the parasympathetic system as well as postganglionic sympathetic axons. They also receive sensory input from within the wall of the gut. Fibers from the cell bodies in these plexuses travel to the smooth muscle of the gut to control motility. Other motor fibers go to the secretory cells. Sensory fibers transmit information from the mucosa and from stretch receptors to motor neurons in the plexuses and to postganglionic neurons in the sympathetic ganglia. The parasympathetic and sympathetic fibers that synapse on enteric plexus neurons appear to play a modulatory role.

Multiple neurotransmitters, neuromodulators, and autocrine factors are present in the GI system. Autacoids are endogenous molecules that have powerful physiologic and pharmacologic effects but do not fall into traditional autonomic or hormonal groups. Two important amineautacoids, histamine (H) and serotonin (5-hydroxytryptamine, 5-HT), and numerous peptide autacoids are present. Both of these amine-autacoids are discussed in previous chapters; histamine in the respiratory system (Chapter 35) and 5-HT in the central nervous system (Chapter 19). Other well-documented autacoids are cytokines (Chapter 32) and prostaglandins (Chapter 34).

As previously discussed (Chapter 35), stimulation of histamine type 1 receptors results in mucous secretion in the respiratory system and contraction of several types of smooth muscle. In contrast, stimulation of histamine type 2 (H2) receptors results in gastric acid secretion in the stomach. Serotonin is produced from the amino acid tryptophan and stored in vesicles in the enterochromaffin cells of the gut as well as neurons in the ENS. In addition to its activity as a central nervous system neurotransmitter (Chapters 12 and 19), 5-HT has a physiologic role as a neurotransmitter in the ENS and perhaps a role as a local hormone that modulates gastrointestinal smooth muscle activity. Fourteen 5-HT receptor subtypes have been characterized, and subtypes 2, 3, and 4 play roles in GI function or emesis. After release, both histamine and 5-HT may be metabolized by monoamine oxidase. Finally, dopamine (D), which has been previously discussed (Chapters 4, 12, 17, and 18), indirectly modulates gastric motility. Stimulation of dopamine type 2 (D2) receptors located on cholinergic neurons in the ENS has an inhibitory effect on acetylcholine (ACh) release, and thus decreases peristalsis.

These transmitters, modulators, and their receptors provide numerous important drug targets, and many of the drugs used in gastrointestinal disease have been discussed in earlier chapters of this book. Those drugs will be reviewed briefly in this chapter. Drugs used in GI disorders may be divided into those for acid-peptic disorders, motility promoters (prokinetics), those used to prevent vomiting (antiemetics), drugs used for treatment of inflammatory bowel disease, and other miscellaneous agents (Figure 36–2).

Ulceration and erosion of the lining of the gastrointestinal tract are common problems. Mucosal erosions or ulcerations arise when the caustic effects of pepsin, acid, or bile overwhelm the defensive factors such as mucus, prostaglandins, and bicarbonate. Cells lining the stomach include mucus-producing cells, parietal cells, and gastrin-containing cells. Parietal cells contain receptors for gastrin, histamine, and acetylcholine (Figure 36–3). When ACh or gastrin bind to parietal cell receptors, they cause an increase in cytosolic calcium, which in turn activates protein kinases that stimulate acid secretion from a H+/K+–ATPase (proton pump) on the canalicular surface. This proton pump exchanges intracellular H+ for K+ present in the lumen of the stomach. In close proximity to the parietal cells are gut endocrine cells called enterochromaffin-like cells. These cells have receptors for gastrin, ACh, and neuropeptides, and are the major source for histamine release. Histamine binds to the H2 receptor on the parietal cell, resulting in activation of adenylyl cyclase, which increases intracellular cyclic adenosine monophosphate (cAMP). The cAMP activates protein kinases that stimulate H+ secretion by the proton pump. Research suggests that the major effect of gastrin upon acid secretion is mediated indirectly through the release of histamine rather than through direct parietal cell stimulation.

Acid-peptic diseases include gastroesophageal reflux(GERD), gastric and duodenal ulcers, and stress-related mucosal injuries. In all of these conditions, mucosal erosions or ulcerations occur. Several drug classes are used in the treatment of peptic disease. Antimuscarinic drugs (Chapter 5) and the eicosanoid analog misoprostol (Chapter 34) have been previously discussed. Other drugs used in peptic disease include H2 antihistamines, antacids, sucralfate, proton pump inhibitors, and antibiotics. Figure 36–3 shows the sites of action of most of the drugs used in the treatment of acid-peptic ulcer disease.

H2 Antihistamines

Four H2 blockers are available; cimetidine is the prototype. Ranitidine, famotidine, and nizatidine differ only in having fewer drug interactions than cimetidine. They are orally active, with half-lives of 1 to 3 hours. Because they are relatively nontoxic, they can be given in large doses. The duration of action of a single dose may be from 12 to 24 hours.

Mechanism and Effects

These drugs produce a reversible pharmacologic blockade of H2 receptors. They are relatively selective and have no significant blocking actions at H1 or autonomic receptors. The only therapeutic effect of clinical importance is the reduction of gastric acid secretion. Blockade of cardiovascular and mast cell H2 receptor–mediated effects can be demonstrated but has no clinical significance when they are used in ulcer treatment.

Clinical Use

In acid-peptic disease, especially duodenal ulcers, these drugs reduce symptoms, accelerate healing, and prevent recurrences. An acute ulcer is usually treated with two or more doses per day, whereas recurrence of ulcers can often be prevented with a single bedtime dose. These antihistamines are also effective in accelerating healing and preventing recurrences of gastric peptic ulcers. In Zollinger-Ellison syndrome, which is characterized by acid hypersecretion, severe recurrent peptic ulceration, gastrointestinal bleeding, and diarrhea, these drugs are helpful but large doses are required. Similarly, the H2 blockers have been used in GERD. In these latter two clinical uses, antihistamines are not as effective as proton pump inhibitors (discussed later). All of the H2 blockers are available over-the-counter.

Toxicity

Cimetidine is a potent inhibitor of some hepatic drug-metabolizing enzymes and may also reduce hepatic blood flow. In high doses, cimetidine also has significant antiandrogen effects. Ranitidine has a weaker inhibitory effect on hepatic drug metabolism; neither it nor the other H2 blockers appear to have any endocrine effects.

Antacids

Antacids are simple physical agents that react with protons (H+) in the lumen of the gut. Aluminum-containing antacids may also stimulate the protective functions of the gastric mucosa. The antacids effectively reduce the recurrence rate of peptic ulcers when used regularly in the large doses needed significantly to raise the stomach pH.

The antacids differ mainly in their absorption and effects on stool consistency. The most popular antacids used in the United States are magnesium hydroxide (Mg[OH]2) and aluminum hydroxide (Al[OH]3). Neither of these weak bases is significantly absorbed from the bowel. Magnesium hydroxide has a strong laxative effect, whereas aluminum hydroxide has a constipating action. These drugs are available as single-ingredient products and as combined preparations. The combination products are usually preferred because they balance the laxative and constipating effects of either single formulation. Calcium carbonate and sodium bicarbonate are also weak bases, but they differ from aluminum and magnesium hydroxides in that they are absorbed from the gut. Because of their systemic effects, calcium carbonate and sodium bicarbonate salts are less popular as antacids than magnesium and aluminum compounds.

Sucralfate

Sucralfate is aluminum sucrose sulfate, a small, poorly soluble molecule that polymerizes in the acid environment of the stomach. This polymer binds to injured tissue and forms a protective coating over ulcer beds. The drug accelerates the healing of peptic ulcers and reduces the recurrence rate. Unfortunately, sucralfate must be taken four times daily. Sucralfate is too insoluble to have significant systemic effects when taken by the oral route; toxicity is very low. Sucralfate is also occasionally used in open wounds as a protective barrier and to minimize excessive exudate.

Proton Pump Inhibitors

Omeprazole is the prototype of the class of inhibitors of the proton pump of gastric parietal cells. Other agents in the group include esomeprazole, lansoprazole, pantoprazole, and rabeprazole. Oral formulations of these drugs are enteric coated to prevent acid inactivation in the stomach. They are rapidly metabolized in the liver, with half-lives of 1 to 2 hours. However, their durations of action are approximately 24 hours, and they may require 3 to 4 days of treatment to achieve their full effectiveness.

Mechanism of Action

These drugs are lipophilic weak bases that diffuse into the parietal cell canaliculi where they become protonated and concentrated more than 1,000-fold. There they undergo conversion to sulfenamides, which react covalently with the proton pump and irreversibly inactivate the enzyme. Proton pump inhibitors are very effective in peptic ulcer disease associated with the bacterium Helicobacter pylori and with nonsteroidal anti-inflammatory drug (NSAID) treatment. They are also useful in the treatment of GERD and Zollinger-Ellison syndrome, the latter a condition usually associated with a gastrin-secreting tumor.

Adverse Effects

The adverse effects of proton pump inhibitors occur infrequently and include diarrhea, abdominal pain, and headache. Chronic treatment with proton pump inhibitors may result in hypergastrinemia. Proton pump inhibitors may decrease the oral bioavailability of vitamin B12 and certain drugs (e.g., digoxin, ketoconazole) that require acidity for their gastrointestinal absorption. Note: Because gastric acid is a major barrier to the colonization and infection of the gut, chronic use of proton pump inhibitors can increase the risk of enteric infections.

Antibiotics

Chronic infection with H pylori is present in the majority of patients with recurrent non-NSAID-induced peptic ulcers, and eradication of this organism greatly reduces the rate of recurrence of ulcers in these patients. The regimens of choice consist of a proton pump inhibitor plus a course of bismuth (Pepto-Bismol), tetracycline, and metronidazole or a course of amoxicillin plus clarithromycin.

Diabetes and other diseases that damage nerves to the viscera frequently cause a marked loss of motility in the esophagus and stomach, resulting in gastric paralysis (gastroparesis). Gastroparesis is associated with delayed stomach emptying, nausea, and severe bloating. Metoclopramide and cisapride are prokinetic drugs; that is, they stimulate motility in the upper GI tract and emptying of the stomach by indirectly stimulating cholinergic activity in the gut wall. Metoclopramide probably acts as an ACh facilitator by antagonizing D2 receptors. Cisapride appears to act as a 5-HT4 agonist, facilitating the release of ACh from cholinergic nerve endings. Adverse effects of metoclopramide with chronic use include symptoms of pseudo-parkinsonism and other extrapyramidal effects and hyperprolactinemia. In high doses, cisapride is associated with a long QT syndrome and has caused fatal cardiac arrhythmias. For this reason, cisapride is now available only on a limited basis.

A variety of drugs are valuable in the prevention and treatment of vomiting during cancer chemotherapy and following general anesthesia. Glucocorticoids (Chapter 23) have been discussed previously. Dopaminereceptorantagonists such as metoclopramide and prochlorperazine, a phenothiazine (Chapter 18), prevent emesis by inhibiting D2 receptors in the postrema area of the medulla.

H1 ANTAGONISTS: Some previously discussed antihistamines (H1 receptorantagonists; Chapter 35), such as diphenhydramine and meclizine, have antiemetic properties and prevent motion sickness. Sedation is a common adverse effect of all of these older (first-generation) antihistamines, as is dry mouth and other anticholinergic effects. Orthostatic hypotension may also occur as a result of α1-receptor antagonism when taking these drugs.

5-HT3 RECEPTOR ANTAGONISTS: The drugs ondansetron, granisetron, and dolasetron are extremely useful in preventing nausea and vomiting associated with chemotherapy and with surgical anesthesia but not motion sickness. These 5-HT3 receptor antagonists have a central antiemetic action in the area postrema of the medulla and also on peripheral sensory and enteric nerves. Alosetron, another 5-HT3 antagonist, is used in the treatment of women with diarrhea associated with irritable bowel syndrome. The adverse effects of ondansetron, granisetron, and dolasetron include diarrhea and headache. Dolasetron has been associated with QRS and QTc prolongation in the electrocardiogram and should not be used in patients with heart disease. Alosetron causes significant constipation in some patients and has been associated with fatal bowel complications.

MARIJUANA DERIVATIVES: Antiemetic properties have also been demonstrated in the active ingredient in marijuana and its derivative, dronabinol (Δ9-tetrahydrocannabinol) and nabilone (Chapter 21).

Steatorrhea, a condition of decreased fat absorption coupled with increased fat excretion in the stool results from inadequate pancreatic secretion of lipase. The abnormality of fat absorption can be significantly relieved by oral administration of pancreatic lipase (pancrelipase) obtained from pigs. Pancreatic lipase is inactivated at a pH below 4; thus, up to 90% of an administered dose will be destroyed in the stomach unless the pH is raised with antacids or drugs that reduce acid secretion.

Laxatives increase the probability of a bowel movement by several mechanisms: an irritant or stimulant action on the bowel wall, a bulk-forming action on the stool that evokes reflex contraction of the bowel, a softening action on hard or impacted stool, or a lubricating action that eases passage of stool through the rectum. Examples of drugs that act by these mechanisms are in Table 36–1.

The most effective antidiarrhealdrugs are the opioids and their derivatives that have been selected for maximal antidiarrheal and minimal central nervous system effects. Of the latter group, the most important are diphenoxylate and loperamide, meperidine analogs with very weak or no analgesic effects. Diphenoxylate is formulated with antimuscarinic alkaloids (e.g., atropine) to reduce the likelihood of abuse; loperamide is formulated alone and sold over-the-counter (OTC) as such. Difenoxin, the active metabolite of diphenoxylate, is also available as a prescription medication. Kaolin is hydrated magnesium aluminum silicate, and pectin is an indigestible carbohydrate from apples. Available in combination as Kaopectate, both kaolin and pectin act as absorbents of bacterial toxins and fluid. Finally, cholestyramine and colestipol, bile salt–binding resins previously discussed in Chapter 26, may decrease diarrhea associated with increased bile acids. Common adverse effects associated with these drugs include constipation. The absorbents and the bile salt resins may decrease the absorption of some drugs, and the resins may also reduce the absorption of lipid-soluble vitamins.

The formation of cholesterol gallstones can be inhibited by several drugs, although none is dramatically effective. Such drugs include the bile acid derivatives chenodiol and ursodiol. Chenodiol appears to reduce the secretion of bile acids by the liver, whereas the mechanism of action of ursodiol is unknown.

Inflammatory bowel disease may be divided into two related conditions: ulcerative colitis and Crohn’s disease. Ulcerative colitis is a nonspecific inflammation of the colon with mucosal damage & bleeding. Crohn’s disease is a recurrent granulomatous inflammation that may affect any part of the small or large bowel. Glucocorticoids (Chapter 23) are used in the treatment of ulcerative colitis and Crohn’s disease. Immunosuppressive agents such as azathioprine, 6-mercaptopurine, methotrexate, and infliximab (Chapter 32) are also used in the treatment of these diseases. These drugs have been discussed in other chapters. Aminosalicylates (e.g., sulfasalazine, balsalazide, mesalamine) also used in the treatment of inflammatory bowel disease. These drugs are not absorbed significantly after oral administration and are designed to release 5-aminosalicylic acid (5-ASA) into various parts of the distal segment of the small bowel and colon. 5-ASA inhibits the synthesis of both prostaglandins and inflammatory leukotrienes. Sulfasalazine (a combination of 5-ASA and sulfapyridine) has a high incidence of adverse effects, which are attributable to the systemic absorption of the sulfapyridine. These effects are dose related and include nausea, gastrointestinal upset, headaches, arthralgia, myalgia, bone marrow suppression, malaise, and severe hypersensitivity reactions. Other aminosalicylates, which do not contain sulfapyridine, are well tolerated.

Drugs that are swallowed pass through parts of the GI system prior to reaching the systemic circulation. Thus, drugs used to treat GI conditions have the potential to interfere with other orally administered drugs, and cause drug-drug interactions. These adverse effects may range from decreased absorption of some drugs resulting in undermedication to decreased biotransformation of other drugs resulting in overmedication. Many drugs used in treating GI dysfunction may be obtained without prescription. The use of these OTC drugs by the patient further complicates the assessment of the drug history. The patient may not consider including such OTC drugs when asked by the health-care provider about “medications.” Examples of such drugs are the antihistamines used in acid-peptic disease.

Nonpharmacologic treatments for emesis are also being investigated. Unconventional types of transcutaneous electrical nerve stimulation (TENS) on acupuncture points are being investigated to prevent emesis following chemotherapy and surgical procedures. Optimal therapy may be a combination of antiemeticdrugs together with TENS.

Adverse Drug Reactions

Acid-peptic drugs

• • Cimetidine inhibits biotransformation of some drugs.
• • Antacids may decrease the absorption of some drugs.
• • Proton pump inhibitors may cause GI distress, decrease B12 absorption, possibly increase GI bacterial infections, and decrease absorption of some drugs.

Prokinetic drugs

• • D2 antagonists can cause extrapyramidal effects. Some drugs that modulate 5-HT receptors cause cardiac dysrhythmias.
• • Long-term use of some laxatives can decrease absorption of fat-soluble vitamins.
• • Several antidiarrheal drugs can decrease absorption of some drugs.

Effects Interfering with Rehabilitation

• • Decreased absorption of drugs can result in reduced blood drug levels and increase the risk of an inadequate clinical effect.
• • Decreased biotransformation of drugs can result in increased blood drug levels and increase the risk of overmedication toxicity.
• • Extrapyramidal motor effects of prokinetic drugs can interfere with functional performance in the clinic.

Possible Therapy Solutions

• • If the patient demonstrates manifestations of undermedication or overmedication, contact the referring health-care provider. A complete drug history of the patient may assist in this determination.
• • If extrapyramidal effects occur with prokinetic drugs, contact the referring health-care provider.

Brief History: The patient is a 63-year-old African American female with a 20-year history of type 2 diabetes mellitus. The patient has hyperglycemia, hypertension, and hyperlipidemia. The patient previously had neuropathic ulcers at the first metatarsal head on the plantar surfaces of both feet.

Current Medical Status and Drug Therapy: The patient is on multiple medications for treatment of her diseases. Two weeks ago, the patient was diagnosed with gastroparesis and she was prescribed metoclopramide as a prokinetic. The patient’s neuropathic ulcer on the plantar surface at the first metatarsal head on the left foot reulcerated last week. She was referred for evaluation and possible foot orthotics to prevent further wound progression.

Rehabilitation Setting: The patient has been seen by the physical therapist on previous occasions for evaluation and treatment of previous neuropathic ulcerations. She arrives today as scheduled for the evaluation. The patient is first observed in the waiting room; She has difficulty initiating sit-to-stand activity and is assisted by her spouse. When the patient finally stands, she has a wide base of support with her upper extremities in low guard position, suggesting decreased initial stability in standing. The patient also has difficulty initiating ambulation, and is again assisted by her spouse. During ambulation, she has a decreased step length resulting in a slow shuffling gait. The patient is finally seated in the treatment area. When asked during the evaluation, she and her spouse suggest that the changes in function observed in the waiting room are recent, although they cannot provide a specific time frame.

Problem/Clinical Options: Multiple antihypertensive and cardiovascular medications may cause orthostatic hypotension, which presents during standing. However, the instability during standing, the difficulty initiating movement, and the slow shuffling ambulation are manifestations of parkinsonism. These manifestations are recent as was the prescription for metoclopramide as a prokinetic. This drug inhibits dopaminergic receptors in the GI system. An adverse effect of this drug is parkinsonism resulting from inhibition of dopamine receptors in the motor areas of the brain. The health-care professional prescribing the metoclopramide should be immediately informed of these adverse effects.

Antacids

Aluminum Hydroxide Gel1 (Amphojel, ALternaGEL, Others)

Oral: 300-, 500-, 600-mg tablets; 400-, 500-mg capsules; 320, 450, 675 mg/5 mL suspension

Aluminum hydroxide and magnesium hydroxide combination preparations1 (Maalox, Mylanta, Gaviscon, Gelusil, others)

Oral: 400- to 800-mg combined hydroxides per tablet, capsule, or 5 mL suspension

Calcium Carbonate1 (Tums, Others)

Oral: 350-, 420-, 500-, 600-, 650-, 750-, 1000-, 1250-mg chewable tablets; 1250 mg/5 mL suspension

H2 Histamine Receptor Blockers

Cimetidine (generic, Tagamet, Tagamet HB1)

Oral: 100-,1 200-, 300-, 400-, 800-mg tablets; 300 mg/5 mL liquid

Parenteral: 300 mg/2 mL, 300 mg/50 mL for injection

Famotidine (Generic, Pepcid, Pepcid AC1)

Oral: 10-mg tablets,1 gelcaps1; 20-, 40-mg tablets; powder to reconstitute for 40 mg/5 mL suspension

Parenteral: 10 mg/mL for injection

Nizatidine (Axid, Axid AR1)

Oral: 75-mg tablets1; 150-, 300-mg capsules

Ranitidine (Generic, Zantac, Zantac 751)

Oral: 75,1, 150-, 300-mg tablets; 150-mg effervescent tablets; 150-, 300-mg capsules; 15 mg/mL syrup

Parenteral: 1-, 25- mg/mL for injection

Selected Anticholinergic Drugs

Atropine (Generic)

Oral: 0.4-mg tablets

Parenteral: 0.05, 0.1, 0.3, 0.4, 0.5, 0.8, 1 mg/mL for injection

Belladonna Alkaloids Tincture (Generic)

Oral: 0.27–0.33 mg/mL liquid

Dicyclomine (Generic, Bentyl, Others)

Oral: 10-, 20-mg capsules; 20-mg tablets; 10 mg/5 mL syrup

Parenteral: 10 mg/mL for injection

Glycopyrrolate (Generic, Robinul)

Oral: 1-, 2-mg tablets

Parenteral: 0.2 mg/mL for injection

l-Hyoscyamine (Anaspaz, Others)

Oral: 0.125-, 0.15-mg tablets; 0.375-mg timed-release capsules; 0.125 mg/5 mL oral elixir and solution

Parenteral: 0.5 mg/mL for injection

Methscopolamine (Pamine)

Oral: 2.5-mg tablets

Propantheline (Generic, Pro-Banthine)

Oral: 7.5-, 15-mg tablets

Scopolamine (Generic)

Oral: 0.4-mg tablets

Parenteral: 0.3, 0.4, 0.86, 1 mg/mL for injection

Tridihexethyl (Pathilon)

Oral: 25-mg tablets

Proton Pump Inhibitors

Esomeprazole (Nexium)

Oral: 20-, 40-mg delayed-release capsules

Lansoprazole (Prevacid)

Oral: 15-, 30-mg delayed-release capsules; 15-, 30-mg enteric-coated granules for oral suspension

Omeprazole (Prilosec)

Oral: 10-, 20-, 40-mg delayed-release capsules

Pantoprazole (Protonix)

Oral: 20-, 40-mg delayed release tablets

Parenteral: 40 mg/vial powder for IV injection

Rabeprazole (Aciphex)

Oral: 20-mg delayed-release tablets

Mucosal Protective Agents

Misoprostol (Cytotec)

Oral: 100-, 200-mcg tablets

Sucralfate (Generic, Carafate)

Oral: 1-g tablets; 1 g/10 mL suspension

Digestive Enzymes

Pancrelipase (Cotazym, Pancrease, Viokase, Others)

Oral: Capsules, tablets, or powder containing lipase, protease, and amylase activity. See manufacturers’ literature for details.

Drugs for Motility Disorders and Selected Antiemetics

Alosetron (Lotronex)

Oral: 1-mg tablets

Cisapride (Propulsid)

Oral 10-, 20-mg tablets, 1 mg/ml suspension

Dolasetron (Anzemet)

Oral: 50-, 100-mg tablets

Parenteral: 20 mg/mL for injection

Dronabinol (Marinol)

Oral: 2.5-, 5-, 10-mg capsules

Granisetron (Kytril)

Oral: 1-mg tablets

Parenteral: 1 mg/mL for injection

Metoclopramide (Generic, Reglan, Others)

Oral: 5-, 10-mg tablets; 5 mg/5 mL syrup, 10 mg/mL concentrated solution

Parenteral: 5 mg/mL for injection

Ondansetron (Zofran)

Oral: 4-, 8-, 24-mg tablets; 4 mg/5 mL solution

Parenteral: 2 mg/mL for IV injection

Prochlorperazine (Compazine)

Oral: 5-, 10-, 25-mg tablets; 10-, 15-, 30-mg capsules; 1 mg/mL solution

Rectal: 2.5-, 5-, 25-mg suppositories

Parenteral: 5 mg/mL for injection

Tegaserod (Zelnorm)

Oral: 2-, 6-mg tablets

Selected Anti-Inflammatory Drugs Used in Gastrointestinal Disease

Balsalazide (Colazal)

Oral: 750-mg capsules

Budesonide (Entocort)

Oral: 3-mg capsules

Hydrocortisone (Cortenema, Cortifoam)

Rectal: 100 mg/60 mL unit retention enema; 90 mg/applicatorful intrarectal foam

Infliximab (Remicade)

Parenteral: 100-mg powder for injection

Mesalamine (5-ASA)

Oral: Asacol: 400-mg delayed-release tablets; Pentasa: 250-mg controlled-release capsules

Rectal: Rowasa: 4 g/60 mL suspension; 500-mg suppositories

Methylprednisolone (Medrol Enpack)

Rectal: 40 mg/bottle retention enema

Olsalazine (Dipentum)

Oral: 250-mg capsules

Sulfasalazine (Generic, Azulfidine, Others)

Oral: 500-mg tablets and enteric-coated tablets

Selected Antidiarrheal Drugs

Bismuth Subsalicylate1 (Pepto-Bismol, Others)

Oral: 262-mg caplets, chewable tablets; 130, 262, 524 mg/15 mL suspension

Difenoxin (Motofen)

Oral: 1-mg (with 0.025 mg atropine sulfate) tablets

Diphenoxylate (Generic, Lomotil, Others)

Oral: 2.5-mg (with 0.025 mg atropine sulfate) tablets and liquid

Kaolin/Pectin1 (Generic, Kaopectate, Others)

Oral (typical): 5.85 g kaolin and 260 mg pectin per 30 mL suspension

Loperamide1 (Generic, Imodium, Others)

Oral: 2-mg tablets, capsules; 1 mg/5 mL liquid

Selected Laxative Drugs1

Bisacodyl (Generic, Dulcolax, Others)

Oral: 5-mg enteric-coated tablets

Rectal: 10-mg suppositories

Cascara Sagrada (Generic)

Oral: 325-mg tablets; 5 mL per dose fluid extract (approximately 18% alcohol)

Castor Oil (Generic, Others)

Oral: liquid or liquid emulsion

Docusate (Generic, Colace, Others)

Oral: 50-, 100-, 250-mg capsules; 100-mg tablets; 20, 50, 60, 150 mg/15 mL syrup

Glycerin Liquid (Fleet Babylax)

Rectal liquid: 4 mL per applicator

Glycerin Suppository (Generic, Sani-Supp)

Lactulose (Chronulac, Cephulac)

Oral: 10 g/15 mL syrup

Magnesium Hydroxide [Milk of Magnesia, Epsom Salt] (Generic)

Oral: 400, 800 mg/5 mL aqueous suspension

Methylcellulose

Oral: bulk powder

Mineral Oil (Generic, Others)

Oral: liquid or emulsion

Polycarbophil (Equalactin, Mitrolan, Fibercon, Fiber-Lax)

Oral: 500-, 625-mg tablets; 500-mg chewable tablets

Polyethylene Glycol Electrolyte Solution (CoLyte, GoLYTELY, Others)

Oral: Powder for oral solution, makes 1 gallon (approximately 4 L)

Psyllium (Generic, Serutan, Metamucil, Others)

Oral: 3.3-, 3.4-, 3.5-, 4.03-, 6-g psyllium granules or powder per packet

Senna (Senokot, Ex•Lax, Others)

Oral: 8.6-, 15-, 17-, 25-mg tablets; 8.8, 15 mg/mL liquid

Drugs That Dissolve Gallstones

Ursodiol (Actigall)

Oral: 300-mg (Actigall) capsules

1Over-the-counter formulations.