Chapter 8: Drugs for Gastrointestinal Disorders

A vast array of gastrointestinal (GI) disorders can cause discomfort and stomach upset. Some of these disorders are peptic ulcer disease (PUD), gastroesophageal reflux disease (GERD), diarrhea, constipation, and intestinal gas. Most GI disorders, however, are never properly reported because athletes do not like to discuss such conditions. This chapter will focus on the common types of GI disorders; their etiology, signs and symptoms; and treatments that require drug management.

PUD is classified as a chronic inflammatory disorder resulting in the erosion of the mucosa of the stomach or duodenum. Usually, the erosion is a result of gastric acid and pepsin, which are normally available to hydrolyze protein and food so that they can be absorbed by the intestine. However, sometimes the production of gastric acid and pepsin results in ulcer formation. Ulcers also occur in the esophagus and other areas of the GI tract, but not as frequently as in the stomach and duodenum. Risk for developing ulcers increases with age, smoking, alcohol, a history of peptic ulcer disease or GI bleeding, and increased doses of nonsteroidal anti-inflammatory drugs (NSAIDs).^19,35

Duodenal ulcers usually occur in the beginning portion of the duodenum and gastric ulcers usually occur in the lower one-third of the stomach, also called the antrum. PUD is often asymptomatic, but signs and symptoms can include a slight dull ache, discomfort 2 to 3 hours after meals and during the middle of the night, poor appetite, bloating, burping, nausea, and vomiting. Such discomfort can often be relieved by food and antacid medications.

The cause of PUD is multifactoral, ranging from increased acid secretion to factors that decrease the protective mucosal barrier. Neurologic impulses (sight, smell, or taste) can also trigger the secretion of acid. Damage to the mucosal barriers can occur as a consequence of alcohol abuse, cigarette smoking, or continual use of aspirin and NSAIDs. Helicobacter pylori (H. pylori) bacterial infection may also directly inflame and damage the mucosal barrier or alter the regulation of gastric acids. Because there are many factors that can cause ulcers, investigators have divided the etiology into three categories: (1) ulcers associated with H. pylori; (2) ulcers caused by NSAID use; and (3) ulcers caused by acid hypersecretion.¹⁴

Helicobacter pylori

H. pylori is a bacterium of the helicobacter genus. Its mode of transmission is unknown, but it is thought to be from person to person.⁹ H. pylori can be found almost anywhere in the stomach but is usually concentrated in the antrum. Inflammation of the antrum is the most common cause of gastritis,^2,28,40 and elimination of H. pylori from this site usually resolves this condition. The exact cause of gastritis caused by H. pylori is unknown, but it is thought to result from either production of a cytotoxin, a breakdown of mucosal defenses, or adhesion to epithelial cells.⁶ As a result, the lining of the stomach and duodenum weakens and allows the acid to penetrate, causing an ulcer.

Nonsteroidal Anti-inflammatory Drugs

Use of NSAIDs is the most common cause of PUD in patients who are not infected with H. pylori.¹⁹ NSAID use can damage the stomach lining through inhibition of prostaglandin synthesis. Prostaglandins stimulate mucus and bicarbonate secretion, maintain mucosal blood flow, and participate in epithelial regeneration and cell growth. Without this process, the stomach lining would be vulnerable to acid.

Gastric Acid Hypersecretion

Acid secretion in individuals who suffer from PUD has been found to be close to normal. Only when hypersecretion occurs do most individuals suffer from ulcers. The hypersecretion can cause ulcers either by injuring the cells of the mucosa or by activating pepsin. When hypersecretion is the cause of ulcers, it may be the result of Zollinger-Ellison syndrome. Zollinger-Ellison syndrome is a rare condition in which a tumor activates the secretion of gastrin, which then stimulates gastric acid release. Only approximately 0.1 percent of all duodenal ulcers occur from Zollinger-Ellison syndrome.

Peptic Ulcer Disease Drug Treatment and Adverse Effects

Treatment of PUD is directed toward relieving ulcer pain, accelerating ulcer healing, and minimizing ulcer recurrence. The following classes of drugs are used for treatment of PUD: H₂-receptor antagonists, proton pump inhibitors, antacids, sucralfate, bismuth compounds, and antibiotics (Table 8–1). Some of these drug classes are available as over-the-counter (OTC) drugs used to treat PUD. As with all OTC items, it is imperative to follow the doses and indications recommended on the drug label. Not following these recommendations may cause unwanted and perhaps severe adverse effects. Therefore anyone who has any questions about which medication to administer or the proper dose should consult his or her physician or local pharmacist.

H₂ Receptor Antagonists

H₂ receptor antagonists decrease gastric acidity by inhibiting histamine from being released by parietal cells. Histamine activates H₂ receptors along the GI tract to increase acid secretion. Common H₂ receptor antagonists include cimetidine (Tagamet), ranitidine (Zantac), nizatidine (Axid), and famotidine (Pepcid). Multiple dosing has been shown to be more effective than single dosing with respect to suppressing gastric acids.^20,33 These drugs can also treat gastroesophageal reflux and hypersecretory gastric states by increasing the pH of gastric contents.^3,4,17,27

H₂ receptor antagonists rarely cause serious adverse effects. However, mild adverse effects can include diarrhea, constipation, headache, stomach cramps, dizziness, and rash. These drugs should be used with caution in patients who have renal failure or liver damage because they are not effectively cleared by the kidney and liver.

Proton-pump Inhibitors

Proton-pump inhibitors inhibit gastric acid secretion by blocking the H⁺/K⁺ adenosine triphosphatase system found at the surface of gastric parietal cells.^3,4,27,37 Omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex), esomeprazole (Nexium), and pantoprazole (Protonix) are drugs used to effectively treat PUD by blocking the final step of acid production.^3,4,17,27,37

The main adverse effects of proton-pump inhibitors are stomach pain and diarrhea. Additional possible adverse effects include abdominal distress, headaches, muscle aches, chest pain, sedation, gas, nausea, vomiting, and rash.^3,4,27,37

Antacids

Antacids neutralize the acid found in the stomach by buffering it and increasing the stomach's pH. Importantly, antacids have no effect on acid production, unlike the H₂ receptor antagonists and proton-pump inhibitors. Although antacids heal ulcers, they are primarily used for the relief of ulcer pain or dyspepsia when used in combination with other anti-ulcer drugs. Antacids are discussed more thoroughly in this chapter in the context of gastroesophageal reflux disease.

Sucralfate

Sucralfate (Carafate) is an prescription-only agent that, when exposed to acid, forms a viscous paste that adheres to the ulcer crater, forming a protective barrier. The drug binds only to the damaged mucosa and maintains the barrier for up to 6 hours. Sucralfate is effective in the short-term treatment of duodenal ulcers and is comparable to H₂ antagonists. Sucralfate is generally well tolerated; its most frequent adverse effect is constipation.

Bismuth Compounds

Bismuth compounds have been used to treat gastrointestinal disorders for many years. The most common agent used today is bismuth subsalicylate (Pepto-Bismol). The mechanism by which bismuth heals ulcers remains uncertain, but theories include providing a local gastroprotective effect, stimulating endogenous prostaglandins, and suppressing H. pylori infection.

Bismuth subsalicylate preparations may contain varying amounts of salicylate and therefore may cause problems for patients taking aspirin or other salicylate-containing drugs. It may cause salicylate toxicity in individuals who are on aspirin therapy. Patients should also be aware that bismuth reacts with hydrogen in the colon to from a compound that blackens the stool.

Antibiotics

Antibiotics are used in the treatment of H. pylori. Antibiotic drug therapy is associated with various treatment success rates (on average 80 to 95%). The most common antibiotics used for treatment of H. pylori include clarithromycin (Biaxin), metronidazole (Flagyl), and amoxicillin (Amoxil). Adverse effects of these antibiotics are mostly GI symptoms such as diarrhea and nausea. Both clarithromycin and metronidazole are known to cause an abnormal taste in the mouth and headache.

Gastroesophageal reflux disease (GERD) is a common chronic disorder that must be treated for an extended period of time in most individuals. GERD refers to the retrograde movement of gastric contents into the esophagus, usually after eating, because the lower esophageal sphincter (LES) does not close properly. With repeated exposure to gastric reflux, the esophagus can become inflamed.²² In some cases, reflux can cause esophageal strictures, esophageal ulcers, perforations, hemorrhage, aspiration, and motility disorders.^7,30 Only patients who have tissue damage of the esophagus or who suffer from symptoms are said to have GERD.

The most common symptom for individuals with GERD is heartburn.³⁹ Heartburn is usually described as pain in the center of the chest, sometimes mimicking angina, and primarily occurs after eating. It is caused by contact of acidic gastric contents with the inflamed esophageal mucosa.¹³ Other symptoms such as dysphagia, odynophagia (pain on swallowing), bad breath, dry cough, or nocturnal symptoms can occur.¹⁸ Most individuals suffering from GERD do not seek medical treatment initially but try to self-medicate with OTC products to control their symptoms.

Symptoms of GERD can be aggravated by foods, specific body positions (especially lying down), and certain drugs. Foods high in fat can cause GERD because they decrease the LES pressure. Spices, onions, citrus juices, coffee, and caffeine can also cause direct mucosal irritation.¹³ Individuals experience symptoms primarily when they are supine or bending over; however, esophageal reflux can occur in any position. Alcohol and certain drug therapies (verapamil, diazepam, and NSAIDs) can also exacerbate GERD symptoms.^11,32

Gastroesophageal Reflux Disease Drug Treatment and Adverse Effects

Patients who have frequent reflux episodes need to inhibit or prevent gastric acid secretion to promote and facilitate healing. Hence, the goals of therapy are to: (1) eliminate or alleviate symptoms, (2) limit the frequency and duration of GI reflux, (3) promote healing of the mucosa, and (4) prevent complications. H₂ receptor antagonists and proton pump inhibitors used to treat PUD can also treat GERD (see Table 8–1).

Patients are encouraged to alter factors that can cause reflux.²³ They are encouraged to lose weight and wear loose-fitting clothes to decrease gastroesophageal pressure.²² To decrease acid secretions, patients should also refrain from cigarette smoking, eliminate from their diet foods that lower esophageal pressure or stimulate acid secretions,^21,22 avoid lying down after meals, and limit their intake of alcohol.

Antacids

Antacids relieve mild to moderate symptoms of GERD by decreasing gastric acidity, thereby increasing LES pressure.³⁶ Antacids have a rapid onset of action but a short duration. However, if taken with food, the effects of antacids can last up to 3 hours. Generally, antacids are used to provide daytime symptomatic relief for those who have mild to moderate symptoms.¹⁶

The primary neutralizing compounds used in antacid preparations are calcium, aluminum, and magnesium salts and sodium bicarbonate (Table 8–2). Calcium carbonate is a widely used antacid that dissolves slowly in the stomach and can be found in products such as Tums and Mylanta lozenges. Aluminum hydroxide reacts with gastric acid to form aluminum chloride and water. An example of an aluminum-containing antacid is Amphojel. Magnesium hydroxide produces a short-acting neutralizing effect and is found in milk of magnesia. There are also a multitude of combination products that contain various salts. Some magnesium and aluminum combination products are Maalox tablets and Mylanta Double Strength Liquid. Finally, sodium bicarbonate is an antacid that is found in Alka-Seltzer and similar effervescent products.

Antacids or antacid combination products may produce several adverse reactions. Diarrhea, constipation, alterations in mineral metabolism, and acid-base imbalances are possible effects of continued antacid exposure. The most frequent adverse effect of aluminum-containing antacids is constipation, whereas that of magnesium antacids is diarrhea. Antacids may also interact with other drugs to affect solubility and absorption.

Prokinetics

Prokinetic agents decrease the amount of esophageal contact time with gastric acid. This is done by stimulating the motility of the upper GI tract without increasing gastric secretions. Metoclopramide (Reglan) is currently the prokinetic drug of choice. Some adverse effects of metoclopramide include restlessness, somnolence, and dizziness.

Diarrhea is an unpleasant and often embarrassing condition that, if left untreated, usually resolves in a couple of days. It is defined as abnormal frequency and liquidity of fecal discharge compared with normal stools. Diarrhea can be classified as either acute or chronic and may be a result of a GI or non-GI disease.

Acute diarrhea can be of infectious, toxic, drug-induced, or dietary origin. Acute diarrhea occurs with a sudden onset of frequent watery stools accompanied by pain, cramping, flatulence, fever, or vomiting. Most commonly, acute diarrhea is caused by bacterial organisms such as Shigella, salmonella, campylobacter, staphylococcus., and Escherichia coli.¹ It can also be caused by food intolerances, viral infections, and parasites.

Chronic diarrhea, lasting more than 2 weeks, is usually of multifactoral etiology and hard to diagnose. Chronic diarrhea is divided into two classifications: organic and functional. Organic diarrhea may be caused by low hemoglobin concentration, low serum albumin, or high erythrocyte sedimentation rate.^5,8,34 Functional diarrhea may be physiological or psychogenic in nature. Causes include stress-related factors, inflammatory bowel disease, and irritable bowel syndrome.

A thorough history of food ingestion during the week before the onset of diarrhea is crucial to help determine the cause. Possible infectious sources include fruits, vegetables, meats, seafood, and water. The toxins in these sources can cause a sudden onset of loose stools, nausea, and possibly fever.

Traveler's diarrhea can occur after ingestion of food or water that is contaminated with bacteria or parasites. Common causes include undercooked meat and seafood, raw vegetables, fruit, and changes in eating habits. The onset of traveler's diarrhea is usually during the first few days of travel in areas of poor hygiene and sanitation, but it can develop at any time during traveling. To prevent traveler's diarrhea, travelers should not drink tap water or unpasteurized dairy products or eat raw meats, fruits, vegetables, or seafood.

Diarrhea Drug Treatment and Adverse Effects

There are three primary goals in treating diarrhea: (1) prevent excessive water, electrolyte, and acid-base disturbance, (2) identify and treat the cause, and (3) provide symptomatic relief. Treatments include antiperistaltic agents, adsorbents, and bismuth compounds.

The first priority for an athlete with diarrhea is to control the loss of fluids and dehydration. Fluids with electrolytes such as fruit juices and sport electrolyte drinks should be consumed; carbonated beverages, caffeine, and products with high fructose levels should be avoided. Urine color is probably the easiest way to determine hydration status (yellow = dehydration, clear = hydration).

If the diarrhea persists for several days, if there is blood in the stool, or if the athlete has severe abdominal pain and cramps, he or she should consult a physician to determine its etiology. A thorough medical examination may include stool culture, blood test, or sigmoidoscopy. If the diarrhea is from a bacterial infection, it is not recommended to stop the bowel movements with medication because the bacterial organism will be trapped in the GI tract. Viral infections can be either left alone to run their course or treated with medications (Fig. 8–1).

Antiperistaltic Agents

Antiperistaltic agents are effective in relieving cramps and stool frequency by inhibiting peristalsis and prolonging transition time of the intestinal contents. The most commonly used antiperistaltic is loperamide (Imodium). Loperamide is available OTC and is an effective treatment for nonspecific acute diarrhea, traveler's diarrhea, and chronic diarrhea from inflammatory bowel disease. Loperamide slows intestinal motility and allows water and electrolyte reabsorption from the intestinal lumen to the systemic circulation. Another agent, Lomotil, with a similar mechanism of action is available by prescription.

The most commonly reported adverse affects of antiperistaltic agents are dizziness, dry mouth, and skin rash. These agents can worsen the effects of invasive bacterial infection by not allowing evacuation of the damaging bacteria or toxins. Antiperistaltic agents should be used with caution in individuals who have a fever, a history of antibiotic use, or inflammatory bowel disease (ulcerative colitis or Crohn's disease).

Bismuths

Bismuth compounds are used to treat acute and traveler's diarrhea and stomach upset. Bismuth subsalicylate (Pepto- Bismol) is available OTC to treat diarrhea. Usually, bismuth subsalicylate is prescribed in doses of 30 mL or 2 chewable or dissolvable tablets every 30 to 60 minutes up to 8 times a day.

Constipation is usually described as a decrease in the frequency of fecal elimination and difficulty in passing stool, which is usually hard and dry. Constipation results from an abnormally slow movement of the feces through the colon and an accumulation of feces in the descending colon. Although there are several factors in the etiology of constipation, its most common causes include inappropriate diet (low in fiber), lack of exercise, insufficient fluid intake, excessive intake of foods, and resisting defecation impulses. Other causes of constipation include diabetes, multiple sclerosis, parkinsonism, inflammatory bowel disease, and pregnancy. The use of antidiarrheal agents can also cause constipation and may also cause low back pain, abdominal distention, dull headache, and lower abdominal distress.

Constipation Drug Treatment and Adverse Effects

Most nonorganic causes of constipation can be treated by lifestyle modifications. Increasing fiber intake enhances regularity by adding bulk and softening the stool. Increasing fluid intake, especially water intake, helps to alleviate constipation. Aerobic exercise, such as walking, running, or swimming, can decrease the likelihood of constipation. Laxatives and other medications (Table 8–3) can be used in conjunction with lifestyle modification to alleviate constipation. Chronic use of laxatives, referred to as laxative abuse syndrome (LAS) may result in diarrhea, steatorrhea, fluid and electrolyte imbalances, cathartic colon, and liver disease.³¹

Bulk-forming Laxatives

Bulk-forming laxatives, because of their ability to promote fecal evacuation, are the drugs most commonly prescribed for relief of constipation. Bulk-forming laxatives stimulate peristalsis (by distending the bowel) and assist in the passage of the stool. These medications should be taken with plenty of fluids to aid swallowing and to facilitate the drugs' efficacy. These laxatives may also be used to prevent the development of constipation.

The two most common types of bulk-forming laxatives are polycarbophil calcium (Mitrolan, FiberCon) and psyllium (Metamucil, Konsyl). Polycarbophil is normally used for both diarrhea and constipation to restore normal moisture levels and to provide bulk. Psyllium promotes the formation of a soft, water-retaining, gelatinous residue in the bowel.

Bulk-forming laxatives should not be taken by individuals who have intestinal ulcerations, obstruction, or stenosis. Failure to consume adequate water during administration can decrease the drugs' efficacy and may cause esophageal or intestinal obstruction. Abdominal discomfort, diarrhea, and flatulence may also occur.

Fecal Softeners

Orally administrated fecal softeners are mainly used to prevent constipation. Softeners increase the wetting efficiency of the intestinal fluid and mix the aqueous and fatty substances to soften the fecal mass. The fecal mass usually softens within 1 to 2 days after initiation of therapy; however, it may take as long as 3 to 5 days. Softeners do not stimulate bowel movement unless they are combined with stimulant laxatives. Docusate (Colace, Surfak) is the most commonly used type of medication in this category. Fecal softeners are considered safe and effective agents. Some possible adverse effects include diarrhea and abdominal cramping.

Hyperosmotic Agents

The class of hyperosmotic agents includes glycerin (rectal) and lactulose (oral or rectal). Both agents produce an osmotic effect by causing fluid retention in the colon. Glycerin produces an irritant effect on the colon for quick lower bowel evacuation. Because of this effect, glycerin suppositories are widely used in children. Lactulose is an effective agent that increases the water content of the stool, thereby softening the stool and producing an effect within 24 to 48 hours after administration.

Hyperosmotic agents are relatively safe. Glycerin may cause diarrhea, nausea, or vomiting. The most common adverse effects with lactulose are flatulence, belching, and abdominal discomfort such as cramping, nausea, and vomiting. Excessive doses may lead to diarrhea.

Stimulant Laxatives

Stimulant laxatives increase the propulsive activity of the intestine by local irritation of the mucosa or the intestinal smooth muscle. Most of the stimulant laxatives are of botanical origin, containing active ingredients obtained from seed pods, bark, leaves, and roots of various plant sources. Stimulant laxatives are primarily used for acute constipation; before proctologic, radiologic, and endoscopic examinations; and for preparation of barium enemas. However, they should not be used for more than 3 days because they can alter large intestine function.

There are two categories of stimulant laxatives, diphenylmethane and anthraquinone. Bisacodyl (Dulcolax) is the most commonly used diphenylmethane. Bisacodyl is a nontoxic agent that causes peristalsis on contact with the colon mucosa nerve plexus. Bisacodyl can trigger peristalsis within 15 to 60 minutes of rectal administration or within 6 to 10 hours if taken orally.

The exact mechanism of anthraquinone agents to produce peristalsis is unknown but is thought to primarily affect the colon. Aloe, cascara sagrada, senna, aloin, casanthranol, danthron, frangula, and rhubarb are examples of stimulant laxatives based on anthraquinone agents. Of these, senna is the preferred choice. The compounds in the anthraquinones, after absorption in the GI tract, can be found in human milk and pass their effects to the nursing infant.¹⁵ Therefore caution is advised for breast-feeding mothers.

Most stimulant laxatives can cause severe abdominal cramping, diarrhea, flatulence, electrolyte and fluid deficiencies, and hypokalemia. Individuals may also suffer from allergic reactions, change in heart rate, skin rash, disorientation, and color changes to the urine and feces.

Saline Laxatives

Saline laxatives are composed of soluble salts that draw water from the wall of the small intestine into the feces, then stimulate and increase intestinal motility. Saline laxatives produce stools that are liquid or semi-liquid in nature and are indicated when preparing for GI examinations or when stool specimens are needed. It can also be used for cases of food poisoning and fecal impaction. However, saline salts are not indicated for long-term management of constipation. There are several types of saline salts that are used as laxatives; magnesium sulfate (Epsom salts), magnesium hydroxide (milk of magnesia), magnesium citrate solution, and sodium phosphate (Fleet brand and other premixed enemas). Saline salts have a rapid course of action and should be taken with at least 8 oz of water with oral administration to prevent vomiting.

Long-term use of saline laxatives can cause electrolyte disturbances and may act as a CNS depressants. Individuals with renal impairment can develop toxicity to magnesium ions in saline salts.²⁹ Up to 20 percent of the magnesium in magnesium salts may be absorbed and produce hypotension, muscle weakness, and electrocardiographic changes.³¹ The most common adverse effects include abdominal cramping, nausea, vomiting, and dehydration.

Many individuals complain of belching, abdominal discomfort, bloating, and flatulence, especially after meals. However, the pathogenesis for intestinal gas is largely misunderstood. Gas is thought to arise from three different sources: (1) air swallowing, (2) intraluminal production, and (3) diffusion of gases from the blood.

When we eat, several milliliters of air are deposited into the stomach with every swallow of food or saliva.²⁶ Over the course of a day, several liters of nitrogen (N₂) found in the air enter the stomach with only approximately 400 mL of N₂ passed as gas. The remaining air is thought to escape into the esophagus or become trapped in the stomach. This trapped air results in a "bloated" feeling for many individuals.

Intraluminal gas (H₂, CH₄, and CO₂) can be produced in the upper gut in various quantities. Carbon dioxide (CO₂) is produced from the interaction of hydrogen ions and bicarbonate. Hydrogen and methane (CH₄) are produced from bacterial metabolism. Methane is not produced by everyone, and individuals who produce methane usually have stools that float. Intraluminal gases produced are eventually released through the rectum.

Most gas production can be the result of malabsorption of carbohydrates and proteins. Fruits and vegetables that contain oligosaccharides and polysaccharides cannot be digested by the enzymes of the bowel; resulting in the production of gas.³⁸ Individuals with low levels of lactase, which is used to digest lactose, can develop gas. Other sources of food that can produce gas include specific flours, oats, corn, and potatoes.²⁴ Rice is the only starch that does not produce gas.

Because gases are soluble in lipid and water, diffusion between the lumen and the blood occurs easily. Pressure gradients create the movements of the gases. Most notably, air that is swallowed diffuses into the blood stream of the stomach. Carbon dioxide (CO₂) is extracted into the blood, whereas N₂ diffuses into the lumen. Bacteria in the colon produce CO₂, H₂ and CH₄, which enter the blood, whereas at the same time N₂ diffuses into the colon. The whole process results in gas production in different parts of the GI tract.

Intestinal Gas Drug Treatment and Adverse Affects

There are two classes of antiflatulent products available for intestinal gas; simethicone and alpha-galactosidase. Simethicone (Gas-X, Phazyme) is used as a defoaming agent to relieve gas by reducing the surface tension of gas bubbles found in the GI tract. As the surface tension is reduced, gas bubbles are broken and can be released through belching or flatus.³¹

Beano, an alpha-galactoside, is a relatively new drug used to relieve intestinal gas. Beano has an enzyme that breaks down oligosaccharides (a component of beans, whole grains, peas, and lentils) before they are metabolized by colonic bacteria.¹⁰ Beano should be administered with the first bite of the food to be effective.

In most instances, PUD and GERD sufferers will not seek medical treatment from athletic trainers. However, some individuals might inform the athletic trainer of their signs and symptoms and ask for an opinion. The responsibility of the athletic trainer is to recognize the condition and refer the athlete to the appropriate medical specialist.

Nearly everyone experiences diarrhea and constipation at some point. Because these conditions are often embarrassing to discuss, it is important for the athletic trainer to have a good relationship with the athlete. A trusting relationship will allow the athlete to discuss the condition openly so that a proper medical evaluation can be made. The athletic trainer must be able to properly determine which OTC medication is appropriate for their athlete's signs and symptoms and how to properly administer the doses. As discussed in Chapter 1, the athletic trainer should document all relevant drug information and distribution.

1. A chronic inflammatory disorder of the mucosa of the stomach is called:

   1. PUD

   2. GERD

   3. Irritable bowel syndrome

   4. Kuder-Richardson syndrome

2. Which of the following is NOT a pathophysiological mechanism of GERD?

   1. Relaxation of the lower esophageal sphincter

   2. A low resting lower esophageal sphincter pressure

   3. Odynophagia

   4. Obesity

3. Which of the following compounds is NOT an antacid?

   1. Calcium citrate

   2. Calcium carbonate

   3. Magnesium salts

   4. Aluminum salts

4. Which of the following drugs is classified as a proton pump inhibitor?

   1. Pepcid

   2. Axid

   3. Aciphex

   4. Milk of magnesia

5. Acute diarrhea can be caused by which of the following?

   1. Shigella

   2. H. pylori

   3. Psychogenic origin, S. aureus

   4. Flatulence

6. Select the appropriate drug used to treat constipation:

   1. Loperamide

   2. Docusate

   3. Lansoprazole

   4. Pantoprazole

7. This type of laxative draws water from the wall of the small intestine into the stool and stimulates intestinal motility:

   1. Bisacodyl

   2. Mineral oil

   3. Magnesium sulfate

   4. Senna

8. Which of the following examples of drugs are causes of PUD in individuals who are not infected with H. pylori ?

   1. Lansoprazole

   2. Erythromycin

   3. Bismuth subsalicylate

   4. Ibuprofen

9. This drug is often used to treat traveler's diarrhea:

   1. Pepcid

   2. Imodium

   3. Colace

   4. Senna

10. Which of the following is an alpha-galactoside used to treat intestinal gas?

    1. Beano

    2. Bisacodyl

    3. Simethicone

    4. Ex-Lax