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OTC Advisor TM A National Education Program for Pharmacists Self-Care for Gastrointestinal Disorders
After reading this module, the pharmacist should be able to:
According to the American Gastroenterological Association, symptoms and complaints r4lated to the gastrointestinal (GI) tract are some of the most common reasons why people take nonprescription or prescription medications or seek the advice of health care providers. Widely quoted statistics indicate that 7% of American adults suffer from daily heartburn, 14% experience weekly heartburn, and 44% experience monthly heartburn.''' At any given time, about one in four adults experiences dyspepsia (a heterogeneous group of upper abdominal symptoms that arise from disparate conditions). Constipation is the most common GI complaint in the United; States; about 4.5 million Americans report being constipated most or all of the time. The average adult has a bout of diarrhea about four times a year.' About half of the U.S. population has hemorrhoids (a common anorectical problem) by age 50.6
Self-treatment of these prevalent GI symptoms and complaints with nonprescription medications is common. The pharmacist may be the first health care professional consulted by patients suffering from heartburn, dyspepsia, constipation, diarrhea, or anorectal disorders, so pharmacists must be able to distinguish between patients who are appropriate candidates for self-treatment and those who require referral to a health care provider for more extensive evaluation. When self-treatment is indicated, the pharmacist should be able to recommend the most appropriate nonprescription products.
This module reviews appropriate self-treatment strategies for heartburn, dyspepsia, constipation, diarrhea, and anorectal disorders.
Heartburn and Dyspepsia
Heartburn usually is described as a sensation of burning discomfort or pain behind the breastbone. The sensation may radiate up the entire retrosternal area to the neck, occasionally to the back, and rarely into the arms.''''9 Heartburn frequently occurs within 1 hour after eating, especially after large or fatty meals. It may be accompanied by acid regurgitation (the effortless return of acidic gastric contents to the pharynx, which causes a sour or bitter taste in the mouth. Dyspepsia usually is defined as pain or discomfort centered in the upper abdomen (epigastrium). The discomfort may be characterized by or associated with bloating, early satiety, postprandial fullness, nausea, anorexia, or burping or belching.Patients who experience heartburn or dyspepsia may not distinguish between these symptoms. In fact, there is considerable overlap among the symptoms: many patients experience both heartburn and dyspepsia. Self-treatment of both heartburn and dyspepsia may involve similar lifestyle modifications or pharmacologic therapy with antacids, histamine H2-receptor antagonists, or proton pump inhibitors. Because of these commonalities, heartburn and dyspepsia will be discussed together for the purposes of this module.
Heartburn is most closely associated with the retrograde (backward) movement of acidic gastric contents into the esophagus (gastroesophageal reflux).'-9 Reflux of gastric contents usually is prevented by the lower esophageal sphincter (LES), an area of specialized smooth muscle located above the junction where the esophagus meets the stomach.8'9 The LES ordinarily is constricted; the resting tone of the LES normally is 10 to 30 mm Hg higher than intragastric pressure.' When food is ingested, the LES relaxes briefly (3–10 seconds) during peristalsis to allow the swallowed bolus to enter the stomach.8'9 The LES works in conjunction with the diaphragm to create a physical barrier against reflux.'''
For gastroesophageal reflux to occur, the pressure gradient between the LES and the stomach must be less than normal or absent.''9 Spontaneous, transient relaxations of the LES appear to be the most frequent mechanism for reflux.8 Transient LES relaxations occur independently of swallowing or peristalsis and last substantially longer (up to 45 seconds) than do swallow-induced LES relaxations.8'9'14 Factors that reduce LES tone also predispose patients to reflux; these factors include certain foods (Table 1) and medications (Table 2), gastric distention, and nicotine (smoking). Reflux is more likely to occur if intra-abdominal pressure is increased, during certain maneuvers (such as when a person bends over, lifts heavy objects, or strains to defecate) or secondary to delayed gastric emptying, disorders of gastric motility, obesity, or pregnancy.7"9 The hormonal effects of pregnancy also may reduce LES tone directly.8'9
It is important to note that frequent reflux alone is not necessarily sufficient to provoke symptoms such as heartburn. Everyone experiences some degree of gastroesophageal reflux, especially after
meals. These episodes usually are asymptomatic. The refluxed material is cleared rapidly from the esophagus by a combination of gravity (when a person is upright) and primary peristalsis in response to swallowing.8 The esophagus is further protected from injury by the buffering action of bicarbonate in swallowed saliva and mucus secreted by glands in the esophageal mucosa and submucosa.2 Symptoms such as heartburn are most likely to occur when esophageal defense mechanisms are compromised and acidic gastric contents (especially pH <4) are able to come into prolonged contact with the esophageal mucosa.8 The clearance of refluxed material from the esophagus is hindered when a person lies down (because gravity facilitates clearance) or sleeps. The production of saliva decreases with increasing age, so esophageal clearance is prolonged in older patients, and less saliva is available to neutralize refluxed material.9 Overeating and delayed gastric emptying increase the amount of material available to be refluxed; large volumes of refluxate increase the duration and "reach" (i.e., proximal extent) of reflux episodes.''9 Patients with hiatal hernia (protrusion of the upper part of the stomach through a small opening in the diaphragm, the diaphragmatic hiatus) often experience problems with esophageal emptying.8 A number of foods (Table 1) and medications (Table 2) precipitate heartburn by irritating the esophageal mucosa directly.
Heartburn vs Gastroesophageal Reflux Disease
It can be difficult to differentiate the term "heartburn" from the term "gastroesophageal reflux disease (GERD). GERD describes any symptomatic condition or tissue damage that res is from episodes of gastroesophageal reflux.2 Heartburn is the classic manifestation of GERD. It is so closely associated with the condition that the presence of heartburn and regurgitation as patient's dominant symptoms is a key factor in establishing a diagnosis of GERD. Any patient who experiences heartburn could be considered to have GERD. However, given the frequency with which heartburn occurs in the U.S. population, the term GERD end to be reserved for persons who have moderate to severe, recurring, prolonged episodes of heartburn.
GERD is associated with a number of symptoms in addition to heartburn and regurgitation Up to 30% of patients report dysphagia (the sensation of food being hindered in its passage from the mouth to the stomach). As many as 50% of patients with GERD report dyspepsia, either in association with heartburn or alone. Nausea increasingly is being recognized as a manifestation of GERD.15
Symptoms caused by gastroesophageal reflux are not necessarily limited to the esophagus. Refluxed material may reach the oropharynx or be aspirated by the patient, leading to atypical symptoms that include noncardiac chest pain that mimics angina, chronic cough, and asthma. Other extraesophageal manifestations of GERD include recurrent laryngitis, chronic hoarseness, recurrent sore throat, hiccups, and dental erosions.
When patients with symptoms of GERD undergo endoscopy, about half are found to have evidence of esophageal mucosal injury (reflux esophagitis).8-16 (Patients without endoscopic evidence of esophageal mucosal injury are said to have nonerosive reflux disease [NERD].1') Reflux esophagitis can be complicated further by the development of esophageal ulcers (which occur in about 5% of patients) and esophageal strictures (which occur in 8%—20% of patients and result from the deposition of collagen during esophageal injury and repair).15'16 Odynophagia usually suggests the presence of esophageal ulceration; dysphagia suggests the presence of strictures.8
Another potentially serious complication of GERD is Barrett's esophagus, a condition in which eroded squamous mucosa in the esophagus is replaced with metaplastic gastric epithelium." Barrett's esophagus is a strong risk factor for esophageal adenocarcinoma.
The treatment of heartburn and GERD follows a stepwise approach.8-10 Lifestyle modifications aimed at reducing the likelihood of reflux (Table 3) should be initiated in all patients; although there is little evidence of the effectiveness of these measures, they may be the only treatment needed for some patients.8'10'' 9 Antacids (alone or in combination with the antirefluxant alginic acid) and nonprescription acid suppressants are recognized as appropriate, initial patient-directed pharmacotherapy for episodic heartburn.10
Patients with (1) frequent or moderate-to-severe symptoms that cannot be controlled with lifestyle modifications and nonprescription medications or (2) evidence of tissue damage usually require therapy with prescription-strength histamine H2-receptor antagonists or proton pump inhibitors. These therapies also promote healing of esophagitis.1° GERD typically is a chronic, relapsing condition; symptoms, tissue damage, or both will recur in a substantial number of patients if treatment is stopped.10 Long-term, possibly lifetime, maintenance pharmacotherapy often is required.10 Antireflux surgery may be performed in patients who continue to have severe symptoms, erosive esophagitis, or disease complications despite adequate pharmacologic therapy.
The constellation of symptoms associated with dyspepsia may be caused by a number of foods, medications, GI tract diseases, and pathologic states in other organ systems (e.g., diabetes, thyroid or parathyroid disorders). However, up to 60% of patients experience dyspepsia symptoms with no obvious biochemical or organic cause.13'22 These patients are labeled as having functional dyspepsia (also referred to as idiopathic dyspepsia or non-ulcer dyspepsia)'12'13 The pathophysiology of functional dyspepsia is not well understood. Both physiologic factors (delayed gastric emptying and other abnormalities in gastroduodenal motility, disturbed gastric sensory function, autonomic neuropathy, Helicobacter pylori infection) and psychological factors (including stress) are thought to be involved.3'22
The foods and beverages commonly implicated in dyspepsia are listed in Table 4. A number of factors contribute to food intolerance, including direct mucosal irritation, irritation of a preexisting ulcer, direct stimulation of mucosal sensory receptors, gastric over distention, delayed gastric emptying or altered intestinal motility, and gas production.' There is little objective evidence to support a cause-and-effect relationship between food intolerance and dyspepsia. Nevertheless, avoiding the offending foods or beverages often resolves a patient's symptoms, if only by means of a placebo effect.
A number of medications are capable of causing dyspepsia through known mechanisms (direct mucosal irritation, alterations in gastric motility) as well as-unknown mechanisms. Medications commonly associated with dyspepsia are listed in Table 5.Notable among these are aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), which provoke dyspepsia in approximately 25% of patients and are a leading cause of peptic ulcer disease. An estimated 15 million to 25 million people in the United States use NSAIDs on a regular basis, with the highest prevalence of use among older adults.
Common Organic Causes of Dyspepsia
The most common identifiable organic causes of dyspepsia are peptic ulcer disease, GERD, and gastric cancer.3'12.'3
Peptic Ulcer Disease. Peptic ulcer disease—a group of chronic, recurring inflammatory conditions characterized by ulcerations of the stomach, duodenum, or both—is the cause of dyspepsia in 15% to 25% of patients.'2.'3'26 The classic symptom of peptic ulcer disease is gnawing or burning, nonradiating, epigastric pain that occurs 2 to 3 hours after meals (when the stomach is empty) or at night.26 The pain may be relieved by antacids or food (although gastric ulcer pain may be worsened by ingestion of food, because it stimulates the release of gastric acid).26'2' The pain also may awaken the patient from sleep, usually between midnight and 3:00 AM when gastric acid secretion is maximal.27
The discovery in the 1980s of the relationship between H. pylori and peptic ulcers revolutionized the clinical approach to what was once considered to be a medically incurable condition.2''26 It is now believed that almost all duodenal ulcers (up to 95% of cases) and most gastric ulcers (approximately 70% of cases) are caused by H. pylori infection.13'26 Therefore, current approaches to treating peptic ulcer disease seek to cure the condition by eradicating H. pylori.27 Eradication therapy employs combination drug regimens made up of an antisecretory agent (usually a proton pump inhibitor to promote active ulcer healing) and antibacterial agents (frequently clarithromycin plus amoxicillin or metronidazole), with or without bismuth subsalicylate 2'27 Unless a patient is reinfected, it is rare for an ulcer to recur once H. pylori has been eradicated.2
Use of aspirin and NSAIDs—especially chronic use of high doses or multiple agents—accounts for the majority of gastric ulcers that are not caused by H. pylori.13'26'27 Most NSAID-induced ulcers heal spontaneously when the medication is discontinued, usually within 14 days.24 Antisecretory agents (histamine H2-receptor antagonists, proton pump inhibitors) or sucralfate may be administered to accelerate the healing process.24
Gastric bleeding is a common complication of peptic ulcer disease that occurs in as many as 20% of patients?'26'27 Symptoms of gastric bleeding include occult blood in the stool, with or without anemia; emesis of material that resembles coffee grounds; hematemesis; and melena (black or tar-colored stools). GERD is determined to be the cause of dyspepsia in 5% to 15% of cases.12''3 As noted earlier, more than half of patients with proven GERD have dyspepsia in addition to heartburn; as many as 20% of patients experience dyspepsia only, without heartburn or regurgitation.
Treatment strategies for dyspepsia are not as straightforward or well-defined as they are for heartburn and GERD. Whenever possible, treatment should be directed at the underlying cause of the symptoms (e.g., H. pylori–eradication therapy for patients with suspected peptic ulcer disease).3'22 Patients who experience dyspepsia in relation to specific foods or activities (overeating, smoking) should be encouraged to limit or avoid them. Drugs that are known to cause or contribute to dyspepsia should be discontinued or replaced with a more suitable agent whenever possible.3'2''22
The efficacy of drug therapy for functional dyspepsia has not been proved conclusively, in part because of a high placebo response (up to 80% of -patients)? Antacids are used commonly for rapid, short-term relief of intermittent dyspeptic symptoms.2'3'2' Antisecretory agents are considered to be first-line therapy, especially for patients with more frequent or severe symptoms 3'2''22 Some patients respond to treatment with metoclopramide or tricyclic antidepressants.3'22
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