http://evolve.elsevier.com/Edmunds/NP/
Key drug, as it is the most commonly used except for the combination products.
Antacids are rarely prescribed as first-line treatment. Usually, the patient has been using OTC antacids before coming to the health provider for care. These medications are used commonly for gastroenterologic diseases such as reflux esophagitis and peptic ulcer. The antacids most commonly prescribed have at least one of the following elements as their main ingredient: calcium carbonate, aluminum salts, or magnesium. The ingredient alginate may provide barrier protection and is useful in the management of GERD.
The key antacid is considered to be calcium carbonate because of its widespread popularity, cost-effectiveness, and ease of use. However, combination antacids—in particular, combinations of aluminum hydroxide and magnesium hydroxide—are probably the most commonly used antacids. Antacids vary in sodium content, in magnesium content (a problem in kidney failure), and in the tendency to cause diarrhea or constipation.
Therapeutic Overview of Gastroesophageal Reflux Disease
The pH of saliva is basic, causing the contents of the esophagus to be neutral to basic. Esophageal peristalsis and salivary bicarbonate serve to protect the esophageal mucosa from erosion. The stomach contents are highly acidic, which helps in the digestion of food.
Pathophysiology
The return of stomach contents back up into the esophagus is called gastroesophageal reflux disease (GERD). This reflux frequently causes heartburn, which results from irritation of the esophagus by stomach acid. GERD can lead to scarring and stricture of the esophagus, requiring stretching (dilating) of the esophagus. In all, 10% of patients with GERD develop Barrett’s esophagus, which increases the risk of cancer of the esophagus. A total of 80% of patients with GERD also have a hiatal hernia, in which a portion of the stomach protrudes through the diaphragm (where the esophagus normally passes through). Hiatal hernias are not a cause of GERD. If the patient with a hiatal hernia has GERD, more reflux will occur.
Many factors may lead to GERD. Obesity and smoking are considered risk factors. A very important factor that contributes to GERD is an incompetent lower esophageal sphincter (LES). Reflux of the stomach contents (pH 2) into the esophagus (pH 6) occurs during relaxation of the LES. A decrease in LES pressure allows acidic gastric contents to enter the lower portion of the esophagus. This happens at rest but increases with stress such as that caused by abdominal straining, lifting, or bending. In addition, some people have low basal LES pressure. The highly acidic gastric contents are damaging to the esophageal mucosa, causing inflammation. This mucosal damage may further decrease LES pressure, initiating a self-perpetuating cycle.
Delayed gastric emptying may be caused by gastroparesis or partial gastric outlet obstruction. This can increase GERD because the food stays in the stomach longer. During sleep, peristalsis is decreased, causing an increase in symptoms. Because saliva helps to neutralize stomach contents, anything that decreases salivation such as anticholinergic medications can exacerbate GERD. Hiatal hernias are common and are not a cause of GERD. If the patient with a hiatal hernia has GERD, more reflux will occur.
Disease Process
GERD is one of the most common chronic conditions for which patients in the United States take daily medication. Heartburn and regurgitation associated with GERD were found to produce symptoms at least once per week in 20% of the population and occur at least twice per week in 6% and 3% of the adult U.S. population, respectively. GERD involves the movement of stomach contents back into the esophagus. Most patients have very mild disease, although it is possible for the patient to develop rare complications such as active erosive esophagitis, esophageal adenocarcinoma, and esophageal stricture.
The main symptom of GERD is heartburn that occurs 30 to 60 minutes after meals and when the patient bends over or lies down. Relief is usually reported after antacids are taken. Other symptoms may include nonspecific GI symptoms such as regurgitation of sour or bitter gastric contents, belching, and fullness of the stomach. Atypical symptoms include chronic cough, chronic laryngitis, asthma, sore throat, and noncardiac chest pain. Erosive esophagitis may have more severe symptoms such as pain and dysphagia but also may be relatively asymptomatic. Esophagitis is divided into four grades, which are determined endoscopically. Grade 1 is defined by erythema of the distal esophagus. Grade 2 consists of scattered erosions. Grade 3 involves confluence of erosions involving less than 50% of the diameter of the esophagus; grade 4 involves confluence of erosions involving greater than 50% of the diameter.
Providers must ask specifically about antacids and other OTC remedies when taking a medication history. Many patients will have tried OTC remedies before going to their primary care provider. Most will have tried antacids, OTC histamine blockers, or proton pump inhibitors (see Chapter 27). Many patients do not consider antacids to be a medication and will not mention taking them when asked about medication use.
An upper endoscopy with biopsy is the standard diagnostic procedure for GERD. It confirms the diagnosis and documents the type and extent of tissue damage. Uncomplicated GERD that is responsive to first-line therapy does not require an endoscopy. For most patients, empiric treatment is initiated based on history and physical examination. Acid suppression therapy with antacids, histamine2-receptor antagonists (H2RAs), or proton pump inhibitors (PPIs) are extremely effective in controlling GERD symptoms but can be problematic because of the high associated costs of many of these medications and the need for indefinite therapy duration in most patients. Patients who do not respond to therapy and those with suspected complications should undergo an endoscopic examination.
The differential diagnosis includes peptic ulcer, cholelithiasis, nonulcer dyspepsia, and angina pectoris. Patients may need to be evaluated for Helicobacter pylori infection.
Mechanism of Action
Antacids are weak bases that neutralize gastric hydrochloric acid by combining with it to form salt and water. This process decreases the amount of gastric acid in the stomach, raising the pH. Antacids decrease pepsin activity because pepsin is rendered inactive in alkaline conditions. Antacids also have a number of cytoprotective effects. They may enhance mucosal prostaglandin levels. Aluminum ions inhibit smooth muscle contraction, thereby slowing gastric emptying. This is counterproductive because in GERD, prompt gastric emptying is beneficial. Aluminum binds epidermal growth factor, thus delivering growth factor to the injured mucosa.
Antacids do not protect the stomach by coating the mucosal lining. Alginic acid is not an antacid because in the presence of saliva, it reacts with sodium bicarbonate to form sodium alginate, and it protects the mucosa with its foaming, viscous, and floating properties. This foam may provide a barrier to reflux of stomach contents into the esophagus.
The ability of antacids to neutralize gastric acid has been labeled acid-neutralizing capacity (ANC). This ANC is the quantity of 1 M HCl (expressed in milliequivalents) that can be brought to pH 3.5 in 15 minutes (expressed as mEq/ml). Antacids with high ANC usually are more effective than others.
Treatment Principles
Cardinal Points of Treatment
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