McKenna's Pharmacology for Nursing, 2e

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C H A P T E R 5 7 Drugs affecting gastrointestinal secretions

G astrointestinal (GI) disorders are among the most common complaints seen in clinical practice. Many products are available for the self-treatment of upset stomach, heartburn or dyspepsia. The underlying causes of these disorders can range from dietary excess, stress, hiatus hernia, oesophageal reflux and adverse drug effects to the more serious peptic ulcer disease. This chapter addresses the major conditions often requir- ing drug therapy: peptic ulcer disease and disorders involving increased acid levels and digestive enzyme dys- function (Box 57.1). ULCER DISEASE Erosions in the lining of the stomach and adjacent areas of the GI tract are called peptic ulcers . People with ulcers present with a predictable description of gnawing, burning pain often occurring a few hours after meals. Many of the drugs that are used to affect GI secretions are designed to prevent, treat or aid in the healing of these ulcers. The cause of chronic peptic ulcers is not completely understood. For many years, it was believed that ulcers were caused by excessive acid production, and treatment was aimed at neutralising acid or blocking the parasympathetic system to decrease normal GI activity and secretions. Further research led many to believe that, because acid production was often normal in people with ulcers, ulcers were caused by a defect in the mucus lining that coats the inner lumen of the stomach to protect it from acid and digestive enzymes. Treatment was aimed at improving the balance between the acid produced and the mucus layer that protects the stomach lining. Currently it is believed that chronic ulcers may also be the result of infection by Helicobacter pylori bacteria. Combination antibiotics have been found to be quite effective in treating some people with chronic ulcers. Acute ulcers, or “stress ulcers”, are often seen in situations that involve acute physiological stress, such as trauma, burns or prolonged illness. The activity of the sympathetic nervous system during stress decreases blood flow to the GI tract, leading to weakening of the mucosal layer of the stomach and erosion by acid in the stomach. Many of the drugs available for treating various peptic ulcers act to alter acid-producing activities of the stomach. DIGESTIVE ENZYME DYSFUNCTION Some people require a supplement to the production of digestive enzymes. People with strokes, salivary gland disorders, or extreme surgery of the head and neck may not be able to produce saliva. Saliva is important in beginning the digestion of sugars and proteins and is essential in initiating the swallowing reflex. People with common duct problems, pancreatic disease or cystic fibrosis may not be able to produce or secrete pancreatic enzymes. These enzymes may need to be administered to allow normal digestion and absorption of nutrients. ■■ BOX 57.1  Major conditions for using drugs that affect GI secretions

DRUGS USED TO TREAT GASTRO- OESOPHAGEAL REFLUX DISEASE AND ULCER DISEASE Drugs typically used to affect GI secretions in treating peptic ulcer disease and disorders involving increased GI acid work to decrease GI secretory activity, block the action of GI secretions, or form protective coverings on the GI lining to prevent erosion from GI secretions. Recent research studies have begun questioning the effects that lowering acid levels might have on the home- ostasis of the GI system and on total body homeostasis, including calcium levels (see Box 57.2). The drugs used to treat gastro-oesophageal reflux disease (GORD) and ulcer disease include Histamine-2 (H 2 ) antagonists, which block the release of hydrochlo- ric acid in response to gastrin; antacids, which interact with acids at the chemical level to neutralise them; proton pump inhibitors, which suppress the secretion of hydrochloric acid into the lumen of the stomach; GI protectants, which coat any injured area in the stomach to prevent further injury from acid; and prostaglandins, which inhibit the secretion of gastrin and increase the secretion of the mucus lining of the stomach, provid- ing a buffer. Figure 57.1 depicts sites of actions of these drugs used to treat GORD and ulcer disease. Box 57.3 highlights important considerations related to use of these drugs across the lifespan. H istamine -2 antagonists Histamine-2 (H 2 ) antagonists (Table 57.1) block the release of hydrochloric acid in response to gastrin. These drugs include cimetidine ( Tagamet ), ranitidine ( Zantac ), famotidine ( Pepcidine ) and nizatidine ( Nizac, Tazac ). receptors located on the parietal cells. Blocking these receptors prevents the release of gastrin, a hormone that causes local release of histamine (due to stimulation of hista- mine receptors), ultimately blocking the production of hydrochloric acid. This action also decreases pepsin production by the chief cells. H 2 receptor sites are also found in the heart, and high levels of these drugs can produce cardiac arrhythmias (see Adverse effects). These drugs are used in the following conditions: • Short-term treatment of active duodenal ulcer or benign gastric ulcer (reduction in the overall acid level can promote healing and decrease discomfort). • Treatment of pathological hypersecretory conditions such as Zollinger–Ellison syndrome (blocking the overproduction of hydrochloric acid that is associated with these conditions). Therapeutic actions and indications The H 2 antagonists selectively block H 2