Running head: Commercial Critique Paper
Commercial Critique Paper
Gastroesophageal reflux disease, also known as GERD, is gastroesophageal reflux through the lower esophageal sphincter (LES) into the esophagus or oropharynx that produces symptoms, injury to esophageal tissue, or both. The stomach continuously produces hydrochloric acid that helps in digesting food. GERD is related to failure of the lower esophageal sphincter (LES) to close properly. This results in reflux of acid into the unprotected lining of the esophagus. The pathophysiology of GERD is not completely understood and is complex. The main etiologic factors are believed to be an abnormal LES pressure and increased reflux during temporary LES relaxation. The inner lining of the stomach is protected from the acid “by the presence of prostaglandins present in gastric mucus that inhibit gastric secretion, stimulate bicarbonate ion secretion, and enhance blood flow” (O'Malley, 2010). The stomach is also protected by “tight intracellular junctions and a mucin layer over epithelial cells” (O'Malley, 2010).
Medications used to treat GERD include H2-receptor antagonists, antacids, and proton pump inhibitors in nonprescription and prescription strength. Antacids neutralize stomach acid, include Maalox, Mylanta, and Tums, and may provide quick relief. Antacids will not heal an esophagus damaged by stomach acid. H2-receptor antagonists are medications that work by reducing the amount of acid the stomach produces by blocking an important producer of acid- histamine 2. H2-receptor blockers include cimetidine (Tagamet HB), famotidine (Pepcid AC), or ranitidine (Zantac 75). H2 receptors blockers are slower acting than antacids but last longer. Proton pump inhibitors block acid production and heal the esophagus. Proton pump inhibitors include lansoprazole (Prevacid 24 HR), omeprazole (Prilosec OTC), and Dexilant (dexlansoprazole) (GERD: Treatment and Drugs, 2010). Proton pump inhibitors...
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