Introduction
The digestive system consists of the gastrointestinal tract and other organs of digestion such as “the salivary glands, liver, gallbladder, and exocrine pancreas” (Huether & McCance, 2016, p. 884). Its major function is to break down ingested food, make it ready for the absorption by body cells, take in fluids, and remove wastes. Functional gastrointestinal disorders are common for gastroenterology (Drossman, 2016).
Gastrointestinal (GI) disorders frequently have similar symptoms such as pain in the abdominal or chest area, problems with swallowing or painful swallowing, anorexia, changes in bowel movements, and even GI tract bleeding (Hammer & McPhee, 2014). Thus, knowledge of GI tract peculiarities, its normal pathophysiology, clinical manifestations of GI disorders is critical for correct and timely diagnosing, and the following treatment.
Normal Pathophysiology of Gastric Acid Stimulation and Production
Gastric hydrochloride acid is responsible for the dissolution of food fibers, executes a bactericide function against swallowed microorganisms, and converts pepsinogen to pepsin (Huether & McCance, 2016). It is produced by parietal cells and this process demands the transportation of “hydrogen and chloride from the parietal cells to the stomach lumen” (Huether & McCance, 2016, p. 891). A major process that results in acid formation is the hydrolysis of water.
The Vagus nerve is an impetus for acid secretion. It releases acetylcholine and quickens the secretion of gastrin. Gastric acid secretion can be regulated by gastrin (Waldum, Hauso, & Fossmark, 2014). Gastrin, in its turn, provokes the discharge of histamine. At the next stage, histamine activates histamine receptors that stimulate the production of acid (Huether & McCance, 2016). Moreover, caffeine and calcium can stimulate the secretion of acid.
Pathophysiology of Gastroesophageal Reflux Disease, Peptic Ulcer Disease, and Gastritis
Major GI disorders include gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and gastritis. GERD is “the reflux of acid and pepsin or bile salts from the stomach into the esophagus that causes esophagitis” (Huether & McCance, 2016, p. 915). This condition can be found in about 30% of the American population. In patients with GERD, the content of gastric acid increases.
The risk of developing GERD increases with aging, obesity, hiatal hernia, and treatment with medicines that soften the lower esophageal sphincter (LES) (Huether & McCance, 2016). GERD can be conditioned with anomalies in LES functioning, and motility or emptying. The growth of abdominal pressure as a result of pregnancy, obesity, bending or coughing can stimulate the reflux. The clinical manifestations of GERD are “pyrosis, acid regurgitation, dysphagia, chronic cough, asthma attacks, laryngitis, and upper abdominal pain within 1 hour of eating” (Huether & McCance, 2016, p. 917).
Gastritis is an inflammatory disease of the gastric mucosa. It can be acute or chronic. Unlike GERD, it is a rare disease in the United States with a prevalence of less than 1%. Gastritis develops as a result of the protective mucosal barrier injury. It can be caused by Helicobacter pylori infection or the consumption of different chemicals or drugs (Watari, 2014). Gastritis is characterized by increased gastric secretion. A chronic condition is more characteristic of older adults, which is similar to GERD. Its clinical manifestations are not specific and can be misinterpreted.
PUD is “a break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum” (Huether & McCance, 2016, p. 920). Ulcers are the result of the influence of erosive factors on mucosal protective factors. These erosive factors include non-steroidal anti-inflammatory drugs and Helicobacter pylori. It is a widely-spread disease affecting more than 15.5 million people in the United States (Huether & McCance, 2016).
Due to the erosive factors, gastric acid production increases ant it penetrates the mucosal barrier. The risk of developing PUD increases for people with gastric infections, smokers, and those who drink alcohol. Moreover, advanced age and some chronic diseases can stimulate PUD. The similarity of the three conditions is that they affect GI and can develop as a result of excessive medication. However, the risk factors and prevalence of the diseases are different for all conditions.
Patient Factor Influencing Pathophysiology of GERD, PUD, and Gastritis
One of the patient factors that influence the diseases of GI is the use of drugs that harm the GI tract. Non-steroidal anti-inflammatory drugs are among the most dangerous medications because they can injure the protective mucosal lining and cause GERD, PUD, and gastritis. In case GERD, PUD, or gastritis are conditioned by NSAID, it is necessary to stop their use. For diagnosis, it is necessary to provide laboratory testing and endoscopic evaluation. Appropriate therapy aimed at the elimination of clinical manifestations and the improvement of patient condition should be used. Moreover, it is important to avoid NSAID in the treatment of GERD, PUD, and gastritis in case they caused the diseases.
References
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Hammer, G.D., & McPhee, S.J. (2014). Pathophysiology of disease: An introduction to clinical medicine (7th ed.). New York, NY: McGraw Hill Education.
Huether, S.E., & McCance, K.L. (2016). Understanding pathophysiology (6th ed.). St. Louis, MO: Elsevier.
Neumann, W., Coss, E., Rugge, M., & Genta, R. (2013). Autoimmune atrophic gastritis—pathogenesis, pathology and management. Nature Reviews Gastroenterology & Hepatology, 10(9), 529-541. Web.
Watari, J. (2014). Helicobacter pylori-associated chronic gastritis, clinical syndromes, precancerous lesions, and pathogenesis of gastric cancer development. World Journal of Gastroenterology, 20(18), 5461. Web.
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