Introduction Motility represents the stomach muscle’s contractions that allow the mix and push of contents within the gastrointestinal tract (GI). Motility is a term generally used for reference to any of the various gastro disorders where there is a loss in ability to control muscular activities resulting from endogenous or exogenous triggers (Ghoshal,...
Introduction
Motility represents the stomach muscle’s contractions that allow the mix and push of contents within the gastrointestinal tract (GI). Motility is a term generally used for reference to any of the various gastro disorders where there is a loss in ability to control muscular activities resulting from endogenous or exogenous triggers (Ghoshal, 2016). Such disorders may be considered primary or secondary. These disorders may present in different ways. From constipation, to abdominal distention, and recurrent vomiting, when there is an alteration in the process of digestion and motility, they can have long-term effects on the individual.
Normal Pathophysiology of Gastric Acid Stimulation and Production
The regulation of pepsin and acid secretion demonstrates the complex balance of chemotransmitters as they are sent to the gastric mucosa via various pathways mediating both inhibitory and stimulatory mechanisms (Ghoshal, 2016). These mechanisms contribute to the normal gastroduodenal mucosa to protect itself from injury and enable it to rapidly repair itself if injury does happen. These control pathways are endocrine, neural, autocrine, and paracrine. When gastric acid secretes into the stomach, it facilitates protein digestion as well as the absorption of vitamin b12, calcium, iron, and even drugs like thyroid hormone or itraconazole.
With the lowering of pH through gastric acid, ingested microorganisms are killed and limited bacterial growth in the stomach averts intestinal infections like Clostridium difficile (Ghoshal, 2016). There are three phases of gastric activity. These are cephalic phase, gastric phase, and intestinal phase. These phases are either controlled by the brain, itself, or the small intestine, respectively. All three phases can happen simultaneously (Ghoshal, 2016). A fourth phase, the basal state happens in between meals and is considered an interdigestive phase. The amount of acid secretion varies and is regulated based on number of parietal cells, body weight, time of day, and the individual.
GERD
The key difference between GERD and gastritis is that GERD symptoms occur in the esophagus whereas gastritis symptoms occurs in the stomach. GERDs origin within the gastrointestinal tract is the esophagus with dissimilar symptoms and causes (Podolsky et al., 2015). When an episode of GERD happens, stomach contents rise to the esophagus, generating a burning sensation (heartburn) that can be felt in the chest. This can happen frequently and create long-term changes within the esophagus.
PUD
Peptic Ulcer disease refers to a break in the stomach lining, the lower esophagus, or the first segment of the small intestine. Common causes of the disease are H. pylori bacteria or non-steroidal anti-inflammatory drugs (Podolsky et al., 2015). Because of the break in the stomach lining, gastric secretions can harm the delicate not protected. This can lead to bleeding, blockage of the stomach, poor appetite among other symptoms/complications.
Gastritis
Gastritis can originate from chronic or acute inflammation of the lining of the stomach. It can also be caused by H. pylori bacteria (Podolsky et al., 2015). Excess gastric secretions from the disease lead to symptoms like stomach upset, belching, nausea, and vomiting. The excess gastric secretions do not travel up to the esophagus like GERD.
Patient Factor
Age is a pertinent patient factor. Older patients are more likely to take NSAIDs compared to younger patients. Therefore, the likelihood of their development of gastritis, GERD, and PUD is higher. NSAIDs are the main contributor to creation of all these diseases especially gastritis and PUD. Patient age may contribute to GERD due to the likelihood of stomach acid imbalance in the patient. Again, from GERD, H. pylori bacteria and so forth.
Diagnosis and Treatment
Older patients who take NSAIDs, I would ask them to seek alternative treatments for pain. For example, sometimes lack of bone density leads to chronic (Van & Bladh, 2016). Diminishing NSAID exposure can be a key factor to alleviating all three diseases. A potential treatment option for all three can also be antacids as they nullify some of the gastric acid and reduce the discomfort. If it is an H. pylori infection that is causing the gastritis or PUD, one can use endoscopy and even a biopsy to identify the extent of the damage. “Ingestion of nonsteroidal antiinflammatory drugs (NSAIDs) is very often followed by an acute gastritis. Timed endoscopic studies have shown that the first visible evidence of injury is mucosal hemorrhage, which can occur as rapidly as 1 hour after initial intake” (Benjamin & DiMarino, 2002, p. 439). Then prescribe antibiotics if necessary.
Gastritis Mind Map
References
Benjamin, S. B., & DiMarino, A. J. (2002). Gastrointestinal disease: An endoscopic approach. Thorofare, NJ: Slack.
Ghoshal, U. C. (2016). Evaluation of Gastrointestinal Motility and its Disorders. New Delhi: Springer India.
Podolsky, D. K., Camilleri, M., Fitz, J. G., Kalloo, A. N., Shanahan, F., & Wang, T. C. (2015). Yamada's Textbook of Gastroenterology, 2 Volume Set. John Wiley & Sons.
Van, L. A., & Bladh, M. L. (2016). Textbook of laboratory and diagnostic testing: Practical application at the bedside. F.A. Davis.
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