Disorders of Motility Gastrointestinal Tract

Gastrointestinal Tract: Disorders of Motility
According to Ramsay and Carr (2011), the stomach’s main function is food preparation for digestion as well as absorption by the intestines. In the words of the authors, “acid production is the unique and central component of the stomach’s contribution to the digestive process” (Ramsay and Carr, 2011, p. 977). The parietal cells are responsible for the secretion of acid in the stomach. As Lascelles and Donaldson (2012) point out, the relevance of gastric acid in the digestive process cannot be overstated. This is more so the case given that it comes in handy in the creation of a pH that is ideal or favorable for not only pepsin, but also gastric lipase. It is also important to note that the pancreatic bicarbonate secretion is stimulated by gastric acid. It is food that initiates the secretion of acid. In this case, the taste, smell, or even thought of food does have an impact on what Lascelles and Donaldson (2012) refer to as “vagal stimulation of the gastrin-secreting G cells” (103). Once gastrin is in circulation, histamine is released. It is the said histamine that leads to the parietal cells stimulation and the subsequent secretion of acid. This results in a pH drop which in turn leads to somatostatin release by the antral D cells. As a consequence, the release of gastrin is inhibited. As Lascelles and Donaldson (2012) observe, there are several mechanisms that protect the GI mucosa. To begin with, HCO3 and mucus production leads to the creation of a pH gradient which, in the words of Lascelles and Donaldson (2012) runs “from the gastric lumen (low pH) to the mucosa (neutral pH)” (104). In basic terms, a barrier is created by the mucus to pepsin and acid diffusion. Next, it should also be noted that any acid that diffuses past or beyond the epithelial layer is removed by mucosal blood flow. Excess hydrogen ions, on the other hand, are removed by epithelial cells.
Gastritis, PUD, and GERD, are predisposed by factors that tend to impede or inhibit the mucosal defenses identified above. To begin with, gastritis has got to do with the erosion, irritation, or inflammation of the stomach lining (Taylor, 2012). Gastritis, according to Pooler (2009) could either be grouped as chronic or acute. In essence, acute gastritis, in the words of the author, “is characterized by an acute mucosal inflammatory process, usually transient in nature” (885). As the author further points out, the condition is in most cases associated with bacterial toxins or alcohol, and aspirin as well as other NSAIDs (Pooler, 2009).
On the other hand, when it comes to chronic gastritis, Pooler (2009) points out that the same is “characterized by the absence of grossly visible erosions and the presence of chronic inflammatory changes leading eventually to atrophy of the glandular epithelium of the stomach” (885). PUD, on the other hand, is an erosion of sections of the duodenum or GI mucosa – and hence duodenal and gastric ulcer respectively. In essence, the muscularis mucosae is in this case penetrated as a consequence of the said erosion. The use of NSAIDs or Helicobacter pylori infections are often cited as the key causes of ulcers (Taylor, 2012). In this case, the normal defense as well as repair of the mucosa is disrupted by the said utilization of NSAIDs or Helicobacter pylori infection. In the end, the susceptibility of the mucosa to acid increases. Lastly, GERD is occasioned by the constant reflux of acid into the esophagus (Taylor, 2012). As a consequence of this constant acid reflux, the lining of the esophagus ends up being irritated. When the sphincter at the bottom of the esophagus relaxes in an abnormal format or weakens, then acid reflux becomes commonplace, hence GERD (Taylor, 2012).
Some of the patient factors that could impact the pathophysiology of gastritis, PUD, and GERD include, but they are not limited to behavior, age, ethnicity, gender, and genetics. These have been highlighted in the table below.
Condition
Patient Factor
Gastritis
Behavior – excessive alcohol use.
Excessive alcohol consumption is associated with mucosal lining erosion
PUD
Age – older adults
Older adults are more likely to take osteoarthritis medications or other pain medications, i.e. NSAIDs that could either inflame or irritate the stomach lining.
GERD
Behavior – obesity
Obese persons tend to have increased abdominal pressure.
Some of the symptoms of Gastritis include, but they are not limited to, appetite loss, indigestion, vomiting, abdominal pain as well as bloating, and recurrent stomach upsets and nausea (Taylor, 2012). For a patient who takes excessive alcohol, I would recommend moderate intake of alcohol or cessation of the same thereof. Next, to reduce stomach acid, I would recommend H-2 blockers or proton pump inhibitors. With regard to PUD, some of the symptoms I would be looking out for include nausea, heartburn, belching and bloating, intolerance to fatty foods, as well as stomach pain. For an older adult taking osteoarthritis medication or other pain medications, I would look into prescribing the lowest possible dose of existing medications; or recommend that they instead take COX-2 inhibitors. Further, I would recommend an acid blocker. Lastly, some of the symptoms of GERD, as Pooler (2009) points out, include a lump sensation in the throat, sour liquid or food regurgitation, and chest pains accompanied by a burning sensation. For a patient who is obese, I would recommend that they cut weight by engaging in exercises and/or looking into their diet. Further, I would prescribe lansoprazole (Prevacid) which is essentially a proton pump inhibitor.
References
Lascelles, P.T. & Donaldson, D. (2012). Diagnostic Function Tests in Chemical Pathology. Boston: Kluwer Academic Publishers.
Pooler, C. (2009). Porth Pathophysiology: Concepts of Altered Health States. New York, NY: Lippincott Williams & Wilkins
Ramsay, P.T. & Carr, A. (2011). Gastric Acid and Digestive Physiology. The Surgical Clinics of North America, 91(5), 977-82.
Taylor, R.B. (Ed.). (2012). Fundamentals of Family Medicine. New York, NY: Springer.