Gastrointestinal Tract Disorders of Motility

The Normal Pathophysiology of Gastric Acid Stimulation and Production
In the words of Phan, Benhammou, and Pisegna (2015), “gastric acid secretion by parietal cells occurs in the fundus of the stomach, and is intricately regulated by various neuronal (vagal), paracrine (histamine, somatostatin) and hormonal factors” (387). As the authors further point out, there are two key phases in gastric acid secretion. These are the cephalic phase and the gastric phases. While the former takes place as a consequence of neurological signals and prior to the entry of food in the stomach, the latter phase could be conceptualized as the period involving the activation of gastric activity in the stomach after food is swallowed. More specifically, gastric secretion in the cephalic phase is the result of several factors including, but not limited to the smell, thought or taste of food. Thus, it follows that this is largely a conditioned reflex. Its occurrence is based on our wanting or liking of food. In essence this particular reflex could be inhibited as a result of depressed appetite. When the cerebral cortex is stimulated by the desire for food (smell, sight, or thought), messages are sent to the stomach, parasympathetic nervous system, the medulla and the hypothalamus by the cerebral cortex. Gastric juice is secreted by the gastric glands. Following the entry of food into the stomach, stretch receptors are activated as the stomach stretches. Additional gastric juice is in this case secreted following the receipt of a message by the medulla (from the stretch receptors). In essence, the gastric phase commences following the activation of gastric activity. It is important to note that gastric activity could be stimulated in two ways by the ingested food, i.e. stomach stretching (as has partially been highlighted above) and via increased PH.
According to Krause, Malagelda, and Preuschoff (2005), there are three chemicals that are involved in the stimulation of gastric secretion. These are: gastrin, histamine, and acetylcholine. It is these three chemicals that trigger the secretion of hydrochloric acid through the stimulation of parietal cells. It should be noted that in reaction to gastrin, pepsinogen is secreted by the chief cells. Gastrin is secreted (by the G cells) in even larger quantities following the breakdown of dietary protein into amino acids and peptides. This helps speed up the digestion of proteins.
GERD, PUD, and Gastritis
There are several distinct mechanisms that protect the GI mucosa. In the words of Lacy, Crowell, and DiBaise (2014), “factors that interfere with mucosal defenses predispose to gastritis and peptic ulcer disease” (118).
GERD
In basic terms, GERD is inclusive of the various consequences of acid reflux into the esophagus (from the stomach). It should be noted that as Lacy, Crowell, and DiBaise (2014) observe, this is often a consequence of failure by antireflux barriers such as lower esophageal sphincter (LES). LES could be conceptualized as a valve. However, Krause, Malagelda, and Preuschoff (2005) are of the opinion that GERD ought to be envisioned as the consequence of abnormalities in a system that involves the stomach, LES, and esophagus. While acidic material clearance could be decreased by what the authors refer to as poor esophageal motility, stomach pressure volume could increase significantly as a result of gastric emptying delay. This results in the defeat of the valve mechanism. The role of LES has further been highlighted above. GERD severity, as Lacy, Crowell, and DiBaise (2014) point out, “increases progressively with reflux that is mainly in the postprandial period to that in the upright posture, to that in the supine or that is bipositional reflux” (174).
PUD
Peptic ulcers are characterized by lesions which largely occur as a consequence of the mucosal lining inability to hold against gastric juice’s acidic properties. There are many factors that are responsible for this phenomenon. These include, but they are not limited to prolonged utilization of NSAIDs and infection with H. pylori. Krause, Malagelda, and Preuschoff (2005) note that in addition to mucosal defense issues, PUD could also result from excessive gastric acid secretion. The authors appear to treat the two as distinct causes.
Gastritis (Acute Gastritis)
According to Braun and Anderson (2007), “acute gastritis is a group of disorders that cause inflammatory changes in the gastric (stomach) mucosa. As the authors further point out, the gastric mucosa could be inflamed by a wide range of factors including, but not limited to, the ingestion of alcohol or chemicals (i.e. aspirin). The vulnerability of the mucosa to stomach contents that are acidic could result from gastric mucosa production inhibition. The said inhibition could be as a consequence of gastric toxins exposure. According to Braun and Anderson (2007), “poor gastric perfusion, as can occur with shock or sepsis, is also implicated in acute gastritis” (59).
GERD, PUD, and Gastritis: The Age Factor
There are various patient factors that impact the pathophysiology of gastritis, PUD, and GERD. To begin with, when it comes to GERD, age appears to be a key factor in as far as its pathophysiology is concerned. Various studies have confirmed this assertion. In one such study, Wantabe, Urita, Sugimoto, and Miki (2007) observe that “although GERD symptoms are common in adults of all ages, the prevalence of GERD was highest in the 20-29 years age group and the age group 70-79 years had the lowest prevalence for both males and females” (4220). In seeking to reduce GERD, I would recommend a reduction in consumption of foods that increase the probability of reflux. For a young person, such foods would be inclusive of carbonated beverages, fried foods and chocolate. When it comes to PUD, Lee, Sung, Kim, Lee, Park, and Shim (2016) point out that past studies have indicated that there could be a strong association between peptic ulcer diseases and old age. For this reason, in as far as treatment of PUD is concerned, I would discourage the utilization of NSAIDs and investigate long-term exposure to pain relievers. Lastly, when it comes to gastritis, Lacy, Crowell, and DiBaise (2014) observe that in comparison to young adults, older adults appear to be at an increased risk. In this case, I would encourage some lifestyle adaptations – such as salt consumption reduction and avoidance of spicy foods.
References
Braun, C.A. & Anderson, C.M. (2007). Pathophysiology: Functional Alterations in Human Health. New York, NY: Lippincott Williams & Wilkins.
Krause, G., Malagelda, J.R. & Preuschoff, U. (2005). Functional Disorders of the Gastrointestinal Tract. Washington, DC: IOS Press.
Lacy, B.E., Crowell, M.D. & DiBaise, J.K. (2014). Functional and Motility Disorders of the Gastrointestinal Tract: A Case Study Approach. New York, NY: Springer.
Lee, S.P., Sung, I. Kim, J.H., Lee, S., Park, H.S. & Shim, C.S. (2016). Risk Factors for the Presence of Symptoms in Peptic Ulcer Disease. Clin Endosc., 50(8), 578-584.
Phan, J., Benhammou, J.N. & Pisegna, J.R. (2015). Gastric Hypersecretory States: Investigation and Management. Curr Treat Options Gastroenterol., 13(4), 386-397.
Wantabe, T., Urita, Y., Sugimoto, M. & Miki, K. (2007). Gastro-esophageal reflux disease symptoms are more common in general practice in Japan. World J Gastroenterol., 13(31), 4219-4223.