The gastric acid produced in the stomach is an acid that aids in digestion and made of potassium chloride, hydrochloric acid and sodium chloride. The role of this acid in the stomach is significant and includes the activation of digestive enzymes for protein breakdown ( Rees et al., 2019) . To aid in this digestion, gastric secretion involves the cephalic phase stimulated by smell, taste and even thought of food; gastric phase stimulated by stomach wall distension; and intestinal phase stimulated by histamine and proteins which involves different stimuli that allow for the release of gastric acid by stomach walls.
The process of eating or gastric distension stimulates the production of gastrin and pancreatic pathways involving ghrelin, histamine and somatostatin, and the effects of neurotransmitters including acetylcholine and chemicals in food including proteins and ethanol (Huether & McCane, 2017). The products of gastric secretion include enzymes, mucus, hormones and intrinsic factors. While some products such as mucus and acids are released into the gut, others such as hormones are released into the blood stream.
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The rate and composition of gastric production varies depending on volume and time of the day. In the morning, the rate of production is low while it increases in the evening and mornings. Un pleasant odors and tastes and somatostatin inhibit the gastric production (Huether & McCane, 2017). On the other hand aggression and hostility may increase gastric secretion and comes along with pathology of the gastric. Consequently, stress and other psychological factors play a role in the pathology of the gastric.
GERD is mainly related with the transient lower esophageal sphincter relaxations (TLESRs). This is a failure in the effectiveness of the esophageal sphincter to maintain a proper tone resulting into acid reflux in the patient. Other factors that may contribute to GERD include the reduction in the lower esophageal sphincter, impaired clearance of the esophageal and slow gastric emptying.
PUD involves the development of sores on the upper potion of the small intestines. Bacteria infection, mainly, H. Pylori and extensive use of aspirin and NSAIDs are the common causes of the disease. When they become extreme, peptic ulcers may cause obstruction of food in food passages and result into reflux in a patient ( Rees et al., 2019) . This explains the removal of food in the people with PUD.
Apart from peptic ulcers, bacteria infection may cause gastritis when chronic. The bacterial cause the inflammation of the gastric mucosa. This inflammation interferes with the normal gastric secretion which may increase to result in excesses. The high rate of gastrin production is related with reflux.
Effects of Age
Research indicate an increase in the prevalence of GERD, PUD and gastritis with age. One factor that may increases an individual’s susceptibility to gastric pathology with age is partial atrophy of gastric glands ( Genta & Turner, 2017) . Also, increase in age increases the potential of impacts of predisposing factors to these three diseases including accumulation of the effects of NSAIDS. Also, there is reduced therapeutic efficacy of most ulcer healing drugs with age that means that one becomes more prone to reflux as they get old.
One disorder which the three year old might have high predisposition due to young age is GERD. The development of the esophageal sphincter takes some time to fully and effectively function. Consequently, at this age, the child might not have a fully developed and fictional esophageal sphincter to prevent stomach content from reflux.
On the other hand, age of the patient works to reduce their susceptibility to PUD and gastritis. PUD and gastritis are common among the elderly due to their continuous exposure to predisposing factors including stress and bacteria ( Genta & Turner, 2017) . In terms of bacterial causes, being of young age means that the patient’s immune system is not fully developed to fight bacteria which may increase their proliferation.
Based on the patient’s age, the treatment of the patient would be changes in dietary practices. Proper feeding of the child while holding her in up-right position, elevating the head and thickening on feed with cereal will help reduce throwing up. The baby should be fed on smaller amounts of foods frequently.
In the case of PUD, the child should be put on antibiotics and antacids for about two weeks. Antibiotics are meant for the treatment of any bacterial infections while anti-acids lower the stomach acidity. For gastritis, a similar regime should be followed and monitoring to avoid extreme drug reactions.
References
Genta, R. M., & Turner, K. (2017). Peptic Ulcer Disease and Non-Ulcer Dyspepsia: The Most Predictive Clinical Manifestations of Helicobacter Pylori Gastritis. Gastroenterology , 152 (5), S246.
Huether, S. E., & McCance, K. L. (2017). Understanding Pathophysiology-E-Book .(6 th ed. ) Elsevier Health Sciences.
Rees, C. J., Pollack Jr, C. V., & Riese, V. G. (2019). Peptic Ulcer Disease. In Differential Diagnosis of Cardiopulmonary Disease (pp. 769-778). Springer, Cham.
