Interfering with the production of the mucosal layer of the gastrointestinal tract causes gastric disorders, including peptic ulcer disease and gastroesophageal reflux disease, where helicobacter pylori infection and non-steroidal anti-inflammatory drugs interfere with mucosal membranes. H. pylori infection causes tears on the mucosal membrane, presented as ulcers and inflammation. Non-steroidal anti-inflammatory drugs affect the mucosal membrane through topical and systematic actions causing ulcers and inflammation (Fokunang et al., 2018). These drugs block cyclooxygenase enzyme action to inhibit prostaglandin production and suppress blood flow, mucus secretion, production of hydrogen carbonate, and cell repair and replication, all in the gastrointestinal tract. The drugs contain low pH and are non-ionized in gastric acid, hence easy diffusion across the tract’s walls and into the epithelial cells.
The pathophysiology of peptic ulcer disease and gastroesophageal reflux disease can be impacted by age, where in children, it is notable that they have an anti-reflux barrier whose function is to ensure frequent relaxations and retrograde flow of gastric contents into the esophageal sphincter barrier existing between the esophagus and stomach is impaired as a factor of age and immaturity among children (Khan & Orenstein, 2018). This condition is caused by the lower esophageal sphincter’s incompetence or relaxation. Peptic ulcer disease causes crucial morbidity and mortality in the elderly, frequently presents atypically, and is associated with high complications. The ubiquity of helicobacter pylori increases with age and can be essential in developing ulcers. It is clear that age impacts the pathophysiology of GERD, PUD, and gastritis as it affects children, and GERD is expected in the elderly.
As it is clear that the gastroduodenal contents, including gastric acid, bile acids, and trypsin, easily corrode the gastrointestinal tract walls. This situation worsens even as the corrosion increases and the naturally occurring defenses such as acid clearance and mucosal resistance are ineffective. The acid defense mechanism accompanies it breaks down further. The treatment of gastritis can be of three categories, the first one is that a lifestyle change is necessary to avoid acidic foods and sleep in the proper posture. For example, fatty acids should be removed from the diet since they are precipitating foods, and the head should be elevated when sleeping (Hindiyeh et al., 2020). The second treatment may involve the patient taking prescribed medication that reduces acid secretion and exposure, including proton pump inhibitors and histamine-2 receptor antagonists. The third and final treatment would involve surgery to repair the anti-reflux barrier. Getting an early diagnosis of the disorders is essential for easy treatments.
The physiology of the stimulation and the production of gastric acid is complex and takes place through several stages. Motility disorders are abnormal muscle and nerve contractions causing spasms or lack of motion anywhere along one’s gastrointestinal tract. The alteration of the physiology of gastric acid initiates the pathophysiology of peptic ulcer disease and gastroesophageal reflux disease and gastritis, where age plays a critical role in the development of gastritis and therefore the epidemiology, diagnosis, and treatment is critically affected by the influence of age on gastritis.
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