Most gastrointestinal tract (GIT) conditions present with similar symptoms and signs. This makes it difficult for clinicians to differentiate, identify, and diagnose the exact disorders. According to Huethe and McCance (2017), the presence of ulcerative or inflammatory disorders may lead to disruption of the normal GI motility, secretion, and nutrients absorption. As a result, healthcare providers especially nurses must understand commonly occurring GI conditions such as gastritis, gastroesophageal reflux disease (GERD), and peptic ulcer disease (PUD). Here, the following will be covered: the simulation and production of gastric acid under normal pathophysiology, the effects of the above GIT conditions on the simulation and production of the acid, how gender affects the pathophysiology of the conditions and how they are diagnosed and treated. The paper will be concluded with gastritis’ mind map.
Normal Pathophysiology of Gastric Acid (GA) Stimulation and Production
As per Huether and McCance (2017), GA production is controlled via various stimulatory and inhibitory factors, and it occurs in 3 phases namely; cephalic stage, gastric stage, and intestinal stage. The stimulatory factors include foods such as protein, ethanol, and coffee. Others are hormonal factors, and they include histamine, gastrin, paracrine, ghrelin, and somatostatin (Huether and McCance, 2017). The acid is produced by the epithelial cells and/or glands present in the gastrointestinal lumen. It is synthesized by parietal cells following activation by histamine- a product of enterochromaffin-like (ECL) cells (Huether, & McCance, 2017). The acid finds its way from parietal cells to the GI tract through tiny channels located on the mucous layer (Huether and McCance, 2017). Presence of gastric acid in the stomach provides an acidic PH which helps in killing pathogens as well as providing optimum PH for pepsin enzyme which digests protein.
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Gastroesophageal Reflux Disease
There are a number of changes that are experienced in GA simulation/production with gastroesophageal reflux disease (GERD). These include the relaxation of the lower esophageal sphincter, slowing of esophageal/gastric motility, and gastric emptying delay (Hunt & Yuan, 2016). The other change that occurs is the esophagitis and its severity dependends on the length of the time in which the upper GI is exposed to the chime. The chime/refluxate may cause inflammation and injury to gastrointestinal mucosa and may present as erosion, edema, increased permeability of blood capillary, hyperemia, increased tissue fragility, and in long-term exposure fibrosis may occur which may cause lesions and thickening of the mucosa which interferes with the normal gastric acid secretion (Huether, & McCance, 2017). The disorder is diagnosed by use of clinical presentations, PH monitoring, patient history, and tissue biopsy. Antacids, H2-receptor blockers, and proton pump inhibitors may be used to treat GERD which is more common in males than in females.
Peptic Ulcer Disease
In PUD, the urease enzyme is produced by H.pylori, and the enzyme neutralizes the acidic conditions within the GIT lumen that comes as a result of gastric acid (Huether and McCance, 2017). The enzyme facilitates the production of ammonia which increases the PH of the stomach lumen. This through positive feedback mechanisms leads to increased secretion/production of gastric acid.
Huether and McCance (2017) stated that this disorder is diagnosed using stool tests, medical history assessment, tissue biopsy, urea breath test, physical examination, and endoscopic evaluation. According to Talawah and Woodward (2015), treatment of PUD targets the causes and prevention of associated complications using antibiotics, H2 receptor blockers, antacids, proton pump inhibitors, and resection of ulcers through surgery. The condition can also be managed through behavioral and lifestyle changes such as improved sleeping habit, avoiding smoking and alcohol, and diet modification. Just like GERD, the prevalence of PUD in males is higher than in females.
Gastritis
With gastritis, the resultant inflammation lumen of the stomach causes decreased gastric acid simulation and thus reduced production. Assessing medical history, Physical examination, upper GI endoscopy, X-rays, stool and blood tests are some of the diagnostic methods employed to diagnose the disorder. For acute gastritis which heals spontaneously, no treatment is required except for behavioral modifications such as avoidance of injurious drugs, acidic drinks, and smoking (Huether, & McCance, 2017). Huether and McCance (2017) have antacids, H2-receptor antagonists, and proton pump inhibitors as the therapy options available for this disorder especially for those with chronic gastritis. Antibiotics can be given to treat the underlying cause. There is an increased risk of one developing PUD in Male patients’ with gastritis.
References
Hammer, G. D.,& McPhee, S. J. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7 th ed.). China: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Hunt, R. H., & Yuan, Y. (2016). Acid-NSAID/aspirin interaction in peptic ulcer disease. Digestive Diseases (Basel, Switzerland) , 29 (5), 465-468. doi:10.1159/000332211
Mayo Clinic. (n.d.). Peptic ulcer . Retrieved from http://www.mayoclinic.org/diseases-conditions/peptic-ulcer/home/ovc-20231363
Talawah, N. A., & Woodward, S. (2015). Gastro-oesophageal reflux. Part 1: smoking and alcohol reduction. British Journal Of Nursing , 22 (3), 140-145.
University of Maryland Medical Center. (n.d.). Gastritis . Retrieved from http://www.umm.edu/health/medical/altmed/condition/gastritis
