Essay Example on Gastrointestinal Tract: Functions and Disorders

Introduction

The gastrointestinal tract is composed of different parts which are the mouth, esophagus, stomach, small intestine, colon, anus and other tissues that aid in food digestion. Also, the GI tract is the food ingestion pathway (Elseweidy, 2017). The whole tract is responsible for food ingestion, digestion, absorption, and excretion. Inflammation or ulceration of the GI can disrupt the secretion, motility, and absorption (Carabotti, Lahner, Esposito, Sacchi, Severi & Annibale, 2017). Therefore the advanced nurse practitioners should understand the common disorders for the GI like gastroesophageal reflux disease, gastritis, and peptic ulcer disease.

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Normal Pathophysiology of Gastric Acid Stimulation and Production

Stimulation and inhibition of gastric acid production are due to some factors which can be divided into different phases which are a gastric phase, intestinal phase and cephalic phase (Hunt & Yuan, 2011). The production and secretion of the gastric acid occurs in the cells and glands within the apical surface or mucosa of the epithelial cells in the GI tract (Elseweidy, 2017). hydrochloric acid or the gastric acid is produced from H+-K+ ATPase active transport system that carries hydrogen and chloride ions out of parietal cells while moving the potassium ions into the cells. The stimulation of the hydrochloric acid production and secretion is as a result of three crucial pathways G-cells, enterochromaffin-like (ECL) cells, and release of acetylcholine from the parasympathetic nervous system (Elseweidy, 2017). Histamine which is secreted by ECL is then bound to the H2 receptors on parietal cells thus stimulating the H+-K+ ATPase pump that is used in HCL secretion (Huether et al., 2018). The other pathway is where the G-cells secret the peptide hormone gastrin. The gastrin receptors are bound to the gastrin on the ECL cells which stimulates the histamine release and the binding of gastrin to gastrin receptors on parietal cells. That boosts the H+-K+ ATPase pump to secrete HCL ((Elseweidy, 2017).

The other pathway is where the cephalic phase of digestion stimulates the acetylcholine secretion from the vagus nerve. Then the release of histamine from the ECL is excited by the already secreted acetylcholine. Acetylcholine also stimulates the gastrin-releasing peptide thus leading to gastrin release but inhibits the release of somatostatins (Huether et al., 2018). Somatostatin is produced by the D cells, and they inhibit the production of gastric acid. The inhibition of gastric acid production by somatostatin is due to its hindrance of the gastrin production from the G cells and the histamine from ECL cells. When the acetylcholine binds to the muscarinic receptors on the parietal cells, it stimulates the HCL production (Huether, McCance, El-Hussein, Power-Kean & Zettel, 2018).

Gastroesophageal Reflux Disease (GERD)

GERD is the upward flow or backward flow of stomach contents into the esophagus thus leading to inflammation of the esophagus or esophagitis (Huether et al., 2018). The signs and symptoms of GERD are cough, regurgitation, dysphagia, laryngitis, epigastric pain pyrolysis (Huether et al., 2018). The behavioral risk factors in GERD are smoking, alcoholism and obesity (Talalwah & Woodward, 2013). Esophagitis in GERD is dependent on the exposure time of mucosa to refluxate of chyme like enzymes, bile salts, and acids. The diagnosis of GERD is made from the history, pH monitor, tissues biopsy and clinical manifestation (Hunt & Yuan, 2011). Treatment is done using proton pump inhibitors, antacids, and H2-receptor blockers. Also, alternating behavioral factors can also be used in GERD treatment. Patient education on changing the lifestyle are the first interventions in relieving the intense symptoms in GERD (Talalwah & Woodward, 2013). If GERD persists, there is a likelihood of peptic ulcer disease with lesion coming up.

Peptic Ulcer Disease

PUD is the ulceration or erosion of the esophagus, stomach or duodenum where it mostly occurs. The ulcers are due to an imbalance of the protective secretions with the acid. The lesions may extend deeper into several layers damaging the blood vessels and the GI tract wall (Huether et al., 2018). The prevalence of PUD in the United States in 2011 was 15.5 million, and the risk factors are H. pylori infection, blood group O, advanced age and chronic diseases. Behavioral factors for PUD are smoking, obesity, smoking, and alcoholism among others (Lanas & Chan, 2017). Prostaglandins are essential in a negative feedback loop in HCL production inhibition. Diagnosis can be done through tissue biopsy, stool samples, urea breath test, medical history, and endoscopic evaluation. PUD management is done using antacids, proton pump inhibitors, H2 receptor blockers and using surgical resection of ulcers (Mayo Clinic, n.d.). Behavioral modification can also be used in PUD management.

Gastritis

Gastritis is observed in PUD and GERD and is less than 1% prevalent. However, it is prevalent in older adults. Similar pathophysiology in gastritis happens with NSAID use of drug. The behavioral factors are alcoholism, smoking, STDs and beverage intake. Clinical manifestation is nausea, vomiting, fullness, hiccup, indigestion an loss of appetite (Mohammad, Mohammad, Hamadan, Ahmed & Mohammad, 2016). Diagnosis is made using medical history, blood, and stool test, X-rays, upper GI endoscopy and physical examination. Treatment is done using; proton pump inhibitors, antacids, avoiding NSAIDS, H2-receptor blockers, and modifying lifestyle (Rath-Wolfson, Varona, Bubis, Tatarov, Koren & Ram, 2017).

References

Carabotti, M., Lahner, E., Esposito, G., Sacchi, M. C., Severi, C., & Annibale, B. (2017). Upper gastrointestinal symptoms in autoimmune gastritis: A cross-sectional study. Medicine, 96(1).

Elseweidy, M. M. (2017). Brief Review on the Causes, Diagnosis and Therapeutic Treatment of Gastritis Disease. Altern Integr Med, 6(231)

Huether, S. E., McCance, K. L., El-Hussein, M. T., Power-Kean, K., & Zettel, S. (2018). Understanding Pathophysiology, Canadian Edition-E-Book. Elsevier Health Sciences.Hunt, R. H., & Yuan, Y. (2011). Acid-NSAID/aspirin interaction in peptic ulcer disease. Digestive Diseases, 29(5), 465-468.

Katz, P. O., Gerson, L. B., & Vela, M. F. (2013). Guidelines for the diagnosis and management of gastroesophageal reflux disease. The American journal of gastroenterology, 108(3), 308.Lanas, A., & Chan, F. K. (2017). Peptic ulcer disease. The Lancet, 390(10094), 613-624.

Mayo Clinic. (n.d.). Peptic ulcer. Retrieved from http://www.mayoclinic.org/diseases-conditions/peptic-ulcer/home/ovc-20231363

Mohammad Makki, A., Mohammad Aldaqal, S., Hamadan Alorabi, S., Ahmed Nemri, I., & Mohammad Alajami, M. (2016). Chronic Gastritis in Morbidly Obese Patients with Sleeve Gastrectomy. Electronic Physician, 8(1), 1786-1790. doi: 10.19082/1786

Rath-Wolfson, L., Varona, R., Bubis, G., Tatarov, A., Koren, R., & Ram, E. (2017). Gastritis in patients undergoing sleeve gastrectomy. Medicine, 96(16), e6602. doi: 10.1097/md.0000000000006602

Talalwah, N. A., & Woodward, S. (2013). Gastro-oesophageal reflux. Part 1: smoking and alcohol reduction. British Journal of Nursing, 22(3), 140-146.