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1: Gastrointestinal Tract: Disorders of Motility Jamie is a 3-month-old female who presents with her mother for evaluation of “throwing up.†Mom reports that Jamie has been throwing up pretty much all the time since she was born. Jamie does not seem to be sick. In fact, she drinks her formula vigorously and often acts hungry. Jamie has normal soft brown bowel movements every day and, overall, seems like a happy and contented baby. She smiles readily and does not cry often. Other than the fact that she often throws up after drinking a bottle, she seems to be a very healthy, happy infant. A more precise history suggests that Jamie does not exactly throw up—she does not heave or act unwell—but rather it just seems that almost every time she drinks a bottle she regurgitates a milky substance. Mom thought that she might be allergic to her formula and switched her to a hypoallergenic formula. It didn’t appear to help at all, and now Mom is very concerned. Cases like these are not uncommon. The mother was concerned and thinking her daughter may have an allergy; she changed to a different formula. However, sometimes babies have immature GI tracts that can lead to physiology reflux as they adapt to normal life outside the uterus. Parents often do not consider this possibility, prompting them to change formulas rather than seeking medical care. As in the case study above, GI alterations can often be difficult to identify because many cause similar symptoms. This same issue also arises with adults—adults may present with symptoms that have various potential causes. When evaluating patients, it is important for the advanced practice nurse to know the types of questions he or she needs to ask to obtain the appropriate information for diagnosis. For this reason, you must have an understanding of common GI disorders such as gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and gastritis. To Prepare Review this week’s media presentation on the gastrointestinal system. Review Chapter 35 in the Huether and McCance text. Identify the normal pathophysiology of gastric acid stimulation and production. Review Chapter 37 in the Huether and McCance text. Consider the pathophysiology of gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and gastritis. Think about how these disorders are similar and different. Select a patient factor different from the one you selected in this week’s Discussion: genetics, gender, ethnicity, age, or behavior. Consider how the factor you selected might impact the pathophysiology of GERD, PUD, and gastritis. Reflect on how you would diagnose and prescribe treatment of these disorders for a patient based on this factor. Review the “Mind Maps—Dementia, Endocarditis, and Gastro-oesophageal Reflux Disease (GERD)†media in the Week 2 Learning Resources. Use the examples in the media as a guide to construct a mind map for gastritis. Consider the epidemiology and clinical presentation of gastritis. To Complete Write a 2- to 3-page paper that addresses the following: Describe the normal pathophysiology of gastric acid stimulation and production. Explain the changes that occur to gastric acid stimulation and production with GERD, PUD, and gastritis disorders. Explain how the factor you selected might impact the pathophysiology of GERD, PUD, and gastritis. Describe how you would diagnose and prescribe treatment of these disorders for a patient based on the factor you selected. Construct a mind map for gastritis. Include the epidemiology, pathophysiology, and clinical presentation, as well as the diagnosis and treatment you explained in your paper.
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| Subject | Nursing | Pages | 8 | Style | APA |
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Answer
Gastrointestinal Tract: Disorders
Gastro-esophageal Reflux Disease
Gastro-esophageal reflux disease (GERD) or heartburn is characterized by cardinal symptoms including regurgitation and troublesome heart (MacFarlane, 2018). Barrett’s esophagus is characterized by damage or depletion of lower esophageal cells due to repeated stomach acid exposure (Lifespan, 2013). Risk factors include pregnancy, eating habits, large meals, bending forward, peptic ulcers, hiatal hernia, insufficient digestive enzymes, smoking, alcohol, and asthma (Lifespan, 2013). Other risk factors include diabetes, genetics, high-fat diet, and some medications (MacFarlane, 2018). Age is a determinant factor for development of GERD since the disease is most common among young people (pediatrics and adolescents). Obesity as well as dietary must be addressed among the young (MacFarlane, 2018). Age will determine the dosage for omeprazole, which is used as a proton pump inhibitor to prevent further production of acid, thus, reducing the risk of esophageal cancer (Lifespan, 2013).
Peptic Ulcer
Gastric or peptic ulcers are open sores in the stomach lining that are closely associated with gastritis (Huether & McCance, 2017). Individuals with a history of Helicobacter pylori infection stand at a 10% to 20% risk of developing peptic ulcer disease. As such, about 90 to 100% of patients diagnosed with duodenal ulcer have H. pylori. H. pylori induce gastritis, which progresses to mucosa ulcerations. Epithelial cells undergo the process of apoptosis, comprises the mucosal protective barrier, which exposes the gastric mucosa to pepsin and luminal acid. Impairment of the fibrinolytic activity and occlusion of mucosal end-arteries accounts for the focal nature of peptic ulcers (Jemilohun & Otegbayo, 2016). On the other hand, ingestion of non-steroidal anti-inflammatory drugs increases the risk of the disease (Huether & McCance, 2017; Jemilohun & Otegbayo, 2016). Patients who present with duodenal ulcers tend to secrete twice as much acid compared to controls; since they tend to possess double number of parietal cells. As opposed to gastritis whereby there may be absence of acid, there is hyper-secretion of acid in patients with duodenal ulcers due to H. pylori infection. Antral gastritis leads to reduction of antral somastatin-producing cells resulting in reduced impact on somastatin-mediated inhibition G cells to secrete gastric acid leading to development of hypergastrinemia (Jemilohun & Otegbayo, 2016).
Age is a risk factor in development of peptic ulcers. Young-people especially young children experience a greater risk of H. pylori infection. The infection leads to gastritis and hence development of peptic ulcers (Sipponen & Maaroos, 2015). As such, young people and children diagnosed of peptic ulcers should also be screened for H. pylori infection. Besides, the age the patient will determine drug dosage.
Gastritis
Gastritis is a chronic inflammation of the stomach mucosa caused by an infection or can be autoimmune in origin. H. pylori infection is the major cause of gastritis. The disease can present as an atrophic or non-atrophic condition of the stomach mucosa. Gastritis is described as an aggressive life-long disease (if not treated) the leads to destruction of mucosa lining of the stomach or atrophic gastritis. It can lead to loss of the normal mucosal glands in corpus, fundus, and/or antrum (Sipponen & Maaroos, 2015). Worsening for atrophic gastritis with time contributes to stomach mucosa dysfunction. Dysfunction is characterized by acid-free stomach in worst case scenarios. Worsening for atrophic gastritis with time contributes to stomach mucosa dysfunction. Dysfunction is characterized by acid-free stomach in worst case scenarios (Huether & McCance, 2017). Acid-free stomach and atrophic gastritis increases the risk of gastric cancer and peptic ulcer. On the other hand, acid-free stomach is associated with failure in absorption of vitamin B12 (i.e. on the essential vitamins) and micronutrients such as zinc, iron, magnesium, and calcium. Besides, a patient may not absorb medicines as well as digest and absorb diet very well (Sipponen & Maaroos, 2015).
Age is a key risk factor playing a role in prevalence and pathophysiology of gastritis. H. pylori infection during childhood years is associated with development of gastritis. As such, treatment plan upon diagnosis of gastritis in young children should focus on elimination of H. pylori infection. Comparatively, the prevalence rate of the disease tends to rise by age (Sipponen & Maaroos, 2015). Besides, age of the patient will be important when determining prescription dosage of specific medication to be used.
Mind Map
Figure 1: Mind-Map – Gastritis
References
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Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby. Jemilohun, A.C., & Otegbayo, J.A. (2016). Helicobacter pylori infection: past, present and future. The Pan African Medical Journal, 23, 216. DOI:10.11604/pamj.2016.23.216.8852. Lifespan. (Oct 7, 2013). Pathway uncovered linking heartburn, esophageal cancer. ScienceDaily. Retrieved on Oct 14, 2018 from, www.sciencedaily.com/releases/2013/10/131007151833.htm MacFarlane, B. (2018). Management of gastroesophageal reflux disease in adults: a pharmacist’s perspective. Integr Pharm Res Pract. 7, 41-52. DOI: 10.2147/IPRP.S142932. Sipponen, P., & Maaroos, H-I. (2015). Chronic gastritis. Scand J Gastroenterol., 50(6), 657-667.
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