Nursing case study

Case study 3.1

1) What anatomic problem most likely leads to gastroesophageal reflux?

Gastroesophageal reflux disease (GERD) is the abnormal reflux of gastric contents back up into the esophagus, and is frequently found in those with regurgitation and heartburn issues (Badillo & Francis, 2016). Therefore, it is likely that the anatomic problem that causes GERD is an abnormally high production of gastric juices, or the body not being able to properly digest and empty gastric juices quickly enough (Scott & Gelhot, 1999). This anatomic problem could be an issue with the sphincter in the lower esophagus. For example, if there is a pressure abnormality or transient sphincter relaxation, this can lead to the reflux of gastric juices in the esophagus (DeGiorgi, Palmiero, Esposito, Moscow, & Cuomo, 2006). In a normally functioning esophagus, the sphincter works with the diaphragm, creating a barrier that does not allow for gastric juices to enter the esophagus (Scott & Gelhot, 1999). However, if a sphincter is relaxing at inappropriate times, this can lead to the abnormal reflux that characterizes GERD (Scott & Gelhot, 1999).

2) What is the injury in gastroesophageal reflux?

Ongoing reflux injury triggers hyperplasia, which is an increase in the number of cells being produced (Braun & Anderson, 2017). Hyperplasia is triggered in GERD because as the reflux is consistently happening, it is killing surface esophageal cells (Souza, 2012). This creates a need for more cells quickly to promote tissue healing, which explains why hyperplasia occurs. Hyperplasia and hypertrophy, or increase in cell size, go hand in hand, making hypertrophy likely to happen with GERD as well (Braun & Anderson, 2017). Hyperplasia and hypertrophy are examples of the body’s response/adaptation to stress. The overproduction and enlargement of cell size can to inflammation if uncontrolled, which is a symptom of GERD (Braun & Anderson, 2017). Additionally, when surface esophageal cells die, the tight junctions between the cells are dilated, weakening the epithelial barrier (Souza, 2012). This is what allows acid and pepsin to penetrate deeper and cause greater injury, leading to chronic GERD symptoms, such as heartburn (Souza, 2012).

3) What would the acute inflammatory response look like?

The acute inflammatory response is triggered by the tissue injury incurred in GERD, the hyperplasia described above. The first step in the acute inflammatory response is increasing blood flow to the esophageal area (Braun & Anderson, 2017). Next, the cellular response is triggered, in which the products of healing are alerted to move towards the esophageal area (Braun & Anderson, 2017). At this point, the injured tissue is removed, and formation of new tissue can begin (Braun & Anderson, 2017). Specifically, in the case of GERD, neutrophils infiltrate the esophageal area to prompt healing and repair tissue (Souza, 2012). Hyperplasia in the basal cells commences to replace cells that were killed by the reflux of acid (Souza, 2012).

4) Why might this condition become a chronic problem?

GERD can occur as often as once an hour (Scott & Gelhot, 1999). When occurring this frequently, this constant regurgitation can lead to the epithelial cells in the esophagus being worn down and dying at an abnormally fast rate (DiGiorgi, et al, 2006). If the relaxation issue with the sphincter or pressure abnormality is not resolved, this could lead to recurring reflux issues. Additionally, if epithelial cells are not replaced in a timely manner, acid and pepsin will continue to penetrate this barrier and cause greater damage. When left untreated, the damage will become more severe, and could even result in ulcers (DiGiorgi, et al., 2006).

5) What pathophysiologic changes would most likely occur with chronic gastroesophageal reflux?

GERD can lead to a development of esophagitis (inflammation of the esophagus) (Scott & Gelhot, 1999). Inflammation leads to vasodilation at the site of injury and the release of inflammatory mediators (Braun & Anderson, 2017). Inflammatory mediators help with increasing vascular permeability, promoting clotting factors, initiating phagocytosis, and repairing injured tissue by promoting new cellular generation (Braun & Anderson, 2017). Inflammation can also lead to pyrexia, or an elevated body temperature, which can manifest as a fever (Braun & Anderson, 2017).

6) What would you expect for clinical manifestations?

Clinical manifestations for GERD are likely to be more commonly present after meals and can range from mild to severe (Badillo & Francis, 2016). These include heartburn, acid regurgitation, pain, bloating, nausea, chronic coughing, dental erosion, vomiting, asthma, laryngitis, ulcer development, and gastritis (Badillo & Francis, 2016). The inflammation resulting from GERD can also lead to clinical manifestations, including fever, swelling, redness, heat at the inflamed site, and chronic pain (Braun & Anderson, 2017).

7) What diagnostic tests might be used?

Patients presenting with atypical symptoms, such as dyspepsia, nausea, bloating, and epigastric pain, are eligible for a proton pump inhibitor (PPI) test (Wilson, 2016). In more typical cases, physicians tend to use typical presenting symptoms, such as heartburn, acid regurgitation, and chest pain to diagnose GERD, once cardiac causes have been ruled out (Wilson, 2016). Endoscopy can be used for GERD diagnosis, but should be reserved for patients presenting with more alarming symptoms (Wilson, 2016). These alarming symptoms can include anemia, dysphagia, and unintended weight loss (Wilson, 2016). Endoscopy is invasive, but useful for those who PPI diagnostics have not been adequate or helpful for. (Wilson, 2016).

8) What treatment measures would you anticipate?

One of the most common ways to treat GERD is through lifestyle changes. This can include not going to bed right after eating, elevating the head of the body while sleeping, weight loss in certain cases, avoiding caffeine, taking acid reflux medication when prescribed, and avoiding alcohol, as well as spicy and fatty foods (Wilson, 2016). Proton pump inhibitors are helpful in moderate GERD cases, and should be dosed thirty to sixty minutes prior to eating a meal to be most effective (Wilson, 2016). Histamine 2 receptor antagonists can provide relief from significant nighttime symptoms to supplement the use of PPI medications during the daytime (Wilson, 2016). In severe cases of GERD, surgical intervention may be necessary. Surgery is reserved for patients who exhibit evidence of ulcer development and erosive esophagitis (Wilson, 2016).

References