Gastrointestinal Tract Essay Paper

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 Gastrointestinal Tract Essay Paper.

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 Gastrointestinal Tract Essay Paper.

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 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 Gastrointestinal Tract Essay Paper.


Gastrointestinal Tract

Gastric acid stimulation and production

Parietal and proximal cells located in the stomach are responsible for secreting gastric acid. The acid serves a significant digestive function by lowering the pH in the stomach to create prime conditions for enzymes (such as pepsin and gastric lipase) to act on the food. Additionally, gastric acid secretion is initiated in the mouth, with thought, smell, and taste acting as vagal stimulants for the stomach’s G cells to begin the secretion. Another stimulant is the ingestion of proteins that increase gastric acid production. Even as gastric acid production increases, the acid circulates within the digestive tract to cause histamine release by enterochromaffin-like cells. Histamine release acts on the H2 receptors found on parietal cells, causing further pH reduction even as more gastric acid is released. A negative feedback mechanism is responsible for regulating the acid production such that when a lot of acid is produced and the pH drops below a set threshold then the antral D cells are stimulated to initial somatostatin release that increases pH and inhibits gastric acid action (Shephard, 2016).

Gastric acid production is an inherent ability of all people from birth although the secreted amounts only peak at two-years of age. The peak acid production continues all through childhood and into adulthood and even old age. Still, there are occasions when acid production drops as a result of gastritis as a medical condition. In healthy individuals, the mucosa walls of the gastrointestinal tract produce mucus that act as a protection layer against the acid’s corrosion (Garcia, Cid & Sanchez, 2013). The protection against acid corrosion occurs through three main strategies. The first strategy is mucus and hydrogen carbonate (alkali) production that creates a pH gradient that keeps the acid within the tract. The second strategy is epithelial cells lining the tract walls that use their membrane transport system to remove the hydrogen ions from the acid so that it is neutralized. The final strategy is the presence if capillary blood vessels in the tract walls that collect the acid that diffused through the epithelial membrane and eliminates them from the tract. It is notable that a compromise of any one of these strategies will disturb the mucosal membrane and result in the development of peptic ulcer disease (PUD), gastroesophageal reflux disease (GERD), and other gastric disorders (Wyllie, Hyams& Kay, 2016).

As earlier indicated, interfering with the mucosal layer of the gastrointestinal tract causes gastric disorders that include PUD and GERD. Typically, Helicobacter pylori infection and non-steroidalanti-inflammatory drugs will interfere with the mucosal membrane. H. pylori infection causes tears on the mucosal membrane that are presented as ulcers and inflammation. Non-steroidalanti-inflammatory drugs interfere with the mucosal membrane through topical and systematic action that causes ulcers and inflammation (Vaezi, 2016). In fact, the 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. Besides that, the drugs have low pH (acidic) and are non-ionized in the presence of gastric acid, thus allowing them to easily diffuse across the walls of the tract and into the epithelial cells, reacting chemically with the hydrogen ions in the cells to increase acidity and cause cell corrosion (Marseglia et al., 2015; Maqbool, 2017) Gastrointestinal Tract Essay Paper.

Selected impact and treatment of the disorders

The selected factor is age. It is notable that children have anti-reflux barrier whose function is compromised so that relaxations ensue more frequently and retrograde flow of gastric contents into the esophagus is experienced. In this case, gastritis occurs when the immature lower esophageal sphincter barrier that exists between the esophagus and stomach is impaired as a factor of age and immaturity among children. This implies that the condition is caused by the lower esophageal sphincter’s incompetence or relaxation. The result is that the gastroduedenal contents (that include gastric acid, pepsin, bile acids, and trypsin) find it must easier to corrode the gastrointestinal tract walls. The situation worsens even as the corrosion increases and the naturally occurring defenses (acid clearance and mucosal resistance) are rendered ineffective. This is accompanied by the acid defense mechanism breaks down further (Wyllie, Hyams& Kay, 2016). Gastritis treatment will take either of three forms. Firstly, a change in lifestyle is necessary to include avoiding acidic foods and sleeping in the right posture. For instance, fatty acids should be removed from the diet since they are precipitating foods. Also, the head should be elevated when sleeping. Secondly, the patient should take prescribed medication that reduce acid secretion and exposure to include proton pump inhibitors and histamine-2 receptor antagonists (H2RA). Finally, surgery should be conducted to repair the anti-reflux barrier (Vaezi, 2016). 

Mind map


Garcia, M., Cid, J. & Sanchez, C. (2013). Gastroesophageal reflux in critically ill children: a review. ISRN Gastroenterology, Volume 2013(2013), Article ID 824320. doi: 10.1155/2013/824320. Retrieved from

Maqbool, A. (2017). Cystic fibrosis and gastroesophageal reflux disease. Journal of Cystic Fibrosis, 16, S2-S13.

Marseglia, L., Manti, S., D’Angelo, G., Gitto, E., Salpietro, C. … & Romeo, C. (2015). Gastroesophageal reflux and congenital gastrointestinal malformations. World Journal of Gastroenterology, 21(28), 8508-8515. doi: 10.3748/wjg.v21.i28.8508

Shephard, R. (2016). Physical activity and the gastro-intestinal tract: responses in health and disease. New York, NY: Routledge.

Vaezi, M. (2016). Diagnosis and treatment of gastroesophageal reflux disease. New York, NY: Springer.

Wyllie, R., Hyams, J. & Kay, M. (2016). Pediatric gastrointestinal and liver disease (5thed.). Philadelphia, PA: Elsevier. Gastrointestinal Tract Essay Paper