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.

 

 

 

Gastrointestinal Tract: Disorders of Motility

 

 

 

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Gastrointestinal Tract: Disorders of Motility

Gastric Acid Stimulation and Production with GERD, PUD, and Gastritis Disorders

“The road to health is paved with good intestines!” (Sherry A. Rogers). Gastric acid is generally produced in the stomach and is essential for digestion. Motility disorders are abnormal muscle and nerve contractions causing spasms or lack of motion anywhere along one’s gastrointestinal tract. The stomach, the small and the large intestine, as well as the colon and the rectum, may be unable to perform their functions in the digestive process. Gastrointestinal motility changes depending on feeding, and GI motility is divided into fasting and postprandial contract patterns (Kitazawa & Kaiya, 2019). This motility is controlled by the contractility of smooth muscles of the GI tract, extrinsic and intrinsic neurons and some hormones. This essay will explore the normal pathophysiology of gastric acid stimulation and production and changes occurring in gastric acid stimulation and production with GERD, PUD, and gastritis disorders. Lastly, look at how age impacts the pathophysiology of GERD, PUD, and gastritis.

The Normal Pathophysiology of Gastric Acid Stimulation and Production

Gastric Acid Stimulation

Parietal and proximal cells are located in the stomach and are responsible for secreting gastric acid. This acid plays a crucial digestive function by lowering the PH in the stomach, creating prime conditions for enzymes to act on the food. Gastric acid secretion is initiated in the mouth, with thought, smell and taste acting as vagal stimulants for the stomach’s G cells to start the secretion (Isackson & Ashley, 2020). The ingestion of proteins is also a stimulant increasing gastric production. As the production of gastric acid increases, the acid circulates within the digestive tract causing histamine release by enterochromaffin-like cells. The release of histamine acts on the H2 receptors located on the parietal cells leading to further PH reduction as more gastric acid is released.

Gastric Acid Production

Gastric acid production is an inherent ability of all people from birth through the secreted amounts only peak at two years of age. Peak acid production continues through childhood to old age, but acid production sometimes drops due to gastritis as a medical condition. For healthy people, the mucosa walls of the gastrointestinal tract produce mucus acting as a protection layer against the acid’s corrosion. This protection occurs through three main stages. Firstly, the production of mucus and hydrogen carbonate creates a pH gradient keeping the acid within the tract (Taherali et al., 2018). Secondly, epithelial cells lining the tract walls use their membrane transport system to extract hydrogen ions from the acid to neutralize it. Lastly, capillary blood vessels in the tract walls collect the acid that diffuses through the epithelial membrane and eliminates them from the tract. Such strategies may disturb the mucosal membrane and result in the development of peptic ulcer disease, gastroesophageal reflux disease, and other gastric disorders.

Changes that Occur to Gastric Acid Stimulation and Production with GERD, PUD, and Gastritis Disorders

Interfering with the production of the mucosal layer of the gastrointestinal tract causes gastric disorders, including peptic ulcer disease and gastroesophageal reflux disease, where helicobacter pylori infection and non-steroidal anti-inflammatory drugs interfere with mucosal membranes. H. pylori infection causes tears on the mucosal membrane, presented as ulcers and inflammation. Non-steroidal anti-inflammatory drugs affect the mucosal membrane through topical and systematic actions causing ulcers and inflammation (Fokunang et al., 2018). These 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. The drugs contain low pH and are non-ionized in gastric acid, hence easy diffusion across the tract’s walls and into the epithelial cells.

The Impact of Age on the Pathophysiology of GERD, PUD, and Gastritis

The pathophysiology of peptic ulcer disease and gastroesophageal reflux disease can be impacted by age, where in children, it is notable that they have an anti-reflux barrier whose function is to ensure frequent relaxations and retrograde flow of gastric contents into the esophageal sphincter barrier existing between the esophagus and stomach is impaired as a factor of age and immaturity among children (Khan & Orenstein, 2018). This condition is caused by the lower esophageal sphincter’s incompetence or relaxation. Peptic ulcer disease causes crucial morbidity and mortality in the elderly, frequently presents atypically, and is associated with high complications. The ubiquity of helicobacter pylori increases with age and can be essential in developing ulcers. It is clear that age impacts the pathophysiology of GERD, PUD, and gastritis as it affects children, and GERD is expected in the elderly.

Diagnose and Treatment of GERD, PUD, and Gastritis Disorders based on Age

As it is clear that the gastroduodenal contents, including gastric acid, bile acids, and trypsin, easily corrode the gastrointestinal tract walls. This situation worsens even as the corrosion increases and the naturally occurring defenses such as acid clearance and mucosal resistance are ineffective. The acid defense mechanism accompanies it breaks down further. The treatment of gastritis can be of three categories, the first one is that a lifestyle change is necessary to avoid acidic foods and sleep in the proper posture. For example, fatty acids should be removed from the diet since they are precipitating foods, and the head should be elevated when sleeping (Hindiyeh et al., 2020). The second treatment may involve the patient taking prescribed medication that reduces acid secretion and exposure, including proton pump inhibitors and histamine-2 receptor antagonists. The third and final treatment would involve surgery to repair the anti-reflux barrier. Getting an early diagnosis of the disorders is essential for easy treatments.

Conclusion

The physiology of the stimulation and the production of gastric acid is complex and takes place through several stages. Motility disorders are abnormal muscle and nerve contractions causing spasms or lack of motion anywhere along one’s gastrointestinal tract. The alteration of the physiology of gastric acid initiates the pathophysiology of peptic ulcer disease and gastroesophageal reflux disease and gastritis, where age plays a critical role in the development of gastritis and therefore the epidemiology, diagnosis, and treatment is critically affected by the influence of age on gastritis.

 

 

 

 

 

 

 

References

Fokunang, C., Fokunang, E. T., Frederick, K., Ngameni, B., & Ngadjui, B. (2018). Overview of non-steroidal anti-inflammatory drugs (NSAIDs) in resource limited countries. Moj Toxicol, 4(1), 5-13.

Hindiyeh, N. A., Zhang, N., Farrar, M., Banerjee, P., Lombard, L., & Aurora, S. K. (2020). The role of diet and nutrition in migraine triggers and treatment: a systematic literature review. Headache: The Journal of Head and Face Pain, 60(7), 1300-1316. https://doi.org/10.1111/head.13836

Isackson, H., & Ashley, C. C. (2020). Secretory functions of the gastrointestinal tract. Surgery (Oxford), 38(6), 289-296. https://doi.org/10.1016/j.mpsur.2020.03.010

Khan, S., & Orenstein, S. R. (2018). Gastroesophageal reflux disease. Current and future developments in surgery. Oesophago Gastric Surg, 1, 189.

Kitazawa, T., & Kaiya, H. (2019). Regulation of gastrointestinal motility by motilin and ghrelin in vertebrates. Frontiers in endocrinology, 10, 278. https://doi.org/10.3389/fendo.2019.00278

Taherali, F., Varum, F., & Basit, A. W. (2018). A slippery slope: On the origin, role and physiology of mucus. Advanced drug delivery reviews, 124, 16-33. https://doi.org/10.1016/j.addr.2017.10.014

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