Gastric Disorders Discussion 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. 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. Gastric Disorders Discussion Paper
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Glands in the stomach secrete gastric juices whose purpose is to break down food and kill the bacteria within the intestines. The inner lining of the intestines is very susceptible to the acidic action of the gastric juice. In addition, medications, food, and drinks can also cause acid imbalances in the GIT (Malfertheiner & Mearin, 2017). This paper will, therefore, discuss various aspects allied to the disorders of gastric acid.
Pathophysiology of Gastric Acid Stimulation and Production
The intestinal walls have parietal cells that produce hydrochloric acid, which is a gastric juice. The secretory canaliculus in the parietal cells is where the secretion of gastric acid occurs and it is very acidic with a PH of 8. Gastric acid secretion into the lumen occurs after the stimulation of the hormones, neurons, and pancreas as well (Malfertheiner & Mearin, 2017). For example, the G cells produce gastrin in the pyloric mucosa of the intestines which stimulates the production of gastric acid. Similarly, the parietal cells secrete hydrogen ions which also play different roles. In addition, Histamine 2 receptors stimulate the production of gastric juice (Wirth & Yang, 2016).
The G cells release gastrin when someone eats food, and the gastrin then binds to the CCK2 receptors, which include ECL and parietal cells. The produced gastrin then combines with the parietal cells, which leads to the stimulation of the intracellular calcium to be released and also stimulates release of proton pump. Binding of the gastrin to the ECL cells leads to the formation of histamine. The binding of the histamine to the H2 cells then occurs, which leads to production of the gastric being stimulated (Wirth & Yang, 2016).
Changes after Gastric Acid Stimulation and Production with GERD, PUD, and Gastritis Disorders
GERD occurs when acid reflux from the abdomen to the esophagus occurs. For GERD to occur, the intra-gastric pressure is normally higher when compared to the LES pressure. This normally occurs after an individual consumes food due to the increased intestinal contents which lead to an increase in the acidity and volume; this leads to malfunction of the sphincter. GERD is mainly characterized by heartburn (Malfertheiner & Mearin, 2017).
On the other hand, when H Pylori inflames the intra-mucosa, this can lead to duodenal ulcers and gastritis. This is because the colonization of the intra-mucosa by H Pylori leads to increased acidity, which erodes the intra-mucosa, causing ulceration of the mucosa (Wirth & Yang, 2016).
Peptic ulcer disorder occurs when the digestive juices or acids within the intestinal tract are secreted, causing an open wound on the lining of the intestine; this causes peptic ulcers. In addition, ulcers also occur when there is excessive production of hydrochloric acid (Sipponen & Maaroos, 2015).
Impact of Behavior
The behavior of a person has a significant impact on pathophysiology of gastric acid disorders where for instance feeding habits impact the motility of the gastric. For example, taking hot foods has been shown to cause congestion of the mucosa and lead to secretion of more intestinal acid. Likewise, taking alcohol has been shown to stimulate secretion of acid whereas taking soft drinks lowers the esophageal sphincter pressure, which can cause gastroesophageal reflux (Burns et al, 2017). Taking nicotine and caffeine also lower the pressure of esophageal sphincter, causing hyperchloremia whereas taking food with spices can stimulate gastric acid to be secreted and at the same time irritate the mucosa, which can lead to gastric lesions and gastritis over time (Lissa et al, 2015).
Diagnosis of Gastric Acid Disorders
Upper endoscopy: During this test, an endoscope is inserted in the esophagus and intestinal tract to identify any inflammation in the esophagus or intestinal tract. The test can also be utilized to take tissues for other tests (Archana et al, 2015).
X-ray: An x-ray of the upper gastrointestinal tract is carried out to identify any abnormality in the GIT (Safavi et al, 2016).
Treatment of Gastric Disorders
Antacids: Antacids can be used for neutralizing the gastric acid and also as pain relievers (Malfertheiner & Mearin, 2017).
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Antibiotics for H. pylori: If H Pylori is determined as the cause of gastritis, antibiotics like clarithromycin and metronidazole are used to treat the condition (Archana et al, 2015). Gastric Disorders Discussion Paper
Behavioral modifications: Patients with gastric disorders can be educated on the lifestyle changes to make when it comes to dietary intake in order to lower the risk of gastric disorders. For example, reducing intake of alcohol, carbonated drinks, spicy, fatty, fried and acidic foods can reduce the risk of gastric disorders. In addition, eating small quantities of food can prevent indigestion (Safavi et al, 2016).
Archana D, Wale J & Thanikar V. (2015). H.Pylori Associated Gastritis. Journal of Clinical and Diagnostic. Research. 6(2): 211-214.
Burns M, Amaya A, Bodi C, Ge Z, Bakthavatchalu V, Ennis K, et al. (2017) Helicobacter pylori infection and low dietary iron alter behavior, induce iron deficiency anemia, and modulate hippocampal gene expression in female C57BL/6 mice. PLoS ONE. 12(3): e0173108.
Malfertheiner P & Mearin F. (2017). Functional Gastrointestinal Disorders: Complex Treatments for Complex Pathophysiological Mechanisms. Digestive Diseases. 35(1):1–4.
Safavi M, Sabourian R & Alireza F. (2016). Treatment of Helicobacter pylori infection: Current and future insights. World J Clin Cases. 4(1): 5–19.
Sipponen P & Maaroos H. (2015). Chronic gastritis. Scand J Gastroenterol. 50(6): 657–667.
Wirth H & Yang M. (2016). Different Pathophysiology of Gastritis in East and West? A Western Perspective. Inflamm Intest Dis. 1(3): 113–122. Gastric Disorders Discussion Paper