Gastrointestinal Tract: Disorders of Motility
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 causes 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: Disorders of Motility.
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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.
Write a 2- to 3-page paper that addresses the following: Include an introduction and conclusion paragraph.
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: Disorders of Motility.
Include the following 2 references to be used exactly as 2 of the 4
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Hammer, G. G. , & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education.
This essay focuses on gastric acid stimulation and production. The normal physiology and the pathophysiology of its stimulation and production. It will specifically focus on gastric disorders; gastroesophageal reflux (GERD), Peptic ulcers disease (PUD), and gastritis disorder. It will expound on how these disorders are diagnosed and the treatment modalities. Lastly, there will be a conclusion summarizing the essay
The normal physiology of gastric acid stimulation and production
Gastric acid is a component of gastric juice (Fortes, 2016). The production of the gastric acid is controlled by the nerves and hormones. Parietal cells in the stomach secrete gastric acid. Its production starts with water combining with carbon dioxide in the cytoplasm of the parietal cells to form carbonic acid. The enzyme, carbonic anhydrase converts it into hydrogen ions and the bicarbonate ions. The bicarbonate ions are transported out of the cell into the blood via the transporter protein that is called the anion exchanger. It transports bicarbonate ions out of the cell and exchanges it for a chloride ion. The chloride ions are then transported into the stomach lumen via the chloride channel. The hydrogen ions that had split from the bicarbonate acid is transported to the lumen of the stomach via the H+/ATPase pump (proton pump). Hydrogen ions and chloride ions having different charges attracts each other and reacts forming the gastric acid (Hydrochloric acid). Its production is regulated by; acetylcholine, histamine, gastrin, and somatostatin (Fortes, 2016; Huether & McCance, 2015; Kahrilas, 2013; Hammer & McPhee, 2014).
The gastric acid stimulation occurs in three phases, the cephalic, gastric and intestinal although the three phases can occur simultaneously (Kahrilas, 2013). The cephalic phase occurs before the food gets into the stomach. It is relatively brief The stimuli are; thought of food, taste of food, sight of food and smell of food. The stimuli are processed by the brain. They increase gastric acid production in preparation for food. The gastric phase lasts for 3 to 4 hours. It is triggered by the entry of food in the stomach as it causes distension activating the stretch receptors. The intestinal phase has both an excitatory and inhibitory element. When the food fills the duodenum it causes production of intestinal gastrin which further stimulates the production of gastric acid (Fortes, 2016)Gastrointestinal Tract: Disorders of Motility.
Pathophysiology of gastric acid stimulation and production.
The gastric mucosal lining/barrier protects the stomach luminal surface from digesting itself although some conditions challenge this barrier (Fortes, 2016). During gastroesophageal reflux (GERD), Peptic ulcers disease (PUD), and gastritis disorder causes some changes in the process of gastric acid stimulation and secretion. In GERD which is a condition that results from reflux of the gastric contents to esophagus. It causes an increase in gastric acid stimulation and production which leads to an increase in GERD condition as the defective esophageal increases the amount of the gastric acid that is refluxing in the esophagus (Kahrilas, 2013). In gastritis, the mucosa lining of the stomach gets inflamed causing erosion of the secretory glands. This in turns causes a reduction in gastric acid stimulation and production. The condition therefore reduces (Hammer & McPhees, 20140. In PUD, there is a lesion that occurs in the stomach. In many cases they are as a result of helicobacter pylori bacterium. The infection causes gastritis, when the infection is localized at the pyloric region, it causes acid hypersecretion. The acid-neutralizing mechanisms gets overwhelmed and the duodenum tissues get damaged even further (Fortes, 2016).
Diagnosis and treatment of GERD, PUD and Gastritis.
GERD condition is diagnosed based on the clinical manifestations that the patient presents with (Huether & McCance, 2015). The symptoms; heartburn, chest pain, acid regurgitation, asthma, tooth decay, persistent coughs and earaches are considered. GERD condition is treated using hypnotics, neuroleptics or anti-depressants that helps to weaken lower esophageal sphincter tone (Kahrilas, 2013). In gastritis its diagnosis is achieved by extracting biopsies from the stomach, they are examined in the laboratory so as to confirm Helicobacter pylori infection (Forte, 2016). Its treatment involves the use of antibiotics to eradicate H. Pylori. Use of anti-acids. In case of PUD, the antibiotics should be used together with proton pump inhibitors and histamine blockers (Forte, 2016).
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The gastric acid is produced by the parietal cells of the stomach lining. The stimulation can either be cephalic, gastric and/or intestinal. Gastric disorders interfere with the gastric acid production. GERD and peptic ulcers disease causes hyper production while gastritis causes a decrease.
Forte, J. G. (2016). Gastric function. In Comprehensive human physiology (pp. 1239-1257). Springer, Berlin, Heidelberg.
Hammer, G. D., & McPhee, S. J. (2014). Pathophysiology of Disease: An Introduction to Clinical Medicine 7/E.
Huether, S. E., & McCance, K. L. (2015). Understanding Pathophysiology-E-Book. Elsevier Health Sciences.
Kahrilas, P. J. (2013). GERD pathogenesis, pathophysiology, and clinical manifestations. Cleveland Clinic journal of medicine, 70(5), S4 Gastrointestinal Tract: Disorders of Motility.