Describe the normal pathophysiology of gastric acid stimulation and production.
Gastrointestinal Tract: Disorders of Motility Essay.
Gastrointestinal Tract
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.
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 increases 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. Gastrointestinal Tract: Disorders of Motility Essay 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).
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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 collects 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). Gastrointestinal Tract: Disorders of Motility Essay.
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-steroidal anti-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-steroidal anti-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).
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.
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. Gastrointestinal Tract: Disorders of Motility Essay 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).
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.
References
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 https://www.hindawi.com/journals/isrn/2013/824320/
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 Gastrointestinal Tract: Disorders of Motility Essay.
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 (5th ed.). Philadelphia, PA: Elsevier.
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 Gastrointestinal Tract: Disorders of Motility Essay. 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. Gastrointestinal Tract: Disorders of Motility Essay.
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 Gastrointestinal Tract: Disorders of Motility Essay.
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.
References to use in the paper.
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.
Chapter 13, “Gastrointestinal Disease”
de Bortoli, N., Martinucci, I., Bellini, M., Savarino, E., Savarino, V., Blandizzi, C., & Marchi, S. (2013). Overlap of functional heartburn and gastroesophageal reflux disease with irritable bowel syndrome. World Journal of Gastroenterology, 19(35), 5787-5797. doi:10.3748/wjg.v19.i35.5787
Pathophysiology of Gastric Acid Stimulation and Production Gastrointestinal Tract: Disorders of Motility Essay.
Gastric parietal cells are responsible for the production of gastric acid in the stomach. The gastric acid production is as a result of response hormones, merocrine and paracrine inputs. The gastric acid production is primarily stimulated by the G cells which are located in the pyloric mucosa. For the parietal cells, they are typically stimulated to secrete hydrogen ions into the lumen. Each receptor has a different level of functional importance. Cholecystokinin hormone receptor is bound to the enterochromaffin-like cells (ECL) cells and the parietal cells when gastrin is produced as a response to meals (Hammer, & McPhee, 2014). When the gastrin is bound to parietal cells, it results in activation and translocation of hydrogen and potassium ions and releases if intracellular calcium. Histamine production is promoted by the binding of gastrin to ECL cells. The histamine binds to H2 on parietal cells and increases cyclic AMP production which in turn is followed by the activation and translocation of proton pump at the canalicular membrane. Gastric acid secretion can be inhibited by natural inhibitors such as the release of somatostatin, CCK, and secretin (Huether, & McCance, 2015).
Changes due to GERD, on gastric acid production
During GERD, PUD and gastritis conditions, it is evident that gastric acid stimulation and production undergoes several changes. GERD results from reflux of the gastric materials into the esophagus and in turn causing damages to their walls of the esophagus (Denbow, 2015). The changes in the stimulation and the production of the gastric acid affect the pathophysiology and severity of the conditions (Huether, & McCance, 2015). Gastrointestinal Tract: Disorders of Motility Essay This rise in gastric acid production during the conditions, makes the balance of the acid towards reflux and in turn affect the standard capacity if the mucosa to withstand the amount of acid. Gastritis causes a bacterial infection known as Helicobacter pylori which damages the stomach walls by wearing it out (De Bortoli et al., 2013). The acid stimulation production elevates the number of H. pylori in the stomach.
How H. pyloric affects pathophysiology of GERD, PUD, and gastritis.
pylori are known for its effects on gastric physiology. The bacteria can either increase the production or lower the production of gastric acid depending on the kind of gastritis produced (Hammer, & McPhee, 2014). According to studies, it is suggested that decreased production of gastric acid in severe gastritis corpus can sometimes be beneficial in GERD. The low production of the acid is brought about by H. pylori infection which is characterized by the corpus inflammation. Epidemiological studies have established the negative association between the severity of GERD and H. pylori prevalence (Waldum et al., 2014). Apparently, the results from studies show that H. pylori infection affects the incidence of GERD mostly in Asian countries.
Overproduction of gastric acid characterizes the conditions in most cases. It is clear that excessive acid in the stomach causes duodenal walls damages. As aforementioned, H, pylori are known to bring forth production of acid in the stomach. Therefore removal of the bacteria from the stomach can accelerate the healing of the conditions (De Bortoli et al., 2013). Gastrointestinal Tract: Disorders of Motility Essay.
Diagnosis of GERD, PUD, and gastritis
Physical examination is known to be the most ideal in the exploration of peptic acid conditions in the differential diagnosis. In the physical examination method of diagnosis, stool examination can be used for occult bleeding (Hammer, & McPhee, 2014). This is significant in guiding for prognosis and extensive diagnostic investigation.
Esophagogastroduodenoscopy can also be employed in the diagnosis of the conditions. In this procedure, a diagnostic endoscopy is used to visualize the upper gastrointestinal tract all the way to the small intestines. The procedure does not require any incision, and thus it is correct to term the method as less invasive. The method is modern, and therefore no injuries are adverse. The only adverse effect of the procedure is a sore throat.
Another test that can be used to determine the presence of the conditions is by testing for H, pylori. A serologic test is used for this kind of test to determine whether H, pylori are present Gastrointestinal Tract: Disorders of Motility Essay.
Histological test- this is regarded to as the most functional diagnostic test. In this diagnosis method, the H. pylori organisms are identified to confirm their presence hence establish whether a patient is suffering from the conditions.
Treatment for H. pylori
Antibiotics are administered for 10-14 days in people above 12years in combination with painkillers. Examples include antibiotics such as metronidazole, tetracycline or clarithromycin in combination with analgesics such as bismuth subsalicylate, ranitidine or a proton pump inhibitor. Suppressing acid by the H2 blocker or the proton pump inhibitor in combination with antibiotics significantly help to alleviate ulcer-related symptoms like nausea and abdominal pains which in turn enhances the efficacy of antibiotics (Hammer, & McPhee, 2014).
Summary
Gastric acid is known to be stimulated by the presence of meals in the stomach and sometimes by psychological effects. Gastric acid is responsible for activating pepsinogen into pepsin, as well as maintaining an optimum environment for digestion Gastrointestinal Tract: Disorders of Motility Essay. When gastric acid is produced in excess, it leads to conditions such as PUD, GERD, and gastritis. Such conditions can be lethal because of their adverse effect on the duodenal walls. The conditions, however, can be treated by use of antibiotics in conjunction with analgesics.
References
de Bortoli, N., Martinucci, I., Bellini, M., Savarino, E., Savarino, V., Blandizzi, C., & Marchi, S. (2013). Overlap of functional heartburn and gastroesophageal reflux disease with irritable bowel syndrome. World Journal of Gastroenterology, 19(35), 5787-5797. doi:10.3748/wjg.v19.i35.5787
Denbow, D. M. (2015). Gastrointestinal anatomy and physiology. In Sturkie’s Avian Physiology (Sixth Edition) (pp. 337-366).
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.
Waldum, H. L., Hauso, Ø., & Fossmark, R. (2014). The regulation of gastric acid secretion–clinical perspectives. Acta physiologica, 210(2), 239-256. Gastrointestinal Tract: Disorders of Motility Essay.