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(gender, ethnicity, age, or behavior).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
Glands within the stomach secrete digestive juices known as gastric juices in order to break down the solid food and kill intestinal bacteria. The intestinal inner lining is venerable to the acidic actions (Malfertheiner & Mearin, 2017). Similarly, the foods, drinks, and medications can result in acid imbalances. Accordingly, the focus of this paper is on disorders of gastric acid on the GIT.
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Pathophysiology of Gastric Acid Stimulation and Production
The parietal cells on the intestinal walls produce gastric juices as hydrochloric acid. The secretory canaliculus within the parietal cells is normally extremely acid (PH of 8) and this is the region where secretion of gastric acid into lumen occurs. Gastric acid is secreted into lumen after neuronal, pancreatic, and hormonal stimulation (Malfertheiner & Mearin, 2017). For instance, gastrin produced by the G cells within the intestinal pyloric mucosa elicits production of gastric acid. On the other hand, hydrogen ions are secreted by the parietal cells and they have numerous roles. However, evidence indicates that the production of gastric acid is mainly stimulated by Histamine 2 receptors (Wirth & Yang, 2016).
Gastrin is released by the G cells during meal consumption, and gastrin binds to parietal cells and ECL which are CCK2 receptors. Gastrin combines with the parietal cells and this stimulates the release of intracellular calcium as well as stimulation of the proton pump. The gastrin then binds to the ECL cells and histamine is formed. The histamine then binds to the H2 cells and this stimulates the production of gastric acid (Wirth & Yang, 2016).
Changes after Gastric Acid Stimulation and Production with GERD, PUD, and Gastritis disorders
Gastroesophageal reflux disease occurs (GERD) occurs when there is an acid reflux from the abdomen to the esophagus. GERD occurs when the intra-gastric pressure is higher than the LES pressure and this mostly happens after meal consumption because the intestinal contents increases in both volume and acidity and the sphincter does not function as required. The main symptom of GERD is heartburn. According to Malfertheiner & Mearin (2017), gastritis and duodenal ulcers are caused by inflammation of the intra-mucosa by the H Pylori. H Pylori colonizes the intra-mucosa and the acidity increases; this erodes the mucosa causing ulceration. Peptic ulcer disorder occurs when there is secretion of the digestive juices or acid within the intestinal tract which results to an open wound on the intestinal lining causing peptic ulcer. Production of surplus hydrochloric acid also causes ulcers (Sipponen & Maaroos, 2015). Gastrointestinal Tract: Disorders of Motility
Impact of Behavior on Pathophysiology of Gastric Acid Disorders
Lifestyle behaviors significantly impact etiology and pathophysiology of gastric acid disorders. For instance, eating habits influence gastric motility. For instance, the intake of hot foods congests the mucosa and increase the secretion of intestinal acid (Burns et al, 2017). Similarly, alcohol intake induces acid secretion while intake of soft drinks reduces the pressure under the esophageal sphincter and can cause gastroesophageal reflux. Nicotine intake reduces the pressure and prompts hyperchloremia while intake of spicy foods stimulates secretion of gastric acid and irritates the mucosa, which can gradually cause gastritis and gastric lesions. Intake of food high in fat is also associated with increased risk to GERD and also retards gastric emptying which causes symptoms like heartburn and precocious satiety (Lissa et al, 2015).
Diagnosis of Gastric Acid Disorders
Upper endoscopy: A tube known as an endoscope is inserted through the through in order to examine the inner part of the esophagus and intestinal tract. An endoscopy can detect esophagitis as well as inflammation of the intestinal tract. Endoscopy can also be used to collect a tissue for biopsy to be performed to test for any other complication or H. Pylori (Archana et al, 2015).
Pylori test: A breath test, blood test or stool test can be used to establish the presence of H. Pylori because H. pylori bacterium is among the causes of gastric disorders. In a breath test, the patient drinks a liquid with radioactive carbon and if there is an H. pylori infection there is a radioactive carbon within the breath sample (Archana et al, 2015).
X-ray: An x-ray is performed for the upper gastrointestinal tract in order to create images of the GIT and identify any abnormality. The patient can also swallow a liquid with barium to make the images and ulcers more visible (Safavi et al, 2016).
Treatment of the Gastric Disorders
Antibiotics targeting H. pylori: In case H. pylori are the cause gastritis, antibiotics such as metronidazole or clarithromycin can be prescribed to kill the H. pylori bacterium (Archana et al, 2015).
Antacids: Antacids can be prescribed in order to neutralize the gastric acid. Antacids also relieve the pain caused by the stomach ulcers (Malfertheiner & Mearin, 2017).
Behavioral modifications: The patient will be advised on the behaviors to adopt in order to reduce the risk of gastric disorders. For instance, the patient will be advised to reduce alcohol intake and intake of carbonated drinks because they are associated with increased risk for gastric disorders. The patient will also be advised to avoid intake of fatty, spicy, fried, and acidic foods, and also avoid taking very hot drinks and foods. Lastly, the patient will be advised to eat smaller amounts of foods in order to prevent indigestion (Safavi et al, 2016). Gastrointestinal Tract: Disorders of Motility
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.
Lissa C, Ddine C, Rodrigues C & Colpo E. (2015). Factors associated with chronic gastritis in patients with presence and absence of Helicobacter pylori. ABCD. 25(2).
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. Gastrointestinal Tract: Disorders of Motility
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