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Initial Post: Summarize the pathophysiology of Peptic Ulcer Disease as compared to GERD and explain which one of his symptoms most closely represent. Support with evidence.
Peptic ulcer disease is a break or an ulceration in the mucosal lining of the lower esophagus, stomach, or duodenum which is supposed to protect these organs (McCance, 2018). Peptic ulcers may be an acute finding or can occur chronically. There are risk factors that can increase the occurrence of peptic ulcer disease including, genetics, smoking, COPD, obesity, acute pancreatitis and excessive use of alcohol and/or NSAIDs. According to Yim, Kim & Lee, peptic ulcer disease may also be caused by helicobacter pylori (H. Pylori) infection (2021). The most chronic type of peptic ulcers are known as duodenal ulcers. When duodenal ulcers are present there is chronic intermittent pain in the patient’s epigastric area. The pain begins 30 minutes to 2 hours after eating when the stomach is empty and is relieved with food and antacids.
GERD an acronym for gastroesophageal reflux disease. GERD occurs when there is an increase in acid and pepsin refluxes from the stomach in the esophagus that causes irritation to the esophagus. This irritation is known as esophagitis. The lower esophageal sphincter is typically lower than normal due to transient relaxation and/or weakness of the sphincter (McCance, 2018). Increased abdominal pressure such as vomiting, coughing, lifting, bending, obesity or pregnancy can also contribute to the diagnosis of GERD as well. The symptoms of GERD are as follows: Heartburn due to acid regurgitation, chronic cough, asthma, sinusitis, and/or upper abdominal pain within the first hour of eating.
The symptoms that the patient has presented with are closer to the symptoms that are present in peptic ulcer disease due to the presentation of daily aspirin usage, pain and burning sensation in the mid sternum and epigastric region, and daily alcohol consumption. His occasional coughing could be related to GERD, but his symptoms seem to be more within the category of peptic ulcer disease.
McCance, K.,L., & Huether, S., E. (2018). Pathophysiology: The biologic basis for disease in adults and children (8th ed) St Louis, MO: Mosby Inc; ISBN-13: 978-0323583473.
Yim, M. H., Kim, K. H., & Lee, B. J. (2021). The number of household members as a risk factor for peptic ulcer disease. Scientific Reports, 11(1), 1–10. https://doi-org.su.idm.oclc.org/10.1038/s41598-021-84892-5.
Gastroesophageal Reflux Disease
Gastroesophageal Reflux Disease is a condition cause by abnormalities of lower esophageal function, esophageal motility, gastric motility, and gastric emptying. This occurs when the resting tone of the lower esophageal sphincter is lower than normal. There are a multitude of factors that contribute to this development including vomiting, coughing, lifting, bending and obesity. These influence the tone of the esophageal sphincter due to the increased abdominal pressure they cause.
Disorders such as gastroparesis, gastric ulcers are associated with delayed gastric emptying which lengthens the time span in which reflux is possible and increases the acid content of Chyme. Exaggerating the symptoms of reflux.
The severity of this condition depends on the composition of gastric contents and esophageal mucosa exposure time. When gastric contents are highly acidic or contain bile salts and pancreatic enzymes reflux can be severe. In the individual with weak esophageal peristalsis, reflux chyme remains in the esophagus for a longer period of time causing damage to the mucosa which can eventually become cancerous.
Symptoms of GERD include heartburn, chronic cough, asthma attacks, laryngitis, sinusitis, weight loss and upper abdominal pain within an hour of eating. Symptoms may be exacerbated when laying down or after consuming alcohol or acidic foods.
Peptic Ulcer Disease
Peptic Ulcer Disease occurs when there is a break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum. Peptic ulcers can be singe or multiple, acute or chronic, and superficial or deep. Superficial ulcerations are called erosions because they erode the mucosa by but do not penetrate the muscularis mucosa. True ulcers extend throughout the muscularis mucosa, damaging blood vessels, causing hemorrhage or perforating the gastrointestinal wall.
The chronic use of NSAIDs suppress mucosal prostaglandin synthesis, decreasing bicarbonate secretion and mucin production while increasing the secretion of hydrochloric acid. H. Pylori, a bacterium, typically found in the stomach, interacts with NSAIDs causing disruption of the mucosa, exposing submucosal areas to gastric secretions and auto digestion, leading to erosion and ulcerations.
Symptoms include chronic intermittent epigastric pain, often occurring 30 minutes to 2 hours after eating and in the middle of the night. This pain may be relieved by food or antacids and exacerbated by acidic foods and muscle spasms. Loss of appetite and weight loss are often present in this condition. These symptoms most closely align with they symptoms experienced by the patient in the discussion scenario (McCance & Huether, 2019)
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2019). Pathophysiology: the biologic basis for disease in adults and children (8th ed.). Elsevier