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NSG 5003 Peptic Ulcer Disease & Other diagnostic tests Case Peer Responses

NSG 5003 Peptic Ulcer Disease & Other diagnostic tests Case Peer Responses

NSG 5003 Peptic Ulcer Disease & Other diagnostic tests Case Peer Responses

Case Study: Henry

Explain the pathophysiology of Peptic Ulcer Disease as compared to GERD and explain which one his symptoms most closely represent. Support with evidence.

Peptic ulcer disease is from ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum of the gastrointestinal (GI) tract. Risk factors for peptic ulcer disease include genetic predisposition, H. pylori infection of the gastric mucosa. Modifiable risk factors include non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, smoking, alcohol use. Stress is also a risk factor for PUD to risk for peptic ulcer disease. The ulcers can vary in severity and number and are divided into two categories. Superficial and true alterations Superficial ulcers erode gastric mucosa but do not penetrate the muscularis mucosae; however, true ulcers penetrate the muscularis mucosae and damage blood vessels, bleeding or perforation the GI walls. Frequent NSAID use results in reduced mucin production and increased secretion of hydrochloric acid. The protective qualities of mucin are reduced, and stomach acid’s acidity is increased (McCance & Huether, 2019). Disruption of the mucosa exposes submucosal areas to gastric secretions that are not made to be exposed to acids. This results in auto-digestion, which further complicates the erosion and ulceration (NCBI, 2016).

Gastroesophageal reflux disease (GERD) is the reflux of acid and pepsin from the stomach to the esophagus that causes esophagitis. Patients that are obese, have Hiatal hernias, or take certain medications may be at higher risk. Patients who experience GERD typically experience issues with their lower esophageal sphincter (LES) resting tone, be it a transient or chronic weakness. Decreased gastric emptying, vomiting, and situations that increase intraabdominal pressure can also cause GERD. Gastric ulcers can cause delayed gastric emptying, increasing the likelihood of reflux of acid and chime through the LES and into the esophagus.

Prolonged exposure of the esophagus to the acid can result in mucosal injury and inflammation. Sustained or repeated exposure can cause ulceration and eventual fibrosis and thickening. If left untreated, the patient may be at increased risk for cancer (McCance & Huether, 2019).

Explain the body’s natural protection against peptic ulcers from a pathophysiology standpoint.

To protect against acid and pepsin, the upper GI tract has intercellular tight junctions, a protective layer of mucus, and right mucosal blood flow. The mucus forms the mucosal barrier that protects the tight junctions which make it impermeable to acid when functioning normally. Prostaglandins and nitric oxide stimulate the release of mucus and bicarbonate; they also inhibit acid secretion which together help protect the mucosa form damage (McCance & Huether, 2019).

What diagnostic testing may be used to further evaluate the symptoms and what might this test tell the healthcare provider?

As a primary care provider, I would ask the patient to reduce his weight, alcohol intake, and stop aspirin use. I would also provide a proton pump inhibitor and schedule the patient for a follow up appointment. Studies in the past have proven that reducing weight and potentially aggravating factors can reduce symptoms. I would also encourage the use of alkaline water and discourage the patient from eating three to four hours before bed. If the patient has a resolution of symptoms, I would consider him to have GERD. If the symptoms didn’t resolve, I would test the patient for H. pylori infection with a stool antigen test or by using a device to measure breath samples after swallowing a urea pill as these are recommended for patients on aspirin (Armand, 2020). I would also consider referral the patient to a GI doctor to be scheduled for an upper endoscopy where they could visualize and even biopsy sites of inflammation or injury.


Armand, W. (2020, August 18). H. pylori, a true stomach “bug”: Who should doctors test and treat?Harvard Health Blog.

Badillo, R. (2014). Diagnosis and treatment of gastroesophageal reflux disease. World journal of gastrointestinal pharmacology and therapeutics, 5(3), 105.

McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Elsevier. Retrieved from

NCBI. (2016, August 21). How does the stomach work? [Internet].

PEER #2Amanda Lahman posted Nov 6,2020

The case study this week describes a 58-year-old male who presents with burning abdominal pain which has awoken him. It occurs several times a week and seems to be relieved by a bland diet and exaggerated by spicy foods. He reports drinking 1-2 beers a day and taking an Aspirin daily. He describes a slight weight loss due to decreased appetite. He complains of intermittent epigastric and midsternal burning and tenderness. This patient is be subjected to a gastrointestinal condition that is causing him discomfort and affecting his daily life. The diagnostic testing, diagnosis, and treatment is required to alleviate the symptoms he is experiencing.

Peptic Ulcer Disease (PUD) is characterized by defects in the gastroduodenal mucosa and annually affects 4.5 million people in the United States (Dunlap & Patterson, 2019). The breakdown of gastrointestinal lining is commonly caused by acid erosion. According to Jayne Jennings Dunlap and Sheila Patterson (2019), the acidic environment of the stomach, stress, diet, tobacco use, and alcohol use have been historically causative factors for the development of peptic ulcers (Dunlap & Patterson, 2019). More recently, studies have found new factors that contribute to the development of ulcers in the GI tract. These being helicobacter pylori and continual NSAID use. According to the textbook readings, NSAIDs are known to erode the mucosal lining by suppressing the innate gut barrier and increasing the secretion of hydrochloric acid (McCance & Huether, 2019). Helicobacter Pylori penetrates the protective mucosal lining and causes inflammation while also leaving the stomach and duodenum subjected to the erosive effects of acid. The most common clinical manifestation of Peptic Ulcer Disease is epigastric pain that occurs when stomach is empty and is relieved by eating foods or antacids (McCance & Huether, 2019).

Gastroesophageal Reflux Disease (GERD) is defined as a reflux of bile salts and/or acid that causes inflammation of the esophagus. This condition affects about a quarter of individuals in North America (McCance & Huether, 2019). GERD is commonly caused by weakness and dysfunction of the lower esophageal sphincter. Delayed gastric emptying also contributes to the reflux of gastric contents (McCance & Huether, 2019). The manifestations that occur during episodes of GERD are caused by the inflammation of the esophagus. These symptoms include heartburn, cough, sinusitis, laryngitis, and epigastric pain soon after eating (McCance & Huether, 2019). An article by Caitlyn Dow (2020) outlines the common contributors to GERD. These include spicy and acidic foods, coffee, and alcohol (Dow, 2020). Foods high in fat are known to slow gastric emptying and therefore contribute to the reflux. Dow noted that many people suffering from GERD report discomfort at night. This is due to eating 1-2 hours before lying flat which further facilitates the reflux of gastric juices into the esophagus (Dow, 2020). The long-term effects of esophageal inflammation can lead to erosion, ulceration, and even cancer (McCance & Huether, 2019).

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