Comparative Pathophysiologies of GERD, Peptic Ulcer Disease and Gastritis

Pathophysiology of Gastric Acid Stimulation and Production The human body produces gastric acid in the stomach, primarily to digest proteins (Anand, 2015; Huether & McCance, 2012). It is composed o hydrochloric acid and sodium chloride. It digests proteins through the action of digestive enzymes and allowing digestive enzymes break down the long chains of amino acids from digested proteins. The production of gastric acid us regulated by the autonomous nervous system and a number of hormones, and by positive regulators and negative feedback processes (Anand, Huether & McCance).

But these structures and processes change when diseased conditions, like gastroesophageal relux disease or GERD, peptic ulcer disease and gastritis, develop. Summary GERD includes all the offshoots and by-products of acid reflux and other stomach irritants pushing up into the esophagus (Anand, 2015; Huether & McCance, 2012). The reflux is primarily caused by the failure of the anti-reflux barriers to perform their function. It becomes more severe and progresses when it occurs after a meal when in an upright, supine or both supine and upright positions (Anand, Huether & McCance).

The development of GERD has been associated with the abnormality of a number of factors, which disturb the normal balance of the system (Anand, 2015; Huether & McCance, 2012). One of these is genetics. Much evidence drawn from epidemiologic and family studies corroborates the inherited tendency to develop GERD.

Findings of some of these studies have shown that GERD in both children and adults have both similar and different clinical features; a predisposition to develop any of the different types of GERD; the association of genetic risk factors with obesity and hiatus hernia; and chromosomal relationships in the development of GERD in some patients but not in others. Diagnosis is made based on increased acid secretion.

Acid suppression, an increase or decrease of transient lower esophageal sphincter relaxation, anticholinergic drugs and new and medical and surgical therapies are treatment options (Anand; Huether & McCance; & Dach, 2015). In PUD, epigastric pain is the most common symptom, which is experienced after meals (Anand, 2015; Huether & McCance, 2012). Functional changes may be in the form of bleeding, anemia, quick satisfaction of a meal, unexplained weight loss, active dysphagia or odynophagia, persistent vomiting and a family history of gastrointestinal cancer.

Those with perforated ulcers report on a sudden attack of severe and sharp abdominal pain (Anand, Huether & McCance). Diagnosing uncomplicated PUD includes radiographic and endoscopic tests (Dach, 2015). All patients with peptic ulcers should be tested for H. pylori infection as the selected factor. The preferred diagnostic test is the urease test. Upper gastrointestinal endoscopy is the choice diagnostic test for suspected cases of PUD as this visualizes the ulcer (Dach, 2015). It also establishes the presence and extent of active bleeding. Endoscopy should be performed on PUD patients older than 45.

Treatment should target H. pylori infection, the elimination of non-steroidal anti-inflammatory drugs and the administering of anti-secretory treatment. Urgent surgery may be resorted to when hemostatis is not achieved, and in cases.