NURS 6501 WeeK 8 : Gastrointestinal Alterations
The alimentary canal or gastrointestinal (GI) tract includes the mouth, esophagus, stomach, small intestine, colon, anus, as well as some accessory digestive tissues such as the salivary glands, liver, gall bladder, pancreas, and is the digestion pathway of food after ingestion. (Huether, & McCance, 2017). The digestive system is responsible for the breakdown, digestion, absorption, and excretion of food. Because many of the GI alterations have similar clinical manifestations, differentiating potential causes into a single diagnosis can be difficult. GI inflammatory and ulcerative conditions can disrupt absorption, motility, and secretion (Huether, & McCance, 2017). For this reason, an advanced practice nurse must have an understanding of common GI disorders such as gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and gastritis. The purpose of this paper is to describe the pathophysiology of gastric acid production and explain the differences in regards to GERD, PUD, and gastritis.NURS 6501 WeeK 8 : Gastrointestinal Alterations
Normal Pathophysiology of Gastric Acid Stimulation and Production
Gastric acid secretion is stimulated and inhibited by several factors and can be broken up into phases cephalic phase, gastric phase, and intestinal phase (Huether, & McCance, 2017). Hydrochloric or gastric acid production and secretion occur in the cells and glands within the mucosa or on the apical surface of epithelial cells of the GI tract (Hammer, & McPhee, 2014). Hydrochloric acid (HCl) is produced by parietal cells from the H+-K+ ATPase active transport system, which carries hydrogen and chloride out of parietal cells and moves potassium into the cell. Stimulation of HCl secretion is from three main pathways, enterochromaffin-like (ECL) cells, G-cells, and acetylcholine release from the parasympathetic nervous system (Hammer, & McPhee, 2014, Huether, & McCance, 2017). ECL cells secrete histamine, the histamine then binds on to the H2 receptors on the parietal cells stimulating the H+-K+ ATPase pump of HCl secretion (Hammer, & McPhee, 2014). G cells secrete the peptide hormone gastrin. Gastrin binds to gastrin receptors on ECL cells stimulating the release of histamine and gastrin binds to gastrin receptors on parietal cells stimulating the H+-K+ ATPase pump to secrete HCl (Hammer, & McPhee, 2014). The last pathway is when the cephalic phase of digestion stimulates the parasympathetic secretion of acetylcholine from the vagus nerve (Huether, & McCance, 2017). Acetylcholine stimulates histamine release from ECL cells, the release of gastrin-releasing peptide stimulating gastrin release, and inhibits somatostatin release (Hammer, & McPhee, 2014). Somatostatin is secreted from D cells and inhibits HCl production. HCl production is inhibited by somatostatin because it hinders the release of gastrin from G cells and histamine from ECL cells. The binding of acetylcholine to muscarinic receptors on parietal cells stimulates HCl production (Hammer, & McPhee, 2014).
Gastroesophageal Reflux Disease
Gastroesophageal reflux disease (GERD) is the backflow of stomach contents upwards into the esophagus, causing esophagitis or inflammation of the esophagus (Huether, & McCance, 2017). Sign and symptoms of GERD include acid regurgitation, cough, dysphagia, epigastric pain, laryngitis and pyrosis (Huether, & McCance, 2017). The prevalence of GERD in the US is 18-27%, and risk factors include advanced age, drugs/ chemicals, and the presence of a hiatal hernia. Behavioral factors in GERD such as alcohol ingestion, smoking, and obesity are also risk factors (Huether, & McCance, 2017).
In GERD the lower esophageal sphincter tone is relaxed, there is slowed esophageal motility, or slowed gastric motility or delayed gastric emptying (Huether, & McCance, 2017). Esophagitis severity depends on the exposure time of the mucosa to the refluxate of chyme including acids, bile salts and enzymes. Refluxate can cause injury and inflammation to the mucosa with edema, erosion, hyperemia, increased capillary permeability, tissue fragility and long-term exposure can lead to fibrosis mucosal thickening, and lesions (Huether, & McCance, 2017). GERD is diagnosed from history, clinical manifestations, pH monitoring and tissue biopsy (Huether, & McCance, 2017). Treatment includes the use of proton pump inhibitors, or H2-receptor blockers and antacids. Alternating behavioral factors can also assist in the treatment of GERD. Educating the patient on life style modifications of smoking cessation, weight loss, and avoidance of alcohol are first-line interventions in alleviating bothersome symptoms in GERD (Talawah, & Woodward, 2013). Surgical intervention of laparoscopic fundoplication is a last resort in GERD treatment (Huether, & McCance, 2017). GERD can lead to peptic ulcer disease with lesions in the esophagus.NURS 6501 WeeK 8 : Gastrointestinal Alterations
Peptic Ulcer Disease
Peptic ulcer disease (PUD) is from an erosion, or ulceration in the protective mucosal layers of the duodenum, esophagus or stomach, and occur more frequently in the duodenum (Huether, & McCance, 2017). PUD lesions are from an imbalance of protective secretions and acid and the lesions can extend through several layers of the GI tract lining and can damage blood vessels, or perforate the wall of the GI tract. The most common clinical manifestation of PUD is chronic intermittent epigastric pain on an empty stomach relieved with rapid ingestion of food and or antacids, nausea, heart burn, weight loss and hemorrhage when the lesion extends into the tunica muscularis layer (Huether, & McCance, 2017, Mayo Clinic. n.d.). Huether, and McCance (2017) report the prevalence of PUD in 2011 was 15.5 million US citizens and risk factors include Helicobacter pylori (H. pylori) infection, nonsteroidal anti-inflammatory drugs (NSAIDs), advanced age, chronic diseases, and O blood type. Behavioral factors in PUD such as alcohol ingestion, smoking, obesity and psychologic stress are also risk factors (Huether, & McCance, 2017).
With PUD acid and pepsin concentrations penetrate the mucosal barriers and cause ulcerations. Duodenal ulcers care commonly from H. pylori infections which have a virulence factor cytotoxin associated gene A (CagA) that produces a vacuolating toxin (VacA) which causes apoptosic of gastric epithelial cell and promotes the release of inflammatory cytokines that damage the gastric epithelium (Huether, & McCance, 2017, p. 916). Prostaglandins are an essential part of the negative feedback loop inhibiting HCl production. Chronic use of NSAIDs prevent the cyclooxygenase-1 (COX-1) enzyme from producing prostaglandins, which normally stimulate secretion of mucus (Hunt, & Yuan, 2011). With the protective barrier against HCl inhibited, this increases the risk of gastric epithelium damage.
Diagnostic approaches such as endoscopic evaluation, tissue biopsy, urea breath test, stool samples, as well as medical history and physical are utilized to diagnose PUD (Huether, & McCance, 2017). The goal in the management of PUD is to relieve the causes, and prevent complications. Use of antacids, H2 receptor blockers, proton pump inhibitors, antibiotics, and surgical resection of ulcers are common treatments in PUD (Huether, & McCance, 2017). Self-management of PUD is also every effective, via modification of behavioral factors including alcohol avoidance, dietary changes, smoking cessation, weight loss, and improved sleep habits (Mayo Clinic. n.d.).NURS 6501 WeeK 8 : Gastrointestinal Alterations
Gastritis
Gastritis is often seen in GERD and with PUD. The incidence of gastritis in the US is less than 1% (Huether, & McCance, 2017). Acute gastritis occurs when the protective mucosal barrier of the stomach becomes inflamed or swollen from increased gastric secretion cause by trauma, drugs, chemicals or H. pylori infection (Huether, & McCance, 2017).
The same pathophysiology in gastritis occurs with NSAID drug use. Behavioral factors in gastritis include alcohol or acidic beverages ingestion, smoking, and sexually transmitted diseases are also risk factors (University of Maryland Medical Center, (UMMC), n.d.). Clinical manifestations of acute gastritis are vague abdominal discomfort, loss of appetite, epigastric pain or indigestion, fullness, hiccups, nausea, vomiting, and bleeding (Huether, & McCance, 2017, UMMC, n.d.). Acute gastritis heals spontaneously requiring no treatment other than modifying behavioral activities such as avoiding injurious drugs, consuming minimal amounts of acidic beverages, alcohol, and smoking cessation Huether, & McCance, 2017, UMMC, n.d.). Other treatments include using antacids, and H2-receptor antagonists Huether, & McCance, 2017).
However chronic gastritis is more prevalent in older adults and is usually due to chronic inflammation, epithelial metaplasia, and mucosal atrophy (Huether, & McCance, 2017). Chronic gastritis can be divided up and classified into several different groups by location of lesions. Type A, immune is found in the fundal region, type B, nonimmune is antral, and type C gastritis is associated with reflux of bile and pancreatic secretions into the stomach (Huether, & McCance, 2017). Immune gastritis is rare and is usually associated with other autoimmune diseases, autoantibodies to gastric H+-K+ ATPase can be found (Huether, & McCance, 2017). With chronic gastritis, the mucosa degenerates causing gastric atrophy, and the loss of parietal cells, causing the normal feedback mechanism to become impaired and allowing for elevated plasma levels of gastrin (Huether, & McCance, 2017). Nonimmune chronic gastritis is usually secondary to H. pylori infection, NSAIDS, or associated with behavioral factors such as alcohol and tobacco use and is related to high levels of HCl secretion (Huether, & McCance, 2017).NURS 6501 WeeK 8 : Gastrointestinal Alterations
Diagnosing gastritis usually requires an evaluation of complete medical history, physical exam, upper GI endoscopy, X-rays, blood and stool tests for H. pylori infection (UMMC, n.d.). Treatment of symptoms usually includes to reduce amount of acid in the stomach, antacids, the use of and antacids, proton pump inhibitors, or H2-receptor blockers, Carafate, or to treat the underlying cause with use of antibiotics vitamin B12, avoiding NSAIDS, or implementing life style modifications of smoking cessation, avoidance of alcohol and acidic beverages, and implementing dietary changes (UMMC, n.d.).
Summary
The overlap of clinical manifestations in GERD, PUD and gastritis can make differentiating the exact diagnosis difficult, without blood or stool tests, and endoscopic evaluation. All three digestive alterations can improve with behavioral and lifestyle changes such as dietary changes, avoiding alcohol, nicotine and NSAIDS. Finally, treatments are essentially the same with treating the underlying cause and the use of antacids, proton pump inhibitors, or H2-receptor blockers.
References
Hammer, G. D., & McPhee, S. J. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.). China: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Hunt, R. H., & Yuan, Y. (2011). Acid-NSAID/aspirin interaction in peptic ulcer disease. Digestive Diseases (Basel, Switzerland), 29(5), 465-468. doi:10.1159/000332211
Mayo Clinic. (n.d.). Peptic ulcer. Retrieved from http://www.mayoclinic.org/diseases-conditions/peptic-ulcer/home/ovc-20231363
Talawah, N. A., & Woodward, S. (2013). Gastro-oesophageal reflux. Part 1: smoking and alcohol reduction. British Journal Of Nursing, 22(3), 140-145.
University of Maryland Medical Center. (n.d.). Gastritis. Retrieved from http://www.umm.edu/health/medical/altmed/condition/gastritis NURS 6501 WeeK 8 : Gastrointestinal Alterations