Gastroesophageal reflux disease (GERD)
Pathophysiology
GERD is also known as heartburn, sour stomach, or acid indigestion. This disease is the reflux of gastric secretions (hydrochloric acid and pepsin) into the esophagus. GERD is attributed to delayed gastric emptying, weak lower esophageal sphincter, tight-fitting clothes, bingeing, and escalated acid secretion.
Epidemiology
GERD affects a third of the US population each month, while 5-7% are affected every other day (Clayton & Willihnganz, 2013, p. 519). Pregnant women have the highest incidences of GERD due to elevated intra-abdominal pressure and a relaxed effect of progesterone on the lower esophageal sphincter (Hershcovici & Fass, 2012, p. 179). Nonetheless, its prevalence is positively correlated with age.
Symptoms
According to Clayton and Willihnganz (2013), the main symptoms usually are regurgitation, burning sensation, belching, and bloating. However, other less common symptoms include chest pain, hiccups, nausea, and lumps in the throat.
Treatment
Treatment is imperative in GERD because it aims to decrease the frequency and duration of reflux, prevent recurrence and heal the injured tissue (Clayton & Willihnganz, 2013). Treatment entails weight management, which entails losing excess weight. It also entails identifying foods that cause an increase in acid production, avoiding or moderating smoking, and consumption of alcohol. In addition, health care providers advise patients on the consumption of small but frequent meals. Treatment also includes maintaining an upright position for 2 hours after consumption of food, avoiding food consumption before bedtime, and wearing loose-fitting clothes, especially around the abdominal area. Lozenges, antacids, and alginic acid therapy are effective among patients with infrequent heartburn.
Peptic Ulcer Disease
Pathophysiology
This disease is a result of an imbalance between the acid contents of the stomach and the body’s defense barriers, subsequently resulting in ulcerations in the GI tract. PUD includes gastric and duodenal ulcers. Even though Helicobacter pylori is not part of the gastric antrum of almost every patient with duodenal ulcers, it is partly responsible for causing the disease. But, ulcers attributed to this microorganism are easy to treat and recur less often (Rubin & Reisner, 2014, p. 361).
The actual mechanism through which H. pylori leads to duodenal is unknown completely. However, formulated theories suggest that the production of cytokines by the inflammatory cells as a response mechanism to infection result in the release of gastrin and suppression of somatostatin secretion. In addition to the release of histamine metabolites, the cumulative effects trigger the secretion of gastric acid. H. Pylori, on the other hand, leads to 75% cases of gastric ulcers. It is important to note that individuals with gastric ulcers secrete less acid than normal persons and individuals with duodenal ulcers. Therefore, the ulceration in this disease may be attributed to other factors (Rubin & Reisner, 2014).
Epidemiology
10% of Americans are believed to get the disease at some point in their lives (Clayton & Willihnganz, 2013). Duodenal ulcers are more prevalent among adults between the ages of 30 and 60 than gastric ulcers, which mainly affect individuals in their middle age. Duodenal ulcers affect more men than women, but gastric ulcers affect men and women in a similar pattern.
Gastritis
Pathophysiology
Gastritis is an inflamed stomach lining, which is otherwise called the gastric mucosa. Gastritis is either acute or chronic. It is attributed to a spectrum of factors:
Dietary indiscretions, steroids, reflux of duodenal contents, nonsteroidal anti-inflammatory drugs, alcohol, ingestion of poisons or corrosive substances, caffeine, food allergies, use of aspirin, cigarette smoking, and vaso-constriction attributed to stress response (Timby & Smith, 2014, p. 731).
The causative factor for chronic gastritis is the helicobacter pylori. Autoimmune gastritis results when the body attacks itself, specifically the lining of the stomach. The aftermath is an eroded lining. This kind of gastritis is due to autoimmune disorders and a lack of vitamin B12 (Silbernagl & Lang, 2010).
Triggering factors that include seeing, smelling, and eating food cause the parietal cells within the stomach to increase the production of hydrochloric acid. The release of histamine and acetylcholine by the parasympathetic vagus nerve also triggers the parietal cells. The increased acid production catalyzes the conversion of pepsinogen to pepsin. The resultant is a chemical mixture in the stomach that can digest the stomach wall (Timby & Smith, 2014, p. 731). It is important to note that pepsin on its own does not have a major effect on the stomach wall.
Treatment
Treatment of gastritis is dependent on the causative agent. Health care workers deliver emergency treatment in cases of poison ingestion. Individuals eat with restriction in acute cases and IV fluids are given correct dehydration. Antiemetics control nausea and vomiting while antibiotics treat the infection.
Factor
The pathogenesis of GERD, PUD, and gastritis is influenced by the behavior of an individual. Unhealthy behavior linked to substance abuse triggers the occurrence of these diseases, and so does their treatment.
Similarities among the three disorders
The behavioral risk factor associated with substance abuse prevail in all three conditions.
All the three disorders interlink because one is a precedent of the other. Gastritis is the initial disease that results in heartburn and later in ulceration.
Differences
Each of the diseases discussed in this paper affects particular age groups, though some may overlap. GERD, for instance, is common among children while gastritis is common among older adults. Ulceration is not a characteristic of GERD as compared to PUD and gastritis.
Mind Map-Gastritis
References
Clayton, B., & Willihnganz, M. (2013). Basic Pharmacology for Nurses (16th ed.). Missouri: Elsevier Inc.
Hershcovici, T., & Fass, R. (2012). Gastroesophageal Reflux Disease.
In C. Hawkey, J. Bosch, J Richter, G. Garcia-Tsao & F. Chan. (Eds.). (2012). Textbook of clinical gastroenterology and hepatology (2nd ed.) (p. 177-193). Oxford: Blackwell publishing Ltd.
Rubin, E., & Reisner, H. (2014). Essentials of Rubin’s Pathology (6th ed.). Baltimore: Wolters Kluwer.
Silbernagl, S., & Lang, F. (2010). Color Atlas of Pathophysiology (2nd ed.). Kirchhentellinsfurt: Georg Thieme Verlag KG.
Timby, B., & Smith, N. (2014). Introductory Medical-surgical Nursing (11th ed.). Philadelphia: Wolters Kluwer Health.