****USE CURRENT RESOURCES LESS THAN 5YRS OLD****
Jamie is a 3-month-old female who presents with her mother for evaluation of “throwing up.” Mom reports that Jamie has been throwing up pretty much all the time since she was born. Jamie does not seem to be sick. In fact, she drinks her formula vigorously and often acts hungry. Jamie has normal soft brown bowel movements every day and, overall, seems like a happy and contented baby. She smiles readily and does not cry often. Other than the fact that she often throws up after drinking a bottle, she seems to be a very healthy, happy infant. A more precise history suggests that Jamie does not exactly throw up “she does not heave or act unwell” but rather it just seems that almost every time she drinks a bottle she regurgitates a milky substance. Mom thought that she might be allergic to her formula and switched her to a hypoallergenic formula. It didn’t appear to help at all, and now Mom is very concerned.
*Select a patient factor: genetics, ethnicity, age, or behavior. Consider how the factor you selected might impact the pathophysiology of GERD, PUD, and gastritis. Reflect on how you would diagnose and prescribe treatment of these disorders for a patient based on this factor.
Write a paper to include:
*Introduction
*Describe the normal pathophysiology of gastric acid stimulation and production. Explain the changes that occur to gastric acid stimulation and production with GERD, PUD, and gastritis disorders.
*Explain how the factor you selected might impact the pathophysiology of GERD, PUD, and gastritis. Describe how you would diagnose and prescribe treatment of these disorders for a patient based on the factor you selected.
*Construct a mind map for gastritis. Include the epidemiology, pathophysiology, and clinical presentation, as well as the diagnosis and treatment you explained in your paper.
*Conclusion
Gastrointestinal Tract: Disorders of Motility
Introduction
Some of the classic symptoms of GERD include regurgitation and heartburn. If the patient is complaining of a burning sensation that arises from the stomach and travels to the neck or chest, this is most likely as a result of GERD. PUD (Peptic Ulcer Disease) is characterized by discomfort and pain that is localized in the central abdomen. Gastritis is the erosion, irritation, or inflammation of the stomach lining (Correa, 2012).
Pathophysiology
Gastric acid stimulation and production is determined by histamine that is secreted by ECL (enterochromaffin-like cells). These cells are based in the oxyntic gland. ECL are stimulated by the nervous and endocrine system. The production and stimulation of gastric acid is controlled in three phases (Blaser, 2010).
Cephalic phase; the thought, taste, smell, or sight of food causes hypothalamus, amygdala, and cerebral cortex impulses to send impulses via the vagus nerve, which triggers gastric acid secretion and production.
Gastric phase; food that is in the stomach triggers reflexes, which stimulates gastrin secretion. This results to gastric acid secretion and production (Correa, 2012).
Intestinal phase; food in the small intestines/ duodenum makes the duodenal mucosa to produce gastrin. This still stimulates secretion of small gastric acid amounts. However, food in the small intestine primarily prevents gastric acid secretion via other mechanisms (Correa, 2012).
The stomach acid produces gastric acid as well as other digestive enzymes that are vital for food digestion. The stomach is lined by a mucosa that is resistant to digestion by these acids through secretion. As a result of imbalances, the acid may act on the gastric mucosa and digest them, which results to PUD or gastritis. In GERD (gastro esophageal reflux disease), the acid refluxes above the cardiac sphincter thereby burning the mucosa’s lining on the lower oesophagus (Blaser, 2010).
Factor, diagnosis, and treatment
GERD
GERD’s prevalence peaks between 1-4 months of age. It however resolves by 6-12 months of age. No definite peak onset age or gender predilection beyond infancy has ever been established. Regurtation is common in 40-65% of healthy infants but reduces to 1% by 1 year of age.
Regardless of the fact that scintigraphy best quantifies gastric aspiration and emptying, endoscopy and esophageal biopsy, esophageal 24-hour pH probe, and barium fluoroscopy are commonly used. There is no single definitive study for diagnosing GERD. There is a need to consult with a pediatric gastroenterologist (Correa, 2012). Some of the medications that can be used for treatment include prokinetic agents, H2-receptor antagonists, lansoprazole, and omeprazole.
Gastritis
Stimulated acid output is less among the elderly. However, gastritis may prevail die to smoking and H. pylori infection (Blaser, 2010). The disease is diagnosed through endoscopy. The disease can be treated though eradicating H. pylori if present and acid-suppressive drugs.
PUD
Older people are at a higher risk of suffering from PUD. This is as a result of a combination of factors. Aging is linked to reduced prostaglandin, bicarbonate, and mucus production, which predisposes PUD development. The elderly also suffer from cardiovascular diseases and arthritis, which leads to the use of NSAIDs and aspirin. There is also a higher prevalence of H. pylori during old age. Moreover, the elderly are more prone to higher smoking rates and cumulative smoke exposure years. PUD is diagnosed through endoscopy and serum gastrin levels. It can be treated through eradicating H. pylori if present and acid-suppressive drugs (Blaser, 2010).
Mind map for gastritis
Conclusion
Regardless of the fact that PUD, GERD, and gastritis are closely related, it is important to seek the real disease and its cause so as to ensure the appropriate treatment. Age plays a crucial role in the pathogenesis of the three diseases and it determines the diagnosis and treatment. Keen diagnosis is necessary to ensure proper treatment.
References
Blaser, M. J. (2010). Gastric Campylobacter-like organisms, gastritis, and peptic ulcer disease. Gastroenterology, 93(2), 371-383.
Correa, P. (2012). Chronic gastritis: a clinico-pathological classification. The American journal of gastroenterology, 83(5), 504-509.