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.
Cases like these are not uncommon. The mother was concerned and thinking her daughter may have an allergy; she changed to a different formula. However, sometimes babies have immature GI tracts that can lead to physiology reflux as they adapt to normal life outside the uterus. Parents often do not consider this possibility, prompting them to change formulas rather than seeking medical care. As in the case study above, GI alterations can often be difficult to identify because many cause similar symptoms. This same issue also arises with adults adults may present with symptoms that have various potential causes. When evaluating patients, it is important for the advanced practice nurse to know the types of questions he or she needs to ask to obtain the appropriate information for diagnosis. For this reason, you must have an understanding of common GI disorders such as gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and gastritis.
Review this week’s media presentation on the gastrointestinal system.
Review Chapter 33 in the Huether and McCance text. Identify the normal pathophysiology of gastric acid stimulation and production.
Review Chapter 35 in the Huether and McCance text. Consider the pathophysiology of gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and gastritis. Think about how these disorders are similar and different.
Select a patient factor different from the one you selected in this week’s Discussion: genetics, gender, 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.
Review the Mind Maps Dementia, Endocarditis, and Gastro-oesophageal Reflux Disease (GERD) media in the Week 2 Learning Resources. Use the examples in the media as a guide to construct a mind map for gastritis. Consider the epidemiology and clinical presentation of gastritis.
Write a 2- to 3-page paper that addresses the following:
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.
The gastrointestinal tract is composed of four distinct regions that perform different functions. These regions are the esophagus, the stomach, the intestines and the colon. The esophagus is responsible for conveying food from the mouth to the stomach where it is crushed and digested by enzymes. The nutrients are absorbed within the intestines into the blood stream and afterwards water is absorbed within the colon before the waste is eliminated from the body.
Normal pathophysiology of Gastric Acid Secretion and Production
The gastric phase begins as food is entering and distending into the stomach. When the food distends into the stomach, there occurs a parasympathetic reflex to the brain which activates the secretion of gastric juices. After digestion is complete in the stomach, the chime goes into the small intestines and hence the intestinal phase takes over. When the pH of the chime falls below 2, the gastric secretion in the lower part of the stomach is inhibited.
There are various nerve pathways that act for the inhibition and secretion mechanisms by checking on the release of chemo transmitters into gastric mucosa. These chemo transmitters are vital in regulating the gastric secretion of pepsin and hydrochloric acid. The secretion of these acids occurs in three phases; cephalic, intestinal, and gastric. These three phases sometimes occur simultaneously. The cephalic phase is triggered by taste, thought, sight, smell, and swallowing of food (Huether & McCance, 2012). These triggers send a nervous impulse to the medulla oblongata causing parasympathetic reflex to travel via the vagus nerve thus stimulating the secretion of pepsin and hydrochloric acid in the stomach. Gastrin hormone is then released from the lower part of the stomach traveling through the bloodstream and causing a further secretion of pepsin and hydrochloric acid in the middle and upper parts of the stomach.
Changes that occur to gastric acid stimulation and production with GERD, PUD, and gastritis disorders
An imbalance in gastric acid secretion within the stomach causes the erosion of the mucosa lining and often leads to the development of gastrointestinal system disorders such as PUD, GERD, and Gastritis. These gastrointestinal disorders develop when chemo transmitters fail to carry out their roles efficiently. This causes more gastric acids to continue to be secreted long after the food has left the upper stomach (Kahrilas, 2011). The excess acid corrodes the stomach lining and causes ulcers. When the excess acid trickles down to the abdomen, it induces the development of PUD and when it is regurgitated to the esophagus region it could cause GERD.
Genetics as a factors that might impact the pathophysiology of GERD, PUD, and gastritis
Clinical research shows that genetics is a factor that can make a patient to be more susceptible to GERD. Genes with the ability to alter the production and secretion of gastric acid are said to influence the development of GERD. The DNA pair pathway has also been found to influence the development of GERD. The presence of the Lewis antigen (Le-b) and H antigen in the bloodstream will provide receptor sites for the attachment of the Helicobacter Pylori which causes the development of PUD and Gastritis.
Diagnosis and Treatment
Gastroesophageal Reflux Disease (GERD) is diagnosed by three main tests namely; endoscopy, esophageal pH monitoring, and manometry. For mild symptoms, the test used is endoscopy. This test is conducted by inserting a flexible tube light and camera through the throat into the esophagus and checking for any inflammations (esophagitis). Esophageal pH monitoring testing method measures the amount of acid sampled from the esophagus over a 24-48 hours period. This test is essential for a doubtless diagnosis especially in asymptomatic cases. This test is also used to determine if the patient should be surgically treated (Yaghoobi, Farrokhyar, Yuan & Hunt, 2010). Manometry is used to test and identify the problems associated with valve pressure and motility in the esophagus. Although GERD is a chronic disease, it is usually manageable. The treatment entails the active reduction of the amount of acid secreted in the stomach. Over the counter and prescription antacids are used to manage this condition.
- pylori infection and NSAIDs are the main causes for the development of PUD. This condition is diagnosed through various methods such upper GI series X-ray, H. pylori testing, endoscopy and gastroscopy. PUD is treated through various procedures which include but not limited to prophylactic treatment of H. pylori, and limiting the use of NSAID (Kahrilas, 2011). Preventive measures and lifestyle changes such as reduction of alcohol intake levels and avoidance of hard drugs and stressors reduces the incidences of PUD.
Acute gastritis is manifested through symptoms such as gnawing, burning pain, epigastric pain, nausea, vomiting blood, and loss of appetite. This condition is caused by a wide range of factors such as H. pylori bacterial infections, certain medications like aspirin or corticosteroids, drinking or eating corrosive substances, excessive alcohol intake and extreme stress. Diagnosis entails various tests such as complete blood count, stool test for blood, gastroscopy, small bowel and upper GI x-ray tests. Acute gastritis is treated by antacids that reduce acidity in the stomach and promote healing. Gastritis caused by stress is normally managed by behavioral therapy while that caused by certain medications are treated by avoidance of these medications (El-Zimaity, 2008).
Mind Map for Gastritis
El-Zimaity, H. (2008). Gastritis and gastric atrophy. Current opinion in gastroenterology, 24(6), 682-686.
Huether, S. E., & McCance, K. L. (2012). Understanding pathophysiology (Laureate custom Ed.). St. Louis, MO: Mosby.
Kahrilas, P. J. (2011). GERD pathogenesis, pathophysiology, and clinical manifestations. Cleveland Clinic journal of medicine, 70 Suppl 5, S4-S19.
Yaghoobi, M., Farrokhyar, F., Yuan, Y., & Hunt, R. H. (2010). Is there an increased risk of GERD after Helicobacter pylori eradication?: a meta-analysis. The American journal of gastroenterology, 105(5), 1007-1013;