Gastrointestinal Motility Disorders (Gastritis, PUD and GERD)

Gastrointestinal Motility Disorders (Gastritis, PUD and GERD). Currently, many persons are unable to differentiate the various types of gastrointestinal motility disorders. Such a state of confusion is undesirable given that these conditions are very common.Among the commonly occurring gastrointestinal disorders that are existent in the contemporary world are gastritis, peptic ulcer disease (PUD) and gastro-esophageal reflux disease (GERD). In essence, this paper focuses on differentiating the pathophysiological mechanisms of these gastrointestinal motility disorders. Moreover, the discussion aims at highlighting the impact of a specific patient factor (genetics) on the pathophysiology, diagnosis, and treatment of these disorders. Finally, the paper will further enhance the understanding of these conditions by offering a visual representation of one of the gastrointestinal disorders (gastritis)in the form of a mind map.

Epidemiology of Gastrointestinal Motility Disorders (GERD, PUD and Gastritis)

According to Buttaro,Trybulski, Polgar-Bailey, and Sandberg-Cook, (2013),GERD is the most prevalent of all gastrointestinal disorders since it affects 10% of the total adult population, which translates to 4-5million physician visits yearly.As for the gastritis, it accounts for1.8-2.1 million visits to physicians in the USA.

On the contrary, approximately 500000 is the estimated number of persons in the USA that suffer annually from PUD and $ 10billion is the cost used for managing these persons yearly (Buttaro et al., 2013).

 Normal Pathophysiology of Gastric Acid Stimulation and Production

Normally, three substances are responsible for stimulation of gastric acid (H+) secretion by gastric parietal cells: Acetycholine (Ach) (increases parietal cell’s secretory activity to stimulate hydrochloride acid (HCL) production), histamine (stimulate the parietal cells to secrete HCL), and gastrin (secreted into the circulation and travels to the parietal cells where it stimulates production of HCL). Gastric acid secretion occurs in three phases namely, cephalic (30%), gastric (60%) and intestinal (10%) phases. Central to the regulation of this gastric acid secretion pathway is the somatostatin hormone, which acts as an inhibitor to the secretory pathway. The presence of food and gastric acid also stimulates cytoprotective mechanisms (mucosal bicarbonate and mucus secretion), which protect the gastric mucosa from the acid’s erosive nature (Huether & McCance, 2017).

However, in gastrointestinal motility disorderstates such as gastritis, PUD and GERD the hemostatic mechanisms become abnormal in the event of exposure to etiological factors in at-risk individuals. Upon exposure, individuals start to experience excessive gastric acid secretion and deficient cytoprotective mechanisms, which contribute to the development of gastric disorders (Copstead-Kirkhorn & Banasik, 2014).

Clinical Presentation

Primarily, individuals with gastritis present with clinical manifestations such asabdominal discomfort (burning or gnawing feeling), anorexia, nausea, headache,lassitude, vomiting, andhiccupping (Porth, & Gaspard, 2015).

On the other hand, PUD patients manifest with several signs and symptoms that are worth noting. They include post prandial epigastric pain, radiating to the right shoulder often relieved with consumption of food or fluids, discomfort between meals (duodenal ulcers, eating usually alleviates discomfort whilein gastric ulcers, pain often worsens after meals), hematemesis, melena, dizziness and syncope (Hinkle, Brunner, Cheever, & Suddarth, 2014).

Finally, in GERD, patients present with clinical manifestations such as heartburn, dysphagia, regurgitation that may lead to aspiration or bronchitis, coughing, hoarseness of voice, nausea, vomiting and wheezing (Nahikian-Nelms, & Sucher,2015).

Impact of Genetics on the Pathophysiology of Gastrointestinal Motility Disorders

Hinkle, Brunner, Cheever, and Suddarth(2014) are of the opinion that gastritis, GERD and PUD are more likely to occur in persons that have a family history of any of these conditions. Central to this vulnerability are conditions such as Helictobacter pylori infection, Crohn’s disease and Zollinger-Ellison syndrome are familial and therefore predisposing individuals who have first-degree relatives with these disorders.

Impact of Genetics on the Diagnosis and Treatment of Gastrointestinal Motility Disorders

Diagnosis

Primarily, genetics has alimited influence on the choice of tests used to diagnose these conditions. Of the essence to the diagnosis of these disorders in genetic predisposed persons are various tests. Other than history taking, physical examination, they include H. pylori testing, barium swallow, endoscopy, gastric secretion analysis, complete blood count and stool for occult blood (Huether & McCance, 2017).

Treatment

Central to the management of these disorders is the collaborative management approach that combines pharmacological, surgical and non-pharmacological interventions. Primarily, the pharmacological interventions comprises of medications such as H2 receptor blockers(Cimetidine, ranitidine (Zantac), nizatidine, famotidine– they decrease HCl production), Sucralfate(mucosal barrier protector), Antacids (to neutralize acid), Omeprazole (proton pump inhibitor that restricts HCl production), Misoprostol (synthetic PG E1 for cytoprotection)and analgesics (Woo, & Robinson, 2016).

Surgery is also an option for patients with extreme worsened conditions, which would benefit significantly from procedures such as gastrojejunostomy, and vagotomy (Hinkle, Brunner, Cheever, & Suddarth, 2014).

Non-pharmacological interventions on the contrary entail measures such as dietary management (taking balanced diet, 3 meals per day, aversion of irritating substances such as nicotine, alcohol, spices, gas producing foods, caffeine, pepper, acidic foods (green leafy vegetables), soda, fried and oily foods as well as plenty of milk consumption), and physical as well as mental rest (Buttaro et al., 2013).

Mind Map of Gastritis

 

 

 

References

Buttaro, T., Trybulski, J., Bailey, P., Sandberg-Cook, J. (2013). Primary care a collaborative practice (4th ed.). [VitalSource Bookshelf Online]. Retrieved from https://digitalbookshelf.southuniversity.edu/#/books/978-0-323-07501-5/

Copstead-Kirkhorn, L., & Banasik, J. L., (2014). Pathophysiology (5th ed.).

Hinkle, J. L., Brunner, L. S., Cheever, K. H., & Suddarth, D. S. (2014). Brunner & Suddarth’s textbook of medical-surgical nursing

Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (Laureate customed.). St. Louis, MO: Mosby.

Nahikian-Nelms, M., & Sucher, K. (2015). Nutrition therapy and pathophysiology.Boston, MA: Cengage Learning.

Porth, C., & Gaspard, K. J. (2015). Essentials of pathophysiology: Concepts of altered health states. Philadelphia: Wolters Kluwer.

Woo, T. M., &Robinson, M. V. (2016). Pharmacotherapeutics for advance practice nurse prescribers. Philadelphia: F.A. Davis Company

 

 

 

 

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