Gastrointestinal Tract: Disorders of Motility
The stomach plays a central role in the digestive tract handling digestion and regulating secretion and motility. This paper highlights the pathophysiology of gastric acid stimulation and production in light of gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and gastritis.
Gastric acid stimulation and production
The stimulation of gastric acid production often takes place in three different phases: cephalic, gastric and intestinal. The first is the cephalic phase which is extrinsic and occurs via the vagus nerve which is stimulated when food is seen, smelled, thought of or tasted. Impulses are sent from the hypothalamus, amygdala and the cerebral cortex through the vagus nerve thereby triggering gastric acid secretion (Sembulingam & Sembulingam, 2012). In the gastric phase, the local receptors in the stomach wall lining are stimulated. The presence of food in the stomach sends triggers the secretion of gastrin which stimulates the production of gastric acid. The endocrine system produces the hormone gastrin which is produced by gastrin cells found in the pyloric gland. The hormone gastrin is produced in the stomach upon detection of the presence of protein in the stomach. In the intestinal phase, acid production is caused by stimuli which originate from the duodenum or jejunum. In the duodenum, food causes the mucosa to produce gastrin which secretes gastric acid (Cluysenaer & Tongeren, 2012).
In GERD, decreased elimination of acid as a result of poor motility in the esophagus can contribute to the disease. Some studies have concluded that there is a link between increased gastric acid secretion and GERD (McColl & Gillen, 2009). More so, when the emptying of the acidic contents is delayed, a build-up is likely to be experienced resulting to an increase in the pressure if the reservoir or stomach such that the valve is defeated. In gastritis, the high levels of acidity result in inflammation of the lining of the stomach as high levels of acidity may cause the deterioration of the lining. Peptic ulcer disease is attributed to gastric acid secretion and the presence of H. pylori bacteria (Shils & Shike, 2006).
Impact of Behavior
Behavior largely has an impact on the pathophysiology of GERD, PUD, and gastritis. High levels of gastric acid in the stomach can be attributed to certain lifestyle characteristics. These include substance abuse, alcoholism and excessive intake of beverages which are likely to cause acidity including citric juices and coffee. Others include ingestion of poisons and abuse of drugs which leads to high levels of toxicity in the stomach (Floyd, Mimms, & Yelding, 2007).
GERD Diagnosis and Treatment
They include heartburn, vomiting or regurgitation, and coughing. Diagnosis can be done through tests such as a gastrointestinal endoscopy. An important aspect of diagnosis is to monitor the pH levels of the patient is order to determine the cause of GERD. Treatment of the disorder is aimed at managing the symptoms of the disease and preventing recurrence or worsening of the condition. The first aspect is modification of way of life through encouraging weight loss, reducing the intake of alcoholic substances and beverages such as citric juices and coffee. The patient must equally adhere to eating small meals frequently rather than large meals at once. Pharmacotherapy will entail the administration of antacids such as magnesium hydroxide, antoginists of H2 receptor such as nizatidine and cimetidine (Woo & Robinson, 2015).
Gastritis Diagnosis and Treatment
A common symptom associated with gastritis is stomach pain, heartburn, abdominal upsets and unusually dark stools. The inflammation of the stomach lining is attributed to several aspects including the long term usage of anti-inflammatory drugs which cause the depletion of the stomach lining, increased acidity in the stomach as a result of poor expulsion of the acid, high levels of bile in the stomach and in many cases the bacteria Helicobacter pylori, commonly referred to as H. pylori leads to gastric ulcers. Testing includes the performance of an endoscopy to examining the lining of the stomach as suggested by DiMarino and Benjamin (2002) in order to obtain samples to detect H. pylori. Stool tests are also done to identify the presence or absence of blood in excreta. Treatment involves administering antacids such as calcium carbonate and Milk of Magnesia (magnesium hydroxide). The patient must reduce intake of alcoholic substances and beverages such as coffee. Changes in the diet are intended to reduce levels of acidity hence foods rich in fiber are advised. The presence of H. pylori is treated using antibiotics.
Peptic Ulcer Disease Diagnosis and Treatment
Diagnosis can be done through gastric analysis such as placement of a nasogastric in some portion of the affected tract (Bayless & Diehl, 2005). Symptoms to look out for include bleeding, satiety at an early stage of eating and continuous vomiting. The test for presence of H. pylori must be undertaken. Fecal tests can equally be done. In order to clearly visualize the ulcers, an endoscopy is required as this may reveal the size of the ulcers and help identify possible bleeding. Lifestyle change is required including the avoidance of substance abuse and stress. Antacids, with aluminum hydroxide or magnesium hydroxide, can be prescribed unless the patient is diagnosed with renal failure (Woo & Robinson, 2015).