Pathophysiology of Gastric Acid Stimulation and Production
The gastrointestinal tract is inclusive of the mouth, pharynx, esophagus and stomach, the large and small intestines. The stomach, which is a saclike organ, functions to organize food for digestion and absorption by the intestines; the production of acids, to aid in the digestive process, is essential because acids immerse food bolus that is stored in the stomach, thus facilitating dejection. Normal gastric acid stimulation and production are essential to the efficient functioning of the digestive system (Lowry, Bhakta, & Nag, 2011). Changes in normal gastric acid stimulation and production result in Gastroesophageal reflux ...view middle of the document...
Once food is eaten, the G cells respond by secreting gastrin through that joins to CCK2 receptors on ECL and parietal cells. This joining of gastrin and parietal cells causes the release of calcium which activates the proton pump (Lundell, 2011). The combination of gastrin and ECL cells results in the creation of histamine that eventually joins to H2 receptors. The gastric mucosal barriers function to protect the surface of the stomach from self-digestion. However, dysfunction of the mucosal barriers can lead to gastric disease conditions recognized by inflammation of the stomach lining. Overtime, the presence of gastric acid and enzymes that are exist in gastric secretion cause digestive disease such as GERD, PUD and gastritis (Huether & McCance, 2014).
Changes in Gastric Acid Stimulation and Production in GERD, PUD and Gastritis
Changes in gastric acid stimulation and production in GERD, PUD and Gastritis conditions impact their pathophysiology and severity. GERD is a digestive disease condition that affects the lower esophageal sphincter (LES).GERD causes the acid in the stomach or the food content of the stomach to reflux into the esophagus. This reflux causes irritation of the esophagus’s lining. During normal digestive process, the lower digestive sphincter (LES) opens to allow food into the stomach and closes to prevent food and acidic juices from flowing back into the esophagus. The weakening of the LES results in the return of food and gastric acid into the esophagus.
Peptic ulcer disorder (PUD) is characterized by painful open sores or ulceration caused by disruption of the “protective lining” of the stomach, lower esophagus or duodenum (Huether & McCance, 2014). The exact cause or causes of peptic ulcer is unknown, but what is certain is the fact that increased gastrin secretion results in extreme secretion of gastric acid. This excess secretion of gastric gas results in gastric and duodenal ulcers, GERD and abdominal pain and diarrhea PUD can be labelled as acute or chronic based on it pathophysiology. The colossal increase of gastric acid happens as a result of increased parietal cells experiencing an upsurge in secretion of gastric acid (Huether & McCance, 2014).
When the gastritis mucosa is inflamed a condition known as gastritis results. Gastritis can also be acute or chronic and it may affects the fundus or antrum and in some cases both. According to Schubert & Peura (2008), gastritis occurs suddenly or overtime and is characterized by exasperation, destruction or soreness of the stomach’s lining. Gastritis is influenced by the over-production and secretion of insulin and gastric acid, which interferes with the ability of the mucosal lining of the stomach to provide defense. Changes in the gastric secretion can result in abdominal discomfort, epigasgastric tenderness and bleeding (Huether & McCance, 2014)
Impact of Selected Patient factor on Pathophysiology on GERD, PUD and Gastritis...