Acid secretion present from birth and reaches adult levels (by weight) at the age of 2 years. In older patients who develop chronic gastritis, acid formation decreases, but otherwise it is maintained throughout life.
Gastric acid is produced by the parietal cells in the proximal two-thirds (body) of the stomach. Gastric acid aids in digestion, by ensuring an optimum pH for pepsin and gastric lipase and stimulates bicarbonate secretion of the pancreas. Acid secretion is initiated by Food: the thought of and the smell or taste of food causes a vagal stimulation of gastrinsezernierenden G-cells in the distal third of the stomach (antrum). Once protein reaches the stomach, gastrin releasing addition. Circulating Gastrin triggers the release of histamine from cells in the gastric body enterochromaffinähnlichen. Histamine stimulates the parietal cells via their H2 receptors. The parietal cells to secrete acid and the consequent drop in pH causes the D-cells of the antrum of releasing somatostatin which in turn inhibits the release of gastrin (negative feedback control). Acid secretion present from birth and reaches adult levels (by weight) at the age of 2 years. In older patients who develop chronic gastritis, acid formation decreases, but otherwise it is maintained throughout life. Normally, the gastrointestinal mucosa is protected by a number of different mechanisms: 1. mucosal production of mucus and HCO3 establishes a pH gradient between the gastric lumen (low pH) and the mucosa (neutral pH). The mucus serves as a barrier for the diffusion of acid and pepsin. 2. Epithelial cells eliminate a surplus of protons (H +) by membrane transport systems and so-called have. Tight junctions, which prevent the back diffusion of H + ions. 3. The blood circulation in the mucosa removed the excess of acid, which is diffused through the epithelial layer. Several growth factors (e.g., EGF, epidermal growth factor;. IGF-I, insulin-like growth factor I), and prostaglandins have been held responsible for mucosal repair and the maintenance of mucosal integrity. Factors that interfere with these defense mechanisms of the mucous membrane (v. A. NSAIDs and Helicobacter pylori infection) predispose to gastritis and peptic ulcer disease one. NSAIDs supports a mucosal inflammation and ulceration (sometimes with gastrointestinal bleeding) both locally and systemically. By inhibition of prostaglandin production by blocking the enzyme cyclooxygenase (COX) NSAIDs reduce the blood circulation in the stomach, reducing the formation of slime and HCO3- secretion and affect cellular repair mechanisms and cell replication. Since NSAIDs constitute weak acids and are present in nonionized form at the pH of the stomach, they diffuse freely through the mucosal barrier in the epithelial cells of the stomach, where H + ions are released and result in other cellular damage. Because the acid production of the stomach via the COX-1 isoforms running, NSAIDs, which act as selective COX-2 inhibitors, have less adverse effects on the stomach than other NSAIDs.