Gastric Antacids

As the name indicates, these agents are used to neutralize excess gastric acid secretion. In the digestion of food, the important constituents of gastric juice are pepsin (a  proteolytic enzyme) and hydrochloric acid. Pepsin is produced from pepsinogens which are located in mucous neck cells of the oxyntic gland area, mucous neck cells of the pyloric gland, and in  Brunner’s gland. It has a molecular weight of 35,000 and is most active at pH 2.0. Hydrochloric acid is secreted by the oxyntic (or parietal) cells of the stomach. This secretion is under the control of acetylcholine, histamine, and gastrin. Gastrin, a heptadecapeptide was first reported in 1905 by Edkins. It contains seventeen amino acids out of which, only four at the acid end are concerned with its role in the stimulation of acid secretion. It is released from the antrum of the stomach while secretin and pancreozymins are released from the duodenal wall in response to a fall in pH and stimulate the secretion of pancreatic juices. Pentagastrin, one of the gastrin analogs, is a powerful stimulant of acid secretion. All three bases i.e.,  histamine, acetylcholine, and gastrin, through an interlinked mechanism control the turnover of gastric acid. Gastric antacids neutralize excess gastric acid secretion by the mechanism which propagates through.

  1. non-receptor mediated events or 
  2. receptor-mediated events. 

Examples include H2 – receptor blocking agents like cimetidine, ranitidine, etc. 

Gastric acid plays a very important role in the formation of a proteolytic enzyme, pepsin from an inactive precursor and pepsinogen. Gastric acid also provides lower pH to make the pepsin activated. Besides this, it also helps in inducing the release of secretin. 

Gastric acid secretion is governed by histamine receptors, muscarinic receptors, and gastrin receptors. Histamine, acetylcholine, and gastrin promote the secretion of gastric acid by activating these respective receptor sites. Histamine is released by mast cells located in the lamina propria, acetylcholine is released by postganglionic vagal neurons, and gastrin is released from the G cells located in the gastric mucosal antrum. 

H+  – K+  – ATPase pump is involved in the secretion of gastric acid. It is located in the apical membrane of the parietal cell. The release of gastric acid (i.e. intracellular hydrogen ions) occurs through this pump by one-to-one exchange with luminal potassium ions. It is an energy-dependent process. Cyclic AMP and calcium ions stimulate this proton pump resulting in the secretion of gastric acid, while prostaglandins, somatostatin, calcitonin,  glucagon, dopamine, and vasoactive intestinal peptide inhibit gastric acid secretion. Usually, the basal acid secretion is high in the night hours with low levels of acid secretion occurring during the daytime. 

The mucus is the thick, viscous, physiological barrier that protects the gastric mucosa from the attack of pepsin and gastric acid. It is secreted from the surface epithelium columnar cells and the mucous neck cells of the cardiac, oxyntic, and pyloric gland areas. It is secreted along with an alkaline fluid. It consists of glycoproteins and mucopolysaccharides. It increases the life span of gastric epithelial cells by providing a tenacious, slimy, and alkaline coat over the inner surface of the gastric mucosa. 

One of the serious complications of hyperacidity is a peptic ulcer which results due to the digestive action of pepsin and hydrochloric acid on the inner wall of the stomach and duodenum. This results due to the failure of the protective mechanisms of mucosa to prevent the autodigestion process. The feeling of gastric irritation is further potentiated due to increased spasms of GIT. The goals of peptic ulcer treatment are to reduce pain, accelerate

the healing rate, prevent complications, and prevent ulcer recurrence. Peptic ulcer consists of a  group of ulcerative disorders affecting the upper gastrointestinal tract. It is thought to occur from an imbalance between the effects of destructive factors (acid, pepsin, bile salts) and protective factor (mucus, bicarbonate, blood flow, epithelial cell regeneration, and prostaglandin synthesis). Depending upon their location, ulcers can be classified as – 

  1. Esophageal ulcers: They affect the esophagus. 
  2. Gastric ulcers: They affect gastric mucosa. 
  3. Duodenal ulcers: They affect duodenum, and 
  4. Stress-induced or drug-induced ulcers. 

When an ulcer is formed, the gastric acid present in the stomach causes pain and spasm.  This, in turn, inhibits the healing process. The severity of hyperacidity ranges from gastritis  (mucosal inflammation) to peptic ulcer. Most peptic ulcers are chronic and periodically visit the patient. Recurrence is associated with the development of complications, such as bleeding, perforation, penetration, and obstruction. Depending upon the severity and location of an ulcer, one can start the treatment. The main objectives of  treatment are: 

  1. Relaxation of the GIT smooth muscles (i.e. spasmolytic action). It is brought about by anticholinergic agents. However, they are now replaced by more potent and specific  antisecretory agents which have fewer side effects, and 
  2. Reduction in the gastric acid secretion rate (i.e. antacids and H2 – blockers). 

If drug treatment fails to achieve satisfactory results, bed rest and surgery may be needed to manage this chronic, relapsing condition. People with hyperacidity should avoid taking alcohol, coffee, cigarette smoking (stimulants of acid secretion), and mucosa irritating diet.

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