Heartburn Medicines Information

 

Heartburn Medicines

Gastric Antacids 
Antacids are weak bases that react with gastric hydrochloric acid to form salt and water. They are employed in the treatment of hyperchlorhydria and peptic ulcer, collectively known as acid-peptic disease. Peptic ulceration can occur at the outlet of the stomach (pyloric ulcer), or in the duodenal bulb, where it is usually single. Gastric ulcer is becoming more common as the population lives longer, or “stress” like brain injury, trauma, burns, drugs, and severe infections may cause peptic ulceration.

Heartburn Medicines Classification

Antacids are divided into two classes: (i) systemic antacids of which sodium bicarbonate is the only example; and (ii) non-systemic antacids, which either form insoluble products in the small intestine or contain a non-absorbable cation, e.g., calcium carbonate, magnesium hydroxide, magnesium trisilicate, and aluminium hydroxide. This category of antacids is preferred as cationic portion is not absorbed from the intestine and the pH is raised to only about 4, whereby peptic digestion continues normally. They are often referred to a non-systemic buffer antacids.

SYSTEMIC ANTACID
Sodium Bicarbonate: Sodium bicarbonate (baking soda) is the only systemic antacid that has been used clinically. It has a rapid onset and short duration of action since it is highly soluble, and offers rapid relief of pain.

NON-SYSTEMIC ANTACIDS 
Calcium Carbonate: Calcium carbonate is a non-systemic antacid, and its reaction with HCl in the stomach is not as rapid as of sodium bicarbonate, and for this reason it produces a more prolonged reduction in gastric acidity.

Magnesium Hydroxide: Powered magnesium oxide in a water suspension is hydrated to magnesium hydroxide. Magnesium hydroxide mixture (milk of magnesia) is used primarily as an antacid-laxative mixture in young children.

Magnesium Trisilicate: Magnesium trisilicate is a hydrate magnesium silicate.

Aluminium Hydroxide: Aluminium hydroxide is the prototype aluminium and is the most commonly used agent of this group.
The advantages of aluminium hydroxide are its relative palatability and its lack of serious toxic effects.

Milk: Milk is a weak antacid and also possesses some protective action, and a “milk drip” containing aluminium hydroxide gel administered through a Ryle’s tube into the stomach may promote healing of the ulcer.

Anticholinergic Drugs: Anticholinergic drugs like propantheline reduce the inter and postprandial secretion of gastric juice, these phases are partly under cholinergic control.

H2 Antagonists

Cimetidine: Cimetidine was the first histamine H antagonist available for clinical use, and contains an imidazole ring. It reduces fasting and stimulated acid and pepsin secretion by competitively antagonizing the action of histamine on H2-receptors.

Ranitidine: It has a thiazole ring. The elimination half-life is 2.5 to hours. Like Cimetidine, it has a low incidence of toxicity. Side effects include confusion, a low incidence of toxicity.

Famotidine: It contains a furan ring structure.

Roxatidine: It is a new antagonist, 4 times more potent than Cimetidine.

Carbenoxolone Sodium: Carbenoxolone is a derivative of glycyrrhizinic acid, a constituent of liquorice root. It accelerates the healing of gastric ulcers, but the mode of action is controversial.

Proton Pump Inhibitors

Omeprazole: It inhibits gastric acid secretion by blocking the HtK triphosphatase (ATPase) enzyme system (the “proton pump”) of the gastric parietal cells.

Lansoprazole: It is a proton pump inhibitor, and inhibits the ultimate step in gastric acid secretion. It is used for short-term treatment of gastric and duodenal ulcer, reflux oesophagitis, stricturing and erosive oesophagitis. In combination with antibiotics Lansoprazole may be used for eradication of H. pylon infection.
Pantoprazole is another proton pump inhibitor with similar actions and uses.

Colloidal bismuth promotes healing of duodenal ulcers. The anti pepsin activity may be partly responsible, but in addition bismuth may react with necrotic tissue in the ulcer crater, denaturing the protein and creating a physical barrier protecting the viable tissue.