Suppresses gastric acid secretion by inhibiting the gastric H,K-ATPase or the proton pump. Proton pump inhibitors are used to promote healing of gastric and duodenal ulcers and to treat GERD, including erosive esophagitis, which is either complicated or unresponsive to treatment with H2 receptor antagonist. They are also the mainstay in the treatment of pathological hypersecretory conditions, such as the Zollinger-Ellison syndrome. Drugs: Omeprazole, lansoprazole, pantoprazole, esomeprazole, rabeprazole, dexlansoprazole
Act selectively on H2 receptors in the stomach, blood vessels, and other sites, but they have no effect on H1 receptors. They are competitive antagonists of histamine and are fully reversible. However, recurrence is common after treatment with H2 antagonists is stopped. Patients with NSAID-induced ulcers are advised to be treated with PPIs, because these agents heal and prevent future ulcers better than H2 antagonists. Drugs: Cimetidine, famotidine, nizatidine, ranitidine
Bacteriostatic agent that inhibits protein synthesis by binding reversibly to 50s ribosomal subunits of sensitive organisms including H. pylori.
Has bactericidal property which action is to interfere with the last step of bacterial cell wall synthesis, resulting in exposure of the osmotically less stable membrane which leads to cell lysis. Penicillins are only effective against rapidly growing organisms that synthesize a peptidoglycan cell wall such as H. pylori.
Has antibacterial activity against all anaerobic cocci and both anaerobic gram-negative bacilli and anaerobic spore-forming gram-positive bacilli. It is clinically effective in trichomoniasis, amebiasis, and giardiasis, and in a variety of infections caused by obligate anaerobic bacteria, and microaerophilic bacteria such as Helicobacter and Campylobacter spp.
Inhibit bacterial protein synthesis by binding to the 30S bacterial ribosome and preventing access of aminoacyl-tRNA to the acceptor (A) site on the mRNA-ribosome complex. They enter gram-negative bacteria, such as H. pylori, by passive diffusion through channels formed by porins in the outer cell membrane and by active transport that pumps tetracyclines across the cytoplasmic membrane.
Suppresses action of H. pylori by promoting ulcer healing due to inhibition of pepsin activity, increase in mucosal prostaglandin production and mucus and bicarbonate secretion. It is largely unabsorbed and is excreted in feces. In the colon it reacts with hydrogen sulfide and forms bismuth sulfide, which blackens the stools.
a. Bismuth subsalicylate
Nonabsorbable medication that binds to gastric mucosa and ulcerated tissue. These properties favor healing and provide cytoprotective effects. When exposed to gastric acid the sulfate ions bind to proteins in the damaged gastric tissue of ulcer craters and stimulate angiogenesis, delivery of growth factors and formation of granulation tissue.