A proton pump inhibitor that converts to active metabolites that irreversibly bind to and inhibit hydrogen-potassium adenosine triphosphate, an enzyme on the surface of gastric parietal cells. Actively secretes hydrogen ions for potassium ions, resulting in an accumulation of hydrogen ions in gastric lumen.
Treatment of gastroesophageal reflux disease (GERD), duodenal ulcers, and hypersecretory conditions (Zollinger-Ellison disease); eradication of Helicobacter pylori infection (with amoxicillin and clarithromycin), H. pylori eradication to reduce risk of duodenal ulcer
Rapidly absorbed from the GI tract after passing through the stomach relatively intact. Protein binding: 96%. Metabolized extensively in the liver. Primarily excreted in urine. Unknown if removed by hemodialysis. Half-life: 1–2 hr (increased with hepatic impairment).
Rapidly absorbed after PO administration. Highly bound to plasma proteins (>95%) and albumin. Undergoes extensive first-pass metabolism in liver. Excreted mainly in feces and, to a lesser extent, in urine. Unknown if removed by hemodialysis. Half-life: 27.7 hr.
Hypertension, fatigue, dizziness, insomnia, rash, pruritus, folliculitis, increased glucose (<250 mg/dl: 9%), increased LDL-cholesterol, hypertriglyceridemia, hyperbilirubinemia, increased AST, increased ALT, increased alkaline phosphatase, arthralgia, extremity pain, increased creatine kinase, increased creatinine, nasopharyngitis, cough, influenza, sinusitis, herpes zoster, lymphadenopathy, anogenital warts
Use with caution in patients taking medications that cause rhabdomyolysis or other risk factors for creatine kinase elevations and/or skeletal muscle abnormalities due to the risk of myopathy (e.g., statins).
(ranitidine hydrochloride: Apo-Ranitidine[can], Ausran[aus], Novo-Ranitidine[can], Rani-2[aus], Ranihexal[aus], Zantac, Zantac-75, Zantac-150, Zantac-300, Zantac EFFERdose, Zantac-25 EFFERdose, Zantac-150 EFFERdose, Zantac-150 Maximum Strength; ranitidine bismuth citrate: Pylorid[aus], Tritec)
Treatment of duodenal ulcer, Zollinger-Ellison syndrome, benign gastric ulcers, hypersecretory conditions, gastroesophageal reflux disease, erosive esophagitis, stress ulcers; unapproved: treatment of GI symptoms associated with NSAID use in rheumatoid arthritis
Rapidly absorbed from the GI tract. Protein binding: 15%. Widely distributed. Metabolized in the liver. Primarily excreted in urine. Not removed by hemodialysis. Half-life: PO, 2.5 hr; IV, 2–2.5 hr (increased with impaired renal function).
! Symptoms of overdose may vary from CNS depression, characterized by sedation, apnea, cardiovascular collapse, and death, to severe paradoxical reactions, such as hallucinations, tremor, and seizures.
! Other serious effects may include involuntary movements, impaired motor coordination, loss of balance, blepharospasm, facial grimaces, feeling of heaviness in the lower extremities, depression, nightmares, delusions, overstimulation, sleep disturbance, and anger.
An antihyperglycemic that stimulates release of insulin from beta cells of the pancreas by depolarizing beta cells, leading to an opening of calcium channels. Resulting calcium influx induces insulin secretion.
Rapidly, completely absorbed from the GI tract. Protein binding: 98%. Metabolized in the liver to inactive metabolites. Excreted primarily in feces with a lesser amount in urine. Unknown if removed by hemodialysis. Half-life: 1 hr.
An antihypertensive that depletes stores of catecholamines and 5-hydroxytryptamine in many organs, including the brain and adrenal medulla. Depression of sympathetic nerve function results in a decreased heart rate and a lowering of arterial B/P. Depletion of catecholamines and 5-hydroxytryptamine from the brain is thought to be the mechanism of the sedative and tranquilizing properties.
Characterized by slow onset of action and sustained effects. Both cardiovascular and CNS effects may persist for a period of time following withdrawal of the drug. Mean maximum plasma levels were attained after a median of 3.5 hr. Bioavailability was approximately 50% of that of a corresponding intravenous dose. Protein binding: 96%. Half-life: 33 hr.
Bacteriostatic binds to protein L2 on the ribosomal 50S subunit, inhibits peptidyl transfer and blocks P-site interaction to prevent formation of this subunit; therefore, inhibits bacterial protein biosynthesis.
Active internal bleeding, AV malformation or aneurysm, bleeding diathesis, history of cerebrovascular accident, intracranial neoplasm, recent intracranial or intraspinal surgery or trauma, severe uncontrolled hypertension