Drugs Information Center(DIC)

Ranexa is an anti-anginal medication. It works by improving blood flow to help the heart work more efficiently. Ranexa is used to chronic treat angina (chronic chest pain) when other medications have not helped the condition. It should be used in combination with another medicine (eg, amlodipine, beta-blockers, nitrates). You should not take Ranexa if you have liver disease, hypokalemia (low levels of potassium in your blood), or a personal or family history of "Long QT syndrome." Ranexa should not be taken together with certain medicines to treat heart rhythm disorders, malaria, infections, mental illness, pain, cancer, or stomach disorders. Before you take Ranexa, tell your doctor about all other medications you are using. Ranexa is not for use during an acute (emergency) attack of angina. Continue using any other medicines prescribed by your doctor (such as nitroglycerin) to treat acute angina. Chronic angina is often treated with a combination of different drugs. To best ...

Methotrexate is a folic acid antagonist derived from aminopterin. It inhibits dihydrofolate reductase, the enzyme required in the pathway supplying methyl donor groups for DNA, RNA and protein synthesis. Methotrexate has been used for the treatment of diseases characterised by inflammation or cellular proliferation. In 1985 the first randomised, placebo-controlled trials were published that demonstrated the short-term efficacy of low-dose weekly methotrexate in rheumatoid arthritis (RA). Methotrexate is now the most widely used disease-modifying antirheumatoid drug (DMARD) in the developed world. It was first used in the treatment of psoriatic arthritis (PsA) in 1951, and has been shown to be of clinical benefit in this condition. However, methotrexate toxicity remains an important issue when considering its use, and is one of the main reasons for discontinuation. The most common adverse effects are gastrointestinal, such as anorexia, nausea, stomatitis and diarrhoea. CNS toxicity incl...

Therapeutic Class Calcium Channel Blocker Cardiovascular Agent Dihydropyridine Mechanism of Action Amlodipine besylate is a long-acting dihydropyridine calcium channel blocker that exerts its effect by blocking the transmembrane influx of calcium ions into cardiac and vascular smooth muscles. It also reduces peripheral vascular resistance and lowers blood pressure by causing a direct vasodilation in the peripheral arteries of the vascular smooth muscle. Its therapeutic effect on vasospastic angina is through inhibition of coronary spasm . Pharmacokinetics about 30 h to 50 h Hepatic Oral: time to peak concentration, 6 h to 12 h Protein binding: approximately 93% Renal: 60% as metabolites, 10% unchanged Bioavailability: 64% to 90% Impaired hepatic function: 56 h Effect of food: bioavailability not altered Patient Advice Patient should avoid activities requiring coordination until drug effects are realized, as drug may cause dizziness. This drug may cause palpitations, peripheral edema, f...

Indications: Treating anxiety and panic disorder. Do NOT use Alprazolam if: you are allergic to any ingredient in Alprazolam or other benzodiazepines (eg, diazepam) you have acute narrow-angle glaucoma, severe liver disease, or a mental state where contact with reality is lost (psychosis) you are taking an azole antifungal (eg, itraconazole, ketoconazole), delavirdine, or sodium oxybate (GHB) Before using Alprazolam : Some medical conditions may interact with Alprazolam . Tell your doctor or pharmacist if you have any medical conditions, especially if any of the following apply to you: if you are pregnant, plan to become pregnant, or are breast-feeding if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement if you have allergies to medicines or other substances if you have glaucoma or a predisposition for glaucoma, liver problems, lung problems or chronic obstructive pulmonary disease (COPD), muscle problems, depression, suicidal tenden...

A peripherally acting mu-opioid receptor antagonist, wasapproved by the US FDA to accelerate thetime to gastrointestinal recovery followingbowel resection surgery. It is the firstpharmacotherapy to be approved for thisapplication. Ileus — a temporary impairment ofgastrointestinal function — is a complicationthat affects almost all patients that undergomajor bowel surgery. It results in abdominaldiscomfort, nausea and vomiting, and is amajor reason for prolonged hospitalization. The pathophysiology of post-operative ileus(POI) is complex. An important contributoryfactor is the activation of m-opioid receptors in the gastrointestinal tract by endogenous opioidsthat are released in response to the stress causedby surgery, as well as by opioid analgesics thatare the most common treatment for pain inpatients undergoing surgery1,2. Activation ofthese peripheral m-opioid receptors leads to anincrease in colonic muscle tone and a reductionin propulsive activity in the gastrointestinaltract. C...

Today i recieve a article from Doctor's Guide regarding Desmopressin and i want to share with healthcare professionals. Health Canada is informing healthcare professionals that all intranasal formulations of desmopressin (DDAVP) are no longer indicated for the treatment of primary nocturnal enuresis (PNE) due to an increased risk of hyponatremia with the intranasal formulations.· All intranasal formulations of desmopressin are now contraindicated for the treatment of PNE.· All patients using intranasal formulations of desmopressin for treatment of PNE should be reassessed to determine their need for continued treatment and to discuss other options. If ongoing treatment is considered necessary, patients should be switched to the lowest starting dose of an oral formulation, with the dose increased only if necessary to control symptoms. Fluid intake and desmopressin dosage should be adjusted carefully in order to reduce the possibility of water retention and hyponatremia, especially i...

FDA notified healthcare professionals that a BOXED WARNING and Medication Guide are to be added to the prescribing information to strengthen existing warnings about the increased risk of developing tendinitis and tendon rupture in patients taking fluoroquinolones for systemic use.Fluoroquinolones are associated with an increased risk of tendinitis and tendon rupture. This risk is further increased in those over age 60, in kidney, heart, and lung transplant recipients, and with use of concomitant steroid therapy. Physicians should advise patients, at the first sign of tendon pain, swelling, or inflammation, to stop taking the fluoroquinolone, to avoid exercise and use of the affected area, and to promptly contact their doctor about changing to a non-fluoroquinolone antimicrobial drug. Selection of a fluoroquinolone for the treatment or prevention of an infection should be limited to those conditions that are proven or strongly suspected to be caused by bacteria. Subscribe to Drugs Info...

Drug errors contribute to morbidity. They also cost the country's health care system. So, doctors should keep in mind these points while prescribing medicines. Drug errors may involve: The wrong choice of a drug or a prescription for the wrong dose, frequency, or duration. An error in reading the prescription by the pharmacist so that the wrong drug or dose is dispensed. Incorrect instructions to the patient. Incorrect administration by a health care practitioner or patient. Incorrect storage of a drug by the pharmacist or patient, altering the drug's potency. Use of outdated drug, altering the drug's potency. Confusion of the patient so that the drug is taken incorrectly. Unscrupulous replacement of a drug with an inferior, diluted, or inactive product. Errors in prescribing are common, especially for certain populations. The elderly ), women of childbearing age, and children are particularly at risk. Drug interactions particularly affect those taking many drugs. To minimi...

The aminoglycoside antibiotics have the narrowest therapeutic range of any of the antimicrobial drugs. Their use requires precision of administration; optimal use requires monitoring serum levels. Accumulation of these compounds causes nephrotoxicity and ototoxicity, which can be delayed in onset and from which full recovery may not ensue. All of these compounds demonstrate a slow terminal elimination phase, and drug is excreted in the urine for weeks after discontinuation of therapy. This slow elimination phase contributes to accumulation of any of these compounds. Penicillins, particularly carbenicillin, piperacillin, and ticarcillin, can physically complex with these agents and, therefore, cannot be mixed in the same intravenous infusion. This same phenomenon occurs in patients with ESRD such that co administration of these penicillins results in a decreased serum level of aminoglycoside.More precise guidelines are offered because of the narrow therapeutic index of aminoglycosides.

As with any tightly protein bound drug, Nsaids can displace other protein bound pharmacologic agents causing transient increases in concentrations of free drug in the serum. It is important to point out that all of these anti inflammatory agents are inhibitors of prostaglandin synthesis and in a variety of disease states, particularly congestive heart failure, liver disease, hemorrhage, systemic lupus erythematosus with renal involvement, and chronic renal failure, prostaglandins appear to be important in maintaining renal blood flow. In addition, it is now clear that both COX-1 and COX-2 have physiologic and pathophysiologic roles in renal function. As a consequence, prostaglandin inhibition, either COX-1 or COX-2, can result in decrements in renal function. Therefore, any of the nonsteroidal anti-inflammatory drugs could cause worsening renal function in patients with the aforementioned diseases. Thus,before prescribing Nsaids it is mandatory to know the Kidney profile of the patient...

The disposition of phenytoin and valproic acid shows important changes in patients with decreased renal function and hypoalbuminemic conditions. These changes are a manifestation of decreased protein binding with a concomitant increase in the volumes of distribution of these drugs. This phenomenon has been closely investigated with phenytoin, and it is likely that parallels can be drawn with valproic acid. Both drugs are highly protein bound; so in patients with renal dysfunction or with hypoalbuminemia, displacement from serum proteins occurs with a concomitant increase in the volume of distribution. The clinical importance of this phenomenon is that the patient with renal dysfunction manifests the same concentration of free drug in serum at a lower total blood concentration than does the subject with normal renal function. Since most clinical laboratories measure only total concentration of drug in the blood, the importance of the phenomenon is in the proper interpretation of a blood...

Many of the neuromuscular blocking agents are eliminated by the kidney and require dose adjustment in patients with renal dysfunction. For some of these drugs no data are available to allow development of guidelines for use in patients. Use of any of these drugs in the patient with renal failure requires caution, and it has been recommended that a peripheral nerve stimulator be employed to assess the degree of neuromuscular blockade. Short of this, the clinician must be aware that a patient with renal dysfunction may have slow recovery from anesthesia owing to both retention of anesthetic agents eliminated by the kidney or to additional factors that again are related to renal function. For example, patients with renal disease who either accumulate aminoglycoside antibiotics to high concentrations or who are potassium depleted may have prolonged respiratory suppression in the face of anesthetic agents as a result of the "curare like" effect that can occur with these antibiotic...

Most of the analgesics are eliminated by the liver and renal dysfunction has little influence on their disposition. It has been noted, though poorly documented, that patients with renal and hepatic dysfunction manifest an increased sensitivity to a variety of the analgesic agents, particularly to narcotics. Whether this increased sensitivity is related to changed distribution to the sites of activity, additive effects of retained endogenous toxins, or to truly increased sensitivity is unclear. Usually, beginning doses of these agents are reduced in patients with renal and liver dysfunction until the individual patient demonstrates his or her own dose response relationship.