Posts

Showing posts from July, 2008

Stop your NSAID medicine if you have any of the following symptoms

nausea more tired or weaker than usual itching your skin or eyes look yellow stomach pain flu-like symptoms vomit blood there is blood in your bowel movement or it is black and sticky like tar unusual weight gain skin rash or blisters with fever swelling of the arms and legs, hands and feet Subscribe to Drugs Information Center by Email

Get emergency help right away if you have any of the following symptoms

Shortness of breath or trouble breathing Chest pain Weakness in one part or side of your body Slurred speech Swelling of the face or throat Subscribe to Drugs Information Center by Email

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Side Effects

Serious side effects include: heart attack stroke high blood pressure heart failure from body swelling (fluid retention) kidney problems including kidney failure bleeding and ulcers in the stomach and intestine low red blood cells (anemia) life-threatening skin reactions life-threatening allergic reactions liver problems including liver failure asthma attacks in people who have asthma Subscribe to Drugs Information Center by Email

Naproxen

Naproxen is a proprionic acid derivative related to the arylacetic acid group of nonsteroidal anti-inflammatory drugs. Indications : Rheumatoid arthritis Osteoarthritis Ankylosing spondylitis Juvenile Arthritis Immediate ReleaseAfter administration of NAPROSYN tablets, peak plasma levels are attained in 2 to 4 hours. After oral administration of ANAPROX, peak plasma levels are attained in 1 to 2 hours Naproxen-containing products are not recommended for use in patients with moderate to severe and severe renal impairment (creatinine clearance < 30 mL/min) Naproxen has been studied in patients with rheumatoid arthritis, osteoarthritis, juvenile arthritis, ankylosing spondylitis, tendonitis and bursitis, and acute gout. Improvement in patients treated for rheumatoid arthritis was demonstrated by a reduction in joint swelling, a reduction in duration of morning stiffness, a reduction in disease activity as assessed by both the investigator and patient, and by increased mobility as demon

Highly Drug-Resistant HIV

Integrase is a viral enzyme that is essential for HIV type 1 (HIV-1) replication; it catalyzes the insertion of proviral DNA into the host-cell genome. Raltegravir is an integrase inhibitor and specifically inhibits proviral DNA-strand transfer, with potent in vitro activity against HIV-1. In most patients with highly drug-resistant HIV, the resistance develops because of sequential exposure to HIV drugs in the context of incomplete virologic suppression. The genetic barrier to drug resistance for several of the most important HIV agents is low, requiring only a single point mutation to confer loss of activity. Drug-resistant virus can also be transmitted from person to person, although the transmission of strains resistant to multiple classes of drugs is rare. Subscribe to Drugs Information Center by Email

Desmopressin increases risk for hyponatremia.

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

Antipsychotics

FDA is notifying healthcare professionals that both conventional and atypical antipsychotics are associated with an increased risk of mortality in elderly patients treated for dementia-related psychosis. In April 2005, FDA notified healthcare professionals that patients with dementia-related psychosis treated with atypical antipsychotic drugs are at an increased risk of death. Since issuing that notification, FDA has reviewed additional information that indicates the risk is also associated with conventional antipsychotics. Antipsychotics are not indicated for the treatment of dementia-related psychosis. Antipsychotic drugs are not approved for the treatment of dementia-related psychosis. Furthermore, there is no approved drug for the treatment of dementia-related psychosis. Healthcare professionals should consider other management options. Physicians who prescribe antipsychotics to elderly patients with dementia-related psychosis should discuss this risk of increased mortality with

Fluoroquinolone Antimicrobial Drugs

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

Amantadine

Class of drug: Treatment for Parkinson’s disease, antiviral agent. Mechanism of action: Anti-Parkinson action: promotes release of dopamine in substantia nigra. Antiviral action: prevents viral penetration of influenza A virus into target host cells. Indications/dosage/route: Oral only . Parkinson’s disease Ð Adults: 100 mg b.i.d., may be titrated up. Maximum: 400 mg/d. Influenza A: Ð Adults: 200 mg/d, single or divided dose. Adjustment of dosage: Kidney disease: reduce dose as follows. Creatinine clearance 30–50 mL/min: initial 200 mg, then 100 mg/d; creatinine clearance 15–29 mL/min: initial 200 mg, then 100 mg q.i.d.; creatinine clearance <15 mL/min: 200 mg q7d. • Liver disease: None • Elderly: Dosage should be divided as twice daily administration. Contraindications: Hypersensitivity to amantadine, untreated angle-closure glaucoma. Warnings/precautions: Use with caution in patients with the following conditions: Psychiatric disorders, liver or kidney disease, history of epilep

Drug Errors

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

Most common Drug Interactions

Aspirin . This common, over-the-counter pain reliever also thins the blood. Aspirin may cause internal bleeding if combined with a prescription blood thinner such as warfarin (Coumadin). It can also decrease the effectiveness of some gout medications and increase the strength of certain diabetes drugs. Antibiotics . Some forms of these infection-fighting drugs can lose their power if combined with antacids or other products containing calcium. In addition, certain antibiotics can hamper the effectiveness birth control pills and greatly increase the effects of warfarin. Probenecid , a drug used to treat gout, can increase blood levels of several different types of antibiotics. In some cases, doctors may even use this interaction to their advantage: For extra punch against germs, doctors sometimes prescribe this drug along with antibiotics. Antidepressants . Newer antidepressants known as SSRIs, such as fluoxetine and paroxetine, shouldn't be mixed with older mood-lifters known as MA

Immunosuppressive Agents

Major classes of agents employed in immunosuppressive therapy: Corticosteroids Cytotoxic Agents T-cell suppressive agents Antibodies Mechanism of action: Cytotoxic Agents- suppress bone marrow function 1. Cyclophosphamide: a. Primarily suppresses B-cell production; lowers humoral immunity b. Used to treat severe rheumatoid arthritis c. Not normally used for graft rejection 2. Azathioprine a. Primarily suppresses T-cell production b. Used for graft rejection c. Normally used in combination with corticosteroids 3. Mycophenolate Mofetil (CELLCEPT) a. Mechanism of action: inhibits inosine monophosphate dehydrogenase; an enzyme required for de novo purine synthesis b. Selective because T and B cells rely on de novo pathway c. Suppresses lymphocyte proliferation and B-cell antibody production d. Can be used to inhibit transplant rejection T-Cell Suppressor Agents 1. Cyclosporine and Tacrolimus a. Mechanism of action: block proliferative response of T-cells to antigen by inhibiting calcineuri

Infliximab

Infliximab is a chimeric IgG 1K monoclonal antibody. Its approximate molecular weight is 149,100 daltons. It is composed of human constant and murine variable regions. Infliximab binds specifically to human TNF-α. Biological effects of infliximab TNF-α induces proinflammatory cytokines that include IL-1 and IL-6. These cytokines enhance leukocyte migration by increasing endothelial layer permeability and expression of adhesion molecules by endothelial cells and leukocytes, activation of neutrophil and eosinophil functional activity, and induction of acute phase and other liver proteins. Infliximab neutralizes the biological activity of TNF-α by binding with high affinity to the soluble and transmembrane forms of TNF-α and inhibits binding of TNF-α with its receptors. A related cytokine that utilizes the same receptors as TNF-α, TNF-beta (lymphotoxin α) is not neutralized by infliximab. It has been found to downregulate IL-18 but not IL-12 and IL-13. It upregulates the expression of CX

Dabigatran etexilate

Image
Dabigatran is a direct thrombin inhibitor, for the prevention of venous thromboembolic events in patients who have undergone total hip- or knee-replacement surgery. Venous thromboembolism (VTE) — occlusion of veins by blood clots — is the third most common cause of cardiovascular-associated death, after heart attacks and stroke. Without preventive treatment, patients undergoing hip- or knee-replacement surgery are at high risk of developing VTE2. Indeed, many clinical studies have demonstrated the importance of primary thromboprophylaxis in reducing morbidity and mortality for such patients. The serine protease thrombin is the final mediator in the coagulation cascade that leads to the production of fibrin, the main protein component of blood clots. Thrombin is also a potent activator of platelets. Consequently, thrombin has been a popular target for the development of novel anticoagulants. Several peptidic direct thrombin inhibitors (DTIs) have been approved for clinical use in the p

Lead Poisoning

Lead is widespread in the environment, reflecting the many uses we have for it. Exposure to lead has decreased dramatically since its use in house paints and gasoline was banned. Lead and its compounds are quite toxic. Metallic lead generally converted to Pb2+ in the body. Lead can damage the brain, liver, and kidney. Extreme cases can be fatal. Lead poisoning is especially harmful to children. Some children develop a craving that causes them to eat unusually things, and children with the syndrome called ‘pica’ eat chips of peeling lead-based paints. Large amount of Pb2+ in a child’s blood can cause mental retardation, behavior problems, anemia, hearing loss, developmental delays, and other physical and mental problems. Adults can excrete about 2 mg of lead per day. If intake exceeds excretion, however, lead builds up in the body and chronic irreversible led poisoning results. Subscribe to Drugs Information Center by Email

Quicksilver --- Slow Death

Mercury is the only common metal that is a liquid at room temperature. Dentists use it to make amalgams for filling teeth, and laboratory workers employ mercury and its compounds in a variety of ways. Farmers use seeds treated with compounds of mercury. Mercury vapor is quite hazardous when inhaled, particularly when exposure takes place over a long period of time. By some as yet unknown mechanism, the body converts the inhaled mercury to Hg2+ ions. All compounds of mercury, except those that are essentially insoluble in water, are poisonous no matter how they are administered. Because mercury is cumulative poison (it takes the body about 70 days to rid itself of half of a given dose), chronic poisoning is a threat to those continually exposed. The antidote for mercury, the compound, a derivative of glycerol, is called British antilewisite (BAL). It acts by chelating (from the Greek chela meaning “claw”) Hg2+ ions. Thus tied up, the mercury cannot attack vital enzymes. The effects

Cyanides: Agents of Death

They act quickly, and it takes only a small amount to kill. The average fatal dose is only 50 or 60 mg of gaseous hydrogen cyanide or of a solid salt containing the cyanide ion. Cyanide blocks the oxidation of glucose inside the cell by forming a stable complex with iron (III) ions in oxidative enzymes called cytochrome oxidases. These enzymes normally act by providing electrons for the reduction of oxygen in the cell. Cyanide blocks this action and brings an abrupt end to cellular respiration, causing death in minutes. Any antidote for cyanide poisoning must be administered quickly. Providing 100% oxygen to support respiration can sometimes help. Sodium nitrite is often given intravenously to oxidize iron atoms in the enzymes back to the active Fe3+ form. Sodium thiosulfate is then used if time permits. The thiosulfate ion transfers a sulfur atom to the cyanide ion, converting it to the relatively innocuous thiocyanate ion.