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Standard dosage: 250 mg every 12 hours, or 500 mg daily of the slow release preparation Diamox-SR ; . Start acetazolamide 24 hours before starting your ascent and continue it for three days at the higher altitude. A recent study in the British Medical Journal, however, found that for altitudes over 4, 000 meters 13, 123 feet ; , a total daily dose of 750 mg was effective, whereas 500 mg was not. Side effects include frequent urination polyuria ; and a tingling sensation of the face and lips paresthesia ; . Use acetazolamide with caution if you have an allergy to sulfa drugs because acetazolamide is a sulfa derivative. A trial course of the drug before going to a remote location is advisable. 2. Dexamethasone Decadron ; --Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS. It may be a useful drug, however, for those who need to ascend abruptly to very high altitudes--for example, those going on a mountain rescue mission--or for those climbers allergic to acetazolamide. The drug is usually used for the treatment of AMS see the Treatment Section on the following page ; . Prophylaxis dosage: 2 to 4 mg every 6 hours, begun the day of ascent, continued for three days at the higher altitude, then tapered over five days. Side effects: weaning from dexamethasone may increase risk of depression. 3. Nifedipine--In someone who has a history of HAPE, use either the 20 mg slow-release capsule available in Europe and Asia under various brand names ; every 8 hours, or the 30 mg slow-release available as Adalat-CC or Procardia-XL in North America ; every 12 hours. All climbers above 10, 000 feet should also carry standby treatment doses of the rapid-acting 10 mg capsules. 4. Aspirin--Pretreatment with aspirin before travel to high altitudes appears to decrease the incidence and severity of headaches, the main symptom of mild AMS. Take one aspirin tablet every four hours for three doses before arrival. After arrival, take two tablets three times daily for three days.
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Gavras I, Mulinari R, Gavras H, et al. Antihypertensive effectiveness of the nifedipine gastrointestinal therapeutic system. J Med 1987; 83 6B ; : 20-3. Gebara OC, Jimenez AH, McKenna C, et al. Stress-induced hemodynamic and hemostatic changes in patients with systemic hypertension: effect of verapamil. Clin Cardiol 1996; 19 3 ; : 205-11. Gel'tser BI, Kotel'nikov VN and Varnina MV. [Osmo-adalat in the treatment of isolated systolic and systolic-diastolic arterial hypertension in aged patients]. Ter Arkh 2000; 72 9 ; : 17-20. Gemici K, Baran I, Bakar M, et al. Evaluation of the effect of the sublingually administered nifedipine and captopril via transcranial doppler ultrasonography during hypertensive crisis. Blood Press 2003; 12 1 ; : 46-8. Gencosmanoglu O, Timurkaynak T, Boyaci B, et al. Effect of verapamil, trandolapril and fixed-dose combination of the two on ambulatory blood pressure values in essential hypertension. [Turkish]. Turk Kardiyoloji Dernegi Arsivi 2000; 28 8 ; : 475480 + 446. George C, Grippat J and Safar M. Second line treatment of essential hypertension after beta-blockade. A randomised trial in 558 patients initially treated with bisoprolol 10mg. Drug Invest 1990; 2 3 ; : 150-154. Germano G, Damiani S, Ciavarella M, et al. Detection of a diurnal rhythm in arterial blood pressure in the evaluation of 24-hour antihypertensive therapy. Clin Cardiol 1984; 7 10 ; : 525-35. Germano G, Ramponi C, Caparra A, et al. Comparative study of the effects of.
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Additional fluids should be administered with caution to avoid cardiac overload. 5. 5.1 PHARMACOLOGICAL PROPERTIES Pharmacodynamic properties ATC code: C08CA05 Pharmacotherapeutic group: Calcium antagonists. Nifedipine is a calcium antagonist and has a spasmolytic effect on the vascular wall of mainly coronary arteries. As a result of the relaxation of arterial muscle, nifedipine reduces peripheral resistance, leading to an improvement of peripheral blood flow whilst decreasing after-load. Therefore, Nifedipine Pharmamatch retard is effective in angina pectoris and hypertension. In a clinical study, the effect of Nifedipine retard prolonged-release tablets on cardiovascular and cerebrovascular morbidity was studied. The primary end-point was the combination of stroke, MI including sudden death ; , heart failure or death from any other cardiovascular cause composite end-point ; . This randomised, double blind, prospective study was carried out on an average population of patients with hypertension that, besides a blood pressure of 150 95 mm Hg higher or a systolic blood pressure of 160 mm Hg, presented with at least one other cardiovascular risk factor. A total of 6321 patients 55-80 years ; were treated during 3 to 4.8 years with Nifedipine Retard or a standard combination of diuretics hydrochlorothiazide 25 mg + amiloride 5 mg ; . The results show that Nifedipine Retard demonstrates both a comparable antihypertensive effect and a comparable effect on the above-mentioned composite end-point. Separate analysis of the individual end-points show little differences in incidence between the groups treated with nifedipine or diuretics of stroke 2.0% versus 2.3% ; , MI 2.9% versus 2.7% ; and death caused by any other cardiovascular disease 0.4% versus 0.4% ; . The incidence of heart failure shows a difference between both treatments 0.9% versus 0.3% ; . Considering the design of the study, no conclusions can be drawn from the results of the separate analysis. Moreover, the number of reported symptomatic adverse events was higher in the group treated with nifedipine than in the control group. This could mainly be attributed to the increased incidence of peripheral oedema. The number of severe adverse events, as well as the number of reported metabolism-related adverse events such as hypokalaemia, hyponatraemia and hyperuremia, was lower in the group treated with nifedipine. 5.2 Pharmacokinetic properties Absorption Nifedipine is rapidly and almost completely absorbed 90% ; . Bioavailability is approximately 40-60%. Nifedipine Pharmamatch retard is formulated in such way that it releases the active substance in the intestine with a practically constant rate over a 16 to hour time period. Therefore, the tablets are appropriate for once-daily administration. An almost constant release rate provides a relatively constant concentration of active substance in plasma, without major differences between maximal and minimal levels. It takes some time lagtime of 2-4 hours ; before the active substance escapes from Nifedipine Pharmamatch retard tablets. Moreover, as is the case for all oral administrations, the active substance undergoes a first pass effect. Steady-state concentrations are already reached after administration of the second Nifedipine Pharmamatch retard tablet. Co-administration of grapefruit juice reduces the first pass effect on nifedipine see section 4.5 ; . The pharmacokinetic properties of nifedipine in the Nifedipine Pharmamatch retard tablet are linear in a dose range of 30-180 mg. Based on the results of the bioequivalence studies, Nifedipine Pharmamatch retard tablets 30 mg and 60 mg can be considered to be bioequivalent to the reference product Afalat OROS under fasting and fed conditions.
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| Adalat retard 10Grapefruit Juice Drug Interactions Grapefruit juice interferes with the metabolism of some drugs that use the cytochrome P450 3A4 metabolic pathway. When grapefruit juice is administered concurrently, or in some cases, up to 4 hours before or after ingestion of one of these drugs, there can be a significant increase in active metabolite of the drug. amlodipine Norvasc ; indinavir Crixivan ; lovastatine Mevacor ; atorvastatin Lipitor ; buspirone Buspar ; nifedipine Adaat ; carbamazepine Tegretol ; Procardia ; cerivastatin Baycol ; nimodipine Nimotop ; cyclosporine Neoral, Sandimmune ; * simvastatine Zocor ; triazolam Halcion ; diltiazem Cardizem, Tiazac, Dilacor ; verapamil Calan, Isoptin ; felodipine Plendil, Renedil ; * Grapefruit juice may be potentially useful to boost cyclosporine levels in transplant patients, reducing the amount of the drug that must be administered.
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Chapter Acknowledgement Introduction Research methodology Brief history of ADR Overview of ADR Elaborate explanation of ADR mechanisms Study of ADR institutions across the world Reasons behind introduction of ADR in India The Arbitration and Conciliation Act, 1996 Lok Adalats as a unique ADR measure in India Implementation of ADR in India Conclusion Bibliography Page no. 03 04 05 ADR originated in the USA in a drive to find alternatives to the traditional legal system, felt to be adversarial, costly, unpredictable, rigid, over-professionalised, damaging to relationships, and limited to narrow rights-based remedies as opposed to creative problem solving. The American origins of the concept are not surprising, given certain features of litigation in that system, such as: trials of civil actions by a jury, lawyers' contingency fees, lack of application in full of the rule "the loser pays the costs". Beginning in the late nineteenth century, creative efforts to develop the use of arbitration and mediation emerged in response to the disruptive conflicts between labor and management. In 1898, Congress followed initiatives that began a few years earlier in Massachusetts and New York and authorized mediation for collective bargaining disputes. In the ensuing years, special mediation agencies, such as the Board of Mediation and Conciliation for railway labor, 1913 ; renamed the National Mediation Board in 1943 ; , and the Federal Mediation and Conciliation Service 1947 ; were formed and funded to carry out the mediation of collective bargaining disputes. Additional state labor mediation services followed. The 1913 New lands Act and later legislation reflected the belief that stable industrial peace could be achieved through the settlement of collective bargaining disputes; settlement in turn could be advanced through conciliation, mediation, and voluntary arbitration.2 At about the same time, and for different reasons, varied forms of mediation for non-labor matters were introduced in the courts. When a group of lawyers and jurists spoke on the topic to an American Bar Association meeting in 1923, they were able to assess court-related conciliation programs in Cleveland, Minneapolis, North Dakota, New York City, and Milwaukee. Conciliation in a different form also appeared in domestic relations courts. An outgrowth of concern about rising divorce rates in the postwar 1940's and the 1950's, the primary goal of these programs was to reduce the number of divorces by requiring efforts at reconciliation rather than.
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Rather than limiting the number of donor exposures, was associated with a decreased risk of platelet alloimmunization. Precautions and Contraindications Patients with thrombotic thrombocytopenic purpura TTP ; should not be transfused with platelets because of a significantly increased risk of thrombosis. Similarly, platelet transfusion is relatively contraindicated in the setting of heparin-induced thrombocytopenia HIT ; , type 2, in the absence of clinically significant bleeding. Platelet transfusion can be considered for these patients, but only if clinically significant bleeding occurs. Response to platelet transfusion may be blunted in a large variety of clinical settings, which are listed in Table 4. Because platelets must be stored at room temperature 20C to 24C [68F to 75.2F] ; to ensure posttransfusion viability, there is a significantly increased risk of bacterial contamination, as compared with refrigerated blood product storage. For this reason, particular attention must be paid to the development of fever hyperpyrexia ; , chills, rigors, or hemodynamic instability hypotension ; during platelet infusion because of the risk of a septic transfusion reaction. Beginning March 1, 2004, bacterial testing of platelets was mandated by voluntary standardsetting organizations to help mitigate this risk. Dosing and Administration A conventional platelet dose for an adult is a pool of 4 to RDP units, or 1 SDP unit. The RDP pool size is established by the individual hospital transfusion service. Platelets must be transfused through a blood administration set containing a nominal 170 m 150 to 260 m ; filter, and RDP must be infused within 4 hours of pooling. Rh-negative patients should receive Rh-negative platelets, if available. Platelets are labeled Rh positive or negative because of red blood cell contamination of the platelet.
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I'm sure you've heard the saying, "The simpler, the better." This statement rings true for health plans, providers, and patients; we're all interested in making healthcare delivery as simple, effective and efficient as possible. At Avera Health Plans, we monitor our efficiency and quality by reviewing the utilization of services provided to our members. We have several ways to do this, including pre-certification, concurrent review, discharge planning and case management. Increasingly, employers are also looking for ways to boost efficiency in the healthcare their employees receive. One strategy employers are exploring for improving efficiency is streamlining the pre-certification process or removing it entirely for certain services. In response to employer and member needs, current low denial rates, legal requirements, projected enrollment increases and the benefits of Care Coordination, AHP has decided to reduce the list of services requiring pre-certification for all members of Avera Health Plans and Avera Health Plans of Minnesota. At the same time, we've identified this change as an opportunity to more fully integrate the care management approach of Care Coordination in order to ensure the continued delivery of necessary services for our members and providers. Beginning January 1, 2003, services requiring pre-certification will include case types, rather than individual procedures. The case types will include inpatient hospital admissions, inpatient chemical substance abuse admissions, inpatient behavioral health admissions, organ transplant services and in-network benefit requests for out-ofnetwork providers. This approach reduces.
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To alleviate the suffering of many patients with migraine, clinicians need to be aware of the commonly accepted indications for preventive therapy and initiate effective therapy in those patients. Although many agents are available for the preventive treatment of migraine, only a few have proven efficacy. Once an agent has been chosen, clinicians should initiate therapy with a low dose and titrate the dose slowly up until clinical benefits are achieved in the absence of adverse events or until limited by adverse events. Because a clinical benefit may take as long as 2 to months to manifest, each treatment should be given an adequate trial. Once preventive treatment is under way, interfering medications, such as overused acute medications such as ergotamine, should be avoided. After a period of stability, clinicians should consider tapering or discontinuing treatment. Patient and clinician need to engage in an ongoing dialogue in which patient expectations and goals for therapy are taken into account when agents are chosen, titrated, or discontinued.
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