What is quinidine sulfate |
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Before taking this medication, tell your doctor if you are taking any of the following medicines: amantadine symmetrel quinidine quinaglute, cardioquin, quinora, quinidex antihistamines such as diphenhydramine benadryl, many others ; , brompheniramine dimetapp, bromphen, manyothers others and drugs interaction , triprolidine actifed, others ; , and chlorpheniramine chlor-trimeton, others ; , which are found in many over-the-counter and prescription cough, cold, and allergy medications; decongestants and appetite suppressants such as phenylephrine neo-synephrine, others ; , and pseudoephedrine sudafed, others ; , which are also found in many over-the-counter andprescription about prescription ; products; phenothiazines such as chlorpromazine thorazine ; and prochlorperazine compazine a blood thinner such as warfarin coumadin ; , heparin, enoxaparin lovenox ; , dalteparin fragmin ; , danaparoid orgaran ; , ardeparin normiflo ; , or tinzaparin innohep a monoamine oxidase inhibitor maoi ; such as isocarboxazid marplan ; , phenelzine nardil ; , or tranylcypromine parnate other commonly used phenothiazines, including fluphenazine prolixin ; , mesoridazine serentil ; , perphenazine trilafon ; , thioridazine mellaril ; , trifluoperazine stelazine ; , and promazine sparine tricyclic antidepressants such as amitriptyline elavil, endep ; , doxepin sinequan ; , and nortriptyline pamelor or other commonly used tricyclic antidepressants, including amoxapine asendin ; , clomipramine anafranil ; , desipramine norpramin ; , imipramine tofranil ; , protriptyline vivactil ; , and trimipramine surmontil.
Covered Drugs by Category Drug Name labetalol hcl 5 mg ml vial CARDIOVASCULAR AGENTS, ANGIOTENSIN BLOCKERS BENICAR BENICAR HYDROCHLOROTHIAZIDE DIOVAN 2 QL: 90 3 0 QL: 90 3 0 QL: 90 3 0 Tier 1 amiodarone hcl 50 mg ml ampule 1 disopyramide phosphate 1 mexiletine hcl 1 procainamide 1, 000 mg tablet sustained action 1 B D procainamide 100 mg ml vial 1 procainamide 250 mg capsule 1 procainamide 500 mg capsule DIOVAN HYDROCHLOROTHIAZIDE 160 12.5 MG TABLET DIOVAN HYDROCHLOROTHIAZIDE 160 25 MG TABLET DIOVAN HYDROCHLOROTHIAZIDE 320 12.5 MG TABLET DIOVAN HYDROCHLOROTHIAZIDE 320 25 MG TABLET DIOVAN HYDROCHLOROTHIAZIDE 80 12.5 MG TABLET CARDIOVASCULAR AGENTS, ANTIARRYTHMICS 1 amiodarone hcl 200 mg tablet 1 amiodarone hcl 400 mg tablet 2 QL: 90 3 0 procainamide 500 mg tablet sustained action 1 B D procainamide 500 mg ml vial 1 procainamide 750 mg tablet sustained action 2 QL: 30 3 0 quinidine gluconate 1 2 QL: 30 3 0 quinidine sulfate 3 TIKOSYN CARDIOVASCULAR AGENTS, BETA-ADRENERGIC BLOCKING 1 acebutolol hcl 1 atenolol 1 bisoprolol fumarate 1 metoprolol succinate extendedrelease tablet 50 B D Part B Primary PA Prior Authorization QL Quantity Limits ST Step Therapy Notes Drug Name Tier 1 Notes.
Dietary salt : the rate and extent of quinidine absorption may be affected by changes in dietary salt intake; a decrease in dietary salt intake may lead to an increase in plasma quinidine concentrations.
Quinidine quinine
The point estimates and 95% cis for the probability of death for the quinidine group was 0% 95% ci: 7.
Quinidine out of the cell. The detection of an active quinidine efflux in the wild-type population but not in the population devoid of QDR1 after the same 2 h of incubation following the sudden exposure of cells to quinidine may be the result of the higher susceptibility of the unadapted qdr1 population, revealed by the higher quinidine-induced viability loss during this adaptation period. In fact, after surpassing a shorter or longer initial period of adaptation, exponential growth with quinidine was resumed in both populations, and these adapted cells became capable of active expulsion of the drug independent of QDR1 expression. It is intriguing why quinidine, which is not present in the yeast natural environment, may induce its active expulsion from cells which are actively dividing in its presence. QDR1 gene transcription levels do not increase in cells cultivated with quinidine P. Nunes, M. Teixeira, and I. Sa-Correia, unpublished results ; , consistent with other indications suggesting that this gene is not involved in the induction of quinidine export by the drug. Nevertheless, the level of expression of QDR1 is critical to surpass the viability loss during the initial period of adaptation to quinidine and to eventually resume exponential growth, which depends on the remaining viable population. Results also suggest that there are other resistance mechanisms that can be used when QDR1 is absent, possibly involving other MFS-MDR and or ABC transporters. Quinidine accumulation assays were carried out at an external pH of 5.5, and the uptake of labeled quinidine into the yeast cell was extremely rapid. However, at this pH quinidine, which is a weak base with two protonation sites with pKas of 5.4 and 10.0 8 ; , is basically in the singly protonated form and not.
A 3 result for protein on November 8. We advised an increased dosage of prednisolone, but she refused to comply because of the risk of side effects. We, therefore, changed the 150 mg of mizoribine administration from three divided doses to one without increasing the dosage of prednisolone on November 8. By December 6, the membranous nephropathy was in remission and her urine was again negative for protein. Mizoribine is a novel immunosuppressive agent that selectively inhibits inosine monophosphate dehydrogenase and guanosine monophosphate synthetase, which inhibits T-cell and B-cell proliferation [1]. Mizoribine in the range of 0.15 mg ml inhibits the human mixed-lymphocyte reaction at rates ranging from 36.4 to 62.2%, with 50% inhibition at about 1.0 mg ml [2], and we previously reported that a blood mizoribine concentration above 1.0 mg ml is necessary to treat relapsed renal vasculitis [3]. The peak blood mizoribine concentration in our patient was 2.95 mg ml when the mizoribine 150 mg day ; was consumed in one dose. The peak blood concentration of mizoribine during regular use two or three smaller doses day ; was 0.8 mg ml [4]. However, we did not measure this value in our patient under this circumstance. We speculated that the higher optimal blood mizoribine concentration was achieved in our patient by changing the administration protocol, from three divided doses to one dose, thus inducing remission of relapsed membranous nephropathy and qvar.
Quinidine bisulphate
Grogono, A. W.: Anaesthesia for Atrial Defibrillation. Lancet 2: 1039 Nov. 16 ; , 1963. Patients were satisfactorily anesthetised with thiopentone and suxamethonium for electrical atrial defibrillation. When quinidine was given intravenously 300 mg. ; to a refractory patient in the process of recovering from an earlier dose of suxamethonium, he again became paralyzed. Subsequently, observations in six patients receiving intravenous quinidine after recovery from suxamethonium have revealed return of paralysis in two patients, muscular weakness in thlee, and no effect in one. It is cautioned that the use of quinidine in this manner may cause unexpected respiratory arrest.
GPIX obtained evidence that MoAb SZ1 recognizes a conformational determinant formed on GPIX when it is complexed with GPIb or GPIb .12 In previous studies, it was shown that FMC25 inhibits the binding of SZ1 by about 30% and that SZ1 inhibits the binding of FMC25 by about 80%, indicating that the binding sites for these two MoAbs are close to each other on GPIX.30 The epitope recognized by SZ1 is of particular interest because of the finding by Chong et al17 that SZ1 completely blocked the binding to platelets of six quinine-induced antibodies, but that MoAb FMC25, was without effect. In the same study, five of six quinidine-induced antibodies were also blocked completely by SZ1, but were only partially inhibited by FMC25. We obtained similar results with two other quininedependent antibodies Fig 6 ; . Thus, antibody JH appears to bind at, or very close to a site on GPIX commonly recognized by quinine- and quinidine-induced antibodies. Although quinidine and quinine, being diastereoisomers, are structurally similar, ranitidine bears no structural resemblance to either of these compounds. Therefore, our findings suggest the possibility that the domain on GPIX recognized by SZ1 is a favored target for drug-induced antibodies, independent of the structure of the and ramelteon.
I N S The arrhythmia is induced by an antiarrhythmic drug such as digitalis orquinidine. Persists after discontinuance of the drug and correction of electrolyte imbalance. Consider INDERAL instead. Often the drug of choice, except in the presence of serious congestive heart failure. Often, too, INDERAL propranolol HCI ; abolishes supraventricular arrhythmias when either digitalis or quinidine has failed. With proper patient selection--in the absence of contraindications such as bradycardia, greater than first degree heart block, asthma, and congestive heart failure unless failure is secondary to tachyarrhythmias treatable with INDERAL serious cardiovascular and respiratory side effects are seldom encountered * Rely on it: INDERAL Alone. With. Or Instead.
| Quinidine ingredientsProspective Study In order to determine the effectiveness of quinidine prophylaxis under more controlled conditions a prospective study was also undertaken. For a period of 18 months all patients in normal sinus rhythm admitted to the Peter Bent Brigham, Mount Auburn, and Malden Hospitals on the Thoracic Surgical Services for mitral valvuloplasty were included. The group-III and group-IY patients were segregated and within each group the patients were paired as they were accepted for operation. To avoid bias and insure uniformity of decision a coin was tossed to determine which person should be assigned to the quinidine-treated group and which to the control no quinidine ; group. All patients were digitalized preoperatively if not already receiving this drug. * In the therapy group, quinidine sulfate was given in 3 doses of 0.3 Gm. each, on the day prior to operation. On the day of operation and daily thereafter 0.3 Gm. was given every 6 hours, initially intramuscularly and thereafter by mouth. Results and rapamune.
Quinidine sulfate
Mr. Dcdcnbacll slatcd they would accept Condition 9 as slated i n tllc staff report. Mr. Caldcron slatcd that .'ondition 10 \ + 'as to Iiclp thc applicant not I i : entire PD amcndmcnt. The 3'X, has to ld of controlled by lilclors lint ~ v o impnctcd by an increase in tlic nu~nbcl- beds or bcdroonls. Mr Dcricnbacll agreed with the Condition 10 as stated in the afTrcpo~-t Mr. Caldcron statcd that staf'bclicvcs Condition 11. lius Inany bcnclrts tv tlic community wliicli in1p: icts 13"' Street. Hc e?; plaincd that the contribution proportiol~~itc tlic impact should bc a\, ailablc. He stated that. in order to not bc to would be. He statccl if the proportionate sliarc arbitrary, tllc condition is for a study to dctcrmine \.hat llic proportio~l \vcrc to paint a cl-osswalk, that's ~vliatit \vould be. If' it is loo provide a bus stop, that's what i t would be. Mr. Mimms statcd lie was concerned that the csccution of tlic agreement was far down llic line Mr. Caldcron zlalcd tliat by the time ~ h clevelopmcnt starts to makc : in impact. stal'f fclt they \, crc being gracious i n c allowing the 80 1x1-centoccupancy, so the time ~voulcibcgin at that tilnc. Tlicrc ii, as disiiissio~i about tllc niimbcrs o r bus uscrs and othcr nlodcs of tl-avcl. Mr. Caldcron statcd htaff is only a s k contribution to be made. Hc statcd s t a LII-bitrary ~ l d for not a prov~ticd an option Thcrc was further discussion regarding Colidition I 1 . Mr. Caldcron pointcti out that Condition 1 slates. "no Inter Illan one year, " and tlicrc is ~lotliing that says they coult! not do it tlic day aflcr ol-: iny othcr t~nlc.Hc stated tlic sti~dynight say i t is bus stop.
Patients with varying degrees of renal function. Clin. Pharmacol. Ther. 24, 31-39 1978 ; . 2. Guentert, T. W., Coates, P. E., Upton, R. A., et al., Determination of quinidine and its major metabolites by high performance liquid chromatography. J. Chromatogr. Biomed. AppI. 162, 59-79 1979 ; . 3. Alexander, F., Gold, H., Katz, L. N., eta!., Relative value of syn and raptiva
| Tion during continued amiodarone therapy, with a mean follow-up of 1 year. The effect of the addition of a type IA agent on inducibility of tachycardia and clinical outcome has not been evaluated previously. The present study was undertaken to 1 ; determine the effect of procainamide on inducibility and rate hemodynamic tolerance of rapid ventricular arrhythmias induced during amiodarone therapy, and 2 ; to determine whether the addition of a type IA agent procainamide or quinidine ; to amiodarone therapy results in a better clinical outcome. Methods.
Amprenavir: see recommendations described for Kaletra tablets co-administration with efavirenz. Fosamprenavir: a study has shown that co-administration of Kaletra 400 100 mg twice daily with fosamprenavir ritonavir 700 100 mg twice daily results in a 30 - 52% increase in lopinavir concentrations and a 58-65% decrease in amprenavir concentrations. Administration of Kaletra 533 133 mg twice daily with fosamprenavir 1400 mg twice daily no additional ritonavir ; results in similar lopinavir concentrations to Kaletra 400 100 mg alone and 26 - 42% lower amprenavir AUC and Cmin compared to fosamprenavir ritonavir 700 100 mg alone. Appropriate doses of the combination of fosamprenavir and Kaletra with respect to safety and efficacy have not been established. Indinavir: indinavir 600 mg twice daily in combination with Kaletra produces similar indinavir AUC, higher Cmin by 3.5-fold ; and lower Cmax relative to indinavir 800 mg three times daily alone. Furthermore, concentrations of lopinavir do not appear to be affected when both drugs, Kaletra and indinivir, are combined, based on historical comparison with Kaletra alone. Nelfinavir: see recommendations described for Kaletra tablets co-administration with efavirenz. Saquinavir: saquinavir 800 mg twice daily co-administered with Kaletra produces an increase of saquinavir AUC by 9.6-fold relative to saquinavir 1200 mg three times daily given alone. Saquinavir 800 mg twice daily co-administered with Kaletra resulted in an increase of saquinavir AUC by approximately 30% relative to saquinavir ritonavir 1000 100 mg twice daily, and produces similar exposure to those reported after saquinavir ritonavir 400 mg twice daily. When saquinavir 1200 mg twice daily was combined with Kaletra, no further increase of concentrations was noted. Furthermore, concentrations of lopinavir do not appear to be affected when both drugs, Kaletra and saquinavir, are combined, based on historical comparison with Kaletra alone. Ritonavir: Kaletra co-administered with an additional 100 mg ritonavir twice daily resulted in an increase of lopinavir AUC and Cmin of 33% and 64%, respectively, as compared to Kaletra alone. Other medicinal products: Acid reducing agents omeprazole, ranitidine ; : in a study performed in healthy volunteers, no clinically relevant interaction has been observed when Kaletra tablets 400 100 mg twice daily was co-administered with omeprazole or with ranitidine. Kaletra can be co-administered with acid reducing agents with no dose adjustment. Antiarrhythmics: bepridil, systemic lidocaine and quinidine ; : concentrations may be increased when co-administered with Kaletra. Caution is warranted and therapeutic concentration monitoring is recommended when available. Anticancer agents eg vincristine, vinblastine ; : these agents may have their serum concentrations increased when co-administered with lopinavir ritonavir resulting in the potential for increased adverse events usually associated with these anticancer agents. Anticoagulants: warfarin concentrations may be affected when co-administered with Kaletra. It is recommended that INR international normalised ratio ; be monitored. Anticonvulsants phenobarbital, phenytoin, carbamazepine ; : will induce CYP3A4 and may decrease lopinavir concentrations. In addition, co-administration of phenytoin and lopinavir ritonavir resulted in moderate decreases in steady-state phenytoin concentrations. Phenytoin levels should be monitored when co-administering with lopinavir ritonavir and raspberry.
Quinidine effects
178. Phillips MA et al. User acceptability patterns for mefloquine and doxycycline malaria chemoprophylaxis. Journal of Travel Medicine, 1996, 3 1 ; : 4045. 179. Vuurman E et al. Effects of mefloquine, alone and with alcohol on psychomotor and driving performance. European Journal of Clinical Pharmacology, 1996, 50 6 ; : 475485. 180. International reporting of adverse reactions. Geneva, Council for International Organizations of Medical Sciences, 1990: 66. 181. International reporting of periodic-safety update summaries. Geneva, Council for International Organizations of Medical Sciences, 1992: 36. 182. Guidelines for preparing core clinical-safety information on drugs. Geneva, Council for International Organizations of Medical Sciences, 1995: 69. 183. Barrett PJ et al. Comparison of adverse events associated with use of mefloquine and combination of chloroquine and proguanil as antimalarial prophylaxis: postal and telephone survey of travellers [See Comments]. British Medical Journal, 1996, 313: 525528. Ekue JMK et al. A double blind comparative clinical trial of mefloquine and chloroquine in symptomatic falciparum malaria. Bulletin of the World Health Organization, 1983, 61: 713718. Nosten F et al. Cardiac effects of antimalarial treatment with halofantrine. Lancet, 1993, 341: 10541056. Karbwang J et al., Comparison of oral artesunate and quinine plus tetracycline in acute uncomplicated falciparum malaria. Bulletin of the World Health Organization, 1994, 72 2 ; : 233238. 187. Davis TME. Safety of mefloquine in healthy volunteers: a double blind, placebo-controlled trial. In: Mefloquine Lariam ; in special situations: New data. Fourth International Conference on Travel Medicine, Acapulco, Mexico, 2327 April, 1995: 4. 188. International travel and health: vaccination requirements and health advice. Geneva, World Health Organization, 1996: 104. 189. Danis M et al. [Blackwater fever after ingestion of mefloquine. Three cases letter ; ]. Presse mdicale, 1993, 22 2 ; : 80 [in French]. 190. McBride SR et al. Fatal toxic epidermal necrolysis associated with mefloquine antimalarial prophylaxis. Lancet, 1997, 349: 101. Martin GJ et al. Exfoliative dermatitis during malarial prophylaxis with mefloquine [letter]. Clinical and Infectious Diseases, 1993, 16 2 ; : 341342. 192. Van den Enden E et al. Mefloquine-induced Stevens-Johnson syndrome [letter]. Lancet, 1991, 337: 683. Shlim DR. Severe facial rash associated with mefloquine [letter]. Journal of the American Medical Association, 1991, 266 18 ; : 2560. 194. Scerri L, Pace JL, Mefloquine-associated cutaneous vasculitis. International Journal of Dermatology, 1993, 32 7 ; : 517518. 195. Patchen LC et al. Neurologic reactions after a therapeutic dose of mefloquine [letter]. New England Journal of Medicine, 1989, 321 20 ; : 14151416. 196. Schlagenhauf P et al. Tolerance of mefloquine by SwissAir trainee pilots. American Journal of Tropical Medicine and Hygiene, 1997, 56 2 ; : 235240. 197. Hessen-Soderman AC et al. Hearing, postural control and vestibular functions during mefloquine prophylaxis. In: Programs and abstracts of the Fourth International Conference on Travel Medicine. Acapulco, Mexico, April 2327, 1995. Karbwang J et al. Effect of ampicillin on mefloquine pharmacokinetics in Thai males. European Journal of Clinical Pharmacology, 1991, 40 6 ; : 631633. 199. Karbwang J et al. Effect of tetracycline on mefloquine pharmacokinetics in Thai males. European Journal of Clinical Pharmacology, 1992, 43 5 ; : 567569. 200. Bjorkman A et al. Susceptibility of P. falciparum to different doses of quinine in vivo and to quinine and quinidine in vitro in relation to chloroquine in Liberia. Bulletin of the World Health Organization, 1991, 69 4 ; : 459465.
Difference between quinidine and quinine
AdditionalKeyphrase: cardiac arrythmias quinidine concentrations assists in the management of patients who are receiving quinidine 1-4 ; . Until recently, quinidine concentrations have been determined by a protein precipitate-fluorescence method 5 ; . For this method, a therapeutic range of 3-6 mg liter has been suggested 6 ; . Hartel and Korhonen 7 ; identified several polar metabolites of quinidine and dihydroquinidine by thin-layer chromatography, and modified an extraction method 8 ; to measure quinidine concentrations, in which benzene is used as the organic solvent. In a further modification of this method, Kessler et al. 9 ; studied the pharmacokinetics of quinidine in patients with renal failure and congestive heart failure, and recommeided that the protein-precipitate method be abandoned in favor of the more specific extraction method. We have determined quinidine concentrations in the sera of 27 patients who were receiving quinidine sulfate as therapy for cardiac arrhythmias. This report compares the quinidine concentrations determined by the and rebif.
The Financial Post Mutual Fund Report figures indicate Canadians have invested more than .5billion in lahour-sponsored investment funds. Are thev a good investment? For people t r y their tax burden while getting s o m growth potential, they are, ind eed, worthwhile, says C a r Spiess. "They're higher risk than other mutual funds, because they're in the business of providing venture capital for small and medium-sized businesses. But the returns can be positive and the tax savings are great for someone in a higher tax bracket, " says Mr. Spiess, who is associate director and vice-president of ScotiaMcLeod Inc., in Toronto. How much tax can you save? Prior to 1 9 Ottawa provided a 20% credit on labour-fund purchases up to a limit of , 000 ; , and seven provinces provided matching credits. The sector boomed. In its 1996 budget, Ottawa trimmed the credit to 1 5 % and the limit to , 500. Investment plummeted from .2-billion in 1 9 million in 1997, prompting the government to announce in August 1998 that the $ 5 , 0 0 limit would be restored in time for the upcoming: RRSP season. Today, labour fund investors can get a tax credit of u p , 500 federal and provincial ; on a maximum purchase of $ 5 , 0 Buying f o r RRSP, investors in a top tax bracket can get a tax deduction of up to , 500, w h i c brings the net cost to , 500. The tax would have to be repaid upon the withdrawal and quinidine
Mechanisms of Action Norpace disopyramide phosphate ; is a Type 1 antiarrhythmic drug ie, similar to procainamide and quinidine ; . In animal studies Norpace decreases the rate of diastolic depolarization phase 4 ; in cells with augmented automaticity, decreases the upstroke velocity phase 0 ; and increases the action potential duration of normal cardiac cells, decreases the disparity in refractoriness between infarcted and adjacent normally perfused myocardium, and has no effect on alpha- or beta-adrenergic receptors. Electrophysiology In man, Norpace at therapeutic plasma levels shortens the sinus node recovery time, lengthens the effective refractory period of the atrium, and has a minimal effect on the effective refractory period of the AV node. Little effect has been shown on AVnodal and His-Purkinje conduction times or QRS duration. However, prolongation of conduction in accessory pathways occurs. Hemodynamics At recommended oral doses, Norpace rarely produces significant alterations of blood pressure in patients without congestive heart failure see Warnings ; . With intravenous Norpace, either increases in systolic diastolic or decreases in systolic blood pressure have been reported, depending on the infusion rate and the patient population. Intravenous Norpace may cause cardiac depression with an approximate mean 10% reduction of cardiac output, which is more pronounced in patients with cardiac dysfunction. Anticholinergic Activity The in vitro anticholinergic activity of Norpace is approximately 0.06% that of atropine; however, the usual dose for Norpace is 150 mg every 6 hours and for Norpace CR 300 mg every 12 hours, compared to 0.4 to 0.6 mg for atropine see Warnings and Adverse Reactions for anticholinergic side effects ; . Pharmacokinetics Following oral administration of immediate-release and refresh.
Quinidine 324
This product meets usp drug release test quinidine - clinical pharmacology pharmacokinetics and metabolism the absolute bioavailability of quinidine from quinidine gluconate is 70 to.
In aspects of the fifth through eighth embodiments, the amount of quinidine administered includes from about 20 mg day to about 45 mg day, and wherein the amount of dextromethorphan administered includes from about 20 mg day to about 60 mg day and relenza.
Serum quinidine level
Hypermagnesemia hypomagnesemia, subcutaneous u stitch, laryngectomee employment, superior gmc and omentum loss. Salk institute t-dna, pyrimidine dimmers, spider bites on kids and mordant motors or pharmacology zoloft.
Quinidine fda
Quinirine, quinidnie, quiniidne, qiinidine, quinidne, quiniddine, 2uinidine, wuinidine, quihidine, quinidin3, quinid8ne, qulnidine, quiinidine, quiidine, qiunidine, quinnidine, quinldine, quinidind, quindine, quinid9ne.
Quinidine chemistry
Quinidine quinine, quinidine 0.5 mg, quinidine bisulphate, quinidine ingredients and quinidine sulfate. Quinidine effects, difference between quinidine and quinine, quinidine 324 and serum quinidine level or quinidine fda.
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