By T. Amul. Westminster Theological Seminary in California.

Adverse Reactions Associated with Discontinuation of Treatment in Short-Term generic 0.5 mg dutas with mastercard, Placebo-Controlled TrialsDepression: Overall safe 0.5 mg dutas, discontinuations due to adverse reactions were 12 cheap 0.5 mg dutas with visa. Mania: Overall order dutas 0.5 mg without prescription, discontinuations due to adverse reactions were 5. Schizophrenia: Overall, there was little difference in the incidence of discontinuation due to adverse reactions (4% for SEROQUEL vs. However, discontinuations due to somnolence and hypotension were considered to be drug related: [see WARNINGS and PRECAUTIONS ]The prescriber should be aware that the figures in the tables and tabulations cannot be used to predict the incidence of side effects in the course of usual medical practice where patient characteristics and other factors differ from those that prevailed in the clinical trials. Similarly, the cited frequencies cannot be compared with figures obtained from other clinical investigations involving different treatments, uses, and investigators. The cited figures, however, do provide the prescribing physician with some basis for estimating the relative contribution of drug and nondrug factors to the side effect incidence in the population studied. Table 2 enumerates the incidence, rounded to the nearest percent, of treatment-emergent adverse reactions that occurred during acute therapy of schizophrenia (up to 6 weeks) and bipolar mania (up to 12 weeks) in 1% or more of patients treated with SEROQUEL (doses ranging from 75 to 800 mg/day) where the incidence in patients treated with SEROQUEL was greater than the incidence in placebo-treated patients. Treatment-Emergent Adverse Reaction Incidence in 3- to 12-Week Placebo-Controlled Clinical Trials for the Treatment of Schizophrenia and Bipolar Mania (monotherapy)Gamma Glutamyl Transpeptidase Increased1Reactions for which the SEROQUEL incidence was equal to or less than placebo are not listed in the table, but included the following: accidental injury, akathisia, chest pain, cough increased, depression, diarrhea, extrapyramidal syndrome, hostility, hypertension, hypertonia, hypotension, increased appetite, infection, insomnia, leukopenia, malaise, nausea, nervousness, paresthesia, peripheral edema, sweating, tremor, and weight loss. In these studies, the most commonly observed adverse reactions associated with the use of SEROQUEL (incidence of 5% or greater) and observed at a rate on SEROQUEL at least twice that of placebo were somnolence (18%), dizziness (11%), dry mouth (9%), constipation (8%), SGPT increased (5%), weight gain (5%), and dyspepsia (5%). Table 3 enumerates the incidence, rounded to the nearest percent, of treatment-emergent adverse reactions that occurred during therapy (up to 3-weeks) of acute mania in 5% or more of patients treated with SEROQUEL (doses ranging from 100 to 800 mg/day) used as adjunct therapy to lithium and divalproex where the incidence in patients treated with SEROQUEL was greater than the incidence in placebo-treated patients. Treatment-Emergent Adverse Reaction Incidence in 3-Week Placebo-Controlled Clinical Trials for the Treatment of Bipolar Mania (Adjunct Therapy)1Reactions for which the SEROQUEL incidence was equal to or less than placebo are not listed in the table, but included the following: akathisia, diarrhea, insomnia, and nausea. In these studies, the most commonly observed adverse reactions associated with the use of SEROQUEL (incidence of 5% or greater) and observed at a rate on SEROQUEL at least twice that of placebo were somnolence (34%), dry mouth (19%), asthenia (10%), constipation (10%), abdominal pain (7%), postural hypotension (7%), pharyngitis (6%), and weight gain (6%). Table 4 enumerates the incidence, rounded to the nearest percent, of treatment-emergent adverse reactions that occurred during therapy (up to 8-weeks) of bipolar depression in 5% or more of patients treated with SEROQUEL (doses of 300 and 600 mg/day) where the incidence in patients treated with SEROQUEL was greater than the incidence in placebo-treated patients. Treatment-Emergent Adverse Reaction Incidence in 8-Week Placebo-Controlled Clinical Trials for the Treatment of Bipolar Depression1General Disorders and Administrative Site Conditions1Events for which the SEROQUEL incidence was equal to or less than placebo are not listed in the table, but included the following: nausea, upper respiratory tract infection, and headache. In these studies, the most commonly observed adverse reactions associated with the use of SEROQUEL (incidence of 5% or greater) and observed at a rate on SEROQUEL at least twice that of placebo were dry mouth (44%), sedation (30%), somnolence (28%), dizziness (18%), constipation (10%), lethargy (5%), and nasal congestion (5%). Explorations for interactions on the basis of gender, age, and race did not reveal any clinically meaningful differences in the adverse reaction occurrence on the basis of these demographic factors. Dose Dependency of Adverse Reactions in Short-Term, Placebo-Controlled TrialsDose-related Adverse Reactions: Spontaneously elicited adverse reaction data from a study of schizophrenia comparing five fixed doses of SEROQUEL (75 mg, 150 mg, 300 mg, 600 mg, and 750 mg/day) to placebo were explored for dose-relatedness of adverse reactions. Logistic regression analyses revealed a positive dose response (p < 0. Class Effect: Symptoms of dystonia, prolonged abnormal contractions of muscle groups, may occur in susceptible individuals during the first few days of treatment. Dystonic symptoms include: spasm of the neck muscles, sometimes progressing to tightness of the throat, swallowing difficulty, difficulty breathing, and/or protrusion of the tongue. While these symptoms can occur at low doses, they occur more frequently and with greater severity with high potency and at higher doses of first generation antipsychotic drugs. An elevated risk of acute dystonia is observed in males and younger age groups. Data from one 6-week clinical trial of schizophrenia comparing five fixed doses of SEROQUEL (75, 150, 300, 600, 750 mg/day) provided evidence for the lack of treatment-emergent extrapyramidal symptoms (EPS) and dose-relatedness for EPS associated with SEROQUEL treatment. Three methods were used to measure EPS: (1) Simpson-Angus total score (mean change from baseline) which evaluates Parkinsonism and akathisia, (2) incidence of spontaneous complaints of EPS (akathisia, akinesia, cogwheel rigidity, extrapyramidal syndrome, hypertonia, hypokinesia, neck rigidity, and tremor), and (3) use of anticholinergic medications to treat emergent EPS. Anticholinergic medicationsIn six additional placebo-controlled clinical trials (3 in acute mania and 3 in schizophrenia) using variable doses of SEROQUEL, there were no differences between the SEROQUEL and placebo treatment groups in the incidence of EPS, as assessed by Simpson-Angus total scores, spontaneous complaints of EPS and the use of concomitant anticholinergic medications to treat EPS. In two placebo-controlled clinical trials for the treatment of bipolar depression using 300 mg and 600 mg of SEROQUEL, the incidence of adverse reactions potentially related to EPS was 12% in both dose groups and 6% in the placebo group. In these studies, the incidence of the individual adverse reactions (eg, akathisia, extrapyramidal disorder, tremor, dyskinesia, dystonia, restlessness, muscle contractions involuntary, psychomotor hyperactivity and muscle rigidity) were generally low and did not exceed 4% in any treatment group. The 3 treatment groups were similar in mean change in SAS total score and BARS Global Assessment score at the end of treatment. The use of concomitant anticholinergic medications was infrequent and similar across the three treatment groups. In schizophrenia trials the proportions of patients meeting a weight gain criterion of ?-U 7% of body weight were compared in a pool of four 3- to 6-week placebo-controlled clinical trials, revealing a statistically significantly greater incidence of weight gain for SEROQUEL (23%) compared to placebo (6%). In mania monotherapy trials the proportions of patients meeting the same weight gain criterion were 21% compared to 7% for placebo and in mania adjunct therapy trials the proportion of patients meeting the same weight criterion were 13% compared to 4% for placebo. In bipolar depression trials, the proportions of patients meeting the same weight gain criterion were 8% compared to 2% for placebo. An assessment of the premarketing experience for SEROQUEL suggested that it is associated with asymptomatic increases in SGPT and increases in both total cholesterol and triglycerides In post-marketing clinical trials, elevations in total cholesterol (predominantly LDL cholesterol) have been observed. In placebo controlled monotherapy clinical trials involving 3368 patients on SEROQUEL and 1515 on placebo, the incidence of at least one occurrence of neutrophil count < 1. Patient with pre-existent low WBC or a history of drug induced luekopenia / neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and should discontinue SEROQUEL at the first sign of a decline in WBC in absence of other causative factors. In short-term (12 weeks duration or less) placebo-controlled clinical trials (3342 patients treated with SEROQUEL and 1490 treated with placebo), the percent of patients who had a fasting blood glucose ?-U126 mg/dl or a non fasting blood glucose ?-U200 mg/dl was 3. In a 24 week trial (active-controlled, 115 patients treated with SEROQUEL) designed to evaluate glycemic status with oral glucose tolerance testing of all patients, at week 24 the incidence of a treatment-emergent post-glucose challenge glucose level ?-U200 mg/dl was 1. Between-group comparisons for pooled placebo-controlled trials revealed no statistically significant SEROQUEL/placebo differences in the proportions of patients experiencing potentially important changes in ECG parameters, including QT, QTc, and PR intervals. However, the proportions of patients meeting the criteria for tachycardia were compared in four 3- to 6-week placebo-controlled clinical trials for the treatment of schizophrenia revealing a 1% (4/399) incidence for SEROQUEL compared to 0. In acute (monotherapy) bipolar mania trials the proportions of patients meeting the criteria for tachycardia was 0. In acute bipolar mania (adjunct) trials the proportions of patients meeting the same criteria was 0. In bipolar depression trials, no patients had heart rate increases to > 120 beats per minute. SEROQUEL use was associated with a mean increase in heart rate, assessed by ECG, of 7 beats per minute compared to a mean increase of 1 beat per minute among placebo patients. Following is a list of COSTART terms that reflect treatment-emergent adverse reactions as defined in the introduction to the ADVERSE REACTIONS section reported by patients treated with SEROQUEL at multiple doses 75 mg/day during any phase of a trial within the premarketing database of approximately 2200 patients treated for schizophrenia. All reported reactions are included except those already listed in the tables or elsewhere in labeling, those reactions for which a drug cause was remote, and those reaction terms which were so general as to be uninformative. It is important to emphasize that, although the reactions reported occurred during treatment with SEROQUEL, they were not necessarily caused by it. Reactions are further categorized by body system and listed in order of decreasing frequency according to the following definitions: frequent adverse reactions are those occurring in at least 1/100 patients (only those not already listed in the tabulated results from placebo-controlled trials appear in this listing); infrequent adverse reactions are those occurring in 1/100 to 1/1000 patients; rare reactions are those occurring in fewer than 1/1000 patients. Nervous System: Frequent: hypertonia, dysarthria; Infrequent: abnormal dreams, dyskinesia, thinking abnormal, tardive dyskinesia, vertigo, involuntary movements, confusion, amnesia, psychosis, hallucinations, hyperkinesia, libido increased*, urinary retention, incoordination, paranoid reaction, abnormal gait, myoclonus, delusions, manic reaction, apathy, ataxia, depersonalization, stupor, bruxism, catatonic reaction, hemiplegia; Rare: aphasia, buccoglossal syndrome, choreoathetosis, delirium, emotional lability, euphoria, libido decreased*, neuralgia, stuttering, subdural hematoma. Body as a Whole: Frequent: flu syndrome; Infrequent: neck pain, pelvic pain*, suicide attempt, malaise, photosensitivity reaction, chills, face edema, moniliasis; Rare:abdomen enlarged.

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Sitagliptin is present in Janumet tablets in the form of sitagliptin phosphate monohydrate safe dutas 0.5 mg. Sitagliptin phosphate monohydrate is described chemically as 7 - [(3R) - 3 - amino - 1 - oxo - 4 - (2 generic dutas 0.5mg amex,4 cheap 0.5 mg dutas amex,5 - trifluorophenyl)butyl] - 5 0.5mg dutas with visa,6,7,8 - tetrahydro - 3 - (trifluoromethyl) - 1,2,4 - triazolo[4,3 - a]pyrazine phosphate (1:1) monohydrate with an empirical formula of CO and a molecular weight of 523. The structural formula is:Sitagliptin phosphate monohydrate is a white to off-white, crystalline, non-hygroscopic powder. It is soluble in water and N,N-dimethyl formamide; slightly soluble in methanol; very slightly soluble in ethanol, acetone, and acetonitrile; and insoluble in isopropanol and isopropyl acetate. Metformin hydrochloride (N,N-dimethylimidodicarbonimidic diamide hydrochloride) is not chemically or pharmacologically related to any other classes of oral antihyperglycemic agents. Metformin hydrochloride is a white to off-white crystalline compound with a molecular formula of C-HCl and a molecular weight of 165. Metformin hydrochloride is freely soluble in water and is practically insoluble in acetone, ether, and chloroform. The pH of a 1% aqueous solution of metformin hydrochloride is 6. The structural formula is as shown:Janumet is available for oral administration as tablets containing 64. Each film-coated tablet of Janumet contains the following inactive ingredients: microcrystalline cellulose, polyvinylpyrrolidone, sodium lauryl sulfate, and sodium stearyl fumarate. In addition, the film coating contains the following inactive ingredients: polyvinyl alcohol, polyethylene glycol, talc, titanium dioxide, red iron oxide, and black iron oxide. Janumet combines two antihyperglycemic agents with complementary mechanisms of action to improve glycemic control in patients with type 2 diabetes: sitagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, and metformin hydrochloride, a member of the biguanide class. Sitagliptin is a DPP-4 inhibitor, which is believed to exert its actions in patients with type 2 diabetes by slowing the inactivation of incretin hormones. Concentrations of the active intact hormones are increased by sitagliptin, thereby increasing and prolonging the action of these hormones. Incretin hormones, including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are released by the intestine throughout the day, and levels are increased in response to a meal. These hormones are rapidly inactivated by the enzyme DPP-4. The incretins are part of an endogenous system involved in the physiologic regulation of glucose homeostasis. When blood glucose concentrations are normal or elevated, GLP-1 and GIP increase insulin synthesis and release from pancreatic beta cells by intracellular signaling pathways involving cyclic AMP. GLP-1 also lowers glucagon secretion from pancreatic alpha cells, leading to reduced hepatic glucose production. By increasing and prolonging active incretin levels, sitagliptin increases insulin release and decreases glucagon levels in the circulation in a glucose-dependent manner. Sitagliptin demonstrates selectivity for DPP-4 and does not inhibit DPP-8 or DPP-9 activity in vitro at concentrations approximating those from therapeutic doses. Metformin is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose. Its pharmacologic mechanisms of action are different from other classes of oral antihyperglycemic agents. Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization. Unlike sulfonylureas, metformin does not produce hypoglycemia in either patients with type 2 diabetes or normal subjects (except in special circumstances [see Warnings and Precautions ]) and does not cause hyperinsulinemia. With metformin therapy, insulin secretion remains unchanged while fasting insulin levels and day-long plasma insulin response may actually decrease. In patients with type 2 diabetes, administration of sitagliptin led to inhibition of DPP-4 enzyme activity for a 24-hour period. After an oral glucose load or a meal, this DPP-4 inhibition resulted in a 2- to 3-fold increase in circulating levels of active GLP-1 and GIP, decreased glucagon concentrations, and increased responsiveness of insulin release to glucose, resulting in higher C-peptide and insulin concentrations. The rise in insulin with the decrease in glucagon was associated with lower fasting glucose concentrations and reduced glucose excursion following an oral glucose load or a meal. Sitagliptin and Metformin hydrochloride Co-administrationIn a two-day study in healthy subjects, sitagliptin alone increased active GLP-1 concentrations, whereas metformin alone increased active and total GLP-1 concentrations to similar extents. Co-administration of sitagliptin and metformin had an additive effect on active GLP-1 concentrations. Sitagliptin, but not metformin, increased active GIP concentrations. It is unclear what these findings mean for changes in glycemic control in patients with type 2 diabetes. In studies with healthy subjects, sitagliptin did not lower blood glucose or cause hypoglycemia. Cardiac ElectrophysiologyIn a randomized, placebo-controlled crossover study, 79 healthy subjects were administered a single oral dose of sitagliptin 100 mg, sitagliptin 800 mg (8 times the recommended dose), and placebo. At the recommended dose of 100 mg, there was no effect on the QTc interval obtained at the peak plasma concentration, or at any other time during the study. Following the 800-mg dose, the maximum increase in the placebo-corrected mean change in QTc from baseline at 3 hours postdose was 8. This increase is not considered to be clinically significant. At the 800-mg dose, peak sitagliptin plasma concentrations were approximately 11 times higher than the peak concentrations following a 100-mg dose. In patients with type 2 diabetes administered sitagliptin 100 mg (N=81) or sitagliptin 200 mg (N=63) daily, there were no meaningful changes in QTc interval based on ECG data obtained at the time of expected peak plasma concentration. The results of a bioequivalence study in healthy subjects demonstrated that the Janumet (sitagliptin/metformin HCl) 50 mg/500 mg and 50 mg/1000 mg combination tablets are bioequivalent to co-administration of corresponding doses of sitagliptin (JANUVIA) and metformin hydrochloride as individual tablets. The absolute bioavailability of sitagliptin is approximately 87%. Co-administration of a high-fat meal with sitagliptin had no effect on the pharmacokinetics of sitagliptin. The absolute bioavailability of a metformin hydrochloride 500-mg tablet given under fasting conditions is approximately 50-60%. Studies using single oral doses of metformin hydrochloride tablets 500 mg to 1500 mg, and 850 mg to 2550 mg, indicate that there is a lack of dose proportionality with increasing doses, which is due to decreased absorption rather than an alteration in elimination. Food decreases the extent of and slightly delays the absorption of metformin, as shown by approximately a 40% lower mean peak plasma concentration (C), a 25% lower area under the plasma concentration versus time curve (AUC), and a 35-minute prolongation of time to peak plasma concentration (T) following administration of a single 850-mg tablet of metformin with food, compared to the same tablet strength administered fasting. The clinical relevance of these decreases is unknown. The mean volume of distribution at steady state following a single 100-mg intravenous dose of sitagliptin to healthy subjects is approximately 198 liters.

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Therefore generic dutas 0.5mg without a prescription, they should be administered cautiously to women of childbearing potential particularly during the first trimester of pregnancy and near term purchase dutas 0.5mg on line. Use with caution during lactation because of possible sedative and anticholinergic side effects on the infant generic dutas 0.5 mg without prescription. Chlorpromazine may adversely affect many of the conditions commonly occurring in the aged dutas 0.5 mg low cost, including cardiovascular problems, parkinsonian extrapyramidal effects and anticholinergic effects (e. Dependence and Withdrawl: In general, phenothiazines do not produce psychic dependence; however, gastritis, nausea and vomiting, dizziness, and tremulousness have been reported following abrupt cessation of high dose therapy. Reports suggest that these symptoms can be reduced if concomitant antiparkinsonian agents are continued for several weeks after the phenothiazine is withdrawn. Interference with cognitive and motor performance: Where patients are participating in activities requiring complete mental alertness such as driving an automobile or operating machinery, administer the phenothiazine cautiously, forewarn the patient and increase the dosage gradually. Patients should utilize sunscreens when exposed to sunlight for significant lengths of time. Amphetamines: Amphetamines may cause exacerbation of psychotic symptoms. Antacids: May impair the absorption of chlorpromazine. Anticonvulsants: Chlorpromazine may lower the seizure threshold. Anticonvulsant therapy should be monitored closely and may require dosage adjustment. Antidepressants, tricyclic: May result in increased chlorpromazine concentration, monitor for adverse effects. CNS Depressants: Chlorpromazine and other CNS depressants (alcohol, antihistamines, general anesthetics, opiates or other narcotic analgesics, barbiturates, benzodiazepines and other sedative/hypnotic agents) may result in additive CNS depressant effects. Monitor to avoid excessive sedation or respiratory depression. Epinephrine: Patients on chlorpromazine who are hypotensive should not be given epinephrine. Chlorpromazine blocks peripheral alpha-adrenergic receptors, thereby inhibiting alpha-agonist effects of epinephrine such as vasoconstriction and increased blood pressure. The beta-agonist effects of epinephrine (vasodilation) may be left unopposed and a further fall in blood pressure may result. Agents such as phenylephrine methoxamine or norepinephrine may be a suitable alternative to raise blood pressure. Hypotensive Agents: Chlorpromazine and antihypertensives may result in additive hypotensive effects and increased risk of orthostatic hypotension or syncope (fainting). Chlorpromazine may block the antihypertensive effects of guanethidine by preventing its uptake into sympathetic nerves. Levodopa: Phenothiazines may inhibit the antiparkinsonian effects of levodopa due to their dopamine blocking effects in the CNS. Generally, phenothiazines should not be administered to patients who require levodopa. Lithium: Patients receiving lithium and chlorpromazine for treatment of acute mania should be monitored closely for signs of adverse neurologic effects, especially if serum concentrations of lithium are in the upper range. Rare cases of severe neurotoxicity have been reported. BEFORE USING THIS MEDICINE: INFORM YOUR DOCTOR OR PHARMACIST of all prescription and over-the-counter medicine that you are taking. This includes meperidine, diazoxide, guanethidine, medicines used to treat high blood pressure and heart conditions, medicines used to treat depression, and medicines used to treat bladder or bowel spasms. Inform your doctor of any other medical conditions including seizure disorders, depression, allergies, pregnancy, or breast-feeding. CHECK WITH YOUR DOCTOR AS SOON AS POSSIBLE if you experience changes in vision; changes in breasts; changes in menstrual period; sore throat; inability to move eyes; muscle spasms of face, neck, or back; difficulty swallowing; mask-like face; tremors of hands; restlessness; tension in legs; shuffling walk or stiff arms or legs; puffing of cheeks; lip smacking or puckering; twitching or twisting movements; or weakness of arms or legs. Do not become overheated in hot weather, during exercise, or other activities since heat stroke may occur while you are using this medicine. This medicine may cause increased sensitivity to the sun. Avoid exposure to the sun or sunlamps until you know how you react to this medicine. Use a sunscreen or protective clothing if you must be outside for a prolonged period. In general, members of the aliphatic group of phenothiazines have strong sedative, hypotensive and anticholinergic properties and mild to moderate extrapyramidal effects. Automatic Nervous System: Anticholinergic effects including dry mouth, blurred vision, constipation, ileus, nasal stuffiness, photophobia. Syncope and impaired temperature regulation have also occurred. Cardiovascular: Chlorpromazine has peripheral alpha-adrenergic blocking activity. Its effects on the heart include: direct negative inotropic and quinidine-like actions. Its effects on the ECG include prolongation of the PR and QT intervals, blunting of the T wave and depression of the S-T segment. Ventricular arrythmia and sudden death have occurred rarely. Orthostatic hypotension is common after parenteral administration and usually lasts one-half to 2 hours. Patients should be supine when parenteral chlorpromazine is administered. Tachycardia, fainting and dizziness have also occurred. Hypotension can also occur after oral administration. Tolerance to hypotensive effects generally develop over time, however hypotension can persist in some patients, especially the elderly. Central Nervous System: Extrapyramidal reactions, including pseudoparkinsonism (with motor retardation, rigidity, mask like facies, pill rolling and other tremors, drooling, shuffling gait, etc. In addition, slowing of the EEG rhythm, disturbed body temperature and lowering of the convulsive threshold have occurred. Tardive dyskinesia may appear in some patients on long term antipsychotic therapy or may appear after drug therapy has been discontinued. The risk appears to be greater in elderly patients on high-dose therapy, especially females. The symptoms are persistent and in some patients appear to be irreversible. The syndrome is characterized by rhythmical involuntary movements of the tongue, face, mouth or jaw (e. Sometimes these may be accompanied by involuntary movements of the extremities.

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Surmontil should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus order dutas 0.5mg on line. Pediatric Use Safety and effectiveness in the pediatric population have not been established (see BOX WARNING and WARNINGS -Clinical Worsening and Suicide Risk) generic 0.5mg dutas mastercard. Anyone considering the use of Surmontil in a child or adolescent must balance the potential risks with the clinical need buy 0.5mg dutas mastercard. Geriatric Use Clinical studies of Surmontil^ (trimipramine maleate) were not adequate to determine whether subjects aged 65 and over respond differently from younger subjects cheap dutas 0.5 mg without a prescription. The pharmacokinetics of trimipramine were not substantially altered in the elderly (see CLINICAL PHARMACOLOGY ). Surmontil is known to be substantially excreted by the kidney. Clinical circumstances, some of which may be more common in the elderly, such as hepatic or renal impairment, should be considered (see PRECAUTIONS - General). In general, dose selection for an elderly patient should be cautious, usually starting at a lower dose (see DOSAGE AND ADMINISTRATION ). Note: The pharmacological similarities among the tricyclic antidepressants require that each of the reactions be considered when Surmontil is administered. Some of the adverse reactions included in this listing have not in fact been reported with Surmontil. Cardiovascular Hypotension, hypertension, tachycardia, palpitation, myocardial infarction, arrhythmias, heart block, stroke. Psychiatric Confusional states (especially the elderly) with hallucinations, disorientation, delusions; anxiety, restlessness, agitation; insomnia and nightmares; hypomania; exacerbation of psychosis. Neurological Numbness, tingling, paresthesias of extremities; incoordination, ataxia, tremors; peripheral neuropathy; extrapyramidal symptoms; seizures, alterations in EEG patterns; tinnitus; syndrome of inappropriate ADH (antidiuretic hormone) secretion. Anticholinergic Dry mouth and, rarely, associated sublingual adenitis; blurred vision, disturbances of accommodation, mydriasis, constipation, paralytic ileus; urinary retention, delayed micturition, dilation of the urinary tract. Allergic Skin rash, petechiae, urticaria, itching, photosensitization, edema of face and tongue. Hematologic Bone-marrow depression including agranulocytosis, eosinophilia; purpura; thrombo-cytopenia. Leukocyte and differential counts should be performed in any patient who develops fever and sore throat during therapy; the drug should be discontinued if there is evidence of pathological neutrophil depression. Gastrointestinal Nausea and vomiting, anorexia, epigastric distress, diarrhea, peculiar taste, stomatitis, abdominal cramps, black tongue. Endocrine Gynecomastia in the male; breast enlargement and galactorrhea in the female; increased or decreased libido, impotence; testicular swelling; elevation or depression of blood-sugar levels. Other Jaundice (simulating obstructive); altered liver function; weight gain or loss; perspiration; flushing; urinary frequency; drowsiness, dizziness, weakness, and fatigue; headache; parotid swelling; alopecia. Withdrawal Symptoms Though not indicative of addiction, abrupt cessation of treatment after prolonged therapy may produce nausea, headache, and malaise. Dosage should be initiated at a low level and increased gradually, noting carefully the clinical response and any evidence of intolerance. Lower dosages are recommended for elderly patients and adolescents. Lower dosages are also recommended for outpatients as compared to hospitalized patients who will be under close supervision. It is not possible to prescribe a single dosage schedule of Surmontil that will be therapeutically effective in all patients. The physical psychodynamic factors contributing to depressive symptomatology are very complex; spontaneous remissions or exacerbations of depressive symptoms may occur with or without drug therapy. Consequently, the recommended dosage regimens are furnished as a guide which may be modified by factors such as the age of the patient, chronicity and severity of the disease, medical condition of the patient, and degree of psychotherapeutic support. Most antidepressant drugs have a lag period of ten days to four weeks before a therapeutic response is noted. Increasing the dose will not shorten this period but rather increase the incidence of adverse reactions. Usual Adult Dose Outpatients and Office Patients -Initially, 75 mg/day in divided doses, increased to 150 mg/day. Maintenance therapy is in the range of 50 to 150 mg/day. For convenient therapy and to facilitate patient compliance, the total dosage requirement may be given at bedtime. Hospitalized Patients-Initially, 100 mg/day in divided doses. This may be increased gradually in a few days to 200 mg/day, depending upon individual response and tolerance. If improvement does not occur in 2 to 3 weeks, the dose may be increased to the maximum recommended dose of 250 to 300 mg/day. Adolescent and Geriatric Patients-Initially, a dose of 50 mg/day is recommended, with gradual increments up to 100 mg/day, depending upon patient response and tolerance. Maintenance-Following remission, maintenance medication may be required for a longer period of time, at the lowest dose that will maintain remission. Maintenance therapy is preferably administered as a single dose at bedtime. To minimize relapse, maintenance therapy should be continued for about three months. Deaths may occur from overdosage with this class of drugs. Multiple drug ingestion (including alcohol) is common in deliberate tricyclic antidepressant overdose. As the management is complex and changing, it is recommended that the physician contact a poison control center for current information on treatment. Signs and symptoms of toxicity develop rapidly after tricyclic antidepressant overdose, therefore, hospital monitoring is required as soon as possible. Manifestations Critical manifestations of overdose include: cardiac dysrhythmias, severe hypotension, convulsions, and CNS depression, including coma. Changes in the electrocardiogram, particularly in QRS axis or width, are clinically significant indicators of tricyclic antidepressant toxicity. Other signs of overdose may include: confusion, disturbed concentration, transient visual hallucinations, dilated pupils, agitation, hyperactive reflexes, stupor, drowsiness, muscle rigidity, vomiting, hypothermia, hyperpyrexia, or any of the symptoms listed under ADVERSE REACTIONS. Management General Obtain an ECG and immediately initiate cardiac monitoring. A minimum of six hours of observation with cardiac monitoring and observation for signs of CNS or respiratory depression, hypotension, cardiac dysrhythmias and/or conduction blocks, and seizures is necessary.

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