By T. Quadir. Lake Forest Graduate School of Management.
In the short-term 0.1mg clonidine with amex, placebo-controlled trials in Major Depressive Disorder order clonidine 0.1 mg mastercard, the incidence of reported EPS-related events order 0.1 mg clonidine overnight delivery, excluding events related to akathisia, for adjunctive aripiprazole-treated patients was 8% vs. Objectively collected data from those trials was collected on the Simpson Angus Rating Scale (for EPS), the Barnes Akathisia Scale (for akathisia), and the Assessments of Involuntary Movement Scales (for dyskinesias). In the adult Schizophrenia trials, the objectively collected data did not show a difference between aripiprazole and placebo, with the exception of the Barnes Akathisia Scale (aripiprazole, 0. In the pediatric (13 to 17 years) Schizophrenia trial, the objectively collected data did not show a difference between aripiprazole and placebo, with the exception of the Simpson Angus Rating Scale (aripiprazole, 0. In the adult Bipolar Mania trials with monotherapy aripiprazole, the Simpson Angus Rating Scale and the Barnes Akathisia Scale showed a significant difference between aripiprazole and placebo (aripiprazole, 0. Changes in the Assessments of Involuntary Movement Scales were similar for the aripiprazole and placebo groups. In the Bipolar Mania trials with aripiprazole as adjunctive therapy with either lithium or valproate, the Simpson Angus Rating Scale and the Barnes Akathisia Scale showed a significant difference between adjunctive aripiprazole and adjunctive placebo (aripiprazole,0. Changes in the Assessments of Involuntary Movement Scales were similar for adjunctive aripiprazole and adjunctive placebo. In the pediatric (10 to 17 years) short-term Bipolar Mania trial, the Simpson Angus Rating Scale showed a significant difference between aripiprazole and placebo (aripiprazole,0. Changes in the Barnes Akathisia Scale and the Assessments of Involuntary Movement Scales were similar for the aripiprazole and placebo groups. In the Major Depressive Disorder trials, the Simpson Angus Rating Scale and the Barnes Akathisia Scale showed a significant difference between adjunctive aripiprazole and adjunctive placebo (aripiprazole, 0. Changes in the Assessments of Involuntary Movement Scales were similar for the adjunctive aripiprazole and adjunctive placebo groups. Similarly, in a long-term (26-week), placebo-controlled trial of Schizophrenia in adults, objectively collected data on the Simpson Angus Rating Scale (for EPS), the Barnes Akathisia Scale (for akathisia), and the Assessments of Involuntary Movement Scales (for dyskinesias) did not show a difference between aripiprazole and placebo. In the placebo-controlled trials in patients with agitation associated with Schizophrenia or Bipolar Mania, the incidence of reported EPS-related events excluding events related to akathisia for aripiprazole-treated patients was 2% vs. Objectively collected data on the Simpson Angus Rating Scale (for EPS) and the Barnes Akathisia Scale (for akathisia) for all treatment groups did not show a difference between aripiprazole and placebo. 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. A between group comparison for 3-week to 6-week, placebo-controlled trials in adults or 4-week to 6-week, placebo-controlled trials in pediatric patients (10 to 17 years) revealed no medically important differences between the aripiprazole and placebo groups in the proportions of patients experiencing potentially clinically significant changes in routine serum chemistry, hematology, or urinalysis parameters. Similarly, there were no aripiprazole/placebo differences in the incidence of discontinuations for changes in serum chemistry, hematology, or urinalysis in adult or pediatric patients. In the 6-week trials of aripiprazole as adjunctive therapy for Major Depressive Disorder, there were no clinically important differences between the adjunctive aripiprazole-treated and adjunctive placebo-treated patients in the median change from baseline in prolactin, fasting glucose, HDL, LDL,or total cholesterol measurements. The median % change from baseline in triglycerides was 5% for adjunctive aripiprazole-treated patients vs. In a long-term (26-week), placebo-controlled trial there were no medically important differences between the aripiprazole and placebo patients in the mean change from baseline in prolactin, fasting glucose, triglyceride, HDL, LDL, or total cholesterol measurements. In 4-week to 6-week trials in adults with Schizophrenia, there was a slight difference in mean weight gain between aripiprazole and placebo patients (+0. In 3-week trials in adults with Mania with monotherapy aripiprazole, the mean weight gain for aripiprazole and placebo patients was 0. The proportion of patients meeting a weight gain criterion of ?-U 7% of body weight was aripiprazole (2%) compared to placebo the 6-week trial in Mania with aripiprazole as adjunctive therapy with either lithium or valproate, the mean weight gain for aripiprazole and placebo patients was 0. The proportion of patients meeting a weight gain criterion of ?-U 7% of body weight with adjunctive aripiprazole was 3% compared to adjunctive placebo 4%.
No appreciable affinity was exhibited for other receptor/binding sites tested discount 0.1mg clonidine amex, including the cholinergic muscarinic receptor (IC50 >1 ~lM) purchase 0.1mg clonidine. The mechanism of action of ziprasidone generic clonidine 0.1mg fast delivery, as with other drugs having efficacy in schizophrenia, is unknown. As with other drugs having efficacy in bipolar disorder, the mechanism of action of ziprasidone in bipolar disorder is unknown. Antagonism at receptors other than dopamine and 5HT 2 with similar receptor affinities may explain some of the other therapeutic and side effects of ziprasidone. The multiple-dose pharmacokinetics of ziprasidone are dose-proportional within the proposed clinical dose range, and ziprasidone accumulation is predictable with multiple dosing. Elimination of ziprasidone is mainly via hepatic metabolism with a mean terminal half-life of about 7 hours within the proposed clinical dose range. Steady-state concentrations are achieved within one to three days of dosing. Ziprasidone is unlikely to interfere with the metabolism of drugs metabolized by cytochrome P450 enzymes. Absorption: Ziprasidone is well absorbed after oral administration, reaching peak plasma concentrations in 6 to 8 hours. The absolute bioavailability of a 20 mg dose under fed conditions is approximately 60%. The absorption of ziprasidone is increased up to two-fold in the presence of food. Distribution: Ziprasidone has a mean apparent volume of distribution of 1. It is greater than 99% bound to plasma proteins, binding primarily to albumin and ~a1-acid glycoprotein. The in vitro plasma protein binding of ziprasidone was not altered by warfarin or propranolol, two highly proteinbound drugs, nor did ziprasidone alter the binding of these drugs in human plasma. Thus, the potential for drug interactions with ziprasidone due to displacement is minimal. Metabolism and Elimination: Ziprasidone is extensively metabolized after oral administration with only a small amount excreted in the urine (<1%) or feces (<4%) as unchanged drug. Ziprasidone is primarily cleared via three metabolic routes to yield four major circulating metabolites, benzisothiazole (BITP) sulphoxide, BITP-sulphone, ziprasidone sulphoxide, and S-methyl-dihydroziprasidone. Approximately 20% of the dose is excreted in the urine, with approximately 66% being eliminated in the feces. Unchanged ziprasidone represents about 44% of total drug-related material in serum. In vitro studies using human liver subcellular fractions indicate that S-methyl-dihydroziprasidone is generated in two steps. The data indicate that the reduction reaction is mediated by aldehyde oxidase and the subsequent methylation is mediated by thiol methyltransferase. In vitro studies using human liver microsomes and recombinant enzymes indicate that CYP3A4 is the major CYP contributing to the oxidative metabolism of ziprasidone. Based on in vivo abundance of excretory metabolites, less than one-third of ziprasidone metabolic clearance is mediated by cytochrome P450 catalyzed oxidation and approximately two-thirds via reduction by aldehyde oxidase. There are no known clinically relevant inhibitors or inducers of aldehyde oxidase. Intramuscular Pharmacokinetics Systemic Bioavailability: The bioavailability of ziprasidone administered intramuscularly is 100%. After intramuscular administration of single doses, peak serum concentrations typically occur at approximately 60 minutes post-dose or earlier and the mean half-life (T m) ranges from two to five hours. Exposure increases in a dose-related manner and following three days of intramuscular dosing, little accumulation is observed.
In order to provide a meaningful estimate of the proportion of individuals experiencing adverse events cheap clonidine 0.1mg on line, events were grouped in standardized categories using MedDRA terminology 0.1 mg clonidine amex. The stated frequencies of adverse reactions represent the proportion of individuals who experienced at least once safe 0.1 mg clonidine, a treatment-emergent adverse event of the type listed. Treatment-emergent adverse events were defined as adverse experiences, which started or worsened on or after the date of the first dose through seven days after study medication discontinuation. There was no attempt to use investigator causality assessments; i. It is important to emphasize that, although the reactions occurred during treatment with Latuda, they were not necessarily caused by it. The label should be read in its entirety to gain an understanding of the safety profile of Latuda. 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 studies. Similarly, the cited frequencies cannot be compared with figures obtained from other clinical investigations involving different treatment, uses and investigators. The cited figures, however, do provide the prescriber with some basis for estimating the relative contribution of drug and nondrug factors to the adverse reaction incidence in the population studied. The following findings are based on the short-term placebo-controlled premarketing studies for schizophrenia in which Latuda was administered at daily doses ranging from 20 to 120 mg (n = 1004). Commonly Observed Adverse Reactions: The most common adverse reactions (incidence ?-U 5% and at least twice the rate of placebo) in patients treated with Latuda were somnolence, akathisia, nausea, parkinsonism and agitation. Adverse Reactions Associated with Discontinuation of Treatment: A total of 9. There were no adverse reactions associated with discontinuation in subjects treated with Latuda that were at least 2% and at least twice the placebo rate. Adverse Reactions Occurring at an Incidence of 2% or More in Latuda-Treated Patients: Adverse reactions associated with the use of Latuda (incidence of 2% or greater, rounded to the nearest percent and Latuda incidence greater than placebo) that occurred during acute therapy (up to 6-weeks in patients with schizophrenia) are shown in Table 6. Table 6: Adverse Reaction in 2% or More of Latuda-Treated Patients and That Occurred at Greater Incidence than in the Placebo-Treated Patients in Short-term Schizophrenia StudiesNote: Figures rounded to the nearest integerBody System or Organ ClassDictionary-derived TermBased on the pooled data from the placebo-controlled, short-term, fixed-dose studies, among the adverse reactions that occurred with a greater than 5% incidence in the patients treated with Latuda, the apparent dose-related adverse reactions were akathisia and somnolence (Table 7). Table 7: Dose-Related Adverse EventsPercentage of Subjects Reporting Reaction* Somnolence includes adverse event terms: hypersomnia, hypersomnolence, sedation, and somnolenceIn the short-term, placebo-controlled schizophrenia studies, for Latuda-treated patients, the incidence of reported EPS-related events, excluding akathisia and restlessness, was 14. Akathisia appeared to be dose-related and the greatest frequency of parkinsonism and dystonia occurred with the highest dose of Latuda, 120 mg/day (Table 8). All EPS events, excluding Akathisia/RestlessnessIn the short-term, placebo-controlled schizophrenia studies, data was objectively collected on the Simpson Angus Rating Scale for extrapyramidal symptoms (EPS), the Barnes Akathisia Scale (for akathisia) and the Abnormal Involuntary Movement Scale (for dyskinesias). The mean change from baseline for Latuda-treated patients was comparable to placebo-treated patients, with the exception of the Barnes Akathisia Scale global score (Latuda, 0. The percentage of patients who shifted from normal to abnormal was greater in Latuda-treated patients versus placebo for the BAS (Latuda, 16. In the short-term, placebo-controlled clinical trials, dystonia occurred in 4. Laboratory Test Abnormalities and ECG Changes in Clinical StudiesLaboratory Test AbnormalitiesIn a between-group comparison of the pooled data from short-term, placebo-controlled studies, there were no clinically important changes in total cholesterol measurements; triglycerides or glucose from Baseline to Endpoint [see Warnings and Precautions (5. There were also no clinically important differences between Latuda and placebo in mean change from baseline to endpoint in routine hematology, urinalysis, or serum chemistry. Latuda was associated with a dose-related increase in prolactin concentration [see Warnings and Precautions (5. A creatinine shift from normal to high occurred in 3. The threshold for high creatinine value varied from ?-U 1.
Most women lie about acquaintance rape because they have regrets after consensual sex clonidine 0.1mg without prescription. Acquaintance rape really happens - to people you know 0.1mg clonidine with amex, by people you know trusted clonidine 0.1mg. Drinking or dressing in a sexually appealing way are not invitations for sex. Women who subscribe to "traditional" views of men occupying a position of dominance and authority relative to women (who are seen as passive and submissive) may be at increased risk. In a study where the justifiability of rape was rated based on fictional dating scenarios, women with traditional attitudes tended to view the rape as acceptable if the women had initiated the date (Muehlenhard, in Pirog-Good and Stets, 1989). Drinking alcohol or taking drugs appears to be associated with acquaintance rape. Koss (1988) found that at least 55 percent of the victims in her study had been drinking or taking drugs just before the attack. Women who are raped within dating relationships or by an acquaintance are seen as "safe" victims because they are unlikely to report the incident to authorities or even view it as rape. Not only did a mere five percent of the women who had been raped in the Koss study report the incident, but 42 percent of them had sex again with their assailants. The company one keeps may be a factor in predisposing women to an increased risk of sexual assault. An investigation of dating aggression and the features of college peer groups (Gwartney-Gibbs & Stockard, in Pirog-Good and Stets, 1989) supports this idea. The results indicate that those women who characterized the men in their mixed-sex social group as occasionally displaying forceful behavior towards women were significantly more likely themselves to be victims of sexual aggression. Being in familiar surroundings does not provide security. Just as with the victim, it is not possible to clearly identify individual men who will be participants in acquaintance rape. As a body of research begins to accumulate, however, there are certain characteristics which increase the risk factors. Acquaintance rape is not typically committed by psychopaths who are deviant from mainstream society. It is often expressed that direct and indirect messages given to boys and young men by our culture about what it means to male (dominant, aggressive, uncompromising) contribute to creating a mindset which is accepting of sexually aggressive behavior. Such messages are constantly sent via television and film when sex is portrayed as a commodity whose attainment is the ultimate male challenge. Buying into stereotypical attitudes regarding sex roles tends to be associated with justification of intercourse under any circumstances. Other characteristics of the individual seem to facilitate sexual aggression. Research designed to determine traits of sexually aggressive males (Malamuth, in Pirog-Good and Stets, 1989) indicated that high scores on scales measuring dominance as a sexual motive, hostile attitudes towards women, condoning the use of force in sexual relationships, and the amount of prior sexual experience were all significantly related to self-reports of sexually aggressive behavior. Furthermore, the interaction of several of these variables increased the chance that an individual had reported sexually aggressive behavior. The inability to appraise social interactions, as well as prior parental neglect or sexual or physical abuse early in life may also be linked with acquaintance rape (Hall & Hirschman, in Wiehe and Richards, 1995). Finally, taking drugs or alcohol is commonly associated with sexual aggression. Of the men who were identified as having committed acquaintance rape, 75 percent had taken drugs or alcohol just prior to the rape (Koss, 1988). The consequences of acquaintance rape are often far-reaching. Once the actual rape has occurred and has been identified as rape by the survivor, she is faced with the decision of whether to disclose to anyone what has happened. In a study of acquaintance rape survivors (Wiehe & Richards, 1995), 97 percent informed at least one close confidant. The percentage of women who informed the police was drastically lower, at 28 percent.
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