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| ملتقى أصحاب الإكتئاب أكره مرض الإكتئاب بنفس القدر الذي أحب به مريض الإكتئاب .. فهو أرق الناس وأصفاهم وأصدقهم .. و من لا يدمع قلبه حين يعايش مريض الإكتئاب ، فإن قلبه من حجر ، أو أشد قسوة " |
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أدوات الموضوع |
24-08-2016, 05:57 AM
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#1 | ||||
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عضـو مُـبـدع
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دواء الاكتئاب الجديد برينتلكس Brintllex
https://goo.gl/images/aGmz7K صورة
http://www.altibbi.com/%D9%85%D9%82%...%A7%D8%A8-2740 المصدر: نفساني
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16-11-2016, 01:27 PM
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#4 | |
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عضو نشط
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الاعراض الجانبية للداوء
جفاف الفم , ترجيع , غازات , دوخة , اسهال ,ضعف جنسي , امساك , غثيان الاسم العلمي للدواء : Vortioxetine تحياتي طلو |
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16-11-2016, 01:42 PM
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#6 | |
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عضو نشط
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الحركة الدوائية للدواء :
After oral administration, vortioxetine is absorbed in the gastrointestinal tract and exhibits peak plasma concentrations in about seven to 11 hours (Tmax). Its bio-availability is 75%. Consumption of food does not affect the bioavailability, and taking vortioxetine with food has not been shown to increase its peak concentration (Cmax). The steady-state concentration is achieved in about two weeks. Vortioxetine has a linear and dose-proportional pharmacokinetic profile with single daily dosing of 2.5 mg to 60 mg.10 Vortioxetine is extensively metabolized primarily through oxidation via CYP2D6, CYP3A4/5, CYP2C19, CYP2C9, CYP2A6, CYP2C8, and CYP2B6 and subsequent glucuronic acid conjugation. CYP2D6, the primary enzyme, converts vortioxetine into its primary inactive metabolite, the carboxylic acid metabolite.10 Since vortioxetine primarily goes through CYP2D6, the probability of interactions with CYP2D6 inhibitors and inducers affecting its concentration is high. The half-life of vortioxetine is approxima  y 66 hours.10 Vortioxetine is primarily eliminated in urine (59%) and feces (26%), with a negligible amount of unchanged vortioxetine in the urine.10 Key measures of absorption and metabolism are summarized inالميكانيكا الدوائية : Vortioxetine’s mechanism of action is not fully understood. Vortioxetine binds with high affinity to the serotonin transporter (Ki = 1.6 nM) and its antidepressant actions are believed to be secondary to enhancing serotonin in the central nervous system through inhibition of reuptake. Vortioxetine also displays binding affinities to other serotonin (5-HT) receptors, including 5-HT3, 5-HT1A, and 5-HT7, with Ki values of 3.7 nM, 15 nM, and 19 nM, respectively. There is moderate affinity toward serotonin receptors 5-HT1D and 5-HT1  with Ki values of 54 nM and 33 nM, respectively. Vortioxetine’s binding affinity is dose-proportional: Raising the dose will cause more binding to the receptors of interest at an increase of 15% for every 5 mg up to the maximum dosage. Based on the receptor binding affinities, vortioxetine displays reuptake blockade of the serotonin transporter, agonist activity at the 5-HT1A receptor, partial agonist activity at the 5-HT1B receptor, and antagonism at the 5-HT1D, 5-HT7, and 5-HT3 receptors. It has not been determined whether the antidepressant effects of vortioxetine are related to its binding at various 5-HT receptors.5,10,12Based on receptor affinity studies, vortioxetine primarily binds to the serotonin transporter (SERT). Although valid pharmacological studies have yet to prove additional clinical benefits for additional serotonin modulation by vortioxetine, various postulated benefits may exist for wide-spectrum binding at serotonin receptors in addition to serotonin transporter blockade. Vortioxetine acts as an agonist at the 5-HT1A receptor and a partial agonist at the 5-HT1B receptor, both of which function as autoreceptors for serotonergic neurotransmission. Agonist and partial agonist activity at these two receptors can lead to further serotonin release and could theoretically cause additional antidepressant activity. Antagonistic activity at the 5-HT7 receptor is hypothesized to potentiate the effects of SERT inhibition by additional release of serotonin through downstream mechanisms. Activity at the 5-HT3 receptor is more closely associated with regulation of nausea and emesis; however, many interneurons in the brain are regulated by 5-HT3 receptors and when blocked can lead to increases in serotonin, dopamine, norepinephrine, acetylcholine, and histamine.5,13 In animal studies, vortioxetine led to increases in extracellular levels of all five neurotransmitters in major regions of the brain associated with depression, including the prefrontal cortex and hippocampus.5 Additional in vivo testing is necessary to determine whether this multimodal action produces an additional clinical benefit. |
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16-11-2016, 01:53 PM
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عضو موقوف
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اقتباس:
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16-11-2016, 02:14 PM
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#10 | ||
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عضو نشط
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اقتباس:
الدواء من الانواع الجديدة من الادوية التي تؤثر على الميلاتونين في المخ الدواء يحفز مستقبلات الميلاتونين 1 و 2 ويثبط مستقبلات 5 اتش تي 2 سي فالتالي يزيد من الدوبامين والنورادرينالين في الفص الامامية في المخ عمر النصف للدواء جدا قصير من 1 الى 2 ساعة قرات انه يزيد BDNF الاعراض الجانبية الم في البطن كثرة التعرق ترجيع اسهال دوخة امساك الم في الظهر يرفع انزيمات الكبد الدواء ممتاز جدا مقارنة مع الادوية الاخرى المضادة للاكتئاب خصوصا في الاعراض الجانبية ( قليل الاعراض الجانبية مقارنة بالادوية الاخرى ) الدواء ليس افضل ولا اسوء من الادية الاخرى لعلاج الاكتئاب تحياتي طلو |
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16-11-2016, 02:15 PM
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عضو نشط
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مقارنة بين فالدوكسان والادية والاخرى المضادة للاكتئاب
https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0061425/ |
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16-11-2016, 02:36 PM
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عضو موقوف
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اقتباس:
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18-11-2016, 01:16 PM
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عضـو مُـبـدع
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اقتباس:
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| الذين يشاهدون محتوى الموضوع الآن : 1 ( الأعضاء 0 والزوار 1) | |
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