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Antipsikotikler (Nöroleptikler)

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1 Antipsikotikler (Nöroleptikler)
A characteristic feature of schizophrenia is a defect in 'selective attention'. Whereas a normal individual quickly accommodates to stimuli of a familiar or inconsequential nature, and responds only to stimuli that are unexpected or significant, the ability of schizophrenic patients to discriminate between significant and insignificant stimuli seems to be impaired. Thus, the ticking of a clock may command as much attention as the words of a companion; a chance thought, which a normal person would dismiss as inconsequential, may become an irresistible imperative. 'Latent inhibition' is a form of behavioural testing in animals, which can be used as a model for this type of sensory habituation. If a rat is exposed to a 'conditioned' stimulus (such as a bell), followed by an 'unconditioned' stimulus (e.g. a foot shock) that it can avoid (e.g. by pressing a bar), it will quickly learn to press the bar as soon as it hears the bell-the conditioned response. But if it has previously heard the bell several times without any ensuing foot shock, it will learn the conditioned response less quickly, having learned to disregard the bell. Latent inhibition is a measure of the inhibitory effect of pre-exposure to the conditioned stimulus on acquisition of the conditioned response. It is often impaired in schizophrenic subjects and in animals treated with amphetamine or psychotomimetic drugs such as lysergic acid diethylamide (LSD), and is restored by many antipsychotic drugs. Prof. Dr. Ç. Hakan KARADAĞ

2 Şizofreninin Semptomları
Pozitif Semptomlar Delüzyonlar Halüsinasyonlar Düşüncenin bozulması Negatif Semptomlar Küntleşmiş duygulanım Konuşma fakirliği Asosyalite Zevk alamama Schizophrenia (see Lewis & Lieberman, 2000) affects about 1% of the population. It is one of the most important forms of psychiatric illness, because it affects young people, is often chronic and is usually highly disabling. There is a strong hereditary factor in its aetiology, and evidence suggestive of a fundamental biological disorder (see below). The main clinical features of the disease are as follow. Positive symptoms: delusions (often paranoid in nature) hallucinations, usually in the form of voices which are often exhortatory in their message thought disorder, comprising wild trains of thought, garbled sentences and irrational conclusions, sometimes associated with the feeling that thoughts are inserted or withdrawn by an outside agency abnormal behaviours, such as stereotyped movements and occasionally aggressive behaviours. Negative symptoms: withdrawal from social contacts flattening of emotional responses. In addition, deficits in cognitive function (e.g. attention, memory) are often present,2 together with anxiety and depression, leading to suicide in about 10% of cases. The clinical phenotype varies greatly, particularly with respect to the balance between negative and positive symptoms, and this may have a bearing on the efficacy of antipsychotic drugs in individual cases. Schizophrenia can present dramatically, usually in young people, with predominantly positive features such as hallucinations, delusions and uncontrollable behaviour, or more insidiously in older patients with negative features such as flat mood and social withdrawal. The latter may be more debilitated than those with a florid presentation, and the prognosis is generally worse.

3 Dopaminerjik Yolaklar

4 Dopaminerjik Yolaklar

5 Dopaminerjik Reseptörler
İkinci Ulak Selektif Agonist Selektif Antagonist D1 Gs (sAMP↑) Fenoldopam n. caudatus, putamen, n. accumbens, olfaktor tüberkül reseptör sinerjizması (D2 agonistlerin etkilerini güçlendirir) D2 Gi (sAMP ↓) Gq/11 (IP3/DAG ↑) Bromokriptin striatum, hipofiz, motor (ekstrapiramidal), endokrin, emosyonel-kognitif etkiler D3 Gi (sAMP ↓) ? n. accumbens, olfaktor tüberkül, hipotalamus emosyonel-kognitif etkiler D4 AA salıv. ↑ FL metilasyon ↑ Klozapin D4>D3=D2 ve 5-HT2A ve 5-HT2C ant. limbik yapılar (striatumda çok seyrek) emosyonel-kognitif etkiler D5 hipotalamus, hipokampüs Fonksiyonel önemi bilinmemektedir. Dopaminerjik Reseptörler AA: araşidonik asit; FL: fosfolipaz

6 Serotonerjik Reseptörler
İkinci Ulak Selektif Agonist Selektif Antagonist 5-HT1 5-HT1A Gi/o (sAMP↓) Buspiron (pars. ag.) Dorsal rafe nöronlarının somasında (anksiyete) 5-HT1B 5-HT1D Sumatriptan Zolmitriptan 5-HT1e Fonksiyonel önemi bilinmemektedir 5-HT1f Fonksiyonel önemi bilinmemektedir. Serotonerjik Reseptörler 5-HT1C daha sonra yapılan sınıflamada 5-HT2C olarak sınıflandırılmıştır.

7 Serotonerjik Reseptörler
İkinci Ulak Selektif Agonist Selektif Antagonist 5-HT2 5-HT2A Gq/11 (IP3/DAG ↑) Ketanserin Öğrenme ve bellek ↑ 5-HT2B 5-HT2C m-klorofenilpiperazin (m-CPP) m-CPP anksiyeteyi, obsesyonu, psikozu, kognitif bozukluğu ↑ 5-HT3 İyonotropik Ondansetron Granisetron Tropisetron 5-HT4 Gs (sAMP↑) n. accumbens, olfaktor tüberkül, GİS, kalp 5-HT5 ? 5-HT6 5-HT7 Serotonerjik Reseptörler

8 Nöroleptiklerin Etkilerinde Reseptörlerin Rolü
Antipsikotik etki D2 ve D4 5-HT2 Ekstrapiramidal yan etkiler D2 Endokrin yan etkiler Rang & Dale 6th Ed Dopamine theory None The dopamine theory was proposed by Carlson-awarded a Nobel Prize in 2000-on the basis of indirect pharmacological evidence in humans and experimental animals. Amphetamine releases dopamine in the brain and can produce in humans a behavioural syndrome indistinguishable from an acute schizophrenic episode-very familiar to doctors who treat drug users. In animals, dopamine release causes a specific pattern of stereotyped behaviour that resembles the repetitive behaviours sometimes seen in schizophrenic patients. Potent D2-receptor agonists (e.g. apomorphine and bromocriptine; Ch. 34) produce similar effects in animals, and these drugs, like amphetamine, exacerbate the symptoms of schizophrenic patients. Furthermore, dopamine antagonists and drugs that block neuronal dopamine storage (e.g. reserpine) are effective in controlling the positive symptoms of schizophrenia, and in preventing amphetamine-induced behavioural changes. There is a strong correlation between clinical antipsychotic potency and activity in blocking D2-receptors (fig. 38.1), and receptor-imaging studies have shown that clinical efficacy of antipsychotic drugs is consistently achieved when D2-receptor occupancy reaches about 80%.3 There is no consistent biochemical evidence for excessive dopamine synthesis or release in schizophrenia. Furthermore, the production of prolactin, which might be expected to be abnormally low if dopaminergic transmission was facilitated, is normal in schizophrenic patients. One difficulty in interpreting such studies is that nearly all schizophrenic patients are treated with drugs that are known to affect dopamine metabolism, whereas the non-schizophrenic control group are not. Even where it has been possible to allow for this factor, however, most findings have proved negative. The best evidence for increased dopamine release in schizophrenic patients comes from imaging studies (Laruelle et al., 1999). A radioligand imaging technique was used to measure binding of a specific antagonist (raclopride) to D2-receptors in the striatum. Injection of amphetamine caused dopamine release and thus displacement of raclopride, measured as a reduction of the signal intensity. This reduction was greater by a factor of 2 or more in schizophrenic subjects compared with in control subjects, implying a greater amphetamine-induced release of dopamine. The effect was greatest in schizophrenic individuals during acute attacks, and absent during spontaneous remissions-clear evidence linking dopamine release to the symptomatology. An increase in dopamine receptor density in schizophrenia has been reported in some studies, but not consistently, and the interpretation is complicated by the fact that antipsychotic drug treatment is known to increase dopamine receptor expression. The D4-receptor has also attracted attention on account of the high degree of genetic polymorphism that it shows in human subjects, and because some of the newer antipsychotic drugs (e.g. clozapine; see below) turn out to have a high affinity for this receptor subtype. Genetic studies have, however, failed to show any relationship between schizophrenia and D4-receptor polymorphism. Moreover, a specific D4-receptor antagonist proved ineffective in clinical trials. Another variant of the dopamine hypothesis (see Abi-Dargham & Laruelle, 2005) suggests that schizophrenia reflects an imbalance between excessive activation of D2-receptors in subcortical regions (causing positive symptoms) and deficient activation of cortical D1-receptors (causing negative symptoms). It is fair to say that, although dopamine is undoubtedly involved, the details remain far from clear. Glutamate theory Another transmitter implicated in the pathophysiology of schizophrenia is-you will not be surprised to learn-glutamate (see Goff & Coyle, 2001; Moghaddam, 2003). NMDA receptor antagonists such as phencyclidine, ketamine and dizocilpine (Ch. 33) produce psychotic symptoms (e.g. hallucinations, thought disorder) in humans, and reduced glutamate concentrations and glutamate receptor densities have been reported in post-mortem schizophrenic brains-one of the few fairly consistent findings. Although schizophrenia is difficult to diagnose in a mouse, transgenic mice in which NMDA receptor expression is reduced (not abolished, because this is fatal) show stereotypic behaviours and reduced social interaction that are suggestive of schizophrenia and that respond to antipsychotic drugs-evidence that supports the glutamate hypothesis. According to this view, glutamate and dopamine exert excitatory and inhibitory effects, respectively, on GABAergic striatal neurons, which project to the thalamus and constitute a sensory 'gate' (see below). Too little glutamate, or too much dopamine, disables the gate, allowing uninhibited sensory input to reach the cortex. It is also suggested that abnormal glutamate function-specifically reduced NMDA-receptor activation-could account for the cognitive deficit that is increasingly recognised as a central feature of schizophrenia, responsible in part for the negative symptoms of the disorder. One possibility is therefore that excess dopamine receptor activation is mainly responsible for positive symptoms, deficient NMDA-receptor activation for the negative symptoms. Although undoubtedly too simple, this idea is driving current efforts to develop novel antipsychotic drugs that increase NMDA-receptor activation. Other theories Other transmitters that may be important include 5-HT and noradrenaline (norepinephrine). The idea that 5-HT dysfunction could be involved in schizophrenia was based on the fact that LSD (see Ch. 42) produces schizophrenia-like symptoms, and has drifted in and out of favour many times (see Busatto & Kerwin, 1997). Many effective antipsychotic drugs, in addition to blocking dopamine receptors (see below), also act as 5-HT-receptor antagonists. 5-HT modulates dopamine pathways, so the two theories are not incompatible. Many 'atypical' antipsychotic drugs (see below) produce fewer extrapyramidal side effects than dopamine-selective compounds, and combine with 5-HT2A-receptors. Whether 5-HT2A-receptor blockade accounts directly for their antipsychotic effects, or merely reduces undesirable side effects associated with D2-receptor antagonists, remains controversial. In conclusion, the dopamine hyperactivity theory of schizophrenia remains attractive. It is undoubtedly an oversimplification, and relates only to the positive symptoms, but it provides the best framework for understanding the action of antipsychotic drugs, although effects on 5-HT and other receptors may contribute significantly to the clinical profile of some of the newer drugs. The glutamate hypothesis is, however, gaining ground, and there are reasonable hopes that it will lead to the next generation of antipsychotic drugs (see Javitt, 2004).

9 Nöroleptikler D. Diğer Nöroleptikler 1. Tipik nöroleptikler Pimozid
Penfluridol Molindon Oksipertin 2. Atipik nöroleptikler Klozapin D2 etkinliği Olanzapin azaltılmış, Risperidon 5-HT2 etkinliği Sertindol artırılmış Amisülprid olanlar Aripiprazol (ketiapin, seroquel, zotepin) 3. Arada kalan nöroleptikler Sülpirid D2 reseptörlere Remoksiprid ileri derecede Rakloprid selektif olanlar A. Fenotiazinler 1. Alifatik fenotiazinler Klorpromazin (asepromazin, levopromazin, promazin, metotrimeprazin trifluopromazin) 2. Piperidinli fenotiazinler Tioridazin (mezoridazin, perisiyazin, pipotiyazin) 3. Piperazinli fenotiazinler Flufenazin (trifluoperazin, perfenazin, proklorperazin, asetofenazin, karfenazin) B. Yapıca Fenotiazinlere Benzeyenler Klorprotiksen, Tiotiksen Zuklopentiksol, Flupentiksol Loksapin C. Butirofenonlar Haloperidol (melperon, droperidol, benperidol)

10 Klorpromazin NÖROLEPTİK SENDROM (25-50 mg, p.o. veya i.m.)
Hipnoz veya aşırı bir sedasyon hali oluşturmaksızın Spontan hareketlerde yavaşlama Çevreye karşı ilgisizlik Çevreden gelen uyarılara yanıt vermeye isteksizlik Yavaşlama, heyecansızlık İnisiyatif ve merakta azalma Motor fonksiyonlar normal Kognitif yetenekler normal (zihinden hesap yapma, çağrışım vb)

11 Klorpromazin Sedatif Etki Katalepsi (Katatoni) (yüksek dozda)
Prokonvülsan Etki CTZ İnhibisyonu Hipotermi Endokrin Etkiler prolaktin salgısında artış FSH ve LH salgısında inhibisyon Ekstrapiramidal Etkiler Otonom ve Diğer Etkiler a1-blokaj antikolinerjik etki lokal anestezik etki antihistaminik etki 5-HT2 blokajı Vazomotor ve Solunum Merkezi Üzerine Depresan (Zayıf) Etki

12 Nöroleptiklerin Çeşitli Reseptörler Üzerindeki Etkinlikleri
a1 5-HT2 H1 M Klorpromazin + ++ +++ Tioridazin Perfenazin - Haloperidol Klozapin* Sülpirid Pimozid +++ Yüksek afinite; ++ Orta derecede afinite; + Az afinite; ± Çok az afinite; - Etkisiz veya minimal etkili *D4>D3=D2

13 Nöroleptiklerin Yan Etkileri
Doz (mg/gün) Sed. Etki EP Etki Hipo TA Diğer Alifatik fenotiyazinler Klorpromazin +++ ++ Fotosensitizasyon (en fazla) Asepromazin 6-9 Çocuklardaki bulantı-kusma ve ajitasyonda kullanılır Promazin Piperidinli fenotiyazinler Tioridazin + Kardiyotoksisite (en fazla), pigmenter retinopati Mezoridazin 75-300 Kardiyotoksisite Piperazinli fenotiyazinler Flufenazin 2-20 ++++ Perfenazin 8-32 Proklorperazin 75-100 Trifluoperazin 5-20

14 Nöroleptiklerin Yan Etkileri (devam)
Doz (mg/gün) Sed. Etki EP Etki Hipo TA Diğer Yapıca fenotiyazinlere benzeyenler Klorprotiksen 50-400 +++ ++ Tiotiksen 5-30 +/++ Flupentiksol 6-18 Zuklopentiksol 20-30 Loksapin 60-100 + Butirofenonlar Haloperidol 2-20 ++++ Melperon Droperidol Benperidol Diğer Nöroleptikler (TİPİK) Pimozid 2-6 Hepatit yapabilir Molindon 50-225 Oksipertin 80-120 Fotosensitizasyon

15 Nöroleptiklerin Yan Etkileri (devam)
Doz (mg/gün) Sed. Etki EP Etki Hipo TA Diğer Diğer Nöroleptikler (ATİPİK) Klozapin ++ +++ Agranülositoz Plazma prolaktin düzeyinde belirgin artma yapmaz Olanzapin 5-20 + Risperidon 2-8 Sertindol 12-20 QT uzaması, ventriküler aritmi Ketiapin Amisulprid Aripiprazol 15-30 - Ziprasidon Paliperidon There has been a proliferation of atypical antipsychotic drugs since the introduction of clozapine in the late 1980s. The defining characteristic of atypical antipsychotic medications is their low risk of EPS and the related reduced risk of tardive dyskinesia. Although the risk for EPS and tardive dyskinesia appears to be absent only with clozapine, the other atypical drugs present a favorable EPS profile and a 0.5 to 1 percent per year cumulative occurrence of tardive dyskinesia, a marked improvement over conventional agents [7,8] . With the exception of clozapine, there is limited evidence of superior efficacy for any one of these drugs. Many head-to-head comparison trials have been sponsored by pharmaceutical companies; one study found that 90.9 percent of published pharmaceutical-sponsored studies reported results favorable for the sponsor's drug, with contradictory results from different studies comparing the same drugs [9] . There is anecdotal evidence, however, of a differential response for individual patients to particular drugs. The only basis for prediction of patient response is prior response to the same agent. Factors including diagnosis, symptom profile, or specific genetic markers have not proven useful in drug selection. These agents have comparable overall tolerability, but specific side effects seen with each of the drugs differ significantly. In Phase 1 of the CATIE study, a large (n = 1493), randomized, double-blind comparison of antipsychotics for maintenance treatment of schizophrenia, patients were significantly less likely to discontinue treatment with olanzapine than with perphenazine, quetiapine, risperidone, or ziprasidone, but other measures of efficacy and severity of side effects were comparable among them [10] . Treatment choice, therefore, may reasonably be based on individual patient response, side effect profile, and cost.

16 Nöroleptiklerin Yan Etkileri (devam)
Doz (mg/gün) Sed. Etki EP Etki Hipo TA Diğer Diğer Nöroleptikler (ARADA KALANLAR) Sülpirid + - Antiotistik ve antidepresan. Belirgin antiemetik ve antivertigo etki. Kan basıncını yükseltir. Gebelerde ve böbrek yetmezliğinde kontrendikedir. Remoksiprid ? Aplastik anemi yapar. Tedavinin ilk 6 ayında haftada bir, daha sonra ayda bir kan sayımı yapılmalıdır.

17 Yan Etkiler Ekstrapiramidal Yan Etkiler Sedasyon Otonomik Yan Etkiler
Akut distonik reaksiyonlar Akatisia Parkinsonizm Tardif diskinezi Sedasyon Otonomik Yan Etkiler Ortostatik hipotansiyon (-blokaj) Atropin benzeri etkiler: Ağız-boğaz kuruluğu, midriyazis, bulanık görme, konstipasyon, ileus, taşikardi, idrar retansiyonu (anti muskarinik etkili olanlar) Yan Etkiler

18 Dil, yüz, boyun ve sırt kaslarında kasılmalar.
Reaksiyon Özellikleri Riskin Maksimum Olduğu Dönem Öne Sürülen Mek. Tedavi ve Önlemler Akut distonik reaksiyonlar Dil, yüz, boyun ve sırt kaslarında kasılmalar. Konvülsiyonu taklit edebilir, histeri değildir. 1.  5. gün Çocuklarda ve 25 yaş  gençlerde daha sıktır ? Antiparkinson ilaçlar1 Reversibldir, nöroleptik dozu azaltılınca belirtiler hafifler, kesilince ortadan kalkar Akatisia Aşırı hareketlilik, yerinde duramama 5.  60. gün Doz azaltılmalı veya başka ilaca geçilmeli Antiparkinson ilaçlar, benzodiazepinler veya propranolol2 kullanılabilir. Parkinsonizm Bradikinezi, rijidite, tremor, maske yüz 5.  30. gün DAerjik ant. Antiparkinson ilaçlar Tardif diskinezi Oral-fasiyal diskinezi; yaygın koreoatetoz veya distoni Tedavinin başlangıcından aylar veya yıllar sonra Aşırı DAerjik etkinlik İlaç dozunun azaltılması belirtileri şiddetlendirir. Başarılı bir tedavi yöntemi henüz yoktur; bu nedenle profilaksisi önemlidir. Malign nöroleptik sendrom Kaslarda rijidite ve akinezi, bilinç bulanıklığı, ateş, kreatin fosfokinaz  Öldürücü olabilir Haftalar (Nöroleptik kesildikten sonraki birkaç gün boyunca da risk yüksektir) Nöroleptik kesilir Mekanik soğutma Dantrolen3 veya bromokriptin4 (dopaminerjik agonist olarak) Antiparkinson ilaçların yararı yok 1 difenhidramin HCl 25 veya 50 mg i.m.; benztropin mezilat 1 veya 2 mg i.m. veya yavaş i.v. injeksiyonla başlanır, sürdürme tedavisi aynı ilacın oral formu ile birkaç hafta sürdürülür. 2 propranololün nisbeten düşük dozları (20-80 mg/gün) sıklıkla etkindir. Selektif 1 blokörler daha az etkindir. 3 dantrolene yanıt vermekle birlikte, iskelet kası Ca2+ transport sisteminde bir patoloji söz konmusu değildir. 4 bromokriptin mg/gün

19 Yan Etkiler Seksüel Disfonksiyon Nöroendokrin Yan Etkiler
Ejakulasyonun inhibisyonu ( blokaj) Bu etki tioridazinde en belirgindir. İmpotens. Ejakulasyonun inhibisyonuna ve hormonal bozukluklara bağlı olarak Nöroendokrin Yan Etkiler FSH, LH ; Prolaktin  Kadınlar: Amenore, galaktore Erkekler: Jinekomasti, ödem, kilo , libidoda  Yan Etkiler

20 Yan Etkiler Hepatotoksisite Hematolojik Yan Etkiler
Kolestatik sarılık. (Klorpromazin ve diğer alifatik nöroleptikler tarafından oluşturulur. Muhtemelen alerjiktir.) Genellikle ilk 4 hafta içinde ortaya çıkar. Hematolojik Yan Etkiler Lökopeni Nadiren agranülositoz ve aplastik anemi Klozapin nisbeten sık olarak agranülositoz yapar. Alerjik Reaksiyonlar Ürtiker Makülopapüler ve peteşiyal döküntüler Nadiren Stevens-Johnson sendromu Klorpromazin ve diğer alifatik yapılı fenotiazinler  dozda fotosensitizasyonciltte koyu pigmentasyon Yan Etkiler

21 Yan Etkiler Göz Toksik Psikoz Konvülsiyona Eğilim Kardiyotoksisite
Nadiren kornea ve lens opasiteleri, konjontival melanozis Tioridazin - pigmenter retinopati Toksik Psikoz Nöroleptik tedavisi sırasında nadiren oluşabilir. Muhtemelen ilacın antikolinerjik etkisine bağlıdır. Belirtileri atropin zehirlenme belirtilerine benzer. Hastalığın nüksettiği izlenimini verebilir. Konvülsiyona Eğilim Yeni atipik nöroleptiklerden risperidon ve remoksipridin konvülsan etkinliği yoktur veya çok azdır. Kardiyotoksisite Tioridazin  aritmi Malign Nöroleptik Sendrom Yan Etkiler

22 İlacı Kesme Antipsikotik ilaçların uzun süreli tedavinin ardından kesilmesi her zaman basamaklı olmalı ve akut yoksunluk sendromları ya da hızlı nüks riskini engellemek için yakından izlenmelidir.

23 Şizofreninin Negatif Semptomlarını Daha İyi Düzelten İlaçlar
Pimozid Penfluridol Klozapin Olanzapin Risperidon Sertindol Ketiapin Amisulprid

24 Spesiyaliteler Haloperidol NORODOL 2 mg /ml, 20 ml damla
5 mg, 50 tablet 10 mg, 30 tablet 20 mg, 20 tablet 5 mg/ml, 5 ampul 10 mg/ml, 5 ampul Pimozid NÖROFREN 2 mg, 30 tablet Klorpromazin LARGACTİL 100 mg, 30 tablet 25 mg/5 ml, 10 ampul Flupentiksol FLUANXOL 3 mg, 50 tablet 20 mg/ml, 1 depo ampul Asepromazin PLEGİCİL 1 mg/10 damla, 30 ml Melperon BURONON 25 mg, 50 draje 100 mg, 30 draje 50 mg, 5 ampul Trifluoperazin STİLİZAN 1 mg/ml, 5 ampul 1 mg, 2 mg ve 5 mg 30 draje Tioridazin MELLERETTES 10 mg, 30 draje 30 mg/ml, 30 ml damla MELLERİL 25 mg ve 100 mg, 30 draje Mezoridazin LİDANİL 5 mg, 20 draje

25 Spesiyaliteler Sülpirid DOGMATİL 200 mg, 24 tablet SÜLPİR
50 mg, 30 kapsül ZEPRİD 200 mg, 24 ve 48 tablet 25 mg/5 ml, 200 ml oral solüsyon Zuklopentiksol CLOPİXOL 20 mg/ml, 20 ml damla 2 mg, 10 ve 25 mg, 50 tablet 50 mg/ml, 1 ACUPHASE ampul İM 200 mg/ml, 1 DEPO ampul İM Risperidon RİSPERDAL 1 mg, 2 mg, 3 mg ve 4 mg, 20 tablet Klozapin CLONEX 25 mg ve 100 mg, 50 tablet LEPONEX Amisülprid SOLİAN 200 mg ve 400 mg 60 ve 90 tablet Apipiprazol ABİLİFY 10, 15 ve 30 mg 28 tablet Olanzapin REXAOİN 5 mg ve 10 mg, 28 tablet ZYPREXA 2,5; 5; 7,5 mg ve 10 mg, 28 tablet Ketiapin SEROQUEL 25 mg ve 100 mg, 30 tablet 200 mg, 30 ve 60 tablet

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