ࡱ>  #bjbj-- 4:OO< $.....   ,G!B     B..W .. :x,֮. m0.""$   BB   "          :    Antipsychotic Medications Key Antipsychotic Target Dopamine antipsychotics seek to eliminate excess dopamine activity Mechanism unknown, just know association does exist between high dopamine ( psychosis Synthesis Tyr ( (tyrosine hydroxylase TH) ( DOPA ( (aromatic acid decarb. AADC) ( Dopamine Metabolism MAO ( metabolizes dopamine to DOPAC and HVA Transporter dopamine transport affected by cocaine & amphetamines ( produce psychosis Dopamine Pathways General CNS Distribution less widespread than NE & Serotonin Limbic (center) brain has too much dopamine activity Frontal cortical brain has too little dopamine activity, insufficient feedback of glutamate Nigrostriatal Pathway involves movement, habit, learning, dopamine enters substantia nigra & flows to striatum Mesolimbic Pathway involves emotion & affect, motor and sensory processing, dopamine enters limbic area Mesocortical Pathway involves decision-making, cognition, dopamine enters prefrontal cortex Tuberoinfundibular Pathway involves prolactin inhibition, GH release, dopamine enters pituitary Chemoreceptor Trigger Zone dopamine receptors here trigger emesis (vomit) & nausea; multiple receptors and not well protected by BBB Psychosis Treatment Reserpine very antiquated, depletes all catecholamines Insulin Shock & ECT also former treatments Chloropromazine/Haloperidol new former Tx, quell all positive symptoms, patients look more normal Modern antipsychotics generally more active against positive symptoms, block D2 receptors; active against psychosis of any origin Dopamine increased DA worsens psychosis (amphetamines, cocaine) Neurodevelopmental model schizophrenic state shows decreased DAergic activity from VTA to prefrontal cortex (leads to negative symptoms), increased DAergic activity from VTA to limbic region (leads to positive symptoms) Duration will act relatively quickly after initial dosing, but takes months to reach maximum effect Potency - directly related to strength of binding to D2 receptors D2 Receptor dopamine has D1 & D2 receptors, its primarily D2 receptors which are blocked G-protein couple receptor Increased activity of beta-arrestin pathway this means there is some protein synthesis effect of the antipsychotics and therefore explains why it takes some time for max effect Modern Psychosis Treatment 1st Generation try as 2nd line, block dopamine receptors, but SEs: Sedation from blocked histamine receptors as well (chlorpromazine) Hypotension from block alpha receptors as well (chlorpromazine) Motor Effects nigrastriatal pathway blocked, less movement (fluphenazine, haloperidol) 2nd Generation try as 1st line drug, include atypical antipsychotics (prototype Risperidone) Sedation, Hypotension, Motor Effects much milder Aripiprazole newest drug, partial D2 agonist, appears no SEs, but need further testing Clozapine try as last resort, very good at removing positive and negative symptoms, but Agranulocytosis can result from clozapine/olanzapine Weight Gain/DM also a result from clozapine/olanzapine Other Effects Range antipsychotics affect a wide range of receptors, not just dopamine ( unwanted Basal Ganglia (Nigrastriatal) too much blockade = motor side effects; worse w/ haloperidol and 1st gen Limbic/Frontal Cortex where dopamine blockade is therapeutic Hypothalamus & Endocrine (tubuloinfundibular) blockade = more PRL, less GH, unable to regulate temperature (poikilothermic); 1st generation and risperidone Chemoreceptor Trigger blockade = no nausea or vomiting; 1st generation and risperidone Autonomic blockade = hypotension, sedate, antimuscarinic (constipate, dry mouth, blurry eye), QT prolongation; low > hi Metabolic effects blockade of multiple receptors ( DM/weight gain; clozapine/olanzipine worst Pharmacokinetics Absorption erratic and variable; lipophilic Clearance slow clearance from brain relative to plasma Metabolism CYTP450 Half-life drugs generally 6-40 hrs, take once a day Depot Forms for non-compliant patients, T1/2 = 7-10d, injection very slow, no dosing flexibility Oral osmotic paliperidone ER (metabolite of risperidone) can be given via pump Tolerance, addiction and DDIs Tolerance tolerance to sedative effects, no tolerance to prolactin secretion or antipsychotic effects Addiction not addicting (opposite of cocaine) Drug-Drug Interaction potentiates actions of CNS depressants (sedative, analgesic, hypnotic) L-DOPA, Dopaminergic agonists blocked by antipsychotics, since receptor downstream blocked CYT P450 extensive metabolism, affects other drugs metabolized here Extrapyramidal SEs Receptor occupancy need 60% of D2Rs occupied to get therapeutic effects; more than 80% produces EPS Extrapyramidal Side Effects movement effects outside pyramidal columns: Acute Dystonia spasm of facial muscles, twisting neck; can give antimuscarinics Akathisia restlessness; reduce dose or propanolol Parkinsonism bradykinesia & tremor resembling Parkinsons disease; due to DA anatagonism Neuroleptic Malignant Syndrome catatonia, stupor, fever, can be fatal; caused by DA antagonism; d/c drug Tardive Dyskinesia involuntary movements of tongue, face, trunk after long-term treatment and subsequent withdrawal; excess function of DA 2nd Generation Dose Response Curves therapeutic more separated from SEs Clozapine/Olanzapine very low dose response curve, no EPS, but horrible agranulocytosis, metabolic SEs Aripiprazole Partial Agonist binds to dopamine receptor, but doesnt evoke 100% response Inhibits mesolimbic lots dopamine here, but aripiprazole takes its place, less response good! Activates prefrontal to little dopamine here, but aripiprazole is better than nothing good! Few extrapyramidal SEs Oral absorption 3-5 hr peak plasma conc, long life Glutamate Glutamate also works hand-in-hand with dopamine, new target for antipsychotic research; major excitatory NT in CNS CNS Levels decreased limbic and mesencephalic glutamate associated w/ schizophrenia Increased glutamate good for treating schizophrenia NMDA Receptor key glutamate receptor involved in consolidation of learning and memory; also Asp agonized co-agonists glycine/D-serine potentiate response Mg2+ - V-gated blocker of channel; depolarization releases Mg and allows for Ca/Na flux PCP/Ketamine noncompetitive antagonists ( produce negative Sx of psychosis Bottom Line increase glutamate activity, decrease dopamine to treat psychosis; NMDA agonists improves psychosis in schizophrenia New treatments NMDA receptors co-agonists glycine, alanine, D-serine Dopamine D1 and nicotine receptor agonists cognitive benefits QUIZ: Drug Review Risperidone 2nd generation antipsychotic, most common Tx Chlorpromazine 1st generation antipsychotic, causes sedation/hypotension Haloperidol 1st generation antipsychotic, causes motor effects Clozapine last resort; great, but agranulocytosis Aripiprazole very new drug, partial agonist, seems great right now, but need more testing >{   % & 0 : A B i w  ) K a  , 8 f ддддЦИЊthM|hOCJaJhO56CJaJhM|hO56CJaJ jh78hOCJaJ jh5rhOCJaJ jhVKhOCJaJ jhchOCJaJhOCJaJhO5CJaJh"NCJaJh"N5CJaJjhsP5CJUaJ-6{0 i  K  D  E .pNSm & FgdOgdO & FgdO   ( C D ^   + D c o p -9opMV{h!@hO5CJaJh!hO5CJaJhDH5hO5CJaJhOCJH*aJhhO5CJaJhuzhO5CJaJhhOCJaJhM|hOCJaJhM|hO56CJaJhO5CJaJhOCJaJhO56CJaJ**@KRSlm :;<>JTVEQ_`acny{uh!@hOCJH*aJh!@hO5CJH*aJh!@hOCJaJhGhOCJaJhthhOCJH*aJhthhO5CJH*aJhGhO5CJaJhhOCJaJh2hOCJaJhO5CJaJhOCJaJhhO56CJaJ.m ;`K%{$4ml & FgdOgdO & FgdO!KT*E\^opq{#$=%3h5hO5CJaJ jh5hOCJaJhvhO5CJaJh5hOCJaJhvhOCJaJh5hOCJH*aJ jhhOCJaJhO6CJaJhO56CJaJhO5CJaJhOCJaJ034@lmz*kl$()9%&9:O<Fp|56KhGohOCJaJhBhOCJaJh>hOCJaJhuzhOCJaJhOCJH*aJhchO5CJaJhO56CJaJhOCJaJhO5CJaJh[hO5CJaJ:l$&:<p6 v4aY  & FgdO & FgdOgdO !v.34Hakn   Y d g x !!2!@!!!᧙ jhBhOCJaJhBhO5CJH*aJhBhO5CJaJhRhO5CJaJhdT=hO5CJaJh>hOCJaJh5$hOCJaJhOCJaJhO5CJaJh(7hO5CJH*aJ3Y 2!!!!<"N"""#I###gdO & FgdO & FgdO!!!!(";"<"N"Y"]"_"""""""""""##I#V####乮h&hOCJaJhGhOCJaJhOCJH*aJhGhOCJH*aJhO56CJaJhOCJaJhO5CJaJhBhOCJaJ21h:pO/ =!"#$% RZDd2%KKv  C RA:08Disclaimer-No_Citation_KeyRYҪG)dYDF\YҪG)JFIFHHICC_PROFILEappl mntrRGB XYZ  acspAPPLappl-appl rXYZ gXYZ4bXYZHwtpt\chadp,rTRCgTRCbTRCdesc@ocprt8vcgt0ndin8dscmLXYZ tK>XYZ Zs&XYZ (W3XYZ Rsf32 B&lcurvvcgtRRRndin8HW K'P T9textCopyright 2007 Apple Inc., all rights reserved.mluc enUS&~esES&daDK.deDE,fiFI(frFU(*itIT(VnlNL(nbNO&ptBR&svSE&jaJPRkoKR@zhTWlzhCNruRU"plPL,Yleinen RGB-profiiliGenerisk RGB-profilProfil Gnrique RVBN, RGB 000000u( RGB r_icϏPerfil RGB GenricoAllgemeines RGB-Profilfn RGB cϏeNGenerel RGB-beskrivelseAlgemeen RGB-profiel| RGB \ |Profilo RGB GenericoGeneric RGB Profile1I89 ?@>D8;L RGBUniwersalny profil RGBdescGeneric RGB ProfileGeneric RGB ProfiletExifMM*>F(iNHHC     C  " }!1AQa"q2#BR$3br %&'()*456789:CDEFGHIJSTUVWXYZcdefghijstuvwxyz w!1AQaq"2B #3Rbr $4%&'()*56789:CDEFGHIJSTUVWXYZcdefghijstuvwxyz ?~EO&2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QF2~EOh(?QEe6(QOȣi"e6(QOȣi"e6(QOȣi"e6( _#d~U{ggE/Q?*NE+Wiᰳ RUqSNVE/Q?*w E⾿8u&it ^eoaH 2I5W׾h ~$u{ֺق|5Ш˗_3d~TYv}-VT]Eqa- jfh8Fe8몺tK="[ 2)k}PkZNȌv'B.ҕ'}|z. ?>+h-l>*Xxxh >خ[>_z~)@NK$#%aE!UGaJn/ >_#7j_ hrxݼq\^i|NYIw7e J!x:O`խ2Bpq54R,%I)M;T]-ʏ/WrW~5kX -d@$w'99S֟x@k]w-n!מjqI a7? 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