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9. Antipsychotics.docx

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University of Otago
Kristin Hillman

Anti-psychotics Insanity in historical context:  What is madness?  Behaving in an absurd manner  Causes?  Thought to be caused by God etc.  Maybe dementia?  Drugs?  Trauma?  Sensory deprivation?  How was it dealt with?  Locked them up  Exorcism st • How is it dealt with in 21 century?  Institutionalization (lock people up…)  Dealt with nowadays more humane?  work with them behavourally etc. The brain and behaviour relationship • recall the definition of behaviour • if you want to change behaviour, yu must change the brain  Lobotamy  ECT  TMS  Behavioural therapy  Pharmacotherapy/drug therapy • These therapies do help insanity Insanity in current contexts • The term insanity is no longer used in most professional fields  in law, can be used in court (plead insane) • Specific diagnonses are preferred e.g.  Schizophrenia  bipolar disorder  delirium  dementia  All have their own characteristics, and diagnoses… What is psychosis • Dysregulation in information processing within the brain leading to altered mental states • Symptoms can span a range of mental functions:  3 different classes: o Positive symptoms  increase in function o Negative symptoms  decrease in function o Cognitive symptoms  either amped up or decreased…  Presents in conditions such as schizophrenia, mania, dementia, delirium, drug influence and schizoaffective disorder • Drugs can also produce psychotic behaviours…what drugs can produce psychosis  Psychedelics (e.g. hallucinogens, Ketamine)  DA agonists  Amphetamines Schizophrenia: • DSM-IV criteria:  • Typically surfaces in early adulthood • Increased suicide risk  Can be fatal, important to talk about and work through in therapy etc. • Variable course of outcome  Some people can do quite well in therapy, others may not.. • Causes:  Not really known, but dysregulation of thought suggests global, widespread  Don‟t memorize all of chart, idea is to look at all the different components – there is a lot!! Predisposing factors, thought to influence later state o There is this level of functional disruption – neurons aren‟t talking to each other like they should be o One idea - too much DA in brain??? • Dopamine theory of Schizo:  Presentations are due to too much DA in brain (DA hyperfunction)  Anti-psychotic drugs work by antagonizing DA receptors  Should know DA system by now!!! o Synthesis etc o DA tracts (x4)  tuberoinfundibular = hormonal tract…important for side effects for DAergic drugs • Dominant theory is still used and held to this day…  But there are other ideas that are emerging o Serotonin Hyperfunction?  Evidence for this?  1) LSD + psychedelic drugs are sometimes called “psychotomimetics” because they can mimic psychosis behaviour  Maybe these drugs mimic this because they work at the serotonin system? o i.e. 5HT agonist = LSD  2) 5-HT receptor  line of evidence that suggests maybe there is too much serotonin in the brain that gives patients these psychosis features o NMDA Hypofunction?  Evidence for this?  1) Ketamine and PCP = NMDA antagonists  Give these drugs to lab rats etc, they develop a lot of behaviours that look like schizophrenia  2) Create a mouse that has its NMDA receptors taken out, it causes a schizophrenic phenotype in the mouse…suggests NMDA tone • All ties in with functional deficit  can fix these with drugs, but in the chart is also says anatomical features  If anatomical problem, then none of these things are going to work  Have to look at other strategies, (like growth factors etc) Treating Psychosis • Historically patients confined, isolated • early treatments relied on psychosurgery (lobotomy) • 1950s introduced of pharmacotherapy radically changed institutionalized numbers  People were „let out‟ into the world again – de- hospitilisation  Problem? o These people are used to living in an institution – used to having this very structured life (when they go out into the real world they have to learn how to get a job, cook for themselves etc – very very difficult) o Hard to deal with going out into unstructured world o Highlights the point that you really have to have occupational, behavioural therapy in addition to letting them out into the world – important to give supportive networks to go with it so people can adjust back in • There are pharmacotherapeutic approaches:  Traditional/classic anti-psychotics  Atypcial anti-psychotics Traditional/classic anti-psychotics: • 1950s – Chlorpromazine  while it calmed normal people down, try it in psychotic patients to see if it did – it did! • 1960s – Haloperidol • Both drugs led to hug drops in institutionalistion • Use these drugs in combination with behavioural therapy!!  Not what happened historically…huge fail • Mode of action  Decrease in positive psychotic symptoms • Mechanism of action  Antagonist for D2 receptor  Also affects a lot of other receptors - not a highly selective drug • Side effects:  Parkinsoneon motor deficits o Late onset dyskinesia  When you block these D2 receptors, you get hormonal disruption o Prolactin release is disinhibited – for men, breast development, lactation when not feeding child (preg) o Decreased gonadotropic release – sexual side effects and infertility  Also have side effects that relate to inhibition of other receptors: o Dry mouth, blurred vision, mydriasis, hypotension, sedation, antiemetic (drug that‟s used to help you stop throwing up) • Chlorpromazine:  ROA o Oral o IM  Absorption o Erratic  Distribution  Metabolism  Elimination o Protracted elimination period – metab  Good = helps you wean off the drug…rather than just stopping – slow release mechanism • Haloperidol:  Ex
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