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Final exam notes (Chapters + lectures)

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Nussbaum D

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Lecture 9- Bipolar Mood Disorder:  1 or more manic/mixed episodes  1 or more episodes of MDD  Episodes don’t occur concurrently with substance, medication somatic treatments  Not due to a general medical condition  Episodes aren’t better accounted for by schizoaffective, schizophreniform, delusion, psychotic, schizo, NOS  Bipolar I: at least one episode of mania  Bipolar II: and hypomanic episodes  Cyclothymia: less severe  Bipolar NOS: only hypomania  Mania symptoms: irritability, excessive high-risk activities, inflated self-esteem, distractibility, less need for sleep  BP depression can look like MDD and schizo, BPD, ADHD, substance abuse, medical conditions  BP may be comorbid with another axis I disorder  Poorer outcome if comorbid with ADHD, anciety, OCD, panic, impulse control  Suicide high in BP and BP is stable  BP have lower life expectancy, health, 60% have comorbid substance, only 1/3 seek treatment  Usually male, psychotic features, history of alchy, poor occupational status  BP associated with: reduction of PFC volume, decreased glial and neurons in PFC, lower levels of NNA marker for neuronal health  Mood stabilizers: reverse impairment in brain structure and BDNF levels  Lithium in rats: promote neuron growth, protect neurons against toxic agents 1  Lithium in humans: increase NAA (marker for health) and gray matter volume nd rd  2 and 3 messenger system most studied mood stabilizers  ^processes produced by G-coupled protein receptors  Lithum, valproeate, carbamazepine interact with enzymes involved in the system  4 classes of mood stabilizers: lithium, anticonvulsants, atypical antipsychotics, omega 3  Lithium  Anti-manic Anticonvulsants:Carbamazepine (Tegretol) ,Valproic Acid (Depakene) Gabapentin (Neurontin), Lamotrigine (Lamictal) ,Gabapentin (Neurontin) ,Topiramate (Topamax) ,Oxcarbazepine (Trileptal)  Atypical Antipsychotics:Olanzapine (Zyprexa), Risperidone, and others  Omega-3 Fatty Acids  Putative Mechanisms: 1)membrane stabilizers( Lithium),  2)inhibition of intracellular enzyme Glycogen Synthase Kinase-3 (GSK-3, lithium, valproate, laomotringie)  Inhibition of GSK-3 increases b catenin( b catenin increases cell survival and promotes axon growth (but increases amyloid b)  3) Protection from Oxidative Stress due to reduction of excessive metabolic activity (e.g., excitotoxicity due to hyper-stimulation by Glutamate  4) Protein Synthesis Induction (DNA stimulation) to increase cellular protective proteins such as cAMP Response Element Binding Protein (CREB) -> increase in BDNF & bcl-2 (Valproate)  Treatment focus: diminish excitatory activity via GLU metabolism, or through GABA/ 5HT inbihition; use neuroprotectants; counter effects of stress to brain  Lithium: effective in 60-80% of acute episodes---used less now because of safety, compliance is poor, side effects intolerable, patients miss the high with the mood swings  Lithium’s excreted unchanged by the kidneys, not metabolized, thou less effected by liver disease---but may cause kidney damage over log use (decades)  Lithium used in: acute mania, hypomania, maintenance of bp or cyclothymia, mixed states, depression, schizophrenia/affective, or aggressive outburst  Anti manic effects: decreases #, frequency, duration, and intensity of episode, decreases subtle mood changes, tkes 5-10 days for response, 2/3 show great response,  Lithiumfor mania: not as good for mixed, atypical, secondary mania---better for acute mania st  Lithium for depression: 1 choice for acute BP depression  People who respond poorly: mixed states, depressive-manic, personality disorder, mania secondary to general condition  Side effects: no specific antidote for OD, narrow TI, adverse reaction 35-90%, cognitive dysfunction, reduced kidney functioning, vomiting, diarrhea,  Hand tremors, incoordination, nystagmus, muscle weakness, loss if excitement and creativity, weight gain, acne, arrhythmia( rare)  Drug interaction: non-psychotropics may increase plasma levels of lithium  Lithium treatments: take 1-2 weeks, take blood levels every 5 days until stable—then every 6 months, most effective in patients with classic symptoms of mania  Toxicity: early- ataxia, lack of coordination; mid- listlessness, nausea, slurring, diarrhea; moderate- confusion, delirium, ataxia pronounced; severe- changes in consciousness, seizures, coma, death 2  Anticonvulsants: overlap with new atypical antipsychotics  Drugs of both groups are anti-bipolar, treat aggression, violent behaviours, and have affective beneficial actions  Stopped at slide 50/105. Bipolar Chapter notes: Lecture 10- Antipsychotics  Schizophrenia has 5 criteria- A) characteristics B) social and occupational dysfunction C)Duration D) schizoaffective and mood disorder E) substance or general F) relationship/developmental  Criteria A) 2+ for at least a month: delusion, hallucinations, disorganized speech and beh, negative symptoms  Criteria C) duration for at least 6 months  Myth: schizophrenia is rare—uh, no.  Difficult to diagnose because of many symptoms  Downward drift: progressive loss of relationships, inability to maintain ql  Brain changes: Reductions in volume of grey matter in frontal lobe, Alterations in blood flow to certain brain areas  General decreased brain volume & activity, Larger ventricles and basal nuclei, smaller hippocampi and smaller amygdala  Neurobiology: Dopamine Hypothesis version 1 (1959): higher DA= more positive symptoms, antipsych block DA2 receptors  Hypthesis 2 (1991): against increased DA, instead PET show lower cerebral blood flow in frontal area: Prefrontal hypodopamine causes negative symptoms; subcortical hypedopamine causes positive symptoms  Version 3: genes, stress, drug use and frontal- dysfunctional all contribute to psychosis  10-20% d2 and d3 receptors density in straitum  Decreases in d2 and d3 receptors in thalamus and anterior cingulate  Decrease in d1 in PFC (negative + cognitive impairments)   Foussias paper on neuro imaging: compared 12 whitematter tracts: schizo with cog and negative symptoms and schizo without symptoms—deficit patients had higher diffused arcuate fasciculus  Negative symptoms: alogia, affective flattening, avolition  Cognitive symptoms: disorganized thinking, slow thinking, poor concentration and memory, difficulty expression thoughts, words, feelings 3  DA pathway 1: Tuberoinfundibular pathway: hypothalamus Ant pituitary responsible for release of hormone prolactin (lactation)  DA Pathway 2: SNBGresponsible for movement controls (certain types)  DA Pathway 3 mesolimbic: VTANAmediates reward, reinforcement, and positive symptoms  DA Pathway 4 mesocortical: VTAfrontal cortex + cingulate cortex: cognitive impairments, negative symptoms  DA hypothesis testing: Conclusion: the better a drug binds to 2he D receptor and blocks the effect of dopamine there, the better it will be as an antipsychotic.  When DA activity is reduced, psychotic symptoms get better.  Conclusion: psychosis (schizophrenia) is due to some abnormal increase in DA activity, or sensitivity. By bringing that down, you reduce the symptoms, even if you have not cured the actual defect.  Drug attaches to receptorblock DAbut clinical effect isn’t for a few weeksConclusion: the dopamine blockade itself is not the immediate cause of improvement. Bl
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