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University of Toronto Scarborough
Zachariah Campbell

Psychiatric & Degenerative Diseases psychiatric biochemical, born with probability of getting disease degenerative disease alzheimer’s global damage ^ both are problems of cells, not lobe SCHIZOPHRENIA -prevalence: 1% of pop’n -onset usually by 30 -symptoms: delusions, (auditory) hallucinations, lose touch with reality -patients often don’t like to take their meds b/c the meds are strong depressants -schizos do show reduced performance 1) in frontal lobe function 2) in verbal and non-verbal memory -not lateralized - but its hard to know if effect u get in memory problems are caused by meds - schizos also have lighter brains and larger ventricles -lighter brains COULD be caused by reduced synapses from reduced life experience OR again from years on strong meds perspectives on schizo: -Freudian persp. thought it used to be thought to be caused by domineering mother, absent father, etc -neuropsych perspective: damaged part of brain? -> NO, there actually appears to be no physicial damage genetic? -> Possibly as indicated below -while it is 1% of general pop, it is 10-15% of patient’ parents, siblings or children -but psychologists argued that could just be because environment is also shared… SO…twin studies were done -dizygotic (non- identical) twins: rate remains same as regular family members 10-15%, -but in monozygotic (identical) twins: 40-75% (NOT 100%, but still high) -but again psychologists say, its because parents treat monozygotes the same -SO a study was done to disprove this: -researcher found 12 pairs of monozygotic twins where one had schizo and the twins were separated in 1 yr of life -results: 9/12 monozygotic twins separated at birth were concordant for schizo therefore this disease is a neurological disorder with a genetic component -discoveries in schizo research was by chance very often- so we’ve discovered a lot about schizo by giving different kinds of meds for treating other diseases and by chance, it had an effect on schizo’s -> these drugs are often called Neuroleptics- anti psychotic drugs: -1)antihystamines- caused a calming/anti-anxiety effect in schizos -are dopamine ANTAGONISTS -2)phenothyazines- chlorpromazines became the most commonly prescribed -blocked the receptor sites for the biogenic amines (monoamines) -from this they tested which monoamines are most important (see below) -the antipsychotic effectiveness of the meds was directly related to their ability to block dopamine receptors -then became clear that dopamine was the problem -furthermore, they found if they used dopamine receptor stimulators such as AMPHETIMINES (at very high levels) would induce schizo in normal individuals AND asymptomatic schizo’s (they relapse) within 24 hrs -schizos DON’T have MORE dopamine, they have more dopamine RECEPTIORS!!!: 6 times more Dopamine D4 receptors -therefore schizo ppl are born with too many dopamine receptors -treatment: we treat schizo with drugs that reduce the dopaminergic system -but, if reduce too much they may induce parkinson’s-like symptoms (if you ease-up on the meds, they may become psychotic…so you may have to decide what to do with a person) AFFECTIVE (EMOTIONAL NOT INTELLECTUAL) DISORDERS - mania and depression and bipolar -Mania:-feel on top of the world unrealistically -hard to treat b/c patients LOVE the highs and miss them -Depression: -Reserpine (used for high blood pressure) causes monoamines to leak from the synaptic vesicles which then floats in the cytoplasm and get destroyed without ever entering the synaptic cleft therefore, results in less monoamines which causes depression -Aldomet (another BP med) blocks synthesis and release of norepinephrine, and this also lead to depression -therefore, less monoamines, specifically norepinephrine, leads to depression -when looking at brains and doing spinal taps of depressed patients (and in suicide patients), 20-25% of depressed patients have a decrease in a chemical called 5HIAA (5- hydroxy-indol-acetic-acid) (is a metabolite/breakdown product of serotonin (5HT)) -also found that serotonin is low in depressed ppl -therefore less monoamines, specifically norepi and serotonin, leads to depression -treatment (inc serotonin and norepinephrine): -1) tricyclic antidepressants: -block both serotonin and norepinephrine reuptake -results in increase in the amnt of ser and nor in the synaptic cleft -seemed to be very effective in treating dep
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