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Biological treatments for sz (typical antipsychotics (Dopamine antagonists…
Biological treatments for sz
typical
antipsychotics
Dopamine antagonists - bind to but do not stimulate 60-75% of D2 receptors - block their action.
Eliminate
positive
symptoms
eg. chlorpromazine - allows D levels to build up so it's production is reduced. Also used as a sedative + for anxiety
SIDE EFFECTS
- tardive dyskinesia
atypical
antipsychotics
Only
temporarily
bind to D2 receptors - then disassociate to allow normal dopamine transmission. Also act on serotonin receptors
little effect on dopamine systems so do NOT cause tardive dyskinesia
eg. clozapine - also acts on serotonin + glutamate receptors. Helps mood + improves cog. functioning. Also prescribed to suicidal people
eg. risperidone - as effective as clozapine w/out side effects. Binds to D + S receptors - binds more strongly to D receptors so effective in smaller doses
AO3
Effectiveness
TA - Thornley - Chlorpromazine associated with better overall functioning + reduced symptom severity than placebo. Relapse rate lower.
ATA - Meltzer - Clozapine more effective than TA, works in 30-50% of cases where TA failed.
Side effects
Tardive dyskinesia rates higher in TA (30%) than ATA (5%)
TA - Ethical issues - protection from harm. If you are sectioned, you have no choice about your medication - no consent!
ATA - could develop agranulocytosis (fatal) - ATA may be more appropriate but ideal is to get off meds + have permanent solutions
Noll - APs don't work in 1/3 of patients with +ve symptoms. APs led to the dopamine hypothesis but may need to relate to hyp
o
dopaminergia as well
Some people also have +ve symptoms even when dopamine levels are normal - should target glutamate system?
Determinist - Ross + Read - when prescribed APs, reinforced view that there is something wrong with them. Decreases motivation to get better
But reduces stigma - becomes medical disorder, takes away responsibility/blame from the patient