Biological therapy for schizophrenia Flashcards

1
Q

drug therapy

A

Most common treatment for schizophrenia involves antipsychotic drugs. Antipsychotics can be divided into typical and atypical drugs.

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2
Q

Typical antipsychotics

A

Includes chlorpromazine. If taken orally it is administered daily up to a max of 1000mg. For most people dosage is gradually increased to a max of 400 to 800mg.

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3
Q

typical antipsychotics - dopamine antagonists

A

typical antipsychotics like chlorpromazine work by acting as antagonists in the dopamine system. Dopamine antagonists work by blocking dopamine receptors in the synapses of the brain, reducing action of dopamine. This dopamine antagonist effect normalises neurotransmission in key areas of the brain, reducing symptoms like hallucinations.

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4
Q

typical antipsychotics - sedation effect

A

chlorpromazine is an effective sedative. It is often used to calm individuals with schizophrenia and other conditions. Syrup is absorbed faster than tablets so it tends to be given when chlorpromazine is used for sedative properties.

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5
Q

Atypical antipsychotics

A

Aim in developing newer antipsychotics was to improve effectiveness of suppressing the symptoms of psychosis and minimise side effects.

Clozapine + Risperidone

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6
Q

Atypical antipsychotics - clozapine

A

daily dosage is a little lower than for chlorpromazine, typically 300 to 450mg a day. Side effect of a blood condition, so patients have blood tests to monitor. Binds to dopamine receptors, but in addition acts on serotonin and glutamate receptors. It’s believed this helps improve mood and reduce depression and anxiety in patients. Mood-enhancing effects mean sometimes prescribed when an individual is considered at high risk of suicide. This is important as 30 to 50% of people with schizophrenia attempt suicide at some point.

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7
Q

Atypical antipsychotics - risperidone

A

developed to produce drug as effective as clozapine without serious side effects. Dose is built up to daily dose of 4-8mg. Believed to bind to dopamine and serotonin receptors. Risperidone binds more strongly to dopamine receptors than clozapine and is therefore effective in much smaller doses. There is some evidence to suggest that this leads to fewer side effects than other antipsychotics.

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8
Q

Evaluation of drug therapy (brief)

A

:) support evidence, Thornley
:( likelihood of side effects
:( mechanism of antipsychotics unclear

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9
Q

strength of drug therapy

A

evidence to support their effectiveness. Large amounts of evidence that support the idea that typical and atypical antipsychotics are moderately effective in tackling symptoms of schizophrenia. Thornley et al (2003) reviewed studies comparing effects of chlorpromazine to control conditions. Data from 13 trials and 1121 participants showed that chlorpromazine was associated with better overall functioning and reduced symptom severity as compared to placebo. There is also evidence for the benefits of atypical antipsychotics. In a recent review, Meltzer (2012) concluded that clozapine is more effective than typical antipsychotics and other atypical antipsychotics. It is effective in 30-50% of treatment resistant cases where typical antipsychotics have failed. This means that, as far as we can tell, antipsychotics work.

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10
Q

weaknesses of drug therapy

A

one weakness is the likelihood of side effects. Typical antipsychotics are associated with a range of side effects such as dizziness, agitation, sleepiness etc. Long-term use can result in tardive dyskinesia, which is caused by dopamine super sensitivity and causes involuntary facial movements. The most serious effect of antipsychotics is neuroleptic malignant syndrome. This is believed to be caused when the drug blocks dopamine action in the hypothalamus. NMS results in high temperature, delirium and coma, and can be fatal. Estimates of its frequency range from less than 0.1% to 2%. This means that antipsychotics can do harm as well as good and individuals who experience these may avoid such treatments (which makes the treatment ineffective).

the mechanism of antipsychotics is unclear. Our mechanism of how antipsychotics work is tied up to the idea that symptoms of schizophrenia are linked to high levels of dopamine activity in the subcortex of the brain. However, we now know that this original dopamine hypothesis is not a complete explanation for schizophrenia, and in fact dopamine levels in other parts of the brain are too low rather than too high. This means that at least some of the antipsychotics may not be the best treatment to opt for – perhaps some other factor is involved in their apparent success.

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