Biological therapy for SZ Flashcards

1
Q

What is the most common treatment for schizophrenia?

A
  • antipsychotic drugs
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2
Q

What are the two types of antipsychotic drugs used for the treatment of schizophrenia?

A
  • typical antipsychotics (first gen) > used since 1950s
  • atypical antipsychotics (second gen) > used since 1970s
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3
Q

How are antipsychotics use differently for different people with SZ?

A
  • may be required in the short or long term
  • some people can take a short cause of antipsychotics then stop use without return of symptoms
  • other people may require use for life or face likelihood of relapse
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4
Q

What is one type of typical antipsychotic and how can it be taken?

A
  • (since 1950s) Chlorpromazine
  • can be taken as tablets, syrup or by injection
  • taken orally it is administered daily up to max of 1000mg
  • initial does are smaller & for most people dosage is gradually increased to a max of 400-800mg
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5
Q

How do typical antipsychotics like chlorpromazine work?

A
  • strong association with the DA hypothesis
  • they work by acting as antagonists (reduce action of neurotransmitters) in the dopamine system
  • DA antagonists block dopamine receptors in the synapses of the brain which reduces the action of dopamine
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6
Q

What are the effects of chlorpromazine on the dopamine system?

A
  • when an individual begins taking chlorpromazine dopamine levels builds up, but then production is reduced
  • this dopamine-antagonists effect normalises neurotransmission in key areas of the brain reducing symptoms like hallucinations
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7
Q

What effect does chlorpromazine also have?

A
  • sedation effect
  • used to calm individuals not only with SZ but with other conditions
  • used with patients first admitted to hospitals & are very anxious
  • used in syrup form for sedative affect as it is absorbed faster
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8
Q

What are the two atypical antipsychotic?

A
  • Clozapine (300 to 450mg a day)
  • Risperidone
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9
Q

What were the main aims of the atypical antipsychotics?

A
  • to improve effectiveness in suppressing symptoms and minimise side effects
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10
Q

When was clozapine first used and why was it withdrawn?

A
  • first trialled in the 1970s
  • it was withdrawn following deaths of some patients from a blood condition called agranulocytosis
  • 1980s it was discovered to be more effective than typical antipsychotics and used when other treatments failed (treatment resistant cases)
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11
Q

If clozapine is used how do individuals ensure they are not developing agranulocytosis?

A
  • regular blood tests
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12
Q

How does Clozapine work and what are its benefits?

A
  • binds to dopamine receptors in the same way as chlorpromazine does but also > acts on serotonin and glutamate receptors as well
  • this helps improve mood & reduce depression & anxiety
  • & may improve cognitive functioning
  • this mood enhancing effects means it is sometimes prescribed when an individual is considered high risk of suicide > important as up to 50% of people with SZ attempt suicide as some point
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13
Q

Why was Risperidone developed and how can it be taken?

A
  • since 1990s
  • developed to be as effective as clozapine but without serious side effects
  • can be taken in from of tablets, syrup, or an injection that lasts around 2 weeks
  • small does initially given & is built up to to a typical daily dose of 4-8mg & a maximum of 12 mg (more effective so less)
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14
Q

How does Risperidone work?

A
  • like clozapine, risperidone is believed to bind to dopamine & serotonin receptors
  • it binds more strongly to dopamine receptors than clozapine & is therefore effective in much smaller doses than most antipsychotics
  • reduces side effects
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15
Q

What is a strength of antipsychotics?

A
  • evidence to support their effectiveness
  • Thornley et al> reviewed studies comparing the effects of chlorpromazine to control conditions
  • data from 13 trials showed that chlorpromazine was associated with better overall functioning & reduced symptom severity as compared to placebo
  • also evidence for the benefits of atypical antipsychotics > In Meltzer’s review he concluded that clozapine is more effective than typical antipsychotics & other atypical antipsychotic & that it is effective in up to 50% of treatment resistant cases were typical antipsychotics have failed
  • implies that clinical evidence suggests that both typical & atypical antipsychotics are effective in treating symptoms of SZ
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16
Q

What is a counterpoint to effectiveness of antipsychotics?

A
  • Healy has suggests serious flaws in the evidence for effectiveness
  • e.g. most studies are of short term effects only & some successful trials have had their data published multiple times exaggerating the size of evidence base for positive effects (publication bias)
  • also because some antipsychotics have powerful calming effects it is easy to demonstrate that they have some positive effect on people experiencing the symptoms of SZ > not the same as saying that they actually reduce the severity of psychosis
  • evidence base for effectiveness of antipsychotics is not as significant than it first appears
17
Q

What is a limitation of antipsychotics?

A
  • the likelihood of side effects
  • typical AP’s are associated with a range of side effects including, weight gain, dizziness, stiff jaw, sleepiness etc.
  • long term use can result in tardive dyskinesia, which is caused by dopamine super sensitivity which causes involuntary facial movements such as grimacing, blinking & lip-smacking
  • most serious side effect of antipsychotics (typical) is neuroleptic malignant syndrome (NMS)
  • this is believed to be caused when the drug blocks dopamine action in the hypothalamus, an area in the brain associated with the regulation of a number of body systems > NMS results in high temperature, coma & can be fatal
  • AP’S can do harm as well as good > means some may avoid treatment
18
Q

What is another limitation of antipsychotics?

A
  • we do not know why they work
  • understanding of how antipsychotic drugs work strongly links with the original dopamine hypothesis > the idea that symptoms of SZ are linked to high levels of dopamine activity in the subcortex of the brain
  • this hypothesis is not complete and in the updated dopamine hypothesis, we now know that dopamine levels in other parts of the brain are too low rather than too high
  • if this is true, the AP’s should not work so given that there are already questions over the effectiveness > this adds to the argument that they are ineffective
  • means AP’S may not be the best treatment to opt for > other factor involved in apparent success