Biological Therapy For SZ Flashcards

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1
Q

What is a defining characteristic of SZ and related disorders?

A

Psychosis.

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2
Q

What are the two ways antipsychotics can be required?

A

In short term or long term.

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3
Q

How can antipsychotics be divided?

A

Into typical or atypical/ second-generation drugs.

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4
Q

How long have typical antipsychotics been around?

A

Since the 1950s.

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5
Q

What is an example of a typical antipsychotic?

A

Chloropromazine.

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6
Q

How can choloropromazine be taken?

A

As a tablet, injection or syrup.

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7
Q

If chlorpromazine is taken orally how often is it administered and what is the maximum mg?

A

Administered daily up to a maximum of 1000mg although initial doses are smaller and for most people the dosage is gradually increased to a maximum of 400-800 mg.

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8
Q

How do typical antipsychotics work?

A

Acting as antagonists in the dopamine system.

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9
Q

What are antagonists?

A

Chemicals which reduce the action of neurotransmitters.

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10
Q

How do dopamine antagonists work?

A

By blocking dopamine receptors in the synapses of the brain reducing the action of dopamine.

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11
Q

According to the dopamine hypothesis what does the dopamine-antagonist effect do?

A

Normalises neurotransmission in key areas of the brain reducing symptoms like hallucinations.

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12
Q

What is a second effect of chlorpromazine?

A

Sedative.

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13
Q

What is chlorpromazines sedative effect been related to?

A

It’s effect on histamine receptors however it isn’t fully understood how this leads to sedation.

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14
Q

What is chlorpromazine often used for?

A

To calm individuals with SZ and other conditions usually done when patients are first admitted to hospitals and are very anxious.

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15
Q

What is absorbed faster?

A

Syrup which tends to be given when chlorpromazine is used for its sedative purposes.

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16
Q

What is the aim of developing new antipsychotics?

A

Maintain or improve upon the effectiveness of drugs in suppressing symptoms of psychosis and minimise the side effects of drugs sued.

17
Q

When was clozapine developed?

A

1960s

18
Q

When was clozapine first trialled?

A

1970s.

19
Q

When and why was clozapine withdrawn?

A

1970s following the deaths of some patients from a. Blood condition called agranulocytosis.

20
Q

What was discovered about clozapine in the 1980s?

A

It was more effective than typical antipsychotics and so was re marketed as a treatment for SZ to be used when other treatments failed.

21
Q

What do people taking clozapine have to do regularly?

A

Have regular blood tests to ensure they aren’t developing agranulocytosis.

22
Q

How is clozapine not available as due to its potentially fatal side effects?

A

Not available as an injection.

23
Q

What is the daily dosage for clozapine?

A

300-450mg

24
Q

How does clozapine work?

A

Binds to dopamine receptors and acts on serotonin and glutamate receptors which is believed to help improve mood, reduce depression and anxiety and improve cognitive functioning.

25
Q

What do the mood enhancing effects of clozapine mean?

A

It is sometimes prescribed when an individual is at high risk of suicide which is important because 30-50% of people with SZ attempt suicide at some point.

26
Q

Why was risperidone developed?

A

In an attempt to produce a drug as effective as clozapine but without its serious side effects.

27
Q

How can risperidone be taken?

A

As tablets, injections which last around 2 weeks or syrups.

28
Q

How is risperidone initially administered?

A

As a small dose which is built up to a typical daily dose of 4-8mg and a maximum of 12mg.

29
Q

How does risperidone work?

A

Binds to dopamine and serotonin receptors more strongly than clozapine and is therefore given in smaller doses.

30
Q

What is there evidence to suggest about risperidone?

A

This leads to fewer side effects than other antipsychotics.

31
Q

Evaluation:
Evidence for effectiveness

A

There is evidence to support the idea that both typical and atypical antipsychotics are at least moderately effective in tackling symptoms of SZ.
Thornley et al showed data from 13 trials with a total of 1121 ppts showed that chlorpromazine was associated with better overall functioning and reduced symptom severity compared to a placebo.
This shows that antipsychotics work.

32
Q

Counterpoint for evidence of effectiveness

A

Healy suggested flaws with evidence for effectiveness e.g. most studies are short-term effects only and some successful trials have had data published multiple times exaggerating the size of the evidence base for positive effects.
This means that evidence is less impressive than it first appears.

33
Q

Evaluation
Serious side effects

A

Typical antipsychotics are associated with a range of side effects such as dizziness.
Long term use can cause tardive dyskinesia which is due to dopamine super sensitivity and causes involuntary facial movements.
The most serious side effect is neuroleptic malignant syndrome which is believed to be caused when drug the drug blocks dopamine action in the hypothalamus.
NMS causes high temperature, delirium and coma and could be fatal.
This means that antipsychotics do harm as well as good

34
Q

Evaluation
unclear how they work

A

Our understanding of antipsychotics is strongly linked to the dopamine hypothesis however we know that the original dopamine hypothesis isn’t a complete explanation for SZ and the fact that dopamine levels in other parts of the brain are too low rather than too high.
If this is true most antipsychotics should not work.
This means that at least some antipsychotics may not be the best treatment for SZ.