drug therapy

Question 1

what are drug treatments of SZ?

Answer 1

antipsychotics are the biological treatment for SZ

Question 2

what are the two types of antipsychotic?

Answer 2

• typical antipsychotics
• atypical antipsychotics

Question 3

which antipsychotic is newer?

Answer 3

atypical

Question 4

how long have typical AP’s been around and what are they referred to as?

Answer 4

• 1950’s
• first-generation antipsychotics

Question 5

how do typical AP’s work?

Answer 5

• they are dopamine antagonists, they bind to dopamine receptors but don’t stimulate them, reducing the action of dopamine
• by reducing stimulation of the dopamine system, it reduces positive symptoms of SZ, such as hallucinations

Question 6

give an example of a typical AP

Answer 6

chlorpromazine

Question 7

there is a strong association with typical AP’s and..

Answer 7

the dopamine hypothesis

Question 8

how long have atypical AP’s been around?

Answer 8

since the 1970’s

Question 9

how do atypical AP’s work?

Answer 9

• also block dopamine receptors, but only temporarily and then they rapidly dissociate to allow normal dopamine transmission to occur
• fast release from receptor
• also target other NT’s, for example clozapine acts on dopamine, serotonin and glutamate
• risperidone targets dopamine and serotonin
• addresses negative symptoms (avolition) as well as positive symptoms

Question 10

why were atypical AP’s developed?

Answer 10

to improve the effectiveness of drugs in suppressing symptoms and minimising side effects

Question 11

what are the 2 types of atypical AP?

Answer 11

clozapine and risperidone

Question 12

what is the most serious symptom of typical AP’s

Answer 12

tardive dyskinesia

Question 13

what is tardive dyskinesia?

Answer 13

long term use can result in tardive dyskinesia, which is involuntary muscle movements of the tongue, face and jaw

Question 14

what is the most serious symptom of atypical AP’s?

Answer 14

agranulocytosis

Question 15

what is agranulocytosis?

Answer 15

an autoimmune disorder affecting white blood cells

Question 16

evaluation: supporting evidence for effectiveness (typical)

Answer 16

ID: supporting evidence for effectiveness
Q: Thornley conducted a meta-analysis on chlorpromazine trials
EV: he took data from 13 trials, using 1121 patients, comparing the effects of chlorpromazine to control conditions in which patients received a placebo so their experiences were identical except for the presence of chlorpromazine in their medication. chlorpromazine was associated with better functioning and reduced symptom severity. data from three trials showed that relapse rate was lower when the drug was taken.
AN: this increases the practical applications of typical AP’s as there is a large amount of evidence supporting its effectiveness in real world applications

Question 17

evaluation: serious side effects

Answer 17

ID: serious side effects
Q: all antipsychotics carry a risk of side effects to varying degrees
EV: these side effects can range from mild (e.g. weight gain, dizziness) to potentially fatal, such as tardive dyskinesia (characterised by involuntary contraction and relaxation of the facial muscles). Lieberman et al (2005) found that 74% of 1,342 schizophrenic patients discontinued antipsychotic drug treatment within 18 months due to side effects.
AN: therefore, a cost-benefit analysis should be carried out to consider whether the benefit of symptom reduction outweighs the cost of side effects for each specific patient.

Question 18

evaluation: use of antipsychotics depends on the dopamine hypothesis

Answer 18

ID: the development of antipsychotics was mainly based upon the dopamine hypothesis, and so their
use depends on this theory too
Q: all AP’s are dopamine antagonists, which means that they block dopamine receptors in order
to reduce production, as high levels of dopamine have been seen to be a contributing factor to SZ
EV: however, this contradicts the modern version of the dopamine hypothesis, which suggests that abnormally low levels of dopamine in the cortex are responsible for symptoms. therefore, a further reduction in dopamine levels should make symptoms worse, and not better.
AN: this paradox has caused some to question the validity of the use of
antipsychotics, as well as the accuracy of the dopamine hypothesis as an explanation for schizophrenia.