Methods of Modifying - schizophrenia Flashcards

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1
Q

until the 1950’s what was the only treatment available?
What was the first antipsychotic drug?
first generation/second generation?

A

electroconvulsive shock therapy, insulin shock therapy, psychosurgery or institutionalisation = ineffective and terrible side effects.
First antipsychotic drug = Chlorpromazine. Improved symptoms to allow people to be discharged from hospital.
First generation – typical antipsychotics
Second generation – atypical antipsychotics.

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2
Q

Who was chlorpromazine trialed on? What are other typical antipsychotics?

A

trialed on one 24 year old manic patient. Sent home 3 weeks later. Further clinical trials – 38 patients. Mass produced – 1955.
Low potency as large amount has to be administered.
Haloperidol = 50x more powerful than Chlorpromazine.
Fluphenazine = injection. Moved when stabilised with oral medication.

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3
Q

How do typical antipsychotics work?

A

Work as a dopamine antagonist. Work by affecting neurotransmission (blocking the action of dopamine). Antagonist of D2 receptors. Blocks other dopamine receptor sites D1-D5.
After presynaptic neuron releases dopamine into synapse, the receptor on postsynaptic neuron is blocked by chlorpromazine reducing activity in postsynaptic neuron. This causes the presynaptic neuron to increase dopamine into the synapse. Dopamine drops as its depleted and amount in synapse decreased leading to decrease in neural activity.
Reduction in dopamine in mesolimbic pathway – decline in positive symptoms.

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4
Q

what’s a atypical antipsychotic?
What did kapur and Remington find?

A

Clozapine = beneficial impacts on negative symptoms and positive. Act on dopamine and serotonin levels.
Kapur v Remington – only occupy dopamine receptors temporarily and then rapidly break down to allow normal dopamine transmission.
Responsible for the lower levels of side effects.

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5
Q

what are the key differences between typical and atypical?

A

Atypical received at fewer dopamine D2 and more at D1 and D4 than typical.
Atypical also antagonise serotonin, 5-HT2A to same degree as dopamine D2.
Seeman = ‘fast off’ theory – Atypical bind more loosely to D2. Not last long enough to produce side effects in typical antipsychotics.

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6
Q

What supporting research is there for antipsychotic drugs?

A

Cole et al – 75% given typical ‘much improved’ (none got worse) but only 25% given a placebo (48% got worse).
Should a placebo be given to patients with a mental illness? Antipsychotic effective in treatment.

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7
Q

What differences in effectiveness are there for antipsychotics?

A

Ravanic et al – compared Clozapine, Chlorpromazine and Haloperidol in 325 people with schizophrenia in 5 years, Clozapine had highest reduction in positive symptoms, fewer side effects (0.9 per patient) = Haloperidol (2.7 per patient) and Chlorpromazine (3.2 per patient).
Atypical more effective than typical. Fewer side effects. However, typical work for some so not useless.

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8
Q

What about non compliance of antipsychotic drugs?

A

Struggle to adhere to medication schedule. Hospitalised, medicated and discharged. Stop taking meds, become ill again and readmitted - ‘revolving door psychiatry’.
Stop taking due to - Side effects, feel ‘normal’ and don’t feel the need for the medication anymore, forget, don’t trust the medication, lack insight that they’re sick. May not be able to generalise to real world usage.

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9
Q

How can antipsychotics cause psychological harm?

A

Side effects like weight gain – become obese, develop diabetes, heart disease etc. Needs to be assessed whether side effects can be cancelled out by reduction in symptoms. If side effects are worse than symptoms, medication not the best option.

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10
Q

Why may there be a lack of valid consent with antipsychotics?

A

Unable to fully understand the side effects. Take medication – sectioned under mental health act – can’t refuse treatment.

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11
Q

Why may there be a lack of understanding about antipsychotics?

A

Actual method of some work is unknown. Unable to explain why they work for some and not all. It takes years to find the right combination and dosage. Stressful – short term. Millions have benefited, may not be perfect but the best we have right now.

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12
Q

how may fewer people be institutionalised with antipsychotics?

A

Before, hospitalised indefinitely in hospitals, asylums. Seen as an incurable, chronic condition. Chlorpromazine – released from hospital. This impact compared to the impact that penicillin had on the treatment of infection.
People could return to employment = benefits for economy.
Help other schizophrenics recently diagnosed = reduce overall suffering.

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13
Q

what downsides are there to care in the community for antipsychotics?

A

Risk of non-adherence to medication = linked to violent crime.
NCISH – 346 murderers with a history of schizophrenia between 2003 and 2013 = 29% non-adherent to drug treatment.
Theyre monitored less closely than they were in hospital, non-compliance with drugs is higher.

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14
Q

What about the cost of antipsychotics?

A

Long term – cost more as un medicated schizophrenics are more likely to require long term hospitalisation.
Cheapest is Chlorpromazine – side effects so phased out in western world but still used regularly in the developing world.
NHS Drug Tariff, the Regional Drug and Therapeutics Centre = estimate cost of antipsychotics can vary from £19.50 - £3161.60 per patient, per year. Average cost - £1590.55.
Medication until they die – treat symptoms rather than dealing with underlying cause.
NHS limited budget, cheaper treatment, more money for treating others.

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15
Q

What’s the aim of CBT?
What’s it mainly used for?
What may it empower?
How often does it take place?

A

challenge maladaptive thoughts and replace them with constructive thinking that will lead to healthy behaviour.
CBt can mainly be used to reduce the impact of positive symptoms. May not be able to prevent a schizophrenic from experiencing hallucination but help them deal and cope with the symptoms.
May be empowered to be more independent and more confident. May have the knock on effect that negative symptoms may also be reduced.

Usually takes place weekly/fortnightly for 5-20 sessions.

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16
Q

what are engagement strategies?

A

fully engaged and committed to therapy. Preliminary sessions for the opportunity to talk at length. A therapist will try and build a rapport with the client.

17
Q

What is psychoeducation?

A

develop an understanding of their illness, learn about the characteristics, their behavior is a symptom and can be managed. This de-catastrophises and normalises the symptoms. Then therapist and client will investigate specific symptoms, identify the contest and possible trigger factors.

18
Q

What are cognitive strategies?

A

The therapist cannot simply tell the schizophrenic that their thinking is wrong and tell them how to think properly. Get the schizophrenic to think about their own thinking and come to their own conclusions about their maladaptive thinking patterns. Become aware of their errors, address these thoughts, develop more productive thinking styles.

19
Q

What’s Socratic questioning and empirical disputing?

A

curiosity driven questions. Help the schizophrenic identify their errors and challenged the patient to evidence that supports their delusions. The lack of evidence should undermine their delusion.

20
Q

What’s behavioural skills training?
what’s a dysfunctional thought diary?
What’s pleasant activity scheduling?

A

helps them cope with the symptoms, negative secondary symptoms. May include deep breathing and relaxation techniques.
record, rate, rational thought, rate, re-rate original. Do something wouldn’t usually do.
making time for an activity the patient enjoys, based on positive reinforcement, designed to challenge negative symptoms like avolition.

21
Q

What supporting research is there for CBT?

A

+ Kuipers et al = 60 randomly allocate to CBT plus drugs or drugs only – 9 months of therapy, 50% improved when given both compared to 31% of just drugs.
CBT is effective when used with anti-psychotics. 19% increase in beneficial outcomes.

  • Kingdon and Kirschen = not deemed suitable for CBT as they would not fully engage with the therapy.
    Not available to all, older people less suited. Limits effectiveness.
22
Q

why is there difficulty measuring the effectiveness of cbt?

A

Often used in conjunction with antipsychotics as unlikely to benefit from CBT alone due to hallucinations and delusions making communication difficult.
Hard to say how much they improve from the CBT and how much from Anti-psychotics.

23
Q

why is cbt not suitable for all patients?

A

Severe symptoms that are resistant to drug therapies may not access the therapy. Denial, not fully engage.

24
Q

why is good that cbt has a lack of side effects?
what ethical issues are there?
Valid consent?

A

free of any physical side effects compared to antipsychotics which has many.
without Antipsychotics CBT is ineffective. The lack of side effects may be canceled out by the lack of symptom reductio that would result from CBT without medication.
CBT entered into with consent, more ethical and they can withdraw themselves. There is a form of coercion to continue taking the drugs as without their symptoms will return.
Stop CBT, no longer receive any benefit but symptoms still controlled.

25
Q

what social implications are there?
- post code lottery?
- additional cost?
- cost effective?

A

CBT and The Post Code Lottery = Not always available. ‘postcode lottery’, determined by the area in which they live.
NHS = ‘trusts’, manage own area. Offered and taking CBT various from 14-67%.
Social inequality = Go private, reduce NHS places.

  • Additional cost = CBT cost between £1750 and £1800 per patiet. This is an additional cost on top of the drugs.

+ CBT is cost effective = Kuipers et al, Costs involved in CBT likely to be offset by the reduced utilisation of service costs in the future. Long term, recouped as less likely to need emergency psychiatric services

26
Q

how does the biological explanation link to antipsychotics?

A

One type of explanation for schizophrenia are biological explanations which includes the dopamine hypothesis. The dopamine hypothesis states that increases in levels of dopamine in the brain are associated with symptoms of schizophrenia. There are 2 pathways linked to the brain – the mesocortical (negative symptoms) which sends dopamine to the frontal cortex from VTA and the mesolimbic pathway (associated with positive symptom) which sends dopamine around the limbic system. The dopamine hypothesis is a biological explanation because the focus of the theory is on the neurotransmitter dopamine in the brain. This explanation sees the cause of schizophrenia as being biological. One method of modifying schizophrenia is through the use of antipsychotics medication. Typical antipsychotics like chlorpromazine block dopamine receptors. Atypical antipsychotics like clozapine block dopamine and serotonin receptors. The use of antipsychotic medication links with biological explanations of schizophrenia as both see the cause of the condition as being biological (high levels of dopamine) and therefore the solution is also seen as biological (drugs) - this is known as the medical model of schizophrenia.

27
Q

how does the individual differences explanations link to cbt?

A

One type of explanation for schizophrenia are individual differences explanations which include the cognitive explanation. There are a range of cognitive theories, but each one considers the role of internal mental processes and thoughts on behaviour. For example, Beck explained the negative symptoms of schizophrenia in terms of a negative triad – Beck said negative thoughts about the self, the future and the world led to negative symptom like avolition. These explanations are examples of individual differences explanation as they focus on the differences between each person in terms of their mental processes and thinking. Such processes can become faulty in some individuals leading to mental illness. One method of modifying schizophrenia is through the use of CBT. When used for schizophrenia CBT include engagement strategies (e.g discussing the problem), psychoeducation (e.g teaching the client about their condition), cognitive strategies (empirical disputing and behavioural experiments), Socratic questioning, behavioural skills and relapse prevention strategies. CBT links to individual differences as both see the cause as aspects of the individual. They both emphasise free will to challenge delusional thoughts, though methods like empirical disputing – even when a recognised symptom of schizophrenia (delusions of grandeur).

28
Q

how does the social psychological explanation link to family intervention therapy?

A

One type of explanation for schizophrenia is social psychological explanations which include Browns expressed emotion theory. Brown proposed the expressed emotion theory. It consists of hostility, e.g. anger directed towards the schizophrenic, critical comments (you’re so lazy) and emotional over involvement which may be expressed as guilt over the family member’s condition. Brown stated that families where EE was high was more likely to cause patients to relapse suggesting an important role for communication within the family and psychosocial stress in the development of schizophrenia. Expressed emotion is a social psychological explanation as it focuses on the social relationships the schizophrenic has with their family members. These relationships are seen as a causal factor in the worsening of symptoms rather than any biological cause. one method of modifying schizophrenia is using family intervention therapy. This may include – reducing stress and burden on relatives and reducing expressions of anger and guilt by the family. Such interventions are designed to improve communication between the schizophrenic and their family and reduce the chance of psychotic relapse. The use of this therapy links with social psychological explanations as both focus on the important role of the family and how they communicate in the development of schizophrenia. Family therapy often targets behaviours shown by High EE families and tries to modify communications to use less of these damaging communication styles.