Schizophrenia AO1 /2 Flashcards
(12 cards)
What are typical antipsychotics and how do they work?
Developed in 1950s (e.g., chlorpromazine).
Dopamine antagonists: bind to D2 receptors, blocking dopamine transmission.
Reduce positive symptoms (hallucinations, delusions) by lowering subcortical dopamine activity.
Also act on histamine receptors, giving a sedative effect (used in institutions).
Usually taken orally or via injection, often 400–800mg/day.
What are atypical antipsychotics and how are they different?
Developed 1970s–90s to reduce side effects.
Target multiple neurotransmitters: dopamine and serotonin/glutamate.
Examples: Clozapine (targets 5-HT, D2, glutamate), Risperidone (stronger dopamine action).
May help positive and negative symptoms (e.g., avolition, depression).
Given in lower doses, fewer motor side effects (e.g., tardive dyskinesia/NMS).
What are the serious side effects of typical antipsychotics?
Tardive dyskinesia: 30% of users; 75% irreversible.
Neuroleptic malignant syndrome (NMS): dopamine blocked in hypothalamus → fever, coma, death.
Common short-term effects: agitation, weight gain, sedation.
Mechanism mismatch: dopamine levels in cortex may be too low, so further reduction can worsen symptoms (contradicts revised dopamine hypothesis).
What are the risks of atypical antipsychotics like Clozapine?
Agranulocytosis: serious blood condition → immune failure → death.
Requires regular blood tests.
Clozapine is restricted to patients unresponsive to other drugs.
Risperidone avoids this side effect but may be less effective for comorbid depression.
How does CBT help treat schizophrenia?
CBT helps patients identify and challenge irrational beliefs (e.g., paranoid delusions).
Uses reality testing, normalisation, and understanding of symptoms to reduce distress.
Improves emotional regulation and daily functioning by promoting coping strategies.
Often includes therapist-patient dialogue: “Could there be another explanation for the voices?”
What is the goal and process of family therapy?
Aims to reduce expressed emotion (anger, guilt), which can trigger relapse.
Burbach (2018) outlined a 7-phase model: info-sharing → skills training → relapse prevention → maintenance.
Therapy creates a therapeutic alliance, improves family understanding, and fosters collaborative care.
Encourages family to support themselves as well as the patient.
What is a token economy and how is it used to manage schizophrenia?
A form of behaviour modification using operant conditioning, not a therapy but a management strategy.
Used in psychiatric institutions to increase desirable behaviours (e.g., hygiene, social interaction) in patients with institutionalisation.
Patients receive tokens (secondary reinforcers) for completing target behaviours, which are exchanged for primary reinforcers like TV time or snacks.
Immediate reinforcement is key to effectiveness.
What behaviours are targeted in token economies for SZ patients?
Typical behaviours include brushing teeth, making beds, joining group activities.
Rewards include privileges (e.g., walk outside, extra TV).
Based on Ayllon & Azrin (1968), who found significant increases in task completion among institutionalised women when tokens were exchanged for privileges.
Normalises patient behaviour and helps re-integration into the community.
What is the interactionist approach to schizophrenia?
Combines both biological and psychological explanations and treatments of SZ.
Central concept: diathesis-stress model, suggesting SZ arises from a genetic vulnerability (diathesis) + environmental stressor.
Supported by Turkington et al. (2006): antipsychotic drugs treat biological basis; CBT treats psychological symptoms.
Outline the original diathesis-stress model and how it has changed.
Meehl’s (1962) model proposed a single schizogene → schizotypic personality → SZ if exposed to stress (e.g. schizophrenogenic mother).
Now considered outdated: no single gene; modern view sees diathesis as biological or psychological (e.g. trauma), and stress as lifestyle or substance use.
Example: cannabis use + trauma = ↑ risk (Houston et al., 2008).
What does modern research say about the nature of diathesis and stress in SZ?
Ripke et al. (2014): 108 candidate genes; no single schizogene.
Ingram & Luxton (2005): early trauma impacts HPA axis, increasing stress sensitivity.
Houston et al. (2008): cannabis use + trauma = 7x ↑ risk of SZ.
Suggests both diathesis and stress can be biological or psychological.
How does the interactionist approach influence treatment?
Supports combination therapies: antipsychotics (bio) + CBT (psycho).
Biological therapies address distal causes (genes/brain chemistry).
Psychological therapies address proximal symptoms (hallucinations, delusions).
More common in UK; USA favours only biological treatment.
