Mind Map by , created about 4 years ago

psychology exam

Created by drenae20 about 4 years ago
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1 What do we mean by psychotic?
1.1 Community images or stereotypes of being out of touch with reality
1.2 Symptoms that are out of touch with reality
1.3 Disorders where those symptoms dominate
2 Symptom groups in Schizophrenia
2.1 1. Negative symptoms
2.1.1 Avolition
2.1.2 Alogia
2.1.3 Affective flattening
2.2 2. Psychotic symptoms
2.2.1 Delusions
2.2.2 Hallucinations
2.3 3. Disorganisation symptoms
2.3.1 Thought disorder
2.3.2 Bizarre behaviour
3 Schizophrenia Spectrum & other psychotic disorders
3.1 Schizotypal (Personality) Disorder
3.2 Delusional Disorder
3.3 Brief Psychotic Disorder
3.4 Schizophreniform Disorder
3.5 Schizophrenia
3.6 Schizoaffective Disorder
3.7 Psychotic disorder due to (medical condition) - Substance/Medication-Induced Psychotic Dis.
4 What causes psychotic disorders?
4.1 Genetic model
4.1.1 60% of monozygotic twins are concordant for schizophrenia vs. 10% of fraternal twins
4.1.2 This is strong evidence that genes can play a role in causation of schizophrenia
4.1.3 It is also strong evidence that genes are not a sufficient condition for emergence of schizophrenia
4.2 Neurotransmitter models
4.2.1 Neurotransmitters such as dopamine can be overactive (& misdirected) in schizophrenia
4.2.2 'Antipsychotic' medications blocking dopamine receptors can reduce some symptoms
4.2.3 Logical Hypothesis: neurotransmitter dysregulation ‘causes’ schizophrenia
4.3 Neurodevelopmental model
4.3.1 Brain maturation processes (e.g., cell migration, pruning of connections) seem to be less fully realised in people with schizophrenia
4.3.2 Structural brain abnormalities may be evident before onset of the disorder, and may change little over time
5 Psychological models
5.1 Both neuropsychological factors (deficits) and cognitive factors (biases) have been implicated
5.1.1 Information processing deficits: e.g. source monitoring – is this “voice” from me or not?
5.1.2 Reasoning biases: e.g. Jumping to conclusions – deluded individuals use insufficient information before reaching a conclusion
5.1.3 Distorted appraisals: e.g. In paranoia, an “external & personalising” bias – i.e. attribution of negative events to others rather than self or the situation
6 Cannabis & Schziophrenia
6.1 Cross sectional studies show an association between cannabis dependence and schizophrenia
6.2 Longitudinal study: Heavy cannabis users at age 18 were 2.3 times more likely to have a schizophrenia admission by age 33 after controlling for pre-existing psychiatric problems
6.2.1 Implications: Heavy use of mind altering drugs can increase the risk for schizophrenia... ...but only a minority of drug abusers will get the disorder
7 Vulnerability-stress-coping model
7.1 Vulnerability
7.1.1 Contributed to by genetic and biological factors, and other enduring problems
7.1.2 All people can be considered to have vulnerability, but to different degrees
7.2 Stressors
7.2.1 Any factors that tax our ability to cope
7.2.2 May arise from life events stressful to anyone, or from stressors unique to the person, including daily hassles
7.2.3 Can be external to the person(e.g.,exam stress) or internal (e.g., using mind altering drugs; maturational changes)
7.3 Coping
7.3.1 Automatic and deliberate actions taken to restore well-being
7.4 Central idea
7.4.1 The occurrence of episodes of a disorder is dependent on the relative levels of vulnerability, stress and coping responses
7.4.2 The experience of stress automatically leads the person to attempt adaptation
7.4.3 Successful coping is contributed to by both “coping effort” and “competence”
7.4.4 Coping breakdown allows the psychopathology to erupt
7.5 Evidence for vulnerability
7.5.1 Adolescents at high risk for psychosis have detectable neurocognitive deficits Processing speed, sustained attention, memory
7.5.2 People with psychosis have high incidence of impaired sustained attention so do their children so do those who have recovered
7.5.3 Relatives have increased incidence of schizotypal personality traits, auditory processing irregularities
7.6 Does stress precipitate episodes?
7.6.1 Life event stressors are strongly associated with worsening symptoms in the months leading up to relapse of schizophrenia and with onset of depression
7.6.2 Daily hassles are also implicated in relapses ̶ And in symptom exacerbation And in onset of sub-clinical symptoms in the normal population
7.7 Benefits
7.7.1 Explains the episodic nature of psychosis whilst recognising the possibility of enduring deficits in brain structure or function ̶ i.e., incomplete cell migration may be a vulnerability, but an episode of psychosis requires either an increase in stress or a breakdown in current coping to emerge
7.7.2 Can engender hope: people are not simply passive victims of their vulnerability or of stressors ̶ Stress can potentially be managed by coping actions
7.7.3 Prompts a wide range of interventions ̶ e.g., if medication (a way of reducing vulnerability) is insufficient to restore equilibrium, reduction of stressors, or coping skills development can be instituted
8 Evidence-based treatments for Schizophrenia
8.1 ‘Antipsychotic’ medications
8.1.1 Theoretical rationale Excess release of a neurotransmitter can be treated by blocking its receptors (with an alternative chemical). Antipsychotics target dopamine D2 receptors, (and others)
8.1.2 Antipsychotics include: risperidone, olanzapine, amisulpride, aripiprazole, clozapine
8.1.3 Benefits Reduction/cessation of positive (‘psychotic’) symptoms in a majority of patients
8.1.4 Limitations Incomplete remission of positive symptoms in many patients Little benefit for negative symptoms, except for Clozapine Side effects may include akathisia, weight gain, hypersalivation, photosensitivity, impotence, fits, etc.
8.1.5 In general, antipsychotics have similar efficacy in reduction or cessation of positive symptoms in the acute phase: 2/3 patients show considerable gain However, some patients recover from acute phases without medication Maintenance antipsychotic medication following an acute episode is effective in reducing the risk of relapse 14 -21% of patients on medication relapse within 9 months, Vs. 55% of patients on placebo relapse within 9 months
8.2 Family Interventions
8.2.1 Strong evidence for relapse reduction
8.3 CBT for psychosis
8.3.1 Can improve symptoms persisting despite antipsychotic use and possibly other challenges of adaptation
8.4 Social Skills Training
8.4.1 Improves skills, but generalisation to everyday life is difficult
8.5 Supported Employment and similar programs
9 Symptom focussed interventions
9.1 Three types of symptom interventions for hallucinations and delusions
9.1.1 1. Coping Enhancement: builds on the person’s ‘natural’ ways of coping Natural’ ways of coping with hallucinations and delusions
9.1.2 2. ‘Information Processing’ techniques: theoretically- derived ways of avoiding or inhibiting the symptoms Vocalisation and subvocalisation
9.1.3 3. Cognitive Therapy interventions:changing appraisals or beliefs to reduce distress and undermine the power of the symptom Identifies irrational (erroneous) beliefs and thoughts that lead to distress and disruption in the person’s life Belief Modification techniques 1. ‘Analysis of evidence’ technique Elicit evidence given for the delusion; explore alternative explanations for this evidence rather than the delusion itself 2. Challenging belief inconsistencies technique Gentle raising of doubts by noting inconsistencies within the delusional system, or between delusional beliefs and other beliefs 3. Reality test technique Jointly construct a test that will prove the delusion to be true or false to the client’s satisfaction
10 Is symptom reduction or elimination all that is needed in treatment of psychosis?
10.1 Person-focused intervention
10.1.1 Recovery Therapy 1. Engagement and assessment - Flexible and unhurried getting to know you, and goal setting 2. Everyday coping and problem solving practical ways of coping with smaller problems or symptom distress 3. Working with hallucinations and delusions - symptom control, coping, belief modification, prevention 4. Learning about psychosis - developing a more adaptive ‘story’ of what has happened 5. Strengthening adaptive views of self - rediscovering, extending and building a positive sense of self 6. Addressing personal issues and emotional disturbance impeding adaptation Includes: - concurrent disorders (substance use, social phobia) - pre-existing developmental issues such as sexuality - trauma and grief of psychosis 7. Practical relapse prevention -early signs identification, preferably including a significant other 8. Family and social re-integration -includes facilitating a low EE environment -support and facilitation of social roles 9. Completion and follow-up
11 Relapse Prevention
11.1 Rationale for Relapse Prevention
11.1.1 A vulnerability-stress-coping model of disorder suggests that the experience of a disorder may be episodic, depending on relative levels of stress and coping. Interventions to reduce stressors, or boost coping may prevent or forestall further episodes.
11.2 Doesn’t ordinary treatment prevent relapses?
11.2.1 Yes - Good ‘bio-psycho-social’ management goes beyond acute treatment ... It may: reduce exposure to vulnerability via medication; reduce impact of stressors via extra supports; enhance coping, etc. These should reduce the likelihood of further episodes Relapse prevention via monitoring for early warning signs ̶ Interventions to reduce stressors, or boost coping may prevent or forestall further episodes. ...This is “tertiary prevention”.
11.2.2 “Relapse prevention” programs are more specific. They target at-risk sub-groups (selective prevention) or focus on early warning signs of relapse (indicated prevention) and They include specific additional assessment and interventions
11.3 Necessary conditions for relapse prevention using early warning signs
11.3.1 1. ‘Early warning signs’ of relapse need to exist
11.3.2 2. Early warning signs must appear early enough to be detected and acted upon before relapse
11.3.3 3. Realistic and reliable methods for detecting early warning signs must be available
11.3.4 4. Consumers, families, case managers & doctors must be prepared to commit to an action plan that is activated by emergence of early warning signs
11.3.5 5. Interventions need to delay or prevent relapse
11.4 Early warning signs procedure
11.4.1 Establish relapse signature using observations from both patient and others (e.g., family)
11.4.2 Agree on intervention plan, e.g. ̶ ̶ reduce stress (remove, medicate) restore coping (re-institute coping actions, boost supports) treat emerging symptoms (medication, CBT)
11.4.3 Agree on monitoring method -- Observer and or patient questionaires, active monitoring by case working
11.5 CBT interventions in the relapse prodrome period
11.5.1 Key idea: cognitions may accelerate relapse Negative appraisals of prodromal symptoms “I’m noticing the voices more often – I’m going crazy again” Traumatic memories “It was awful going to hospital” Interventions Normalise misinterpretations, reduce catastrophisation, Address key negative beliefs, Boost coping strategies for distress, & prodromal intrusions
11.6 Relapse
11.6.1 A full or partial re-emergence of acute episode symptoms following a period of full or partial recovery
12 Family burden
12.1 The impact of bizarre and unpredictable behaviour
12.2 Stigmatisation by friends and the community
12.3 Perceived blame from professionals
12.4 Loss of former personality and expected futures of the ill relative
12.5 Financial impact (less income,costs of support
12.6 Restrictions on own lives due to caring role