plans Flashcards
DESCRIBE AND EVALUATE THE CLASSIFICATION AND DIAGNOSIS OF SCHIZOPHRENIA
A01
A01:
CLASSIFICATION OF SCHIZOPHRENIA
* SCHZOPHRENIA: a PSYCHOTIC DISORDER involving a BREAK in REALITY which involves a disruption of COGNITION and EMOTION, which affects LANGUAGE, THOUGHT, PERCEPTION and SENSE OF SELF
* 2 MANUALS : ICD 10 AND THE DSM5
* DSM-5: ONE of the POSITIVE features (delusions or hallucination or speech disorganisation)
* ICD-10: TWO or MORE NEGATIVE FEATURES and recognises SUBTYPES of SCHZOPHRENIA e.g. PARANOID SCHIZOPHRENIA = powerful DELUSIONS and HALLUCINATIONS but few other + HEBEATRNIC SCHIZOPHRENIA = DISTURBANCE of MOVEMENT, leaving the sufferer IMMOBILE or OVERACTIVE
POSITIVE SYMPTOMS
* HALLUCINATIONS: they SEE, HEAR, TASTE or EVEN FEEL something that ISN’T REALLY THERE - HEARING VOICES or imagining PEOPLE/ANIMALS/DISTORDED FACIAL EXPRESSIONS
* DELUSIONS: IRRATIONAL BELIEFS e.g. being an important figure - beliefs that have NO BASIS in reality and ACT in a way that makes SENSE TO THEM
NEGATIVE SYMPTOMS
* AVOLITION: finding it DIFFICULT to perform ACTIVITIES that are GOAL-ORIENTED e.g. poor hygiene, lack of energy and inconsistency in work/education
* SPEECH POVERTY: REDUCTION in the AMOUNT and QUALITY OF SPEECH e.g. slurred speech or a delay in the sufferer’s verbal responses during a conversation
DESCRIBE AND EVALUATE THE CLASSIFICATION AND DIAGNOSIS OF SCHIZOPHRENIA
A03
AO3
* RELIABILITY: (CONSISTENCY) INTER-RATER RELIABLITY: the extent to which DIFFERENT ASSESSORS/TWO or MORE MENTAL HEALTH PROFESSIONALS AGREE on the ASSESSMENTS/SAME DIAGNOSIS (DIAGNOSTIC RELIABILTY) - CHENIAUX ET AL: 2 psychiatrists INDEPENDENTLY diagnose 100 patients using the DSM + ICD = POOR INTER-RATER RELIABILITY (1ST - 26 w/ DSM + 44 w/ ICD AND the other - 13 w/ DSM + 24 w/ ICD)
* VALIDITY: the extent to which we are MEASURING what we WANT to measure - the number of VALIDITY ISSUES measured through the CRITERION VALIDITY; do different ASSESSMENT SYSTEMS arrive at the SA
DESCRIBE AND EVALUATE BIOLOGICAL EXPLANATIONS OF SCHIZOPHRENIA
A01
AO1
Genetics: Gottesman (1991) conducted family studies
MZ Twins - Identical twins monozygotic identical
If one twin has sz 48% chance the other twin will have sz
DZ Twins - non identical
If one twin has sz 17%
In terms of parents if both parents have sz you will have a 46% chance of developing sz
And 10% chance of sz with one parent having it.
All these figures compared to 1% in the general population
Candidate genes - single faulty gene that could explain sz
The largest study done by Ripke looked at 37,000 diagnoses of people with sz and found 108 separate genetic variance and found that they are Aetiologically heterogeneous
The role of mutation
SZ can also arise in the absence of a family history via a mutation in the parents DNA e.g the flu in the 2nd trimester but also there is a increased risk of 2% if your father is over 50 in the old man’s sperm
DESCRIBE AND EVALUATE BIOLOGICAL EXPLANATIONS OF SCHIZOPHRENIA
A03
(1) Adoption Studies
P: Supporting evidence from adoption studies
E: Tienari et al (2004) shows that children that are biologically connected to people with Sz are still at high risk even when adopted by non-Sz families. Also, gattsman found that if your aunt had sz you have 2% chance of getting it but if its your identical twin its goes to 48%
A: There is overwhelming evidence for genes making you more vulnerable for being at risk for schizophrenia
(2) curren at al
Evidence for dopamine Curran et al amphetamines increase dopamine and worsen symptoms in people with schizophrenia DOUBLE not all drugs that increase dopamine lead to worse symptoms for example apomorphine
(3)(dopamine hypothesis)
P: Support from drug therapy
E: DA is involved in Sz as dopamine agonists increase dopamine-receptor activity and make Sz worse, antipsychotic drugs which block DA reduce symptoms of Sz
A: there is a direct link between Sz and dopamine which increases validity of theory as DA plays a role in Sz
(4) other neurotransmiters
P: Other evidences show that other neurotransmitters have a central role such as glutamate
E: Several brain scan studies and post mortem showed that paitents with Sz have high levels of glutanate. Several candidate genes of Sz also are involved in glutamate production
A: evidence for dopamine hypothesis is mixed and equally as strong for other neurotransmitters
DRUG THERAPHY A01
Chlorpromazine
- typical antipsychotic, dopamine antagonist (block DA receptors and doesn’t allow message to pass
- this reduces hyperdopaminergia which reduces certain positive symptoms
- Atypical drugs were created to reduce the many side effects that come with this
Risperidone
- developed to avoid a certain blood condition that comes from clozapine
- blocks DA, serotonin and glutamate receptors but stronger on DA
- This makes it more effective in smaller doses and has fewer side effects
clozapine
- Atypical which acts as an antagonist where it blocks DA receptors but also serotonin and glutamate receptors
- effective at improving cognitive functioning and mood
- used when patient doesn’t respond to typical drugs
Risperidone
Drug Theraphy A03
(1 - vidence for effectiveness of antipsychotic drugs/ thornly?)
P: Evidence for effectiveness of antipsychotic drugs
E: Thornly (2003) review studies comparing effects of chlorpromazine to control conditions. 13 trials 1121 ptps overall showed better functioning with the drug. Meltzer (2012) clozapine is more effective than typical antipsychotics and effective in 30-50% of treatment resistant cases where anitpsychotic have failed
A: Shows they’re effective at reducing symptoms, it is better to treat as early as possible
(2 - serious side effects?)
P: serious side effects
E: Typical AP, long term effects associated with tardive dyskinesia (Involuntary facial movements) caused by DA super sensitivity. Very serious sone is neuroleptic malignant syndrome - drug blocks DA in hypothalamus, resulting in high temp, delerium and coma
A: Typical AP can do harm as well as good so many may avoid them, making them ineffective
(3 - unclear mechanism)
P: Unclear mechanism due to dependence on dopamine hypothesis
E: DA hypothesis is an incomplete explanations as explained by the updated version. DA levels in other parts of the brain are too low rather than too high - antipsychotics shouldn’t work
A: AP may have be the best treatment to opt for and there may be other factors involved in their success
Psychological explanations A03
(1 - READ ET AL)
P: Evidence showing that difficult family relations may increase risk of Sz
E: Read et al (2005) reviewed 46 studies of child abuse and Sz and found that 69% of adult woman patients had a history of verbal, physical and sexual abuse. For men, it was 59%
A: shows a clear link between family dysfunction and increased risk of sz
H: Most of the evidence shares a weakness, they are all based on information about childhood, reported after all the symptoms have occurred so they may havterm-24e forgotten or Sz may have distorted their recall
(2 - weakness: schizophrenogenic mother)
P: weak evidence for schizophrenogenic mother
E: Research provided is from clinical observations and early evidence that looked at mothers and gave them “crazy-making” observations.
A: The supporting evidence is weak and may tell us very little about the extent to which childhood and family affect the development of Sz
P: Schizophrenogenic mother leads to parent-blaming
E: After having to see your child descent into Sz and having to bear a life-long responsibility of taking care of them. This theory adds further trauma by “adding salt to the wound”
A: this makes it very hard for a mother to take care of her child and causes her to blame herself for everything
(3 - research support for cognitive explanation)
P: Research support for cognitive explanation
E: Stirling found, comparing 30 people in a control to 30 people with a Sz, that those with Sz performed poorly on cognitive tasks like the stroop test (took twice as long)
A: Supports ‘central control errors’ hypothesis
H: fails to explain the actual cause and offers only part of the explanation on what is happening
