paper 2 essay plans Flashcards
1
Q
rosenhan AO1
A
- ppts - 8, 12, 5/3, 5
- hollow, empty, thud, then stopped signs of SZ
- charged with SZ in remission
- normal behaviour seen as “obsessive”
- follow up 41, 23, 19
- 35/118 patients, 7-52, avg 19
- sticky
2
Q
rosenhan results
A
- 7-52 day stays, mean 19
- 35/118 knew pseudos were fake ‘you’re not crazy - you’re a journalist’
- normal behaviour interpreted as nervous e.g. ‘obsessive note taking’
- pt 2 - 43 by 1 staff member, 23 by a psychiatrist, 19 by a psychiatrist & other staff member
3
Q
rosenhan AO3
A
- diff hospitals but only rep of 70s
- qual and quant, subjective data journals
- pressure on accuracy, not worldwide app
- eco validity, ppl refused into wards
4
Q
ICD/DSM AO1
A
- ICD, coded into sections - F, F20 SZ,
- moniters incidence, prevalence, mortality, morbidity
- available in cultural forms, features and symptoms needed to diagnose disorder
- DSM 5 - 3 sections; how to use, diagnosis, standardised tests and GAF scale
- removed unneccessary disorders - 5-> 1 autism
5
Q
DSM AO3
A
Validity:
- Lahey - good predictive validity for ADHD over 3 years
- BUT Sanchez - 74% of depressed people recieved the correct diagnosis 26% wrongly diagnosed with depression - internal valid shite
Reliability:
- Rosenhan - 7/8 were correctly diagnosed with SZ when presenting same symptoms - inter-rater
- Beck - same symptoms diagnosed as same disorder ab 50% of the time - low inter-rater
6
Q
ICD AO3
A
Validity:
- mason et al predictive validity 13y later but
- Valle et al found the validity to be uncertain
Reliability:
- Ponizovsky 94.2% mood disorder agreement, 83% psychotic - intra-rater reliable
- BUT Nicholls 0.36 rel score <DSM &GOS hospital criteria
7
Q
Types of reliability and validity
A
- intra-rater
- interrater
- aetiological - cause of disorder
- internal - symptoms/disorder match
- construct - operationalised disorder
- predictive - treatments good?
8
Q
name 4 symptoms and 3 features of SZ
A
- affects 1% population
- peak onset mid 20sM, late 20sF
- men more likely to develop negative symptoms
* hallucinations
* delusions
* thought insertions
* disorganised speech/thought
9
Q
difference between pos and neg symptoms of SZ
A
- pos = adds something e.g. hallucinations
- neg = takes something away e.g. anhedonia (diminishes ability to experience pleasure)
10
Q
dopamine hypothesis AO1
A
- hyperdopaminergia causes SZ symptoms
- ↑ dop in mesolimbic causes positive symptoms
- more/more sensitive D2 receptors
- beta hydroxylase low levels
- hypOdopaminergia in PFC
- ↓ dop in mesoCORTICAL causes neg symptoms
11
Q
dopamine hypothesis AO3
A
- donnewee homovanillic BUT SZ could cause dop ↑ - C and E
- lindstroem LDOPA BUT could be a combo of genes and NTs
- backed by drug therapies however diathesis stress might be better
- Falsifiable therefore scientific however reductionist so issue with validity
12
Q
Genetic explanation of SZ AO1
A
- heritable factor of SZ
- 8-16% higher risk for first degree relatives, 17% if DZ twin, higher for MZ
- chromosome 22, 1, 15
- 22q11 deletion linked to delusions and psychotic symptoms
- COMT gene produces an enzyme maintaining dopamine/ serotonin levels - found in dodgy chromosome 22
- adoption studies can separate nature and nurture
13
Q
Genetic explanation of SZ AO3 - hasnt come up
A
- gottesman meta 41 studies, 17% DZ concordance, 48% MZ, BUT not 100% therefore not a full explanation
- International SZ consortium - abnormalities in chrom22,1,15 BUT could be due to dysfunctional negative family communication and the stress
- genes sensitise the brain to dopamine so could be both however focusing only on biological aspects is reductionist
- alternative theory - diathesis stress model more holistic, however application to screening and early intervention
14
Q
cognitive explanation of SZ AO1
A
- SZ = dysfunctional attention system
- preconscious filtering - delusions, paranoia, disorganised thought/speech
- perception and memory - schemas are not activated in new situations; disorganised speech - cant figure out what will happen next
- ## self-monitering - cant tell whats internal/external - hallucinations and paranoia,
15
Q
Cog explanation of SZ AO3
A
- Interactionist - more hol, but hard to establish cause and effect
- Mcguire - temp lobe less active in hals, unable to control inner voice, Butler et al found less activity in frontal lobes, dont pay attention to surroundings
- can be used by CBT to treat SZ however less effective for neg symptoms which may be better explained via the dop hyp
- dickson et al found adolescents had same cog defects but Sitskoorn found relatives same defects no SZ
16
Q
drug therapy SZ AO1
A
- ECT/psychosurgery used but controversial
- tablet / syrup / injection
- typical/atypical
- reduce levels of dopamine in brain by binding to D2 receptors, depolarises neuron
- atypical bind temporarily to D2
- typical binds permanently
- atypical block serotonin
- bind within 48h, takes 10-14 days to improve
17
Q
Drug treatment SZ AO3
A
- Pickar et al - clozapine>neuroleptics and placebos, BUT some are treatment resistent - 25%
- Elmsley risperidone - 84% ppts at least 50% reduction BUT might be due to early part of disorder
- schooler et al - less severe side effects and lower relapse 42% rather than 55% BUT side effects
- better to keep in society, cheaper, cant cure the disorder, only manages symptoms
18
Q
psychoanalysis AO1
A
- dream association - dream diary kept and analysed for manifest content and latent content - sub messages
- free recall - write down every thought
- freudian slips - make a verbal mistake that reflects an unconscious thought/ attitude
- challenges view of parental relationship
- deal with repressed material, reconstructs ego defence mechanism to be healthier
- regression into childhood and roleplay with the therapist as the parent
19
Q
psychoanalysis AO3
A
- malmberg et al - those who did psychotherapy couldnt be released from hospital, drugs can BUT less relapse and needed less further treatment
- Bargenquast - person underwent 2 years of psychoanalysis, reduced symptoms BUT ungeneralisable to TP
- Long waiting lists for treatment, accessibility issue BUT non-invasive treatment eg if dont like idea of chemically altering yourself
- roth and fonagy those in acute stages less able to cope with treatment - emotionally invasive BUT no side effects physically
20
Q
Carlsson AO1
A
- looked at research on dop hyp
- 32 studies used between 1979 and 1999
- used animals, brain scans, SZs, remission patients, post-mortem studies and PCP use
- results - 3 stages - dopamine, glutamate, drug treatments
- PET scans support dopamine - more dop in basal ganglia
- hypoglutamatergia causes psychotic symptoms
- clozapine might be effective for treatment resistent SZs because blocks serotonin not just dope
21
Q
carlsson AO3
A
- generalisable - 32 pieces of reserach broad range
- however research is 20 years old therefroe may be a generational thing might not be relevant today
- PET scans are scientific, objective and easily comparible - reliable
- secondary data standardised procedure issues may be missed - not own research
- types of SZ variations looked at not just one type - valid
- animal research - may have same brain structure but not same cognitive function so ungeneralisable
22
Q
name 3 symptoms and 3 features of depression
A
- prevalence - 3.5 mill in UK
- Gender - twice as common in women - 1/4 women
- age of onset - mid 20s, most common between 25-44
- symptoms include - depressed mood, loss of pleasure, fatiguability
- needs to be shown for at least 2 weeks
23
Q
Monoamine hypothesis AO1
A
- monoamines - serotonin, dopamine, noradrenaline lower levels in D ppl
- serotonin regulates other NTs
- sero associated with sleep and anxiety - causes insomnia
- dopamine associated with reward - causes lack of motivation
- noradrenaline keeps alertness and focus, a lack causes lethargy and lack of focus
- 2 ways a lack is caused:
- pump-like mechanism uptakes NTs too quick
- too much monoamine oxidase enzymes break down too many NTs
24
Q
Monoamine hypothesis AO3
A
- anti depressants do work - Geddes - therefore it shows a bio exp is also credible BUT many30% may not respond well to anti-depressants
- Wender and Klein found rats given low levels of nora made them inactive and sluggish BUT RATS
- Bell found low levels of tryptophan creating sero caused D BUT cause and effect
- scientific - empirical, falsifiable - reductionist bad
25
Q
cognitive explanation of UD AO1
A
- Cognitive triad - neg thoughts about self, world, future
- cognitive errors eg catastrophising, crystal ball, labelling
- cog errors lead to selective attention to the neg
- schemata - core beliefs shaped by early childhood, more negative / traumatic experiences = more negative views on the world
- depressed schemata - affective schema causing sadness, motivational schema leading to lack of motivation
26
Q
Non-biological explanation UD AO3
A
- koster et al 15 depressed teens focused on loser longer in selective attention task BUT yovel and Mineka couldnt find a relationship between UD and selective attention
- moilanen found D teens associated with dysfunctional attitudes and future attitudes - neg triad - BUT macintosh and fisher said too complex, just need neg thoughts of self
- Children of the 90s study dad left caused depression by trauma so schema good BUT genetic dispositions or hormonal imbalances
- evidence based theory - empirical research BUT hard to prove neg thoughts cause depression
27
Q
biological treatment for UD AO1
A
- pump-like mech, monoamine oxidase too much
- more popular bc less controversial than ECT
- increase serotonin and noradrenaline by stopping these processes ^
- SSRIs work by inhibiting reuptake of serotonin
- tricyclics block the reuptake of both sero and nora
- MAOIs inhibit the enzymes that break down the monoamines
- people often react differently so may affect which drug is used to treat
28
Q
biological treatment for depression AO3
A
- Coppen found SSRIs useful but Kuyken found CBT to be better
- WHO stated its a well documented treatment for severe depression over loads of studies BUT piggott found publication bias is common with drug treatments because theyre easier
- quicker and cheaper than therapy - can feel better in 2 weeks BUT not a cure
- Geddes found it effective - 18% relapse, 42% placebo and treatment lasted 3 years BUT side effects like suicide ideation, nausea and insomnia can cause people to come off and relapse - not good if they cant complete treatment
29
Q
psychological treatment for UD AO1
A
- CBT - UD due to maladaptive thought processes
- explores sig life events
- provides the therapist with a frame of reference
- therapist listens to core beliefs, tecahing how to recognise and provide adaptive solutions
- downward arrow technique - question statements until core belief is revealed eg soup bad → failure
- smart targets - specific, measurable, achieveable, relevant and time-bound - reviewed weekly
- therapist helps break cycle by reality testing, encouraging asking questions
- keep a thought diary that can be worked through
- work on ways to banish neg thoughts eg distractions
30
Q
psychological treatment for UD AO3
A
- kuyken found CBT more effective for symptoms and relapse than drug therapies BUT Jarrett found MAOIs and CBT equally effective
- NICE recommends CBT BUT Chan found CBT more effective WITH drugs
- CBT may be preferred sue to no side effects BUT it still may be emotionally invasive and exhausting and requires a desire for change which D ppl will struggle with
- CBT treats the core problem rather than just relieving the symptoms however witing lists may be very long and may take ages to get the treatment
31
Q
Williams et al AO1
A
- is CBMI effective? with I-CBT? does it ease the difficulty of I-CBT?
- 232 ppts originally, but due to exclusion criteria eg if PHQ score under 19, no minors, or suicidal history ended up with 69 ppts in trial or control group
- 77% women in trial group
- 20 mins a day for 7 days of CBMI, then trial group did ICBT for 10 weeks with 6 online lessons, given extra homework and resources
- Results - sig reductions in all prim measures
- PHQ- 7.23 vs WLC 3.26
- BDI-II - 17.52 vs WLC 7.46
- K10 - 11.86 vs WLC 4.17
