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Clinical - Coggle Diagram
Clinical
diagnosis
4 d's definition of abnormality
- Deviance - behaviour deviates from expectations/social norms
- Danger - behaviour that puts an individual or others in harms way
- Dysfunction - the individual cannot function normally in day to day life
- Distress - the extent to which a behaviour puts an individual or others in harms way
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Dysfunction +can put help in place to make a real difference -everyone may be dysfunctional at times
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Distress +if a patient is visiting the doctors it is likely they are not happy and want/need help -emotions can be hidden by an individual
ICD - International classification of diseases - concerned with MHD as well as other diseases (MHD is section F)
ICD-
Reliability
+Reliability- higher reliability than DSM-5 according to kappa values
+Regier- for Sz and mood disorders from ICD better diagnostic system
+Ponizovsky- found ppv increased for Sz and mood disorders from ICD-9 to ICD-10 shows improvement
+open nature of ICD-10 allows for reviews and for clinicians to re-check diagnosis
Validity
+produced by WHO-free to access and is in multiple different languages - non-political body therefore is more likely to present an un-biassed listing of relevant disorders irrespective of treatment
-views on MHD alongside other medical issues- may be reductionist as see MHD as having physiological origin and ignores purely psychological causes
DSM- diagnostic statistic manual of mental health disorders
Reliability
+Brown-reliability of diagnosis improved for PTSD, binge eating disorder
-Ward- found inconsistencies with DSM diagnosis- blamed diagnostic tool- most errors with DSM -low reliability and validity
Validity
-Janson- compared ICD-10 with DSM-IV and found high rate of agreement- both equally valid (concurrent validity)
+DSM looks at cultural differences - DSM-V looks at how disorders relate to each other & cultural guidance on making diagnos is more valid
-DSM produced by APA for US clinicians- may be influenced by interested parties such as pharmaceutical companies
Rosenhan - being sane in insane places (1973)
- 3 women 5 men - pseudopatients trained by Rosenhan in how to address psychiatric health workers and avoid taking medication
- were admitted through a clinical interview at the hospital
- were truthful about lives except from names and address and careers as some where psychologists
- reported same symptoms- hearing an unfamiliar voice repeating the words empty, hollow, thud.
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- Rosenhan approached the head of the hospital he was going to and informed them of the deception
- Rosenhan breifed lawyers to get participants out if anything went wrong.
- once admitted they started acting normally - took a notepad and pen along to record, started asking to be discharged.
- none of the staff recognised pseudopatients were healthy.
- took between 7 and 52 days to be discharged.
- Pseudopatients were discharged with Sz in remission
- observed staff abusing patients, patients refusing medication - patients not treated as people, no doors, staff wouldnt make eye contact - pseudopatients were seen as having notetaking behaviour and oral inquisitive symptoms when they arrived early to the canteen -labelling
conclusion - hospital that diagnosed manic depression (1 out of 12) was a private hospital- may have diagnosed that as easier to treat -wealthier people diagnosed with disorder can have therapy to be treated
Follow on study- Rosenhan contacted hospital and they requested to run the study again but with awareness of pseudopatients- Rosenhan sent in no pseudopatients yet staff believed there were 41 imposters out of 193 real patients
Evaluation
G- used a strong range of hospitals private, state run, old, new
-12 hospitals is small for a country as big as US
-data from a 9th Pseudopatient not recorded as they didnt follow procedure
R - no inter-rater reliability - only one pseudopatient in each hospital
+11 out of 12 diagnoses were Sz may prove diagnosis is reliable after all
A + caused psychiatric hospitals to review their admissions process
+had major influence on reforming DSM
V - Ketty criticised Rosenhan- pseudopatients were faking doesn't say anything about how people with genuine mental health conditions are diagnosed- don't expect deception
-may not have recorded any positive interactions
E -hospital staff were deceieved about symptoms - couldnt consent to withdraw
-contributed to a crisis of public confidence in the american mental health system
Unipolar depression
characterised by a persistently low mood. Has several subtypes classified by severity, length of occurance and whether it has psychotic or other features
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DSM-V - depression can be diagnosed if 5 or more symptoms present for a two week period. Symptoms: significant weight gain or loss, changes in sleeping pattern, fatigue, excessive guilt, loss of concentration, recurrent thoughts of death.
78% of deaths by suicide are male - not as likely to talk as women
women more susceptible to depression -postpartum
more likely to develop if suffering from BPD, substance abuse, anxiety.
has a high prevalence rate.
Biological explanation-Neurotransmitters - Monoamine hypothesis
-depression results from a chemical imbalance in the monamine neurotransmitters in the brain (serotonin and noradrenaline)
- noticed in 1950 that drugs decreased these amine neurotransmitters and brought about symptoms of depression
however- drugs developed that increased serotonin levels and noradrenaline levels didn't improve symptoms for up to 6 weeks.
Eval of Bio explanation
- most evidence is from drug research- strong evidence that low levels of serotonin being the cause of depression
Kirsch- believes anti-depressants cause a placebo effect - may explain mood improvement.
Andreoli- antidepressants that increase noradrenaline levels have been shown to be just as effective as those that increase serotonin
Angoa-Perez - mice were bred without gene for serotonin but didnt show depressive symptoms more complex than just serotonin.
- correlation not causation- aetiological fallacy- causes unknown
- reductionist, diathesis stress model may suggest other things at play
other explanations- cognitive
- Sullivan- 40% more likely to develop if relative has depression- genetic?
Cognitive explanation - operant conditioning - Lewinson - proposed depression occurs because of a lack of positive reinforcement from the environment
Seligman-passive acceptance of failure - the dogs that were exposed to inescapable electric shocks learnt to give up- reflects symptoms of depression
Abramson- those with a maladaptive attributional style tend to put more emphasis on fault within themselves as a factor for their failure. internalise failure in a way that suggests they cannot change
Beck- argued depression due to a pessimistic schema we hold about how the world works - develops during childhood as a result of trauma.
Evaluation of cognitive explanation-
-fails to explain gender bias, why women suffer more with negative thinking, no evidence to show they have more negative schema than men
-doesn't explain suicide an active wish to die- not passive acceptance (learned helplessness)
-don't know what came first tlking negatively about yourself causing depression or depression causing you to speak badly about yourself
+Beck's ideas supported by D'Assandro - found students with negative views about their futures were strongly associated with an increase in depressed mood.
Treatments- drug therapy
- antidepressants most common intervention- work by increasing serotonin and noradrenaline
- Tricyclics - three ring structure- increase noradrenaline and serotonin by blocking re-uptake channels neurotransmitter stays in synapse for longer
-patients on these need to be carefully monitered by doctors
- SSRI-selective serotonin reuptake inhibitors - most common antidepressants e.g- Prozac is an SSRI - first choice as less side effects.
- MAOI-monoamine oxide inhibitor- mops up enzyme so neurotransmitter stays in pro-synaptic axon for longer -side effects as alters all receptors
- NRI - noradrenaline reuptake inibitors, doesn't influence serotonin levels
+less side effects
-newer
Evaluation- those who are depressed most likely have a lack of motivation therefore will struggle to get to the dr's to be prescribed anti-depressant
-treats the symptoms not the cause
-WHO found non-medicated patients with depression enjoyed a better health than those who took anti-depressants
-study in Holland - found 76% of patients who didn't take drugs recovered and never relapsed.
CBT-therapy - an active and direct model
- aims to challenge irrational belief that may be at the root of the depression
- the therapist helps the client recognise faulty cognitions that the client uses to process info about the world, encourages them to challange these cognitions.
- clients encouraged to keep a daily mood diary and to do excercises outside the session and reflect back on their effectiveness
- client learns techniques where they can analyse events and map the emotional response.
Effectiveness Keller- CBT alone 52% effective, CBT an Drugs 85% effective
- participant actively involved in recovery
+not invasive, no side effects, skills learnt useful in every day life
Limitations
-client can become dependent on therapist, less effective for patients with endogenous depression (no apparent cause)
-unpredictable treatment length
Ethics - treatment takes a while to recieve on NHS- well off patients who can pay for treatments will get treatments first
Schizophrenia
Crow- divided symptoms into positive and negative
- positive - add to experience of the patient- hallucinations
- negative - subtracts from the normal behaviour lack of energy, poverty of speech, social withdrawal
Neurotransmitters- postmortem originally used to understand Sz
Owen et al. Postmortem examinations on people who have had Sz
- high density of dopamine receptors on certain parts of the brain than non-suffering patients.
- suggests a higher sensitivity to the action of dopamine than people who have not had Sz
-1960's first associated dopamine with Sz - patients who abused large amounts of amphetamine drugs often showed positive symptoms for psychosis.
- Randrup and Munkvad - raised dopamine levels in the brains of rats by injecting them with amphetamines
-rats behaviour changed - more aggressive, changes in dopamine consistant to patients with Sz
- not everyone who takes amphetimines develops Sz
Parkinsons- associated with low levels of dopamine - to alleviate symptoms patients often prescribed
L-Dopa a known dopamine agonist -when working out how much L-dopa to prescribe patients can suffer symptoms of Sz.
Medication that reduces dopamine and is effective suggests dopamine plays a role in Sz
-not all patients respond to this treatment
Genetics evidence of strong heritable link in development of Sz
- Genain Quads - each diagnosed with Sz but at different levels- all suffered abuse in childhood
-diathesis stress model? - build up of stress, childhood trauma
- Gottesman and Shields - found in Mz twins 42% were both diagnosed with Sz and for Dz twins 9% both diagnosed
-looks at concordance rate for Sz in Mz and Dz twins
-if Sz fully genetic then there would be 100% in Mz twins who share the same genetics.
- Torrey- argued not representative as Mz concordant twins with Sz are more likely to voulenteer
-may be inter-uterine factors that are responsible rather than genetic factors.
Cognitive theory
- when a patient experiences a hallucination they may look to others to confirm what they have seen or heard - when they cannot confirm this they may become wary of them and feel they are keeping something - can create further delusions and paranoia
- Frith - suggests Sz results from the patients increased self-awareness where there is an inability to filter out cognitive noise
- McGuigan - misinterpret inner voice as belonging to someone.
Carlsson - 2000
- literature review of research and current theory- variety of sources investigating neurochemical levels in patients with Sz
- key finding - lots of research evidence supporting the role of low levels of glutamate activity at NMDA receptors
- patients with Sz in remission- dopamine levels normal - side effects of drugs that lower dopamine most present during remission
- thalamic filter - seperates the causes of + and - symptoms, some patients respond better to some drugs than others
Evaluation of Carlsson -
G- no sample group generalisability doesn't apply in the same way - cites 33 studies in his review
R- studies are all lab based and most were peer reviewed (one was not published therefore wasnt peer reviewed)
A - to develop new drugs with fewer side effects
V - secondary study so therefore had to assume that is what happened.
-human participants being administered drugs to bring on psychotic episode different to a homeless person having a psychotic episode -lower validity
-lots of Carlssons evidence from animals, identifying psychotic episode in animals is up to interpretation - humans can tell you if the're hallucinating.