Clinical Flashcards
What are the criterion (symptoms) of Anorexia nervosa?
Criterion A: restriction of energy intake and low body weight- BMI of less than 17kg/m^2 or using DSM-5 tend to accept the ICD-10 definition.
Criterion B: intense fear of gaining weight even if the current body weight is low. This is done by excessive exercise, restriction, binge purging, and the use of laxatives or diuretics. DSM-5 gives no examples but the ICD-10 does
Criterion C: Distortion of body image where the weight is hugely overestimated and emphasis on body weight in the patient’s view of themselves- poor self-image, overuse of body weight in self-evaluation.
DSM-5 uses the three symptoms
What are the subtypes of Anorexia nervosa?
1) Restricting- weight loss through diet, excessive exercise, and fasting within the past three months.
2) Binge type/purging- alternate with purging, with the misuse of laxatives, self-induced vomiting, diuretics or enemas in the past three months.
What are the ratio, onset, and stressor of Anorexia nervosa?
Ratio: females to males (10:1)
Onset: 13-18 years old
Stressors: leaving home or university are examples
What is the prognosis of Anorexia nervosa?
6x as many deaths were expected for females with Anorexia nervosa. The highest mortality rate of all mental disorders. Amenorrhoea (lack of menstruation). High prevalence of the disorder in high-income countries. Dahlgren et al. (2017), the lifetime prevalence rate for females ranged from 1.7%-3.6% and was 0.1% for males.
What are some examples of secondary symptoms of Anorexia nervosa?
Brittle nails, amenorrhoea (lack of menstruation), hair thinning, dry flaky skin, osteoporosis (weaken bones)
What is co-mobility and what is co-mobility for Anorexia nervosa?
Co-mobility is the presence of another/more mental disorder in someone. Anorexia nervosa usually also shows anxiety, depression, and OCD
What is the strength of the diagnosis of Anorexia nervosa?
DSM-5 is reliable. Sysko et al. (2012) measured the test-retest reliability of Anorexia nervosa diagnosis, participants were given a telephone interview, and between three and seven days later, a different assessor telephoned each participant and repeated the assessment. The extent of agreement across the two occasions was described as ‘excellent’. Trained assessors can reliability diagnose AN using the DSM-5 criteria.
What is the competing argument for the strength of the diagnosis of Anorexia nervosa?
Doesn’t support that the view DSM-5 criteria are reliable. Thomas et al (2015) most studies go beyond the official DSM-5 criteria in operationally defining AN. Researcher- defined cut-off point for ‘significantly low weight’ because none is specialised in the DSM-5. Research studies are higher than what they would be in real life (easier to achieve agreement between raters when criteria are defined in detail)
What is a weakness of the diagnosis of Anorexia Nervosa?
The lack of validity. Smith et al (2017) looked at the validity of four severity specifiers. 109 adults diagnosed with AN, higher BMI was linked with greater eating disorders psychopathology. Opposite of what was expected outcomes. Failed to distinguish accurately between people.
What is EPHX2?
It is a gene that codes for an enzyme called epoxide hydrolase that breaks down (metabolises) cholesterol and if there is a fault, the enzyme will misshape and disrupt the metabolism of cholesterol as the cholesterol can’t bind to the enzyme, causing higher chronic cholesterol. This can cause people not to be reminded to eat. Found by Scott-Van Zeeland
What is ITPR3 and how does this affect Anorexia nervosa?
It is a gene that encodes for a protein which is the receptor for inositol triphosphate (detecting sweet and bitter tastes). Dysfunction of the taste pathway so people with AN are indifferent to tastes that others enjoy and that partly motivates eating. A dysfunction causes a misshape of the receptor, so serotonin can’t bind. Found by Scott-Van Zeeland with 1205 AN participants and 1948 control participants
What are the 4Ds of diagnosis?
Deviance
Dysfunction
Distress
Danger
What is deviance?
Behaviours that are unusual. Understand the statistical and social norms of particular social groups and cultures. Failure to conform to social norms can lead to negative attention
What is dysfunction?
Inability to do everyday activities. Looks at what is going on around them and their deterioration.
What is distress?
Emotional pain or anxiety and this may manifest in physical symptoms. Gather quantitative data using scales like Kessler Psychological Distress Scale (K10), which is a 10-item self-report questionnaire taken over 4 weeks.
What is danger?
Careless, hostile, or hazardous behaviour which could jeopardise the safety of the individual and/or others. People could be detained under the Mental Health Act which requires the agreement of 3 professionals and people are taken to a mental health hospital for treatment.
What is the supporting evidence for the 4D model?
It is valid as it is not over or under inclusive like the deviance from social and statistical norms are used with another 4D. However, subjective like cultures in Fiji praise curvy shapes over slimmer ones like in the west.
How does the 4D model lack reliability?
Distress is objective and people may show distress in different ways. However, quantitative data can be gathered with the Kessler Psychological Distress Scale (K10).
How does the 4D model affect labelling?
By labelling someone as dangerous then people are less likely to get diagnosed. It could also have an effect on a ‘self-fulfilling prophecy’ as their behaviour may become dangerous from being labelled dangerous. But labelling doesn’t cause danger.
What is the DSM?
It is made by the American Psychiatric. There are 3 sections. Section 1 is about the guidance of the system. Section 2 gives details of the disorders. Section 3 is a section on new disorders. It is a ruling of best fit and rules out other disorders. It is done by observation and unstructured interviews with Beck Depression Inventory with 21 questions.
What is the kappa score (overall)?
The test is then retested later on or by another clinician. 0.7 felt like a good score.
What are the different types of validity?
Descriptive (symptoms), aetiological (causal factors), concurrent (method), and predictive.
What is the reliability of DSM?
Good. Field trials of DSM-5- kappa score of 0.46 (Regier) and Sartorius= 0.86 of schizophrenia (consistent)
What happens to the agreement (increase/decrease) of the DSM?
The agreement falls (Cooper). Least reliable in the major depressive disorder of the DSM.
Why was the DSM-III better than the DSM-5?
Kupfer and Kraemer (2012) found that the DSM-5 field clinicians say they would ‘work as they usually would’. DSM-III used careful testing and retesting.
What is the validity of the DSM?
Kim-Cohen concurrent validity of conduct disorder as they got interviews from mothers and children, observing children’s anti-social behaviour and questionnaires from teachers. The predictive validity to give accurate treatment.
Why is there low validity in the DSM?
Co-mobility and illness share similar symptoms. There are also cultural variations. Rastafarians- neologism (new words) clinicians may not be aware of this.
What is the ICD?
It involves mental and physical disorders created by the WHO. It is multilingual and is mostly used in the UK. Used by policymakers and organisations. Chapter 5 focuses on mental disorders and is coded as F with F20-F29 representing schizophrenia, schizotypal and delusion disorders. Each section has leftover code allowing new disorders to be added. Comprehensive and inclusive enough without overlap. Clinicians select keywords from interviews like hallucinations a go by alphabetical index or straight to the section.
What is the dopamine hypothesis?
Excitatory neurotransmitters as it increases the likelihood of the next neurotransmitter firing. This is known as the ‘feel-good’ hormone.
What is hyperdopaminergic and how does this impact schizophrenia?
The excess of dopamine. Schizophrenia patients have too much dopamine as it is firing to easily and too often.
What are amphetamines and their effect on non-schizophrenia people?
Increase dopamine energy (drug)- mode of action on dopamine. If a ‘normal’ (non-schizophrenia) person took amphetamines they would experience similar symptoms to a schizophrenia patient like hallucinations. We infer that schizophrenia is the result of excess dopamine.
What do antipsychotics do to dopamine and people with schizophrenia?
It decreases dopamine levels by binding to the postsynaptic receptors neurone which then dopamine can’t bind to the receptors and is then taken up by the reuptake channel. This means the action potential can’t be triggered. The dopamine is displaced and left in the synaptic cleft. This reduces schizophrenia symptoms by acting on dopamine the cause of dopamine is excess dopamine.
What does reduced beta hydroxylase?
The enzyme that breaks down dopamine, if there is less of this then dopamine is more likely to bind to the postsynaptic receptors and then trigger more action potential.
What does the proliferation of D2 receptors do?
If there are more receptors then it is more likely to fire.
What did Davis et al. find with hyperdopaminergic?
It causes positive symptoms, which is adding to someone’s normal function like delusions, disordered thinking, hallucinations, and thought insertion. This is in the mesolimbic pathway (reward pathway)
What did Davis et al. find out about hypodopaminergic?
It causes negative symptoms, which are taking away someone’s normal function like the flat effect, which reduces the range of emotions, and alogia, which is a poverty of speech in catatonic schizophrenia. In the mesolimbic pathway (wakefulness)
What is serotonin?
An inhibitory neurotransmitter
What did Carlsson et al. (2000) find out about serotonin?
Carlsson et al. did a meta-review which analyses the findings of other research on neurotransmitters (secondary data). He found that Clozapine binds to the D1 and D4 receptors but only weakly to the D2 receptors to reduce positive symptoms. Based on existing knowledge D2 is important for schizophrenia. The study suggests this is reductionist as D2 doesn’t work with Clozapine. It also binds with serotonin reducing positive and negative symptoms. Focusing on the interaction between neurotransmitters as serotonin regulates dopamine in the mesolimbic pathway- reward pathway.
What are the 4 key symptoms for schizophrenia?
Thought insertion, hallucinations, delusions, disorganised thinking.
What are the features of schizophrenia?
It has a lifetime prevalence which is 0.3-0.7%. This varies with the ethnicity, nationality and geographic origin of immigrants. Onset is slightly earlier in males than females (early to mid-20s vs late 20s). Males tend to have a poorer prognosis than females. Females are overrepresented in late-onset cases (40+). The prognosis is variable and hard to predict. A minority recover completely, but most experience chronic, episodic impairment and some show progressive deterioration, with increasingly brief periods of remission and severe cognitive deficits. Positive symptoms reduce over time but debilitating negative symptoms often remain.
What is the strength of the diagnosis of schizophrenia?
Made to a high degree of certainty with both the DSM-5 and ICD-10. Field trials of the DSM-5 reported a kappa of 0.46 (good)- Regier et al. 2013- Sartorius et al. 1995- 0.86 kappa score (very good). Only 3.8% of clinicians said they lacked confidence in their diagnosis of schizophrenia using the ICD-10. Schizophrenia is sufficiently detailed and distinguishes other disorders with the same symptoms and features.
What is a weakness of the diagnosis of schizophrenia?
The diagnosis of schizophrenia is not easy as it shares symptoms with various disorders. For example, hallucinations can be experienced by people with depression and post-traumatic stress disorder and can be caused by drug withdrawal, metabolic disorders and sleep deprivation while catatonic behaviour can be symptomatic of major depression or bipolar disorder.
How does culture affect the diagnosis of schizophrenia?
If the client is from a different background than the psychiatrist. Rastafarians often use neologism (new words) which is a play on words like ‘overstand’ for ‘understand’, and a clinician who is unaware of this may see this as a sign of disordered thinking. This means that the diagnosis of schizophrenia requires awareness and sensitivity to culture and linguistic differences.
What did Luhrmann et al. (2015) find out regarding culture?
Interviewed 60 Americans, Indian and Ghanaian people with schizophrenia. They found that 70% of the American people said their voices told them to hurt people while 50% of Ghanaians said their voices were mainly positive.
Classic study: Rosenhan (1973)- Aims
Show the flaws in the process of psychiatric diagnosis. Demonstrated the psychiatrists were unable to distinguish the ‘sane from the insane’ and aimed to provide evidence to support the idea that mental disorders lie not with individuals but with the person making the diagnosis. He gained access to psychiatric wards as a patient and obtain information about how clients/patients were treated by staff and each other.
Classic study: Rosenhan (1973)- Sample
A psychology student, paediatrician, psychiatrist, painter, housewife and three psychologists (3 females and 5 males including Rosenhan)
Classic study: Rosenhan (1973)- Procedure
Each person took on the role of a pseudo-patient (fake). Each person presented themselves at a psychiatric hospital complaining of the same symptoms; hearing same-sex, an unfamiliar voice that was unclear but said ‘empty’, ‘hollow’ and ‘thud’, terms not normally linked to schizophrenia. They gave false information. They approached 12 hospitals in 5 different states and once they were admitted they would behave normally following a period of unsurprising nervousness. In order to be released they had to convince the staff that they were sane by cooperating and following orders. They observed.
What was the follow-up study of the classic study Rosenhan?
The hospitals were told to expect pseudo-patients (fake patients) but none were sent. The staff at the hospitals were to rate every patient from 1-10 (with 1 being that the patient was fake.
What was the mini study of Rosenhan?
Pseudo-patients approached a staff member on the hospital grounds and asked a polite question about their release. Responses were compared with a similar encounter of that between people on the Stanford University Campus.
What were the findings of the initial study?
All pseudo-patients were admitted (seven with schizophrenia and one with bipolar disorder), most released with ‘schizophrenia in remission’. The length of stay was between 7 to 52 days, with 19 being the average. 30% of real patients were suspicious of the pseudo-patients
What were the findings of the follow-up study?
41/193 patients were wrongly reported as fake by at least one member of staff, 23 by at least one psychiatrist and 19 by one member of staff and then one psychiatrist.
What were the findings of the mini-experiment?
4% of pseudo-patients received an answer from a psychiatrist and 0.5% form a nurse. 100% of people on campus stopped and talked.
What were the findings of the mini-experiment?
4% of pseudo-patients received an answer from a psychiatrist and 0.5% form a nurse. 100% of people on campus stopped and talked.
What was the conclusion of Rosenhan’s study?
‘We cannot distinguish the sane from the insane in psychiatric hospitals’
The hospital environment created situational factors leading to depersonalisation and segregation. Overdiagnosis occurred because clinicians avoided calling a sick person healthy. But in the follow-up study, staff erred in the opposite direction to avoid calling a healthy person sick.
What is the strength of Rosenhan’s study (in terms of design)?
Used covert participant observation and collected both qualitative and quantitative data. Staff were unaware the pseudo-patients were researchers, so their behaviour would have been more natural. Therefore, the data had high ecological validity, enhanced by the wealth of the data collected by naturalistic observation.
What is a counter-argument to the strength of Rosenhan’s study?
It could be argued that the validity of the study is poor. Pseudo-patients may have only recorded instances of negative interaction between staff and patients as they were all supporters of Rosenhan. Only one pseudo-patient per hospital so there is no way to check the reliability of the data collected.
What is a weakness of Rosenhan’s study?
Demand characteristics may explain the diagnosis. Psychiatrists admitted pseudo-patients on flimsy evidence because they didn’t expect someone to fake symptoms. They would assume anyone seeking admission must have a good reason to. This may challenge some on the validity of the conclusions.
What is the strength of Rosenhan’s study (in terms of support for the anti-psychiatry movement)?
Szasz (1960) argued that mental illnesses are problems in living not diseases, and therefore it is inappropriate to use a medical model for the diagnosis of mental illness. Rosenhan supports this as it showed that the diagnosis of mental state was invalid. He also argued that labels for mental illness, once given, were ‘sticky’ so patients would forever be labelled ‘schizophrenic’. Shows that psychiatry needs to be reformed, to avoid the misuse of diagnostic labels. A behavioural approach to avoid labels.
What is the issues and debates that relates to Rosenhan’s study?
Ethics- long-term benefits to society but there were risks to the pseudo-patients, clinicians and real patients. For example, the clinicians were made to feel incompetent and real patients may have been discriminated against if clinicians believed they were fake (psychological harm)
What is the application of Rosenhan’s study?
Spitzer saw the DSM-III revision as an opportunity to address the issues raised by Rosenhan, It arguably paved the way for critical reform to the diagnosis process, though it was not Rosenhan’s intention.
What was the aim of the contemporary study: Carlsson et al. (2000)?
Review evidence for and against the dopamine hypothesis. Consider other neurotransmitters (glutamate, serotonin). Explore new antipsychotics (help with treatment resistance)
What was the first point Carlsson made (contemporary study) - dopamine hypothesis revisited?
Evidence still supports this hypothesis, e.g. studies using PET scans show how amphetamine (dopamine agonist) enhances psychotic symptoms. But still doesn’t apply to all people with schizophrenia.
What was the second point Carlsson made (contemporary study) - beyond dopamine?
Glutamate -PCP (‘angel dust’) induces schizophrenia symptoms, an antagonist (stops glutamate) of NDMA (glutamate) receptors. This leads to increase dopamine activity (acts as an accelerator).
What was the third point Carlsson made (contemporary study) - glutamatergic control of dopamine?
Glutamate also affects the release of GABA, with the opposite effect (a ‘brake’, reducing dopamine activity). Therefore low glutamate (hypo glutamatergic) may cause an increase or decrease in dopamine. Normally, there is a balance between ‘accelerator’ and ‘brake’ but the distribution of either can produce schizophrenia-like symptoms
What was the fourth point Carlsson made (contemporary study) - glutamate-dopamine interaction?
Hypo-glutamatergic in cerebral cortex –> negative symptoms
Hypo-glutamatergic in basal ganglia –> positive symptoms
Dopamine + glutamate pathways interact and affect the striatum.
What was the fifth point Carlsson made (contemporary study) - thalamic filter?
It is suggested that the psychotogenic pathway the thalamus may be ‘turned’ on or off depending on which pathway is activated. Normally the inhibitory glutamate pathway dominates.
What was the sixth point Carlsson made (contemporary study) - comparing two experimental schizophrenia models?
- Hyperdopaminergic model - the traditional view of dopamine (increase produces psychotic symptoms) is not challenged by the second model, merely extended.
- Hypoglumatergic model - glutamate can increase or decrease dopamine activity, depending on whether an accelerator or brake is applied.
Haloperidol tackles hyperdopaminergic, and M100907 tackles hypoglutamatergia (affecting GABA via serotonin). People with different symptoms could be treated with different drugs. Or use combined drugs to tackle both problems.
What was the seventh point Carlsson made (contemporary study) - is the therapeutic exhausted?
Understanding mechanisms that moderate dopamine activity may show new ways to stabilise the dopamine system. May avoid some negative effects of current antipsychotics.
What was the eighth point Carlsson made (contemporary study) - concluding remarks?
More attention could be focused on other neurotransmitters (e.g. acetylcholine) and other pathways in the brain.
What is the strength of Carlsson’s study (2000) - research?
Carlsson and Carlsson (1989) gave mice a drug to reduce motor activity followed by MK-801 (reduces glutamate and increases serotonin and dopamine in the nucleus accumbens) MK-801 restarted motor activity but continued to use highly abnormal, psychotic-like behaviour. This suggests that schizophrenia may be caused by glutamate irregularity and also implies that glutamate agonists may be effective treatments.
What is the counterargument for the strength of Carlsson’s study (research)?
This is not the full story. Since the study, two further neurotransmitters (anandamide and nitric oxide) have been identified as important in psychosis and may lead to new treatments (Crippa et al. 2015). It has also been suggested that neurotransmitter imbalances may arise from autoimmune problems (Severance et al. 2018) - this means even glutamate is not the end of the story.
What is a weakness of Carlsson’s study (culture)?
Luhrman (2015) showed that the US participants were more likely to hear violent and frightening voices whereas Ghanaian and Indian people had more positive experiences. It may be that the review didn’t include cultural factors because of conclusions in the reviews are based on animal models. Thus animal models may fail to capture holistic lived experience of schizophrenia, which includes other people’s reactions to their symptoms (truer reflection)
What is a weakness of Carlsson’s study (experiences)?
Some evidence of the dopamine hypothesis was based on people with schizophrenia during acute periods. But people with chronic schizophrenia may respond differently to drugs when they are between episodes (e.g. more side effects). Therefore, research should consider all the phases of the disorder so better conclusions can be made about efficiency and adherence.
What are the issues and debates related to this study?
Gender. On the average most onset of schizophrenia is later in women than it is for men and the prognosis is generally more positive. The main female sex hormone oestrogen has a neuroprotective role, which helps regulate glutamate, serotonin and dopamine (Gogos et al. 2015). This suggests that gender-related oestrogen-based medications may provide yet another pathway for treating schizophrenia.
What is the application of Carlsson’s study?
Development of new drug treatments. Serotonin antagonists and glutamate agonists are effective in reducing both positive and negative symptoms. By tackling more precisely the disturbances of neurotransmitter systems, their action is less likely to have detrimental effects. These advances have helped people who were treatment-resistant or who experienced side effects (e.g. tardive dyskinesia)
What is the strength of the diagnosis of Anorexia nervosa?
DSM-5 is reliable. Sysko et al. (2012) assessed participants by telephone interview using the DSM-5 criteria for AN and repeated this with a different assessor a few days later. The extent of agreement across the two occasions (test-retest reliability) was described by the researcher as ‘excellent’. This suggests that trained assessors can reliably diagnose AN using the DSM-5 criteria.
What is the counterargument for the strength of the diagnosis of Anorexia nervosa?
This does not necessarily support the view that the DSM-5 criteria for AN are reliable. Thomas et al (2015) point out that many studies go beyond the DSM-5 criteria defining AN. Many use a researcher-defined cut-off point for ‘significantly low weight’ because none is specified in the DSM-5. This means that reliability estimates in research studies are likely to be higher than they would be in real-life clinical practice.
