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A comprehensive set of practice flashcards covering schizophrenia, anorexia nervosa, biological/psychological explanations, therapies, and related research from the notes.
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What is schizophrenia as defined in the notes?
A psychotic disorder marked by severely impaired thinking, emotions and behaviours, with sufferers often unable to filter sensory stimuli and may have enhanced perceptions.
What are positive symptoms?
Symptoms that add to normal experience, such as hallucinations and delusions.
What are negative symptoms?
Loss or reduction of normal experiences, such as speech poverty and avolition.
What are hallucinations?
Distorted perception of real stimuli or perceptions of stimuli with no basis in reality; often auditory and linked to dopamine in Broca's area.
What are delusions?
Fixed, false beliefs not grounded in reality; types include persecutory, grandeur, jealousy, erotomania, somatic.
What is speech poverty?
Abnormally low frequency/quality of speech; derailment due to central control dysfunction.
What is avolition?
Subjective reduction in interests, desires and goals and a behavioural reduction in self-initiated acts.
What are the two main classification systems for mental disorders?
DSM-V and ICD-10.
What are the DSM-V criteria for schizophrenia?
At least 2 of delusions, hallucinations, disorganized speech and catatonic symptoms, lasting for at least 1 month.
What are the ICD-10 criteria for schizophrenia?
Clinical picture dominated by relatively stable, often paranoid delusions, usually with hallucinations.
What is a major difference between DSM and ICD criteria?
Different organizations (APA vs WHO), differing numbers and specificity of symptoms, and recognition of subtypes.
What are schizopheria subtypes mentioned in the notes?
Positive schizophrenia with prominent delusions/hallucinations; mixed schizophrenia with mixed or neither prominent; subtypes recognized in ICD-10.
What is co-morbidity in schizophrenia?
High co-occurrence with other disorders; e.g., PTSD and depression are relatively common among SZ patients.
What did Gottesman’s concordance rates show?
Genetic basis suggested by higher concordance in monozygotic twins (about 48%) than dizygotic twins (about 17%), with environmental influences also present.
What did Ripke et al. 2013 find?
Genome-wide study identifying 22 risk loci for SZ; 13 new; indicates SZ is polygenic with many candidate genes.
What is the original dopamine hypothesis?
SZ caused by hyperdopaminergia in subcortical areas.
What is the revised dopamine hypothesis?
SZ involves both hyperdopaminergia and hypodopaminergia in different brain areas; cortex involvement matters.
How is Broca’s area involved in SZ symptoms?
Hyperdopaminergia with excess D2 receptors in Broca's area may contribute to auditory hallucinations.
What is the link between the prefrontal cortex and negative symptoms?
Hypodopaminergia in the prefrontal cortex linked to speech poverty and avolition.
What neural correlate is linked to avolition?
Low activation in the ventral striatum associated with impaired reward evaluation and motivation.
What did Allen et al. (2007) find about self-generated speech?
Misidentification of self-generated speech linked to abnormalities in the anterior cingulate and left temporal cortex.
What did Brown et al. (2002) find about paternal age?
Offspring risk of SZ increases when the father is over 50 years old, suggesting genetic/biological factors.
What are typical antipsychotics and give an example?
First generation dopamine antagonists; e.g., chlorpromazine; often sedative due to actions on other receptors.
What are atypical antipsychotics and give examples?
Second generation drugs with broader receptor targets; e.g., clozapine and risperidone; fewer motor side effects.
What is special about clozapine?
Effective for treatment-resistant SZ and can improve cognitive functioning and mood, but risks agranulocytosis.
What is a key risk of clozapine requiring monitoring?
Agranulocytosis, a dangerous drop in white blood cells.
What is a key advantage of risperidone?
Effective dopamine antagonism at lower doses, useful for patients with less depression or blood-related history.
What is neuroleptic malignant syndrome (NMS)?
A serious, potentially fatal reaction to antipsychotics with fever, rigidity and autonomic dysfunction.
What is the third-variable problem?
Correlational evidence cannot establish causation because a third unmeasured factor could influence both variables.
What is CBT for schizophrenia?
Therapy to understand and challenge delusions/hallucinations, reduce distress, and improve coping rather than cure.
What is family therapy for schizophrenia?
Aims to reduce expressed emotion and family stress, improving medication adherence and relapse prevention.
What is token economy in schizophrenia treatment?
Behavioral system using tokens as secondary reinforcers for desirable behaviours, exchangeable for rewards.
What are ethical concerns with token economies?
Privileges vs rights, potential harm for severe patients, autonomy concerns, and possible coercion.
What is an interactionist approach to treatment?
Combines biological therapies for distal causes with psychological therapies for proximal symptoms.
What are the DSM-IV criteria for anorexia nervosa (A/B/C)?
A: weight loss with BMI below 85%; B: intense fear of gaining weight; C: disturbance in body weight/shape perception and denial of seriousness.
What do twin studies suggest about anorexia nervosa?
High heritability with concordance rates in monozygotic twins much higher than dizygotic twins; estimates vary widely.
What is the EPHX2 gene finding related to anorexia nervosa?
Scott-Van Zeeland 2014 reported variants in EPHX2 associated with AN and BMI relationships; indicates genetic involvement.
What is the serotonin role in anorexia nervosa?
Disturbances in serotonin linked to symptoms; high levels associated with anxiety; SSRIs often ineffective for AN.
What is the dopamine role in anorexia nervosa?
Increased dopamine activity in basal ganglia affects reward processing and may relate to food restriction and anxiety.
What is limbic system dysfunction in anorexia nervosa?
Dysfunctions in emotion-regulation circuits may contribute to AN pathology.
What is deep brain stimulation for anorexia nervosa?
Experimental treatment targeting the nucleus accumbens showing some BMI improvements in small studies.