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What are the three broad features used to define mental disorder?
Distress, dysfunction, and deviance.
Which classification systems are commonly used to diagnose mental disorders?
ICD-11 and DSM-5.
What is schizophrenia?
A severe mental disorder involving disturbances in thought, perception, emotion, and behaviour, especially a loss of contact with reality.
What are the main symptom categories of schizophrenia?
Positive, negative, cognitive, disorganised, and affective symptoms.
What are positive symptoms of schizophrenia?
Abnormal experiences added to normal function, such as delusions, hallucinations, and catatonic behaviour.
What are negative symptoms of schizophrenia?
Loss or reduction of normal functions, including affective blunting, alogia, anhedonia, avolition, and asociality.
What are cognitive symptoms of schizophrenia?
Impaired attention, working memory, episodic memory, and processing speed.
What is needed for a diagnosis of schizophrenia?
At least two key symptoms for most of one month, continuous disturbance for at least six months, dysfunction, and exclusion of mood, substance, or medical causes.
What is the dopamine hypothesis of schizophrenia?
It proposes that abnormal dopamine signalling contributes to schizophrenia, especially excess dopamine activity linked to psychosis.
What is the role of the mesolimbic pathway in schizophrenia?
It is thought to be hyperdopaminergic and is associated with positive symptoms such as hallucinations and delusions.
What is the role of the mesocortical pathway in schizophrenia?
It is thought to be hypodopaminergic and is associated with negative and cognitive symptoms.
Why do D2 antagonist antipsychotics mainly improve positive symptoms?
Because they reduce excess dopamine signalling in the mesolimbic pathway, but may also worsen low dopamine signalling in the mesocortical pathway.
Why may D2 partial agonists such as aripiprazole be useful in schizophrenia?
They can reduce dopamine signalling where it is too high while partially stimulating receptors where dopamine is too low.
What is the glutamate hypothesis of schizophrenia?
It suggests that NMDA receptor hypofunction contributes to schizophrenia, particularly by disrupting excitatory-inhibitory balance.
How can NMDA receptor hypofunction contribute to schizophrenia?
Reduced NMDA activity on GABA interneurons decreases inhibition, causing disinhibition of excitatory pathways and increased downstream dopaminergic activity.
Why is schizophrenia considered a neurodevelopmental disorder?
Because many risk genes act during brain development and abnormal development may create vulnerability long before symptoms appear.
Why does schizophrenia often emerge in late adolescence or early adulthood?
Because this is a critical period of ongoing prefrontal cortex development and synaptic pruning.
What is synaptic pruning and why is it relevant to schizophrenia?
Synaptic pruning is the removal of excess synapses during development; excessive or abnormal pruning may contribute to schizophrenia.
What is the role of microglia in schizophrenia?
Microglia are brain immune cells involved in inflammation and synaptic pruning, and increased microglial activation is linked to schizophrenia.
What evidence supports a genetic contribution to schizophrenia?
Twin studies show higher concordance in monozygotic than dizygotic twins, and GWAS studies have identified many schizophrenia risk loci.
Name some environmental risk factors for schizophrenia.
Prenatal infection, poor prenatal nutrition, obstetric complications, and adolescent cannabis use.
What are the two broad types of mood disorder mentioned in the lecture?
Depressive disorders and bipolar disorder.
What are the two core symptoms required for Major Depressive Disorder?
Low mood and/or loss of interest or pleasure (anhedonia).
How long must symptoms usually last for a diagnosis of MDD?
At least two weeks, nearly every day and most of the day.
Name four common additional symptoms of MDD.
Sleep disturbance, appetite or weight change, fatigue, poor concentration, guilt or worthlessness, psychomotor change, and suicidal thoughts.
Why must mania or hypomania be ruled out before diagnosing MDD?
Because a history of mania or hypomania suggests bipolar disorder rather than major depressive disorder.
What is the classical monoamine theory of depression?
It proposes that depression is linked to abnormalities in monoamine neurotransmitters, especially serotonin, norepinephrine, and dopamine.
What newer idea about depression is highlighted in the lecture?
That depression may involve neural circuit dysfunction and excitation-inhibition imbalance, including reduced GABAergic function.
What are SSRIs and how do they work?
Selective serotonin reuptake inhibitors; they block serotonin reuptake and increase serotonin levels in the synaptic cleft.
What are SNRIs?
Serotonin-norepinephrine reuptake inhibitors that block reuptake of both serotonin and norepinephrine.
Why are TCAs and MAOIs less commonly used today?
Because they have more side effects and can be dangerous in overdose.
Why is ketamine important in depression treatment?
It is a rapid-acting antidepressant that blocks NMDA receptors and promotes glutamate-related synaptic plasticity.
What are two advantages and two disadvantages of ketamine in MDD?
Advantage: rapid action; may help treatment-resistant depression. Disadvantage: tolerance/addiction risk and possible psychosis.
What is ECT used for in depression?
It is mainly used for treatment-resistant depression and can be more effective than medication in some patients.
Name some psychological treatments for MDD.
Cognitive therapy, mindfulness-based cognitive therapy, interpersonal psychotherapy, behavioural activation, and couples therapy.
What are iPSCs?
Induced pluripotent stem cells made by reprogramming adult cells into stem-like cells that can become neurons or brain organoids.
What are brain organoids?
Three-dimensional mini brain-like structures derived from human stem cells that model aspects of brain development and disease.
Why are brain organoids useful in psychiatric research?
They allow study of disease mechanisms, human-specific development, drug screening, biomarker discovery, and personalised medicine.
What schizophrenia-related phenotype was shown in patient-derived organoids in the lecture?
Disrupted cortical layer formation in organoids derived from a patient with a DISC1 mutation.