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Flashcards in 9 - Psychiatric Conditions Deck (22):


- Chronic mental illness
- affects 1% of the population
- males:
> earlier onset (15-25 vs 30 in females)
> more severe conditon
> more pronounced brain abnormalities
> more resistant to treatment

Positive Symptoms (new):
- Hallucinations
- Delusions
- Disorganised Thoughts

Negative Symptoms (lack of characteristics that should be present):
- reduced speech (alogia)
- lack of emotional and facial expression (affective flattening)
- social withdrawal (asociality)
- decreased ability to enjoy themselves (anhedonia)

Cognitive Symptoms (deficits):
- memory
- attention
- planning
- decision making


Stages of Schizophrenia

- premorbid stage
- prodromal stage (brief positive symptoms)
- psychotic phase (indicated by the first psychotic episode) [many positive symptoms]
- stable phase (negative symptoms)

- 20% have only one episode, no impairment
- 35% have several episodes but no impairment
- 10% have impairment after the first episode with exacerbation afterwards
- 35% have impairment which gets worse after each episode


Stigma associated with Schizophrenia

- increased family stress
- reduced employability
- poverty
- homelessness
- difficulty obtaining housing
- shame
- physical, verbal abuse
- suicide


Heritability of Schizophrenia

- if a dominant gene, 2 affected parents would have 75% of an affected child
- if recessive they would have 100%

- actually the rates here are less than 50% so multiple genes are responsible, or some environmental factors also

- if 1 identical twin has schizophrenia, the other has 50% chance of having it
- thus it is not 1 single gene, but several implicating genes


Common disease-common variant
Common disease-rare variant

Common disease-common variant
- SZ is caused by a large number of genetic changes, each with a small effect

Common disease-rare variant
- SZ is caused by some rare but highly affective genetic changes


Environmental Factors

- winter birth (+5% risk)
- having a cat from a young age (+53%)
- complications at birth (+71%)
- living in urban environment (+85%)
- fever in pregnancy (+182%)

- prenatal infections
- perinatal hypoxia
- adolescent drug abuse
- stress

- causing altered gene expression


Developmental triggering

via pruning, where only the essential neuron connections are kept


Anatomical changes in SZ

- reduction in grey matter
- increased ventricular size (15%)
> associated with poor cognition and drug unresponsiveness


Dopamine pathways in SZ

- increased mesolimbic pathway is linked to positive symptoms
- decreased mesocortical pathway is linked to negative and cognitive symptoms


Glutamate and SZ

- low glutamate in CSF
- PCP and Ketamine Induce SZ-like symptoms in normal people and exacerbate them in SZs
- reduced NMDA receptor binding in patients
- glutamate also regulates dopamine


Serotonin and SZ

- linked to negative effects
- modulates dopamine


Acetylcholine and SZ

- cigarette use is 90% in SZ patients (compared to 33% normally)
- nicotine improves working memory and selective attention, withdrawal exacerbates cognitive impairments


Pharmacological treatment of SZ

Typical Antipsychotics
- block all D2 receptors
- reduces positive symptoms
- causes extrapyramidal side effects such as Tardive Dyskinesia (jerky uncontrolled movements of the face)
- increases prolactin, affecting lactation, menstruation and bone density

Atypical Antipsychotics
- less likely to produce extrapyramidal effects and tardive dyskinesia
- reduces positive, negative and cognitive symptoms
- block D2 receptors but with less affinity so are less potent

Side effects:
- metabolic syndromes (high bp, obesity)
- decreased white blood cells


Psychosocial Treatments for SZ

- Psychoeducation programs
- Family intervention
- Social skills training
- Case management


Affective disorders

- disorders that cause changes in mood
> severe mania severe depression

Bipolar Disorder:
- manic episodes and depressive episodes
- onset is late adolescence
- prevalence is 1%
- incidence is 4%
- 30% attempt suicide

Major Depression Disorder:
- prevalence is 15%
- incidence is 1%
- onset is early adulthood
- more prevalent in females only after 13y


Basis of Depression

- genetic predisposition
- changes in brain chemistry
- brain damage due to stress

- negative explanatory style
- learned helplessness
- gender differences

- traumatic events
- cultural expectations
- depression-evoked responses

Genetic Heritability:
- ranges from 17%-80%
- no significant genetic difference between genders, so maybe it's environmental or cultural

Environmental factors:
- in utero issues
- urban upbringing
- maltreatment
- bullying
- cannabis use
- stress
- many risk factors overlap with generalised anxiety disorders
- environment-gene interaction:
> during early life there are periods of rapid brain growth in regions involved in emotion and the stress response, which are sensitive to stressors (amygdala, prefrontal cortex, hippocampus)

Genetic factors:
- serotonin transporter gene 5-HTT
> short allele means more susceptible to depression than the long allele


Basis of bipolar

- monozygotic concordance rate of 0.43
- heritability is 58%

Genetic factors:
- WFS1 (insulin deficiencies)
- FKBP5 (cortisol)
- CRH (cortisol)

Environmental risk factors:
- asthma
- Obesity
- childhood adversity
- head injury

Gene and Environment:
> personal illness, injury or assault
> marital separation or relationship issues
> serious problem with close friend or relative
> childhood abuse


Stress hormones (cortisol) and mood disorders

GR = Glucocorticoid Receptors (cortisol)
CRF = Corticotropin Releasing Factor
ACTH = Adrenocorticotropin Hormone

- there is increased Cortisol and CRF in the CSF of depressed people
- increased Cortisol in Cushing's disease causes depression
- there is decreased Hippocampal and Prefrontal Cortex volume in depressed people
> where GR (glucocorticoid receptors) are

- injecting CRF in rats induces depressive behaviours


Monoamines and mood disorders

- depressed people have lower levels of Serotonin
- 5HT genes linked to depression
- Tryptophan depletion (through diet) reduces synthesis of 5HT causing mood lowering in some
- Lithium (main treatment for bipolar) acts on serotonin receptors


Neurotrophic factors and mood disorders

BDNF = Brain Derived Neurotrophic Factors
- stress reduces BDNF and anti-depressants increase BDNF


Drug treatment for depression

MAO Inhibitors
- inhibit MAO enzyme preventing breakdown of noradrenalin, serotonin and dopamine

Tricyclic Antidepressants
- inhibit the reuptake of noradrenalin and serotonin
- linked to dementia if taken long term

Selective Reuptake Inhibitors
- inhibit reuptake of serotonin only (SSRIs) or serotonin and noradrenalin (SNRIs) [prozac]


Treatment for bipolar

Mood stabilisers
- lithium