9 - Psychiatric Conditions Flashcards

1
Q

Schizophrenia

A
  • 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
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2
Q

Stages of Schizophrenia

A
  • 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
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3
Q

Stigma associated with Schizophrenia

A
  • increased family stress
  • reduced employability
  • poverty
  • homelessness
  • difficulty obtaining housing
  • shame
  • physical, verbal abuse
  • suicide
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4
Q

Heritability of Schizophrenia

A
  • 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

but:

  • 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
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5
Q

Common disease-common variant
vs
Common disease-rare variant

A

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

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6
Q

Environmental Factors

A
  • 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
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7
Q

Developmental triggering

A

via pruning, where only the essential neuron connections are kept

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8
Q

Anatomical changes in SZ

A
  • reduction in grey matter
  • increased ventricular size (15%)
    > associated with poor cognition and drug unresponsiveness
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9
Q

Dopamine pathways in SZ

A
  • increased mesolimbic pathway is linked to positive symptoms
  • decreased mesocortical pathway is linked to negative and cognitive symptoms
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10
Q

Glutamate and SZ

A
  • 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
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11
Q

Serotonin and SZ

A
  • linked to negative effects

- modulates dopamine

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12
Q

Acetylcholine and SZ

A
  • cigarette use is 90% in SZ patients (compared to 33% normally)
  • nicotine improves working memory and selective attention, withdrawal exacerbates cognitive impairments
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13
Q

Pharmacological treatment of SZ

A

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
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14
Q

Psychosocial Treatments for SZ

A
  • CBT
  • Psychoeducation programs
  • Family intervention
  • Social skills training
  • Case management
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15
Q

Affective disorders

A
  • 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
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16
Q

Basis of Depression

A

Biological:

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

Psychological:

  • negative explanatory style
  • learned helplessness
  • gender differences

Socio-cultural:

  • 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

17
Q

Basis of bipolar

A
  • monozygotic concordance rate of 0.43
  • heritability is 58%

Genetic factors:

  • WFS1 (insulin deficiencies)
  • FKBP5 (cortisol)
  • CRH (cortisol)

Environmental risk factors:

  • asthma
  • IBS
  • Obesity
  • childhood adversity
  • head injury

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

18
Q

Stress hormones (cortisol) and mood disorders

A
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
19
Q

Monoamines and mood disorders

A
  • 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
20
Q

Neurotrophic factors and mood disorders

A

BDNF = Brain Derived Neurotrophic Factors

- stress reduces BDNF and anti-depressants increase BDNF

21
Q

Drug treatment for depression

A

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]

22
Q

Treatment for bipolar

A

Mood stabilisers
- lithium

Anticonvulsants

Antipsychotics