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Sophie - Psychology for Medicine - Year 2 > 26.9 - Mood Disorders and Schizophrenia > Flashcards

26.9 - Mood Disorders and Schizophrenia Flashcards

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1
Q

What are mood disorders and what are the main ones?

A
  • Psychiatric diagnosis of low or elated mood with associated symptoms.
  • Main mood disorders: Depression and bipolar disorder
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2
Q

What makes mood disorders different from normal experience?

A
  • More intense
  • More persistent
  • Associated with functional impairment
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3
Q

Describe the classification of depression disorders.

[IMPORTANT]

A

NOTE: Dysthymic disorder is a type of chronic depressive disorder which is often less severe than acute depression.

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4
Q

What are the symptoms of unipolar depression?

A

Physical:

  • Changed appetite
  • Reduced energy
  • Reduced libido
  • Changed sleep pattern

Psychological:

  • Hopelessness
  • Helplessness
  • Low self-esteem
  • Guilt
  • Suicidality
  • Reduced motivation
  • Reduced interest
  • Reduced enjoyment (anhedonia)

There is often diurnal variation of mood (morning worst) and early morning wakening (=terminal insomnia).

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5
Q

Describe the prevalence of unipolar depression.

[IMPORTANT]

A
  • 6% 12 months
  • 15-18% lifetime risk
  • Varies internationally
  • Major worldwide cause of disability
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6
Q

Why does unipolar depression increase mortality?

A
  • Unnatural causes (e.g. suicide)
  • Natural causes
  • Comorbid substance use significantly increases risk
  • Comorbid physical health problems
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7
Q

What is the heritability of unipolar depression?

A

40%

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8
Q

How do life events contribute to unipolar depression?

A
  • 60-80% of people experienced a life event in the 6-12 months prior to first episode
  • Less prominent for subsequent episodes
  • There is likely to be a genetic-environment interaction
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9
Q

Describe gender differences in unipolar depression.

A

The ratio of female:male is 2:1

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10
Q

Draw a table of biopsychosocial factors in depression.

A
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11
Q

Give some example theories for why antidepressants take a couple of weeks to start working.

[EXTRA]

A

Neurochemical model:

  • When the drugs are started, the increase in synaptic serotonin is compensated for by increased pre-synaptic inhibition of the pre-synaptic neuron
  • Once these receptors are saturated, desensitisation occurs and thus there is increased serotonin concentration in the synapse that increases transmission

Cognitive neuropsychological theory:

  • When the drugs are started, there are immediate neurochemical changes
  • This enables new positive associations to be formed
  • These then result in a feeling better after a couple of weeks
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12
Q

What is the structure of a formal CBT program for unipolar depression?

A

Weekly individual sessions of 1 hour x 10-15 + homework

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13
Q

What are 3 big components of CBT for unipolar depression?

A
  • Behavioural activation -> Encouraging the individual to return to activities that bring them joy (e.g. going to the gym)
  • Combating automatic negative thoughts (ANTs) -> Identifying, challenging and replacing these thoughts
  • Combating cognitive errors -> These may include disqualifying positives, jumping to conclusions, catastrophising, etc.
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14
Q

What are some challenges of delivering CBT to patients with depression?

A
  • Depressive symptoms can reduce engagement
  • Non-cognitive maintaining factors e.g. alcohol
  • Accessibility
  • Willingness to engage
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15
Q

What is an interesting new development in terms of CBT for treating depression?

A

Computerised CBT:

  • May improve wellbeing
  • Guided approaches where there is a mix of in person and computerised CBT are likely to be more helpful
  • Recommended for mild-moderate anxiety and depression
  • High attrition rates
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16
Q

Give some experimental evidence for exercise as a treatment for depression.

[EXTRA]

A

(Schuch, 2016):

  • Found that exercise has a large and significant antidepressant effect in people with depression.
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17
Q

Draw how mood changes in bipolar disorder 1, bipolar disorder 2 and cyclothymia.

A

Note: In reality, the mood is much less stable than this and the pattern may not be as clear.

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18
Q

Compare bipolar 1 and bipolar 2.

A
  • Both feature elated mood, increased activity, grandiosity, decreased need for sleep, etc.
  • Bipolar 1 (mania)
    • Impairment in functioning
    • Lasts for more than 1 week
  • Bipolar 2 (hypomania)
    • Change in functioning that is uncharacteristic of the person when not symptomatic. Observable by others.
    • Lasts for more than 4 days
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19
Q

What is rapid cycling bipolar disorder?

A
  • Bipolar where there are at least 4 episodes a year.
  • Patients are much more likely to be in depressed rather than manic phase
  • Treatment is more difficult
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20
Q

Is psychosis part of bipolar?

A

It can be.

21
Q

Do depressive or manic symptoms dominate in bipolar disorder?

A

Depression

22
Q

What is the average delay to diagnosis of bipolar depression?

A

10 years -> This is largely due to mis-diagnosis as unipolar depression.

23
Q

Draw a table of biopsychosocial factors in bipolar disorder.

A
24
Q

Draw a diagram to summarise the pathogenesis of bipolar disorder.

A
25
Q

Describe the suicide risk in bipolar disorder.

A

50% of individuals will attempt.

26
Q

Describe the treatment of mania in bipolar disorder.

A
27
Q

Describe the treatment of depression in bipolar disorder.

A
28
Q

Describe the maintenance treatment in bipolar disorder.

A
29
Q

What evidence is there for schizophrenia being a neurodevelopmental disorder?

A
  • Risk factors are mostly pre- or perinatal
  • ‘Pre-schizophrenic’ children are already impaired in motor, behaviour, and intellectual functions
  • Absence of neurodegeneration
30
Q

To what extent is schizophrenia a genetic condition? Why?

A
  • Definite genetic component - if both parents have scz, your risk is 40%, if identical twin has it, your risk is 60%
  • There is no single gene, but many genes with small effects that altogether increase risk
31
Q

What is the dopamine hypothesis?

A

Excess dopamine underlies positive schizophrenia symptoms
While cognitive and negative symptoms may be due to insufficient dopamine

32
Q

What do fMRI studies show about brain activity in people with schizophrenia?

A
  • Hypofrontality: frontal lobes not as active as normal
  • Failure to activate prefrontal cortex during working memory
33
Q

What are some structural brain changes seen in schizophrenia? How can anti-psychotics further modulate the structure?

A
  • Ventricular enlargement
  • Decreased brain volume and weight:
    smaller volume of cortex, grey matter, hippocampus, thalamus
  • Due to anti-psychotics: larger basal ganglia
34
Q

What are some environmental risk factors for schizophrenia?

A
  • Birth complications
  • Maternal issues - infection, malnutrition
  • Living in urban areas
  • Older father
  • Migration
  • Childhood abuse
35
Q

How much of the population is affected by schizophrenia?

A

~1%

36
Q

Which group gets schizophrenia earlier and more severely - men or women?

A

Men

37
Q

What are examples of negative symptoms?

A
  • Social withdrawal
  • Poverty of speech (lack of conversation)
  • Cognitive deficits
  • Emotional blunting
38
Q

What is the difference between hallucinations and delusions? How are they similar?

A

Hallucinations = fixed false sensory perception without an external stimulus, usually auditory but can be any sensory modality

Delusions = false beliefs that are not culturally appropriate (e.g. religion might not be delusional)

Both are perceived as fully genuine and with complete conviction

39
Q

What are examples of positive symptoms?

A
  • Disordered thinking (disjointed, incoherent, stop and start of ideas)
  • Hallucinations
  • Persecutory ideas (others out to harm them)
  • Delusions
40
Q

What is the difference in duration of positive and negative symptoms?

A

Positive = acute, negative = chronic

41
Q

Schizophrenia is part of a wider group of disorders called…

A

Psychoses

42
Q

What is Schizophrenia?

A

Schizophrenia is a mental disorder that is diagnosed by the presence of two or more of the following symptoms for a significant portion of time during a one-month period:
Delusions
Hallucinations
Disorganized speech
Disorganized or catatonic behavior
Negative symptoms (e.g., decreased motivation and diminished expressiveness)
The symptoms must impact the person’s ability to work or have relationships. The diagnosis is usually made after the first episode of psychosis

43
Q

What are the secondary consequences of decreased glutamate transmission in schizophrenia?

A
  • Lowered GABA interneuron activity - so enhanced dopamine transmission –> positive symptoms
  • Impaired cognitive function –> negative symptoms
    (might have a serotonin affect too?)
44
Q

What is the glutamate hypothesis?

A

There is NMDA receptor hypofunction - so deficiency of glutamate activity
Disinhibited glutamate release

45
Q

What is a newly identified transmitter involved in schizophrenia?

A

Glutamate

46
Q

What are the two possible causes of failure of sensory integrations in delusions in schizophrenia?

A
  • Bottom-up: perceptual or attentional problems
  • Top-down: cognitive impairments and prefrontal dysfunction
47
Q

What is a current model for how delusions occur?

A

There is a failure to integrate sensory perceptions with the internal world
Or failure to distinguish the two

48
Q

Which biological pathways do the schizophrenia risk genes converge on?

A
  • Glutamate synapses and plasticity
  • Immune function
  • Calcium signalling
  • Epigenetic signalling
49
Q
A

Sophie - Psychology for Medicine - Year 2 (12 decks)

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