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Diseases of the Nervous System > Mood Disorders > Flashcards

Mood Disorders Flashcards

1
Q

How can mood disorders be defined?

A

A pathological change of mood state with two extremes - mania and depression

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2
Q

What are the three core features of depression?

A

Diurnal variation (depressed mood), anhedonia (diminished interest) and anergia (lack of energy)

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3
Q

What are the psychotic symptoms of depression?

A

Delusions and hallucinations

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4
Q

What are delusions?

A

False or fixed beliefs that are firmly sustained despite evidence to the contrary, and usually not consistent with individual’s culture or religion

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5
Q

What are hallucinations?

A

A sensory experience (auditory, visual, olfactory, gustatory, tactile) in the absence of an external/objective sensory correlate

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6
Q

Is there evidence for a genetic basis for depression?

A

Increased evidence in first degree relative, the monoamine hypothesis and neuroendocrine dysfunction

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7
Q

What are the environmental factors behind depression?

A

Early social and environmental factors and stress

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8
Q

What drugs are used to treat depression?

A

Antidepressants - SSRIs, NRIs, SNRIs and TCAs

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9
Q

What are psychological treatments for depression?

A

CBT, IT, supportive psychotherapy, psychodynamic psychotherapy

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10
Q

What is bipolar disorder?

A

Short but recurrent episodes of mania/depression with psychotic symptoms

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11
Q

What are the two types of bipolar disorder?

A

I - mania with or without depression

II - depression and hypomania

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12
Q

What is the age of onset of bipolar disorder?

A

15-24

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13
Q

How long does diagnosis of bipolar disorder take?

A

7-8 years as often misdiagnosed as depression, substance abuse or ADHD

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14
Q

How many people have depression worldwide?

A

10.7% (lifetime prevalence approximately 15%)

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15
Q

How is depression diagnosed?

A

On the presence of clinical symptoms occurring for longer than two weeks

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16
Q

What are three causes of depression?

A

1) the monoamine theory of depression
2) altered circadian rhythms
3) dysfunctional HPA axis

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17
Q

What is the monoamine theory of depression?

A

Depression is a result of decreased monoamine (particularly 5-HT) activity

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18
Q

Is there any evidence for the monoamine theory of depression?

A
  • reserpine (XMA) induces depression
  • ⬇️ tryptophan levels induces depression
  • effective antidepressants are MA agonists
  • PET scans show decreased 5-HT1a binding and SERT levels
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19
Q

Is there any evidence against the monoamine theory of depression?

A

should see immediate effects with acute ⬆️ in MA levels brought about by antidepressants, but usually takes 2-3 weeks to see therapeutic effects

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20
Q

What is the generally accepted theory behind the lag in therapeutic action of antidepressants?

A

Initially: ⬆️ in MA levels brought about by antidepressants is opposed by increased activation of presynaptic 5-HT autoreceptors 2-3 weeks: constant activation of 5-HT autoreceptors leads to receptor desensitisation and allows ⬆️ MA levels to have effect

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21
Q

What is the evidence for altered circadian rhythms being implicated in psychiatric disorders?

A
  • insomnia/hypersomnia diagnostic of depressive episode
  • ⬇️ need for sleep is a prodromal marker for a manic episode in bipolar disorder
  • melatonin levels are increased in depression
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22
Q

Is there a significant association between common variants in circadian genes and psychiatric disorders? What does this mean?

A

The PCG GWAS found no significant association between common variants in circadian genes and increased susceptibility to psychiatric disorders This could mean altered circadian rhythms are a consequence of psychiatric disorders rather than a cause

23
Q

Are there and SNPs found to be significantly linked to major depressive disorder (MDD?)

A

SNP in the SLC6A15 gene, encoding a Na-dependent branched chain amino acid transporter (solute carrier 6 family)

24
Q

How is the SLC6A15 gene associated with major depressive disorder?

A

⬇️ SLC6A15 expression within the hippocampus is associated with alterations to hippocampus volume, neuronal integrity and the HPA axis
= a higher susceptibility to major depressive disorder

25
How do polymorphisms in the SLC6A15 gene affect the HPA axis in major depressive disorder?
Presence of the SNP increases ATCH and cortisol answers in the Dex/CRH test therefore leading to HPA axis hyperactivity
26
What structural effect does recurrent depressive episodes have on the hippocampus?
⬇️ hippocampal volume
27
SLC6A15 appears to be a candidate gene for susceptibility to MDD - how is this thought to occur?
via alterations to hippocampal volume and HPA-axis activation
28
what is the concordance rate for monozygotic twins for bipolar disorder?
80%
29
aversive early life events are thought to produce biological vulnerability and susceptibility to mood disorders - what is the evidence for this?
1 - family disadvantages in childhood = increased risk of MDD as an adult (NTFS) 2 - parental loss during childhood = increased risk of mood disorder as adult
30
negative feedback of the HPA axis is mediated by which molecules?
glucocorticoids (e.g. cortisol)
31
which hormone increases in response to stress?
cortisol
32
what is the evidence for HPA axis dysregulation due to dysfunctional glucocorticoid-R mediated -ve feedback in MDD?
1 - in the Dex suppression test, depressed patients exhibit attenuated dexamethosone suppression 2 - in the Dex/CRH test, depressed patients exhibit exaggerated response
33
what is anxiety?
a physical or physiological response to a perceived threat
34
the fight or flight response in the physcial response to threat: true or false?
true
35
the fight or flight response is due activation of the ________ nervous system and peripheral release of ____
sympathetic nervous system activation and peripheral release of NA
36
peripheral release of NA causes what bodily effects in anxiety?
tachycardia and heart palpitations, hyperventilation, sweating and GI symptoms
37
what are the psychological symptoms of anxiety?
dread and fearful anticipation, agitation (leading to motor restlessness and muscle ache), fear of loss of control, irritability and disturbed sleep and depersonalisation
38
how is a normal anxiety in response to a threat characterised?
perception of the the threat is not out of proportion to the likely outcome and the physical/psychological response should subside after event
39
what is pathological anxiety?
excessive/unreasonable responses to a perceived threat that affect an individual's ability to lead a normal life
40
the lifetime prevalence of anxiety disorder is ___%
21
41
anxiety is more common in males than females: true or false?
false - it is twice as common in females
42
anxiety is often comorbid with which other mental health disorders?
depression, bipolar disorder and substance misuse
43
what are the six types of anxiety?
``` 1 - panic disorder with or without agoraphobia 2 - agoraphobia 3 - generalised anxiety disorder 4 - obsessive compulsive disorders 5 - social anxiety disorders 6 - post traumatic stress disorder ```
44
what is the HPA axis?
a hormone cascade activated by stress and resulting in release of corticosteroids from the adrenal glands
45
what inhibits the HPA axis?
negative feedback by glucocorticoids
46
why is negative feedback of the HPA axis required?
to restore normal hormone levels at the end of the stress period and to prevent long-term damaging effects of corticosteroids
47
what is evidence to support the HPA axis dysregulation theory of anxiety?
in PTSD patients, found elevated CRH levels in CSF | in rats given CRH, get dose-dependent increase in time spent in centre/corner of arena (i.e. less exploration)
48
receptors for corticotrophin releasing hormone (CRH/CRF) are G-protein coupled: true or false?
true
49
do CRF-R1 antagonists show anxiolytic effects?
yes - in humans and animals
50
do CRF-R1 antagonists show side effects?
yes - elevated liver enzymes and toxicity
51
which neurotransmitters are implicated in anxiety?
NA, 5-HT and GABA
52
what functions does NA have in anxiety?
physical symptoms via peripheral release and effects within the brain
53
what is the NA hypothesis of anxiety?
an increase in NA release leads to increased anxiety
54
what is the source of NA neurones?
the locus coerelius

Diseases of the Nervous System (6 decks)

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