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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
Q

How do polymorphisms in the SLC6A15 gene affect the HPA axis in major depressive disorder?

A

Presence of the SNP increases ATCH and cortisol answers in the Dex/CRH test therefore leading to HPA axis hyperactivity

26
Q

What structural effect does recurrent depressive episodes have on the hippocampus?

A

⬇️ hippocampal volume

27
Q

SLC6A15 appears to be a candidate gene for susceptibility to MDD - how is this thought to occur?

A

via alterations to hippocampal volume and HPA-axis activation

28
Q

what is the concordance rate for monozygotic twins for bipolar disorder?

A

80%

29
Q

aversive early life events are thought to produce biological vulnerability and susceptibility to mood disorders - what is the evidence for this?

A

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
Q

negative feedback of the HPA axis is mediated by which molecules?

A

glucocorticoids (e.g. cortisol)

31
Q

which hormone increases in response to stress?

A

cortisol

32
Q

what is the evidence for HPA axis dysregulation due to dysfunctional glucocorticoid-R mediated -ve feedback in MDD?

A

1 - in the Dex suppression test, depressed patients exhibit attenuated dexamethosone suppression
2 - in the Dex/CRH test, depressed patients exhibit exaggerated response

33
Q

what is anxiety?

A

a physical or physiological response to a perceived threat

34
Q

the fight or flight response in the physcial response to threat: true or false?

A

true

35
Q

the fight or flight response is due activation of the ________ nervous system and peripheral release of ____

A

sympathetic nervous system activation and peripheral release of NA

36
Q

peripheral release of NA causes what bodily effects in anxiety?

A

tachycardia and heart palpitations, hyperventilation, sweating and GI symptoms

37
Q

what are the psychological symptoms of anxiety?

A

dread and fearful anticipation, agitation (leading to motor restlessness and muscle ache), fear of loss of control, irritability and disturbed sleep and depersonalisation

38
Q

how is a normal anxiety in response to a threat characterised?

A

perception of the the threat is not out of proportion to the likely outcome and the physical/psychological response should subside after event

39
Q

what is pathological anxiety?

A

excessive/unreasonable responses to a perceived threat that affect an individual’s ability to lead a normal life

40
Q

the lifetime prevalence of anxiety disorder is ___%

A

21

41
Q

anxiety is more common in males than females: true or false?

A

false - it is twice as common in females

42
Q

anxiety is often comorbid with which other mental health disorders?

A

depression, bipolar disorder and substance misuse

43
Q

what are the six types of anxiety?

A 
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
Q

what is the HPA axis?

A

a hormone cascade activated by stress and resulting in release of corticosteroids from the adrenal glands

45
Q

what inhibits the HPA axis?

A

negative feedback by glucocorticoids

46
Q

why is negative feedback of the HPA axis required?

A

to restore normal hormone levels at the end of the stress period and to prevent long-term damaging effects of corticosteroids

47
Q

what is evidence to support the HPA axis dysregulation theory of anxiety?

A

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
Q

receptors for corticotrophin releasing hormone (CRH/CRF) are G-protein coupled: true or false?

A

true

49
Q

do CRF-R1 antagonists show anxiolytic effects?

A

yes - in humans and animals

50
Q

do CRF-R1 antagonists show side effects?

A

yes - elevated liver enzymes and toxicity

51
Q

which neurotransmitters are implicated in anxiety?

A

NA, 5-HT and GABA

52
Q

what functions does NA have in anxiety?

A

physical symptoms via peripheral release and effects within the brain

53
Q

what is the NA hypothesis of anxiety?

A

an increase in NA release leads to increased anxiety

54
Q

what is the source of NA neurones?

A

the locus coerelius

Diseases of the Nervous System (6 decks)

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