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Abnormal Psych > Depressive and Bipolar Disorders > Flashcards

Depressive and Bipolar Disorders Flashcards

1
Q

what is disruptive mood regulationdisorder

A

→ Severe recurrent verbal or behavioural temper outbursts out of proportion with intensity to the situation
→ Outbursts inconsistent with developmental level
→ Outbursts 3-5 times a week
→ Mood b/w outbursts is irritable/ angry most of the day, nearly everyday

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2
Q

How long do the symptoms of disruptive mood regulation disorder have to be present before diagnosis

A

criteria met for a year (12 mth) with no period 3+ mths in which all the criteria weren’t met

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3
Q

What is the age of onset for disruptive mood regulation disorder?

A

Age of onset = before 10 but NOT before 6 or after 18 (b/w 6-18)

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4
Q

can disruptive mood regulation disorder occur exclusively during a major depressive episode?

A

NO

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5
Q

What disorders can’t DMRD co occur with?

A

• Cannot co-exist with Oppositional Defiance Disorder, bipolar or intermittent explosive disorder

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6
Q

what do kids with DMRD tend to develop in adulthood

A

tend to develop unipolar depressive disorder, or anxiety disorders, rather than bipolar disorder (if they develop anything at all)

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7
Q

second to anxiety _________ is the largest area of mental order diagnosis

A

Major Depressive Disorder

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8
Q

DSM-5 criteria for depression

A

→ 5 of the following during 2-wk period
• Depressed mood
• Anhedonia
• weight loss (not dieting) or gain
• Insomnia or hypersomnia
• Psychomotor agitation (enhancement) or retardation (slower movement)
• Fatigue/loss of energy
• Feelings or worthlessness or guilt
• Reduced concentration, indecisiveness
• thoughts of death (suicidal idealization)

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9
Q

what is anhedonia

A

• Diminished interest or pleasure

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10
Q

What two symptoms must be present to diagnose MDD

A

depressed mood or anhedonia

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11
Q

what distinguishes depression from bipolar

A

presence of a manic or hypomanic episode

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12
Q

Criteria for Bipolar I is one manic episode lasting at least a week with 3 or more of the following criteria…

A

o Inflated self-esteem/ grandiosity
o Reduced need for sleep
o talkative/ pressure to keep talking
o Flight of ideas/ racing thoughts
o Distractibility
o Increased goal-directed activity/psychomotor agitation
o involvement in activities with high risk (gambling, excessive sexual behaviour, spending money, giving gifts)
o impairment in social or occupational functioning, or requires hospitalization or has psychotic features

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13
Q

is a depressive episode required to diagnose bipolar disorder?

A

NO but it is typically the case

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14
Q

What is the difference b/w bipolar I and II

A

1: with manic episode

2 (milder version of 1):with hypomanic episode

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15
Q

difference b/w manic episode and hypomanic episode

A

• same as manic accept NO marked impairment in social or occupational functioning, or hospitalization to prevent harm to self or others, or psychotic features.

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16
Q

What is the point prevalence for Major depression?

A

5-9%(females), 2-4%(males)

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17
Q

What is the lifetime prevalence of Major depression?

A

10-20% (females), 5-12% (males)

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18
Q

What is the average age of onset for MDD?

A

20s-50s, mean=late 30s

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19
Q

Biases for MDD?

A

No race, SES, or class bias

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20
Q

What is the lifetime prevalence for Bipolar disorder

A

1-2% no sex bias

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21
Q

what is the age of onset for BD

A

Late teens – 20s

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22
Q

Canadian Annual prevalence of mood disorders

A

Females: 6.3%, Males: 4.2%, Overall: 5.2%

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23
Q

Psychodynamic Etiology of depression

A

Anger turned inward at an introjected lost love object

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24
Q

Depressive Etiology: Seligman (cognitive)

A

Attribution based model:

• People with depression have a bias towards internal and negative attribution of events

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25
Q

what are the 3 types of negative attributions for failure described by seligman

A

o Internal reasons: “something about me”
o Global reasons: “Something very big and important about me”
o Stable reasons: “Something unchanging about me”

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26
Q

What is Beck’s theory of depression (cognitive)

A

• Presence of depressogenic schemata (selecting and interpreting events that generate depression)
- characterized by unrealistically negative views and systematic errors in logic

27
Q

What is the negative triad described by Beck

A

Negative thoughts
o Of the self
o Of the world
o Of the future

28
Q

What are the systematic errors in logic described by Beck

A

o Arbitrary interference
o Selective abstraction
o Magnification & Minimization
o Overgeneralization

29
Q

What is Arbitrary Interference

A

tendency to draw negative conclusions in the face of no evidence whatsoever or contrary evidence

30
Q

What is Selective abstraction

A

picking and choosing from among the evidence things that cast your circumstances in a negative light

31
Q

What is Magnification & Minimization

A

minimizing positive and maximizing the impact of the negatives

32
Q

What is Overgeneralization

A

tendency to see one failure in one circumstance as having broad implications for your entire life

33
Q

Who developed CBT

A

Beck

34
Q

What is the amine hypothesis

A
  • Depression = Low levels of amine neurotransmitter activity

* Mania = High levels of amine neurotransmitter activity

35
Q

What are the 3 candidate neurotransmitters for depression

A

o Dopamine
o Noradrenaline
o Serotonin

36
Q

What are tricyclics?

A

Inhibit reuptake (blocks reuptake of neurotransmitters into presynaptic neuron, they are left in the synapse longer and remain active)

37
Q

What are MOA inhibitors

A

Inhibit breakdown (inhibit monoamine oxidase – which breaks down neurotransmitter molecules)

38
Q

What does ECT do?

A

Reduce B-adrenergic receptors; increase serotonergic response, theta-adrenergic receptors (relaxation, inhibition)

39
Q

What does lithium do?

A

Stabilizes serotonergic activity

40
Q

What are precursors?

A

manufacture more neurotransmitter - increased precursors should improve depression

41
Q

What are Metabolites?

A

chemical products left over after neurotransmitters have been broken down - expect them to be lower in depressed patients

42
Q

What evidence was found when giving patients the precursor L-DOPA

A

o Enhances effect of MAO inhibitors (consistent with hypothesis)
o May lead to hypomania in BD

43
Q

What evidence was found with Metabolite: HVA (Homovanillic acid)

A

o HVA is not lower in CSF of depressed patients (as would have been expected)
o We do see a relation of lower HVA and motor retardation

44
Q

What neurotransmitter is implicated in motoric symptoms

A

Dopamine (makes sense because they are implicated in Parkinson’s and other motor disorders)

45
Q

What evidence was found through norepinephrine metabolite MHPG

A

o Lower levels of urinary MHPG in depression than controls

o Especially in bipolar patients

46
Q

What evidence was found through the serotonin Precurser Tryptophan?

A

o May be antidepressant in mild cases

o Moderate-severe doesn’t work

47
Q

What evidence was found through the serotonin Metabolite 5-HIAA

A
  • lower CSF levels of 5-HIAA in depression

- Low CSF levels of 5-HIAA in aggression, impulsivity, suicide

48
Q

what is the theory of permissive serotonin? Evidence?

A
  • Serotonin (master regulator) regulates neural activity of dopamine and norepinephrine
  • Reduced regulation = wider activity changes → mania or depression
  • Serotonin stabilization by lithium in bipolar disorders (stabilizes the swings of dopamine and norepinephrine)
  • Reports of successful treatment with serotonin precursors
49
Q

What are some problems with the evidence we have gathered based on neurotransmission

A
  • the whole spinal cord and other organs also produces metabolites which can be found in the CSF
  • other drugs relieve depression without amine uptake effects
  • Delay between drug effects (neurotransmitter activity levels = 1-2 days) and lifting of depression (3-4 weeks)
50
Q

What are the problems with using drugs that change neurotransmitter levels

A

Equally likely that it’s the changes in affect that cause changes in neurotransmitters
ex. CBT without drugs is more effective

51
Q

what are some structural and functional differences in the brains of depressed patients?

A
  • smaller hippocampal volume

- less left frontal EEG activity (more asymmetry) associated with reduced positive emotions

52
Q

bipolar and unipolar depression are associated with high levels of what?

A

Cortisol (stress hormone)

53
Q

how do cortisol release patterns differ during depression

A

o Release stars earlier in depression (normally 4am – noon, 1am for depression)
o Higher peaks in depression
o Longer release period in depression
o Increased ACTH release by pituitary

54
Q

What is somatostatin and how is it related to depression

A

Gut neuropeptide that inhibits HPA axis - low CSF levels in depression = HPA axis more active = more cortisol

55
Q

what is the concordance rate of 1st degree relatives for depression

A

6 – 40%

56
Q

______ are Good as antidepressants when no comorbid anxiety

A

Omega-3 acids

57
Q

what is ketamine?

A

tranquilizer used in veterinary practice: At lower doses than anesthesia does provide rapid relief of depression unlike SSRIs and MOA inhibitors

58
Q

list drugs for depression

A

SSRIs, MAO inhibitors, Omega-3 acids, ketamine

59
Q

what are the physical treatments for depression

A
  • Electroshock Therapy - memory loss
  • Transcranial Magnetic Stimulation (brain subjected to magnetic feild - similar to ECT, experimental)
  • Deep brain stimulation (brain surgery to inject electrodes)
60
Q

Where are electrodes injected during Deep brain stimulation

A

inside the nucleus accumbens, beneath frontal lobes. (related to release of dopamine)

61
Q

what are psychological treatments of depression?

A
  • Psychodynamic psychotherapy

* Cognitive Behavioural therapy

62
Q

Pharmacological treatment for bipolar

A

• Chlorpromazine
• Haloperidol – dopamine antagonist
• Lithium – works for most patients, very rapid.
- side effects

63
Q

Seligman’s learned hopelessness model of depression the individual becomes depressed when he or she

A

comes to believe that aversive or negative events are caused by something pervasive about themselves.

Abnormal Psych (8 decks)

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