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Z YEAR 2 BRS PSYCH > Mood Disorders > Flashcards

Mood Disorders Flashcards

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1
Q

What is ICD-10 of mood or affective disorders?

A
  • …where the fundamental disturbance is a change in affect or mood to depression (with or without associated anxiety) or to elation.
  • The mood change is usually accompanied by a change in the overall level of activity
  • Most of the other symptoms are either secondary to, or easily understood in the context of, the change in mood and activity.
  • Most of these disorders tend to be recurrent and the onset of individual episodes can often be related to stressful events or situations.
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2
Q

What is the prevalence of bipolar I and II?

A

Lifetime (and 12-month) prevalence estimates of 1.0% (0.6%) for bipolar-I and 1.1% (0.8%) for bipolar-II

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3
Q

What is the lifetime rate of major depressive disorder (MDD)?

A

10-20%

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4
Q

What is the gender distribution of Bipolar I, II and MDD?

A
  • Bipolar-I: F=M
  • Bipolar-II
  • MDD: F>M (2:1 for MDD)
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5
Q

What is the typical cycle of low mood (unipolar and bipolar depression)?

A
  1. Thoughts: whats the point
  2. Feelings: low, flat, irritable
  3. Physiological symptoms: exhaustion
  4. Behaviours: lie in bed all day and ruminate
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6
Q

What is the DSM-5 criteria for depressive episode?

A

Occurrence of 2 weeks or more of depressed mood AND the presence of 4 of 8 out of the symptoms

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7
Q

What are the symptoms for depressive episode?

A
  1. Sleep alterations (insomnia or hypersomnia) 

  2. Appetite alterations (increased or decreased) 

  3. Diminished interest or anhedonia (core) 

  4. Decreased concentration 

  5. Low energy (core) 

  6. Guilt 

  7. Psychomotor changes (agitation or retardation) 

  8. Suicidal thoughts
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8
Q

What would lead to a longitudinal diagnosis of MDD?

A

If no manic or hypomanic episodes in the past are identified, then the diagnosis of a current major depressive episode

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9
Q

What are subtypes in DSM-5 for Major Depressive Disorder (MDD)?

A
  1. .cAtypical features (which represent mainly increased sleep and appetite, along with heightened mood reactivity) 

  2. Melancholic features (defined by no mood reactivity, along with marked psychomotor retardation and anhedonia) 

  3. Psychotic features (the presence of delusions/hallucinations). 

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10
Q

What are core symptoms in depression?

A
  1. Low mood
  2. Anergia
  3. Anhedonia
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11
Q

What are the biological symptoms in depression?

A
  1. sleep
  2. libido
  3. appetite
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12
Q

What are the psychological symptoms in depression?

A
  1. The world
  2. The future
  3. Oneself
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13
Q

What is the typical cycle of high mood?

A
  1. Thoughts: Im the best/I can do all these things
  2. Feelings: elation / excitement
  3. Physiological symptoms: increased energy / race sensation
  4. Behaviours: impulsive/increased activity
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14
Q

What is the DSM-5 for manic episodes?

A

Euphoric or irritable mood with 3 or more of 7 manic criteria

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15
Q

What are the 7 manic criteria?

A
  1. Decreased need for sleep with increased energy
    
2. Distractibility 

  2. Grandiosity or inflated self-esteem 

  3. Flight of ideas or racing thoughts 

  4. Increased talkativeness or pressured speech
  5. Increased goal-directed activities or psychomotor agitation 

  6. Impulsive behaviour (such as sexual impulsivity or spending sprees)
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16
Q

When is a manic episode diagnosed?

A

If such symptoms are present for minimum 1 week with notable functional impairment ( leading to a DSM-5 diagnosis of type I bipolar disorder )

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17
Q

When is a hypomanic episode diagnosed?

A

If such symptoms are present for at minimum 4 days, but without notable functional impairment

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18
Q

When is the DSM-5 diagnosis of type II bipolar disorder made?

A

If not a single manic episode had occurred ever, but only hypomanic episodes are present, along with at least one major depressive episode

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19
Q

What is the DSM-5 diagnosis of unspecified bipolar disorder?

A

If manic symptoms occur for less than 4 days, or if other specific thresholds are not met for manic or hypomanic episodes

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20
Q

When can someone not be diagnosed with hypomainc episode?

A
  1. If psychotic features are present, then hypomania cannot be diagnosed (since such features involve notable impairment by definition)
  2. If a patient is hospitalized, irrespective of duration of manic symptoms, a manic episode is diagnosed, not a hypomanic episode
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21
Q

What is it called when a manic or hypomanic episodes are caused by antidepressants?

A

diagnosis of bipolar disorder is still made in DSM-5 (an important change from DSM-IV where antidepressant- related mania/hypomania was viewed as an exclusion factor)

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22
Q

What is cyclothymia?

A

Mood swings, but not the extremes in depression or mania

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23
Q

What are the major of bipolar 1 first episodes?

A
  • 85% have a depressive as first episode 

  • 10% a manic episode 

  • 3-5% mixed episode 
-Most (90-100%) of patients will develop more episodes after their first manic episode
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24
Q

When are symptoms present in bipolar?

A

47% of time, mostly depressive

25
Q

When can anxiety play a part in bipolar?

A
  • 30-70% of bipolar patients 

  • DSM-5: “Anxious Distress Specifier” 

  • Worse prognosis and outcomes
26
Q

How many people seek help in MDD?

A
  1. 65-70% of people with MDD had visited a health professional in the last 6m but only 15-20% for mental health reason
  2. Among individuals with a 12- month diagnosis of pure MDD only 21% had received any antidepressant treatment within the same period
27
Q

What used to be the reason that bipolar (presence of mania episodes) being different from unipolar (without any history of mania)?

A
  1. Bipolar illness had an early age of onset (mean age of about 19 years vs about the late 20s for unipolar depression) 

  2. Shorter depressive episodes (in average 3m or less in bipolar vs in average 6-12m in unipolar). 

  3. . Recurrent course (more frequent episodes in bipolar than unipolar illness, with rapid cycling, defined as four or more episodes yearly happening in about 25% of bipolar illness cases, but in <1% of unipolar depression cases). 

  4. Genetic specificity (manic episodes were found in families of persons with manic episodes, but not in families of persons with unipolar depression).
  5. Differential treatment (antidepressants for unipolar depression vs neuroleptics and lithium for mania) 

28
Q

Why is bipolar and unipolar not that different in reality?

A
  1. MDD is commonly diagnosed in children, far below the mean onset of the late 20s. 

  2. Brief depressive episodes that occur multiple times yearly are diagnosed in patients with MDD commonly, whereas such course of illness should be rare if MDD was a different illness than bipolar disorder. 

  3. Genetic studies have found high rates of depressive episodes, without mania, in persons with bipolar illness, and also frequent occurrence of bipolar illness in relatives of those with unipolar depression. 

  4. Treatment now overlaps considerably, with neuroleptic agents proven effective not only for mania, but also for depression, both in bipolar and unipolar types. 

  5. Lithium has been well known to be effective not only for mania, but also for depression, both in bipolar and unipolar types. 

29
Q

Is insight preserved in depression and mania?

A
  • preserved in depression and impaired in mania
  • about 50% of patients with severe mania and also most patients with hypomania deny such symptoms [despite the actual presence of those symptoms observed by researchers]
30
Q

How is insight hindered in mania?

A
  • U- shaped curve in relation to severity

- most impaired in hypomania and in severe mania but may be more present in moderate states of mania

31
Q

Is Bipolar or MDD more heritable?

A

Bipolar more

32
Q

Why is important to distinguish bipolar and unipolar?

A
  • antidepressants
    1. appear to be mostly ineffective in acute bipolar depression and in prophylaxis
    2. can cause acute manic/hypomanic episodes
    3. have been shown to worsen the long-term course of bipolar illness in some subjects, especially those with a rapid- cycling course.
    4. in rapid-cycling cases appear to lead to more mood episodes, including depressive states, over time.
33
Q

What is the attention bias like in dperession?

A
  • Prolonged attention to negative pictures - same in remitted / high risk of depression
  • difficulties for depressed people to disengage from negative material.
34
Q

What is fMRI?

A

works by detecting the changes in blood oxygenation and flow that occur in response to neural activity – when a brain area is more active it consumes more oxygen and to meet this increased demand blood flow increases to the active area.
In steps

35
Q

How does fMRI work?

A

1) neural activity is systematically associated with changes in the relative concentration of oxygen in local blood supply;
2) oxygenated blood has different magnetic susceptibility relative to deoxygenated blood;
3) changes in the ratio of oxygenated/de-oxygenated blood (haemodynamicresponse function;
4) can be inferred with fMRI by measuring the blood-oxygen- leveldependent (BOLD) response;
5) fMRI can be used to produce activation maps showing which parts of the brain are involved in a particular mental process

36
Q

What happens in the amygdala in depression attention bias?

A

Sustained amygdala response to negative stimuli

37
Q

What happens in the prefrontal in depression attention bias?

A
  • perigenual anterior cingulate cortex (ACC) (BA 24, 25, and 32) appears to mediate negative attentional biases
  • Increased lateral inferior frontal cortex associated with the impaired ability to divert attention from task-irrelevant negative information
38
Q

What is the memory bias like in dperession?

A
  • Depression: strong evidence for biased memory processes.
  • Preferential recall of negative compared to positive material
  • present in individuals at risk (neuroticism) and in recovered depressed individuals.
39
Q

What is the perceptual biases in depression?

A
  • Increased recognition negative faces

* and/or decreased recognition happy faces

40
Q

What is the facial expression processing in depression?

A
  • Incidental /passive viewing of emotional facial expressions
  • Enhanced emotional response to negative face, even in absence of awareness but not always replicated
41
Q

Where is the amygdala and what does it do?

A
  1. medial temporal lobe region 2. involved in the perception and encoding of stimuli relevant to current or chronic affective goals, ranging from rewards or punishments to facial expressions of emotion to aversive or pleasant images and films
  2. Generally sensitive to detecting and triggering responses to arousing stimuli, exhibits a bias towards detecting cues signalling potential threats, like expressions of fear
42
Q

What happens to facial expression recognition in noradrengeric antidepressants in an acute single dose?

A

-(reboxetine, duloxetine) -better recognition of happy faces

43
Q

What happens to facial expression recognition in serotonergic antidepressants in an acute single dose?

A
  • mirtazapine: decreased recognition of fearful faces

  • SSRI citalopram: mixed results (sometimes found to increase fear recognition)
  • Neurofunctional: both increased and reduced amygdala response to SSRIs
44
Q

What happens to facial recognition 7 days after treatment with noradrenergic and serotonergic antidepressants?

A

reduced recognition of anger and fear

45
Q

What happens to facial recognition 7 days after treatment with noradrenergic and serotonergic antidepressants neurofunctionally?

A
  • reduced amygdala and mPFC response to fear

- Happens IN THE ABSENCE OF ANY CHANGES IN SUBJECTIVE MOOD 


46
Q

What happens to treatment in clinical samples?

A
  1. Early change in positive processing (facial expression recognition after single dose) predicts later response
  2. Clinical response to (gold-standard SSRI) escitalopram after 6 weeks of treatment is associated with early change [at 1 week] in the amygdala, thalamus, ACC, and insula response to fearful faces
47
Q

What happens after 6 weeks in clinical response?

A
  • Elevated baseline ACC activity in depressed patients during tasks that probe affective circuitry
  • but also executive functions, or self-referential processes e.g. resting state
  • Predict positive response to treatment [ ii.e. decrease in depression severity following interventions. Both medication, neurostimulation & CBT]
48
Q

What is another word for serotonin?

A

5-HT

49
Q

What is the monoamine deficiency hypothesis of depression?

A

depressive symptoms arise from insufficient levels of monoamine neurotransmitters serotonin (or 5-hydroxytryptamine , 5-HT), norepinephrine, and/or dopamine

50
Q

What is some indirect evidence for 5-HT hypofunction in depression?

A
  1. 5-HT depletion by the antihypertensive drug reserpine could cause
    depression
  2. Clinically useful antidepressants all increase synaptic monoamine (some selectively 5-HT) concentrations.
  3. Post-mortem evidence of reduced 5-HT levels in brainstem of individuals who committed suicide
  4. Lower levels of 5-HT1A-receptors and 5-HT4-receptors (in living with PET)
  5. Monoamine oxidase A increase in MDD (this used to breakdown serotin)
51
Q

What is some more indirect evidence for 5-HT hypofunction in depression?

A
  1. . Blockade of serotonin synthesis by the tryptophan hydroxylase inhibitor p-chlorophenylalanine prevents the antidepressant effects of both MAOIs and TCAs
  2. Tryptophan depletion ( ➔brain serotonin decreases ) triggers relapse in MDD successfully treated with SSRIs or cognitive behavioural therapy (CBT)
  3. Monoamine depletion correlates with decreased mood both in at risk and MDD in remission.
  4. Depression-related traits; “pessimism” and “dysfunctional attitudes” in MDD, and traits “negativism” and “neuroticism” in healthy, related to 5-HT2A-receptor increased (inversly related to serotonin so Serotonin decreased )
52
Q

What is PET imaging used for?

A

method to investigate brain pharmacology

53
Q

Why is PET better than fMRI?

A
  1. Selective, but invasive
  2. Radioactive
  3. Expensive
  4. Less optimal temporal and spatial resolution
54
Q

How does PET work?

A
  1. Injection of a radioactive pharmaceutical (= tracer = ligand)
  2. The tracer binds to a specific target (e.g. a receptor) and decay is detected + density
55
Q

How do you use PET for the dopamine system?

A

Targets dopamine receptors in brain and then use to quantify how many receptors are there

56
Q

What happens after you give a pharmacological challenge? How do you measure dopamine after this?

A
  1. given pharmacological challenge that releases dopamine from preysnaptic site so dopamine competes with radio tracer so less tracer can bind when system challenged
  2. subtract two scans and different in binding of tracer to receptor
  3. measure of how much dopamine was released from the challenge given
57
Q

Can you use PET for 5-HT and why?

A
  1. Deficiency or problem in releasing serotonin - as not everyone response to SSRIs - repeat serotonin with challenge
  2. Different types of tracers have tried to bind to serotonin receptors in pathway but hasn’t work as mostly antagonist
58
Q

When has a tracer worked for 5-HT?

A

new agonist with challenge (amphetamine) and worked release less serotonin to response to challenge and if more depressed less serotonin released

59
Q

Why did the antagonists PET tracers not work?

A

not sufficiently sensitive to pharmacological challenges

Z YEAR 2 BRS PSYCH (4 decks)

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