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!!!!! BRS YR2 !!!!! > Psych - Mood disorders > Flashcards

Psych - Mood disorders Flashcards

1
Q

What is the fundamental disturbance in mood disorders according to ICD-10?

A

change in affect/mood to depression (with or without associated anxiety) or to elation

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2
Q

What is the mood change in mood disorders often accompanied by, according to ICD-10?

A

accompanied change in overall level of activity

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3
Q

How do other symptoms usually fit into mood disorders according to ICD-10?

A

most other symptoms are either secondary to, or easily understood in the context of, the change in mood and activity

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4
Q

What is the frequency like in mood disorders according to the ICD-10?

A

most mood disorders are RECURRENT

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5
Q

What can trigger individual episodes in mood disorders according to ICD-10?

A

often triggered by stressful events or situations

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6
Q

What resources or criteria are used to classify mood disorders?

A

→ DSM : diagnostic + statistical manual of mental disorders, US manual, latest is DSM-5
→ ICD : international classification of diseases (ICD), WHO manual, latest is ICD-10

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7
Q

What is the lifetime prevalence of bipolar-I?

A

1%

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8
Q

What is the lifetime prevalence of bipolar-II?

A

1.1%

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9
Q

What are the lifetime rates of major depressive disorder?

A

10-20%

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10
Q

What is the gender distribution for bipolar-I?

A

F : M = 1 : 1

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11
Q

What is the gender distribution for bipolar-II?

A

F : M = 2 : 1

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12
Q

What have studies across the country noted about the rates of MDD and the age of onset over time?

A

increasing rate of MDD with an earlier age of onset

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13
Q

What is the DSM-5 criteria for a depressive episode within mood disorders?

A 
occurrence of 2 weeks or more of depressed mood + presence of 4 of these:
→ sleep alterations
→ appetite alterations
→ diminished interest or anhedonia
→ low energy
→ guilt
→ psychomotor changes (e.g. agitation or retardation)
→ suicidal thoughts
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14
Q

What is the diagnosis for someone with no manic or hypomanic episodes in the past, but still current major depressive episodes?

A

longitudinal diagnosis of Major Depressive Disorder (MDD)

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15
Q

What are the features listed in the DSM-5 for MDD?

A

→ Atypical features (which represent mainly increased sleep and appetite, along with heightened mood reactivity)
→ Melancholic features (defined by no mood reactivity, along with marked psychomotor retardation and anhedonia)
→ Psychotic features (the presence of delusions/hallucinations).

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16
Q

What triad of biological symptoms could depression affect?

A

→ libido
→ sleep
→ appetite

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17
Q

What triad of psychological symptoms could depression affect?

A

→ oneself
→ the future
→ the world

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18
Q

What triad of core symptoms could depression present with?

A

→ low mood
→ anergia
→ anhedonia

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19
Q

What is the criteria for mania according to the DSM-5?

A

euphoric or irritable mood with 3 or more of 7 of :
→ Decreased need for sleep with increased energy
→ Distractibility
→ Grandiosity or inflated self-esteem
→ Flight of ideas or racing thoughts
→ Increased talkativeness or pressured speech
→ Increased goal-directed activities or psychomotor agitation
→ Impulsive behaviour (such as sexual impulsivity or spending sprees)

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20
Q

What is the criteria for a manic episode diagnosis according to the DSM-5?

A

→ mania symptoms being present for minimum 1 week

→ with notable functional impairment

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21
Q

What is the criteria for a hypomanic episode diagnosis according to the DSM-5?

A

→ mania symptoms being present for minimum 4 days

→ without notable functional impairment

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22
Q

What leads to a diagnosis of bipolar-I?

A

presence of manic episodes + depressive episodes

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23
Q

What leads to a diagnosis of bipolar-II?

A

→ no manic episodes
→ only hypomanic episodes
→ at least one major depressive episode

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24
Q

What leads to a diagnosis of Unspecified Bipolar Disorder?

A

→ manic symptoms for less than 4 days

→ other thresholds for manic or hypomanic are not met

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25
Q

What features distinguish mania from hypomania significantly?

A

impairment to functionality:
→ psychotic features present
→ hospitalisation

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26
Q

What percentage of people relapse within a year of recovery from mood episodes?

A

50-60%

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27
Q

How are patients between episodes?

A

largely autonomous

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28
Q

What percentage of first episodes are depressive for Bipolar-I?

A

85%

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29
Q

What percentage of first episodes are manic for Bipolar-I?

A

10%

30
Q

What percentage of first episodes are mixed for Bipolar-I?

A

3-5%

31
Q

What are the different long-term statuses of patients with bipolar disorder?

A

→ majority symptom free (53%)
→ depressive symptoms (32%)
→ manic / hypomanic symptoms (10%)
→ cycling / mixed symptoms (6%)

32
Q

How many bipolar patients also have anxiety?

A

30% - 70%

33
Q

What does the DSM-5 call anxiety affecting bipolar patients?

A

Anxious Distress Specifier

34
Q

How does anxiety affect bipolar patients?

A

worse prognosis + outcomes

35
Q

What percentage of people with MDD visit a health professional? How many for mental health reasons?

A

→ 65%-70% visit health professionals

→ 15-20% for mental health reasons

36
Q

How many of those with a 12-month diagnosis of MDD get antidepressant treatment?

A

only 21%

37
Q

What was the main difference identified between bipolar and unipolar identified by the DSM-3?

A

→ bipolar (presence of manic episodes)

→ unipolar (without any history of mania)

38
Q

What were the other differences between bipolar and unipolar in the DSM-3 in the 1980s?

A

→ Bipolar = early age of onset (mean age of 19 rather than late 20s fo unipolar)
→ Shorter depressive episodes (in average 3m or less in bipolar vs in average 6-12m in unipolar).
→ 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).
→ Genetic specificity (manic episodes were found in families of persons with manic episodes, but not in families of persons with unipolar depression).
→ Differential treatment (antidepressants for unipolar depression vs neuroleptics and lithium for mania)

39
Q

What is the newer evidence that shows that bipolar and unipolar may be more similar?

A

→ MDD is commonly diagnosed in children, far below the mean onset of the late 20s.
→ 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.
→ 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.
→ Treatment now overlaps considerably, with neuroleptic agents proven effective not only for mania, but also for depression, both in bipolar and unipolar types.
→ Lithium has been well known to be effective not only for mania, but also for depression, both in bipolar and unipolar types.

40
Q

When is insight preserved in depression and mania?

A

→ preserved in depression

→ impaired in mania

41
Q

What percentage of patients with severe mania deny having symptoms (i.e. having no insight)?

A

50%

42
Q

How does a patient’s insight change with the severity of their mania?

A

→ U-shaped curve with mania
→ severe mania or hypomania = impaired insight
→ moderate states of mania = intact insight

43
Q

What does an acute single dose of noradrenergic antidepressants do?

A

better recognition of happy faces

44
Q

What are some examples of noradrenergic antidepressants?

A

→ reboxetine

→ duloxetine

45
Q

What does an acute single dose of serotonergic antidepressants do?

A

→ decreased recognition of fearful faces for mirtazapine

→ citalopram also causes mixed results (sometimes increases fear recognition)

46
Q

What are some examples of serotonergic antidepressants?

A

→ citalopram

→ mirtazapine

47
Q

What does 7 days of treatment for antidepressants in general result in?

A

reduced recognition of anger + fear

48
Q

something about facial recognition modulation in ECGs

A

honestly have no clue what this is, please review section 2

49
Q

What is the monoamine deficiency hypothesis?

A

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

50
Q

How does an antihypertensive drug prove the MD hypothesis indirectly?

A

antihypertensive drug, RESERPINE causes 5-HT depletion which has caused depression

51
Q

How do antidepressants indirectly prove the MD hypothesis?

A

Clinically useful antidepressants all increase synaptic monoamine (some selectively 5-HT) concentrations.

52
Q

What is the postmortem evidence for the MD hypothesis?

A

Post-mortem evidence of reduced 5-HT levels in brainstem of individuals who committed suicide

53
Q

Which receptors and enzymes provide evidence for the MD hypothesis?

A

→ lower levels of -HT1A-receptors and 5-HT4-receptors

→ Monoamine oxidase increased in MDD

54
Q

What else provides evidence for the MD hypothesis?

A

→ Blockade of serotonin synthesis by the tryptophan hydroxylase inhibitor p-chlorophenylalanine prevents the antidepressant effects of both MAOIs and TCAs
→ Tryptophan depletion (decreasing brain serotonin) triggers relapse in MDD successfully treated with SSRIs or cognitive behavioural therapy
→ Monoamine depletion correlates with decreasing mood both in at risk and MDD in remission
→ Depression-related traits; “pessimism” and “dysfunctional attitudes” in MDD, and traits “negativism” and “neuroticism” in healthy, related to 5-HT2A-receptor increase and serotonin decrease

55
Q

Why can’t the MD hypothesis be proven directly?

A

very difficult to measure serotonin in the living brain

56
Q

How are receptors and transmitters measured in the living human brain?

A

PET imaging

57
Q

What are the differences between PET imaging and fMRI?

A 
PET imaging is :
→ more  Selective
→ more invasive
→ radioactive
→ expensive
→ less optimal temporal and spatial resolution
58
Q

What does PET imaging involve?

A

→ Injection of a radioactive pharmaceutical (tracer, ligand)
→ tracer binds to a specific target (e.g. a receptor)
→ scanning picks up on tracer

59
Q

How do we use PET imaging to quantify dopamine receptors?

A

→ inject Raclopride as the tracer or ligand
→ PET scan establishes dopamine density at baseline
→ present a challenge (e.g. Amphetamine challenge)

60
Q

Why is it difficult to use PET scanning to quantify serotonin receptors?

A

many antagonist PET tracers haven’t been significantly sensitive to pharmacological challenges

61
Q

What has worked in quantifying serotonin receptors with PET scanning?

A

5-HT release is measured using :
→ Agonist radioligand 11C-CIMBI-36
→ Pharma challenge Amphetamine

62
Q

What is the measure of cerebral 5-HT release with depression?

A

→ measurable 5-HT release in healthy

→ no measurable 5-HT release in patients with depression

63
Q

What is an attention bias?

A

Depression is characterised by biases in maintaining/shifting attention = difficulties for depressed people to disengage from negative material

64
Q

What are examples of attention biases?

A

→ Prolonged maintenance of attention over negative pictures

→ reduced attention allocation to positive stimuli

65
Q

How does fMRI work?

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
→ to meet this increased demand blood flow increases to the active area

66
Q

How does fMRI identify attention biases?

A

→ sustained amygdala response to negative stimuli
→ perigenual anterior cingulate cortex of prefrontal cortex appears to mediate negative attentional biases
→ lateral inferior frontal cortex associated with the impaired ability to divert attention from task-irrelevant negative information

67
Q

What is memory bias?

A

→ Preferential recall of negative compared to positive material
→ one of the most robust findings in the depression literature

68
Q

Where is memory bias mostly present?

A

→ people with depression
→ individuals at risk (neuroticism)
→ recovered depressed individuals

69
Q

What is perceptual bias?

A

increased recognition of negative faces and/or decreased recognition of happy faces

70
Q

How does perceptual bias play into MDD?

A

→ robust strong evidence of Emotion Recognition deficits in MDD
→ reduced recognition of all basic emotions except for sadness
→ small effect size: may be confounded by medication
→ Enhanced amygdala response to negative faces

71
Q

What is the function of the amygdala?

A

→ medial temporal lobe region
→ 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
→ amygdala generally is sensitive to detecting and triggering responses to arousing stimuli
→ exhibits a bias towards detecting cues signalling potential threats, like expressions of fear

!!!!! BRS YR2 !!!!! (72 decks)

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