Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Psychiatry > Mood disorders (depression) > Flashcards

Mood disorders (depression) Flashcards

1
Q

How are mood disorders/ diseases classified

A

In accordance to:
1. US manual: DSM
The American Psychiatric Association’s “Diagnostic and Statistical Manualof Mental Disorders”, DSM. The latest is DSM-5 from 2013
2. WHO manual: ICD
We also have WHO’s system: International Classification of Diseases (ICD). Latest is ICD-10 from 1994. ICD-11 currently being implemented

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the current definition of “mood (or affective) disorders” according to ICD-10?

A
  • …where the fundamental disturbance is a change in affect/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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is needed to diagnose a depressive episode?

A

DSM-5 criteria for depressive episode:
Occurrence of 2 weeks or more of depressed mood
AND the presence of 4 of 8 out of the following:

  • Sleep alterations (insomnia or hypersomnia)
  • Appetite alterations (increased or decreased)
  • Diminished interest or anhedonia
  • Decreased concentration
  • Low energy
  • Guilt
  • Psychomotor changes (agitation or retardation)
  • Suicidal thoughts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Under what conditions can a diagnosis of a Major Depressive Disorder be made following a depressive episode?

A

If no manic or hypomanic episodes in the past are identified, then the diagnosis of a current major depressive episode leads to a longitudinal diagnosis of Major Depressive Disorder (MDD).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the types of features for Major Depressive Disorder (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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the core symptoms of depression?

A
  • low mood
  • Anergia
  • Anhedonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What biological features are affected by depression?

A
  • libido
  • Sleep
  • Appetite
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What psychological symptoms are affected by depression?

A
  • The world
  • Oneself
  • The future
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the typical cycle of low mood (seen in unipolar and bipolar depression)

A

thoughts:
“whats the point?” ->
feelings:
- low
- flat
- irritable ->
Physiological symptoms:
- exhaustion ->
Behaviors:
- Lie in bed all day
- Ruminate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the typical cycle of high mood (can be seen in mania)

A

Thoughts:
“I’m the best”
“I can do all these things” ->
Feelings:
Elation excitement ->
Physiological Symptoms:
Increased energy
Race sensation ->
Behaviours:
Impulsive
Increased activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are manic episodes?

A

Euphoric or irritable mood with 3 or more of 7 manic criteria:
- 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)

If such symptoms are present for minimum 1 week with notable functional impairment, a manic episode is diagnosed, leading to a DSM-5 diagnosis of type I bipolar disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the difference between hypomania and mania?

A

Hypomania and mania are periods of over-active and excited behaviour that can have a significant impact on your day-to-day life. Hypomania is a milder version of mania that lasts for a short period (usually a few days) Mania is a more severe form that lasts for a longer period (a week or more)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

If manic symptoms are present for at minimum 4 days, but without notable functional impairment what is the diagnosis?

A

a hypomanic episode is diagnosed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the difference between type 1 and type 2 bipolar disorder?

A

Bipolar I disorder involves periods of severe mood episodes from mania to depression. Bipolar II disorder is a milder form of mood elevation, involving milder episodes of hypomania that alternate with periods of severe depression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

“Unspecified Bipolar Disorder”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

If psychotic features are present, hypomania can still be diagnosed, true or false?

A

FALSE:
If psychotic features are present, then hypomania cannot be diagnosed (since such features involve notable impairment by definition).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

if a patient is hospitalized, irrespective of duration of manic symptoms, a manic episode is diagnosed, not a hypomanic episode, true or false?

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

If manic or hypomanic episodes are caused by antidepressants, then the diagnosis of bipolar disorder is still made in DSM-5, true or false?

A

TRUE:
If manic or hypomanic episodes are caused by antidepressants, then the 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)

20
Q

Are bipolar disorders “mood disorders”?

A

DEBATABLE:
it can be challenged whether Bipolar Disorders are “mood disorders”: Some argue; MDD can be without sad mood and mania without euphoric mood
In fact, mood is variable in the phenomenology of these conditions, and the most consistent clinical features for diagnosis are psychomotor changes.

21
Q

What are the different subtypes for bipolar disorder?

A

Bipolar 1
Bipolar 2
Cyclothymia

22
Q

What is cyclothymia?

A

It is a rare mood disorder. Cyclothymia causes emotional ups and downs, but they’re not as extreme as those in bipolar I or II disorder

23
Q

Describe the difference in illness course between the subtypes of bipolar

A

Bipolar 1:
- More severe (more extreme)- higher peaks (than bipolar 2 or cyclothymia) during manic and depressive episode
Bipolar 2:
- Lower peaks than Bipolar 1 but similar peaks to cyclothymia in manic episodes
- higher peaks in depressive episodes than cyclothymia but similar to Bipolar 1

  • Research studies report around 50-60% relapsing within a year of recovery from a mood episode
  • Patients largely autonomous ‘between episodes’
24
Q

What type of episode is common in Bipolar 1?

A

The majority of first episodes are depressive;

  • 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; it is important to get diagnosed after just 1 manic episode

25
Q

Patients with bipolar disorder can be symptom free for over 50% of the time, true or false?

A

TRUE

26
Q

What is meant by “insight”?

A

Ability to recognise that they’re experiencing psychotic symptoms.

27
Q

Describe the difference in heritability and insight between depression mania?

A
  • In general, insight is preserved in depression, and impaired in mania.
  • Insight is most impaired in hypomania and in severe mania but may be more present in moderate states of mania
  • Heritability more common in mania/ bipolar than depression
28
Q

What is bipolar and unipolar depression?

A

Unipolar depression is another name for major depressive disorder. The term “unipolar” means that this form of depression does not cycle through other mental states, such as mania. In contrast, bipolar conditions cause periods of both depression and mania.

29
Q

What is attention bias?

A
  • Prolonged maintenance of attention over negative pictures
  • Reduced attention allocation to positive stimuli
30
Q

How is attention bias presented in depression?

A

Depression is characterised by biases in maintaining/shifting attention = difficulties for depressed people to disengage from negative material.
- Preferential recall of negative compared to positive material
- Increased recognition of negative faces and/ pr decreased recognition of happy faces

31
Q

What is neurofunctional abnormalities that lead to attention biases seen in depression?

A
  1. Sustained amygdala response to negative stimuli
  2. Prefrontal cortex:
    * perigenual anterior cingulate cortex (ACC) appears to mediate negative attentional biases
    * Increased lateral inferior frontal cortex associated with the impaired ability to divert attention from task-irrelevant negative information
32
Q

How is fMRI used to detect neurofunctional abnormalities?

A

fMRI, 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.

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 theblood-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.

33
Q

How is memory bias tested?

A

Negative memory bias:
Free recall tasks meta-analysis = 10% more neg vs pos words
Higher-level conceptual memory tasks vs purely perceptual tasks

Bias: Toward negative material or Away from positive material

34
Q

Memory biases also present in individuals at risk (neuroticism) and in recovered depressed individuals, true or false?

A

TRUE

35
Q

How can you test for perceptual biases?

A

“Facial Expression Recognition task”= show patient’s different mood states and ask them to categorise them between neg and positive faces

36
Q

What is the mechanism for how the brain causes recognition bias?

A
  • Enhanced amygdala response to negative faces (cuases an emotional response more than a fear response)
  • The amygdala is 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
  • While amygdala generally is sensitive to detecting and triggering responses to arousing stimuli, it exhibits a bias towards detecting cues signalling potential threats, like expressions of fear
37
Q

What role does Serotonin play in depression?

A

Serotonin is a neurotransmitter (a messenger chemical that carries signals between nerve cells in the brain). It’s thought to have a good influence on mood, emotion and sleep.

After carrying a message, serotonin is usually reabsorbed by the nerve cells (known as “reuptake”). SSRIs work by blocking (“inhibiting”) reuptake, meaning more serotonin is available to pass further messages between nearby nerve cells.

It would be too simplistic to say that depression and related mental health conditions are caused by low serotonin levels, but a rise in serotonin levels can improve symptoms and make people more responsive to other types of treatment, such as CBT.

38
Q

What causes the lag in treatment response to antidpressants?

A

A delayed response to antidepressant drug treatment is often linked with the time taken for a variety of adaptive neurobiologic changes to occur, for example, desensitization of serotonin 1A receptors and expression of neurotrophic factors such as brain-derived neurotrophic factor.

39
Q

How is facial expression recognition modulation by antidepressants?

A

Acute single dose:
- Noradrenergic antidepressants (reboxetine, duloxetine): better recognition of happy faces
- Serotonergic antidepressants: decreased recognition of fearful faces

7 days treatment:
- Noradrenergic & serotonergic antidepressants: reduced recognition of anger and fear

Clinical:
- 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.

40
Q

What are (tryptamine) psychedelics?

A
  • Psychedelics are serotonin 2A agonists
  • Stimulate the post-synaptic receptors; increase binding of serotonin
  • but do not affect or increase pre-synaptic production of serotonin
41
Q

Describe the effects and safety of psychedelics

A

Effects:
- Hallucinations
- blissful state
- sense of unity
- spiritual experience
- insight-fullness

Safety:
- Non addictive
- Low physiological & brain toxicity
- Good therapeutic index

Risks:
- Dysphoria/ anxiety
- Nausea
- Headache
- False memories (v. rare)

42
Q

What does has been shown to be effective with psychedelics?

A

Full dose interventions = rapid and enduring mood improvement

43
Q

What is the “monoamine deficiency hypothesis”?

A

The “monoamine deficiency hypothesis” of depression postulates that depressive symptoms arise from insufficient levels of monoamine neurotransmitters serotonin (or 5-hydroxytryptamine , 5-HT), norepinephrine, and/or dopamine.

  • Clinically useful antidepressants (including the tricyclics (TCA) and monoamine oxidase inhibitors (MAOI) and serotonin reuptake inhibitors (SSRI)) all increase synaptic monoamine concentrations.
44
Q

What indirect evidence is there to prove the role of 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 (serotonin receptors) in depression.
  5. Monoamine oxidase A (enzyme that decreases serotonin) increased in MDD (major depressive disorder)- suggests that low serotonin can lead to MDD
  6. Blockade of serotonin synthesis by the tryptophan hydroxylase inhibitor p-chlorophenylalanine prevents the antidepressant effects of both MAOIs and TCAs.
  7. Tryptophan depletion (leads to brain serotonin decrease) triggers relapse in MDD successfully treated with SSRIs or cognitive behavioural therapy (CBT).
  8. Monoamine (serotonin/ dopamine) depletion correlates with decreased mood both in at risk and MDD in remission.
45
Q

the evidence for 5HT deficiency in depression has been challenged- why not just measure sertonin in the living human brain?

A

V. difficult:
The method to investigate brain pharmacology= PET scan:
- Injection of a radioactive pharmaceutical (= tracer = ligand)
- The tracer binds to a specific target (e.g. a receptor)
- selective, but invasive, radioactive and expensive and with less optimal temporal and spatial resolution

46
Q

How do we quantify dopamine receptors using amphetamine-induced dopamine release?

A
  1. First give the patient a tracer ([11C]raclopride) which binds to dopamine receptors
  2. calculate the density
  3. give amphetamine to induce dopamine release
  4. this will decrease tracer binding
  5. calculate the new density and work out the difference between the 2
  6. indicates how much dopamine the person is able to bind to

Psychiatry (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions