Session Seven (Major Depressive Disorder) Flashcards

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1
Q

How do we characterise Major Depressive Disorder (as separate from regular depression)?

A

MDD is a more recurring problem, characterised by 1+ major depressive episodes.

Depression is something that happens to all people and is normally self resolving, MDD is a medical condition, and like any other medical condition it won’t go away on it’s own.

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2
Q

What impact does asking someone about suicidal ideation have on their risk of committing suicide?

A

None at all, may decrease it

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3
Q

What are the key symptoms of depression?

A
  • Depressed mood for most of the day, nearly every day (N.B. in teens this may present as irritability instead)
  • Diminished interest/motivation/pleasure in all or nearly all activities (anhedonia)
  • Significant weight loss or gain, or changes in appetite.
  • Insomnia or Hypersomnioa.
  • Psychomotor retardation or agitation
  • Fatigue/ Loss of energy
  • Feelings of worthlessness or excessive guilt
  • Diminished ability to think and concentrate
  • Recurrent thoughts of death or suicide.
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4
Q

What are the 5 diagnostic criteria for MDD?

A

1) 5+ symptoms, present for the same 2 week period most of the day every day. (must include depressed mood and anhedonia, others can be anything)
2) Symptoms cause impairment or distress
3) Symptoms are not due to a medical condition or a substance
4) Symptoms do not meet the criteria for a mixed manic/depressive episode
5) Symptoms are not better accounted for by bereavement

Symptoms + Impairment + 3 Exclusion criteria (Grief, Bipolar, Other condition)

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5
Q

What are the similarities and differences between Depression and Grief/ Bereavement?

A

Similarities:

  • Intense feelings of sadness
  • Withdrawal from usual activities

Differences:

  • Depression involves a persistent low mood, with grief the sadness comes in waves mixed in with positive memories of the deceased.
  • Depression is characterised by self-loathing and worthlessness, in grief self-esteem is maintained.
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6
Q

How prevalent is MDD?

A

50-80% of people will have more than one episode in their life

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7
Q

Is MDD more common in women or men?

A

Twice as common in women

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8
Q

When does MDD usually first occur?

A

Rapid increase in symptoms in adolescence, most people with MDD have developed it by their 30s.

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9
Q

What is the link between depression and suicide?

A

60% of people who commit suicide have a depressive or mood disorder

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10
Q

How significant a burden on the NHS/economy is depression?

A
  • Leading cause of disability worldwide
  • It is the second leading cause of global burden of disease
  • Costs the UK 9.2 billion per year in direct and indirect costs
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11
Q

What have twin studies taught us about the pathology of depression?

A
  • Heritability sits at about 31-42%
  • Shared environment between the twins accounted for 0% of variability (parenting styles and local environments)
  • Non-shared environment accounted for upwards of 60% (so individual specific events such as bullying)
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12
Q

What have adoption studies taught us about depression?

A

Contradict twin studies, suggest there is little or no genetic linkage.

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13
Q

Why are assisted conception family studies important in psychology?

A
  • Allow us to study the intricate relationship between genes and environment.
  • Families where for example there may be separate genetic, gestational, environmental… parents
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14
Q

What did Lewis et al (2011) tell us about depression based on assisted conception families?

A

AIM:

  • What is the estimated effect of the environment on links between parental and child depression and anxiety.
  • Compare genetically related and unrelated kids

METHOD:

  • 852 families with a child born by assisted conception provided data on parental and child depression symptoms
  • Mix of parents genetically related and unrelated

RESULTS:
- Significant associations were found for both parents, in both genetically related and unrelated cases.

CONCLUSION:
- Environmental factors do account for significant variance, and do so independently of shared genetic factors.

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15
Q

What is the link between depression and anxiety?

A

Significant co-morbidity, one tends to cause the other. E.g. depressed so unmotivated therefore miss work therefore become anxious about losing job.

From a therapy point of view, it is best to work out which came first and which is strongest and treat that one.

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16
Q

What have GWAS studies suggested about the genetic link to depression?

A

GWAS have identified some areas across the human genome where depressive and non-depressive individuals are different, however they haven’t found anything concrete.

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17
Q

Studies into the genetic cause of depression have thrown up mixed results, how can this be explained?

A

Gene-Environment Interaction:

  • Genes for depression are expressed only in the presence of an environmental stressor
  • Genes predispose someone, but environment acts as a trigger

Gene-Environment Correlation:

  • Genes do cause depression, but only in the sense that they influence exposure to environmental stressors
  • Genes make people more likely to behave in a way and do things that are likely to make them depressed
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18
Q

What is the main underlying basis for the serotonin model of depression?

A

Anti-depressants.

They work by acting on the serotonin system, therefore depression must be something to do with serotonin.

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19
Q

How do MAOIs work?

A

Inhibit the enzyme Monoamine Oxidase, which destroys excess 5-HT (another name for serotonin)

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20
Q

How do SSRIs work?

A

Block the re-uptake of Serotonin across the pre-synaptic membrane.

Increase availability of serotonin the synaptic space and therefore increase it’s function.

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21
Q

What issues exist with the serotonin hypothesis?

A
  • Studies only support them being significantly better than placebos at the higher end of the depression spectrum, at lower ends no real point.
  • SSRIs don’t work for everyone
  • SSRIs don’t work immediately
  • SSRIs also work for a bunch of conditions unrelated to Serotonin, and we know they’re active on a wide range of other neurotransmitter symptoms.
  • Logic that “it works therefore that’s the cause” is pretty flawed, for example Morphine can effectively treat a headache but headaches aren’t caused by an opioid depletion.
22
Q

What do tryptophan depletion studies tell us about the link between depression and serotonin?

A

Tryptophan is a vital precursor to Serotonin, giving someone a drink full of Amino Acids but not Tryptophan causes them to compete to cross the BBB, causing profound T depletion and therefore S depletion.

These studies have led to a recurrence in depression symptoms in recovered depression, people previously treated with SSRIs and people who were previously suicidal.

However have no mood effect on healthy volunteers with no D history.

This suggests Serotonin plays some role in depression, but a much more complex one (not as simple as low S causes depression as if this were the case all participants would have developed depression)

23
Q

Given evidence linking depression and serotonin is mixed, what explanations have people given to serotonin’s role in depression?

A

Serotonin (and SSRIs) don’t affect mood per se, but instead work on cognitive and information-processing factors that affect how we perceive the world, and this is what influences mood.

This would go someway to explaining the delayed effect of SSRIs (need time to have an effect on cognition) and why only some people see benefits.

24
Q

Where are the main abnormalities in the brains of depressive individuals seen? What happens to these when symptoms remit?

A

Abnormalities are found in the limbic and PFC structures.

Some of these reverse when symptoms remit, and likely reflect areas of altered physiological activity in order to mediate or respond to the emotional/behavioural/cognitive manifestations of MDEs.

Others persist despite remission and may represent anatomic differences between depressive and control subjects.

25
Q

What does the Amygdala do and what is it’s suggested role in depression?

A

Fight or flight centre, directs attention towards threat and makes judgements regarding them.

At rest depressive individuals show hyperactivity in the amygdala, which correlates with symptom severity and regresses when symptoms do.

Some have suggested this may play a role in interpretation bias seen in people with MDD, causing them to interpret neutral people as threatening or somehow against them.

26
Q

What does the Nucleus Accumbens do and what is it’s suggested role in depression?

A

NA plays a role in the central reward system of the brain.

Evidence suggests MDD sufferers show reduced activity in the NA during the “consummatory” phase of reward processing.

This has potentially huge implications as it might physically stop depressed people enjoying things. When given rewards, healthy subjects show activation in this area but people with depression do not.

27
Q

What does the Hippocampus do and what is it’s suggested role in depression?

A

Hippocampus is involved in episodic, declarative, contextual and spatial learning and memory.

Some evidence suggests it is smaller and less developed in people with a history of depression, possibly due to chronic stress causing reduced neurogenesis.

This could cause them to look back on and focus on past failures, or not be able to formulate a positive view for the future.

28
Q

What does the PFC do and what is it’s suggested role in depression?

A

PFC maintains representations of goals and how we intent to achieve them, as well as regulating out emotions.

Reduced activity in depressives, could be cause of issues with motivation, preventing them from engaging in goal oriented behaviours.

29
Q

What evidence is there linking the Anterior Cingulate Cortex to depression?

A

Structural MRI studies have shown it to be of lower volume but overall increased activity in those with MDD.

Role unclear.

30
Q

What are the complexities of studies into the structure of MDD brains?

A
  • Most of the changes observed disappear with treatment, suggesting they are caused by depression not the cause of depression.
  • Cause vs Correlation vs Consequence?
  • Most of these studies do not control well for co-occuring conditions, previous SSRI treatment, recurrent episodes, genetic background etc.
31
Q

Outline Beck’s Cognitive Theory (1976) and how it relates to abnormal psychology?

A

Beck thought dysfunctional thinking was common to all psychological difficulties, and had a significant effect on people’s mood and behaviour.

3 Levels of Cognition:

  • Cognitive Distortions
  • Cognitive Schemas
  • Automatic Thoughts
32
Q

What are Cognitive Distortions in Beck’s Cognitive Theory? Give some examples

A

Essentially, errors in appraisal of the world that can lead one to depressive thinking:

  • Labelling (e.g. do something stupid therefore you are stupid)
  • Jumping to conclusions
  • Emotional reasoning (something FEELS true therefore it IS true, e.g. today feels like a bad day so it will be a bad day)
  • All or Nothing thinking (either they love me or they hate me)
  • Unnecessary Should/Must thinking
  • Taking things personally
  • Magnification (aka catastrophisation) and minimisation
  • Discarding the Positive
  • Obsessing over the negative
  • Over-generalisation
33
Q

What are Cognitive Schema in Beck’s Cognitive Theory?

A

Schemas = Beliefs about self and the world based on experience, used to organise and interpret new information.

Individuals become consistent with their schemas, prevent disconfirmation and maintain difficulties.

34
Q

What are Negative Automatic Thoughts in Beck’s Cognitive Theory?

A

Short, sharp thoughts that pop into your head at certain times. Features:

  • Can be verbal or images
  • Involuntary
  • Rapid
  • Shorthand
  • Believable
  • Feel true

e.g. “oh god I’m the most awkward person ever”

35
Q

Outline Beck’s Model of Depression?

A

People with depression have a negative cognitive triad. Bad thoughts about:

  • The self
  • The world
  • The future

Depression is also characterised by a pervasive negative appraisal and misinterpretation of experience.

36
Q

How did Beck describe the development of Depression?

A
  • Early experiences lead to…
  • Core beliefs, which can cause…
  • Dysfunctional attitudes/assumptions/rules for living.
  • A Critical Incident then activates these assumptions, leading to…
  • NATs, which cause
  • The Symptoms of Emotional Disorder.

These symptoms then influence our behaviour, affect, cognitions, and physical symptoms.

37
Q

Describe Beck’s Cycle of Depression?

A
  • Situation (e.g. bad feedback at work) affects
  • Thoughts (e.g. I am a failure) affects
  • Emotions (e.g. depression) affects
  • Behaviours (e.g. take time off work to feel better) which in turn affects our Situation (e.g. more bad feedback due to time missed)

Cognitive therapies often aim to break this cycle .

38
Q

What maintenance mechanisms exist in Depression?

A
  • Cognitive distortions and NATs
  • Biased processes (ways people try and control their negative emotions that feel helpful but aren’t e.g. rumination, thought suppression)
  • Behaviours (including coping strategies, aim to avoid negative feelings altogether)
39
Q

Give examples of some biased processes that can help maintain depression?

A
  • Thought Control; strategies that interfere with normal emotional processing e.g. emotional habituation
  • Thought Suppression
  • Rumination; respond to distress by focusing on the symptoms of distress and on the possible causes and consequences of these symptoms
40
Q

Give some examples of behaviours that may lead to depression maintenance?

A

Any coping strategies that aim to reduce emotions and prevent negative outcomes in the short term but can worsen symptoms in the long term. E.g.:

  • Social withdrawal (removes support network)
  • Physical inactivity (leads to more rumination)
  • Emotional avoidance using substances (depressive effects of withdrawal)
  • Safety behaviours (behaviours aimed to reducing danger that backfire because they prevent reality testing, and therefore the disconfirmation of erroneous beliefs)
41
Q

What are the pros and cons of antidepressant use in depression management?

A

Pros:

  • NICE guidance recommends their use when psych therapies aren’t enough
  • Work for a wide variety of conditions

Cons:

  • Don’t work straight away
  • Initial side effects are unpleasant
  • Don’t work for everyone
  • Some evidence suggests they only work for severe depression, not for first episode or mild-moderate depression

In spite of this, still used routinely as psych therapies are totally overrun

42
Q

Outline what CBT for depression aims to achieve?

A

Aims to break the Situation/ Thought/ Emotion/ Behaviour loop by working out which one is most relevant and targeting it.

43
Q

What are some benefits to CBT for depression?

A

Better at avoiding relapse

Can be made highly;y personalised to the patient.

44
Q

What are some steps parts to the STRUCTURE of CBT?

A
  • History and assessment
  • Developing a shared plan
  • Discuss and set SMART goals
  • Try out skills to alter beliefs and behaviours
  • Rinse and repeat
  • Relapse prevention plan and follow up sessions

The setting of a realistic goal is super important in CBT

45
Q

How does CBT target Situations, Thoughts and Behaviours?

A

Situations through Problem Solving.

Thoughts through Cognitive Restructuring.

Behaviours throughBehavioural Activation.

46
Q

Outline the 3 steps to Cognitive Restructuring, used to manage the Thoughts part of the depression cycle?

A

IDENTIFY unhelpful automatic thoughts

EVALUATE evidence for and against these thoughts

CHALLENGE these by constructing automatic and more realistic thoughts.

Often patients will spend a few sessions at each stage.

47
Q

Outline the process of Behavioural Activation, used to manage the Behaviours part of the depression cycle?

A
  • Identify routine, pleasurable and necessary activities.
  • Make these into a hierarchy
  • Schedule activities using an activities diary
  • Implement these (homework)
48
Q

Outline the process of Problem Solving in CBT, used to manage the Situation part of the depression cycle?

A

1) Identify the problem
2) Think of as many solutions as possible
3) Pros and Cons of each
4) Choose a solution
5) Plan
6) Carry it out
7) Evaluate

The process of going through it in this rational way with another person can have benefits itself, and coming up with silly solutions to complex problems can make them seem silly as well, reducing anxiety about them.

49
Q

Outline the Evidence Base for CBT?

A
  • Highly effective across a range of disorders
  • Nice recommended
  • Resistance to relapse in both depression and anxiety when compared to medication
  • Shorter waiting list compared to non-specific psych interventions
  • Can be done in fewer sessions
  • Some evidence it’s actually more effective than psych interventions
50
Q

What are the two other suggested therapies for depression outside of Antidepressants and CBT?

A
  • Mindfullness (notice thoughts and reactions to them, accept and allow these thoughts, shift from analytical to experiential focus, meditation). In many ways opposed to CBT as focus is on accepting emotion not changing it.
  • Deep Brain Stimulation (electrodes placed over subgenual Anterior Cingulate Cortex)