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Psychopathology - 13 mins > Mood Disorders > Flashcards

Mood Disorders Flashcards

1
Q

depression

A

Low sad state which life seems dark and challenging

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2
Q

Mania

A

opposite of depression; state of breathless euphoria or at least frenzied energy in which people believe that the world is theirs for the taking

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3
Q

two groups of disorders centre round depression and maina

A

Depression and bipolar

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4
Q

Major depressive disorder//unipolar depression

FACTS/FIGS

A
  • 18% of people will experience at least once in your life
  • poor > wealthy
  • women twice as likely than men BUT girls = boys
  • 85% recover, some without treatment
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5
Q

Symptoms of MDD (4)

A

1) Cognitive symptoms: Negative views, helplessness.
2) Emotional symptoms: Sad/empty, isn’t context specific, anhedonia
3) Motivational symptoms: No desire for unusual activities, wish to die
4) Behavioural symptoms: Less active, speech slowed

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6
Q

Diagnosing MDD

A
  • 2+ weeks of 5 symptoms (including SAD MOOD AND LOSS OF PLEASURE)
  • May be acc by psychotic eps
  • somatic symts (make sure its due to MDD tho)
  • loss of appetite/sleep
  • inability to concentrate

**MUST HAVE NO HISTORY OF MANIA

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7
Q

Why is it that G=B but W>M

A

Pre pube = less social and hormonal factors playing a role

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8
Q

Grief vs MDD?

A
  • in grief = Predominant emotion is loss and emptiness. There is an ability to be happy/be humorous
  • MDD = Persistent depressive mood and inability to have fun or enjoyment. Can’t be happy
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9
Q

differential diagnosis MDD

A
  • bipolar
  • sadness
  • depression CAUSED by another primary illness (i.e. stroke)
  • ADHD (distractibility and low frustration tolerance)
  • substance use
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10
Q

co morbidity of MDD (5)

A

1) Substance use
2) panic disorder
3) OCD
4) AN/BN
5) BPD

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11
Q

Persistent DD

what?

A
  • For those whose unipolar depression is particularly long lasting (2+ years)
  • Some people have repeated major depressive EPISODES, a pattern technically called ‘persistent depressive disorder with major depressive episodes
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12
Q

Differential diagnosis

PDD

A
  • PD
  • MDD
  • Psychotic disorders
  • Depression/bipolar
  • substance induced depression
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13
Q

premenstral depressive disorder

A
  • For women who have clinically depressive and related symptoms a week before menstration
  • Inclusion to DSM 5 was controversial
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14
Q

should premenstral depressive disorder have been included into the DSM?? controversial

A
  • was under “not otherwise specified”
  • Over diagnosis bc they don’t know exactly what causes it
    pathologising healthy women –> discrimination?
    MONEY TO BE MADE = Prozac –> Sarafem same thing but it was £10 not 0.25p
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15
Q

stress and unipolar depression

A
  • Unipolar depression often seems to be triggered by stressful events
    = Some express the importance of dividing reactive depression (from clear cut stressful events) & endogenous depression (which seems to stem from inside)
    —> Endogenous depression occurs without the presence of stress or trauma. In other words, it has no apparent outside cause.
    –> Reactive depression happens after a stressful or traumatic event takes place.

BUT how can clinicians tell? + DSM says it doesnt help with treatment regardless.

LINK W PTSD
> If MDD follows traumatic event what makes it diff from PTSD?
1) MDD has no avoidance strategies
2) No reoccurant imagery of the trauma

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16
Q 
Models of MDD: 
BIO FACTORS (4) -- a lot of enthusiasm

> what kind of dep do these relate to?

A

1) Genetic factors
2) Biochemical factors
3) Brain anatomy & brain circuits
4) Immune system

17
Q

Genetics in MDD (2)

A

1) Twin studies: double the chance in identical twins

2) Genetic studies have also found that unipolar depression may be related to a set of genes’ chromosomes

18
Q

Biochemical factors in MDD

A
  • Serotonin & norepinphrine
  • body’s endocrine system
    a) Cortisol; abnormally high
    b) Melatonin; seasonal affective disorder.
19
Q

Evidence around biochemical factors in MDD

A
  • evidence comes from the fact you can treat MDD with SRIs (but doesnt work for everyone at all, 40%, just a wide spread belief that it does cos theyre widely used)
  • may work cos they affect glutamate levels

there is a lack of strong evidence supporting a direct correlation between low serotonin signaling and depression
- but has been a lot of evidence around faulty serotonin transportation and expression
BUT
- its actually a faulty glutamate system which may cause depression
- a wealth of data from animal models have shown that different types of environmental stress enhance glutamate release/transmission in limbic/cortical areas and exert powerful structural effects, inducing dendritic remodeling, reduction of synapses and possibly volumetric reductions resembling those observed in depressed patients.
-

20
Q

Brain anatomy + brain circuits in MDD

> What + evidence?

A

1) Serotonin circuit emotion regulation: amygdala + prefrontal cortex
2) Dopamine reward system: ventral striatum + medial prefrontal cortex
- in MDD theres a decreased experience of pleasure or interest in previously enjoyed activities (i.e. anhedonia) such as work or hobbies, and is accompanied by decreased motivation or drive
- thus, altered reward functioning may underlie this
- release dopamine within major components of the brain reward system = more pleasurable behaviour

  • ** among depressed people the blood flow to prefrontal cortex is diminished and hihger in emotion areas
  • the hippocampus is undersized and its production of new neurones is low (Kubera et al. 2011).

BUT EVIDENCE IS MIXED: WHY?

  • single SRI used in most of these studies
  • single neuroimagimg modality
  • only looking at the circuit of interest
21
Q

brain anatomy in BP and despression

A

there are neural correlates for the two

22
Q

Immune system + MDD

A
  • Gut microbioata
  • Inflammation around the body
  • inflammation due to insufficient reg of the immune system. Dysreg affects the negative feedback system + probs with brain areas like hoppocampus
  • mainly studies in rats but they have shown pos results by adding into diet
23
Q

Behavioural models of MDD

A

FOCUS: REWARDS + PUNISHMENTS in lives

  • Linked with depression
  • social rewards: depressed persons receive fewer social rewards than non-depressed people
  • those with depression report fewer rewards than non- depressed participants but when their rewards increased their mood also increased
  • May be a two way relationship  may be depressed persons is a victim of social circumstances but also may be that their flat mood etc help produce a decline in social rewards
24
Q

Cog models of MDD (2)

A

1) Learned helplessness

2) Negative Thinking

25
Q

Learned Helplessness model of MDD

A
  • Lack of control is the basis; dont try and help self bc they feel it will fail

NOW REFERED TO AS:
—-“Attribution helplessness theory”—–
attributing their present lack of control to intertal attributes ie “im inadequate at everything” = helpless to outcomes
SOME HAVE SAID THAT THEY ONLY CUASE DEPRESSION WHEN THEY CAUSE HOPELESSNESS IN A PERSON

26
Q

Evidence for Learned Helplessness model of MDD

A
  • interactions between the serotonin neurons and emotion-related brain regions (EG amygdala) play a key role in the development and/or expression of LH
  • GENERALLY mice showing “helpless” behavior had an overall brain-wide reduction in the level of neuronal activation compared with mice showing “resilient” behavior

limitations = relies a lot on animal research BUT can animals attribute?

27
Q

Negative thinking model of MDD

A
  • Cognitive Triad (themselves, experiences, futures interp in certain ways)
  • Errors in thinking (drawing fast concs on little evidence)
  • Automatic thoughts (steady train of unpleasant thoughts)
28
Q

Evidence for Negative thinking model of MDD

A
  • Lots of evidence for Beck (Possel & Black, 2014)
  • Agree that depressed people hold maladaptive attitues & the more maladaptive attitudes they hold the more depressed they are (Thomas & Altareb, 2012)
  • BUT are these biases cause or consequence?
    a) early negative schemas + inferences mediate the effects of cog vulnerability –> depression

People say you should link bio + cog = more holistic + neurobiological processes that initiate the cognitive bias and attenuated cognitive control, which allows the bias to persist **
- observed differences in cortical activity between healthy individuals and individuals with depression can be individually associated with elements
of biased attention.
- seperate neural mechs for increasing salience of negative stimuli and decrease the salience of positive or rewarding stimuli (maintenance of dep. mood)
- Amygdala HYPERacitivy = biased memory for negative
stimuli

29
Q

Family social perspective of MDD

A
  • basicalllyyy just a lack of social support has been linked with depression
  • isolation and lack of intimacy also linked
30
Q

Multicultural perspective of MDD: gender + culture

A

1) gender: why are women more likely than men?
a) less likely to get detected in men
b) Hormones
c) Body dissatifaction
d) Rumination theory - why am i depressed? Women more likely to ruminate

2) Culture
a) Symptoms can mostly be seen worldwide
b) not much diff in US culture
c) some expression of sympts is diff i.e. in china they have more physical but less cog

31
Q

BIPOLAR what?

A
  • Experience both the lows of depression and the highs of mania
  • emotional rollercoaster; much less common than unipolar depression
Depression = same as in MDD
Mania = complete opposite of depression symptoms

TYPE 1:
- full manic and Major depressive episodes
- weeks of mania followed by a week of wellness followed by weeks of depression
- can have mixed episodes: depression and mania are experienced in the same episode i.e. racing thoughts amidst having depressive thoughts
TYPE 2
- involves a major depressive episode lasting at least two weeks and at least one hypomanic episode (like mania but less severe)
- NO history of manic episodes

***cyclothymic disorder – repeated patterns over period of years of type 2

32
Q

Bipolar facts + figs

A
  • 1 – 3% of the population have bipolar at one point in time
  • 4% suffer with it at some point in their life
  • Men = women
  • Poor > rich
33
Q

what is a manic episode?

A

3+ of these
◦ Inflated self-esteem or grandiosity
◦ Decreased need for sleep
◦ Increased talkativeness or pressure to keep talking
◦ Flight of ideas or racing thoughts
◦ Distractibility
◦ Increase in goal-directed activity or psychomotor agitation
◦ Excessive involvement in risky behaviours
◦ Psychotic symptoms in severe cases

34
Q

Differential diagnosis (5)

A 
MDD
GAD/Panic/PTSD
Subs induced Bipolar
ADHD
PD
35
Q

Aetiology of BIPOLAR - bio exps

A
  • High norepinephrine activity
  • dysregulates ion molecules
  • Smaller basal ganglia and cerebellum + Structural abnormalities in AMG, PFC
  • genetics: 40% MZ twins
36
Q

Psychological models

A

NOT MUCH SUPPORT

37
Q

Online Social Networking and Mental Health

A
  • positive and negative effects
  • normally two ends of same sword
    EG
    may enhance self esteem but may reduce SE
    DOES seem that extreme use of SM = inc risk of depression
38
Q

Apps for mental health

A

Some have found them helpful only if theyre made well and meet user needs

  • despite the benefits of accessibility, cost-effectiveness, identification of triggers, anonymity, and ability to tailor content to individual needs, consumer engagement remains a hurdle for uptake and continued use
39
Q

Rethinking serotonin in depression

A
  • Functional fixedness
  • Calypsol AKA ketamine; works on glutamate
  • No mania so harder to see obvs effects
  • Seems to protect against stress; THUS we could give it to people who are @ high risk of developing depression
  • ATM we only have masking symptoms - why not put something in place to prevent it?
  • SSRIs work cos serotonin plays a modulating role on glutamate

Psychopathology - 13 mins (14 decks)

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