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Pyschology > Mood Disorders > Flashcards

Mood Disorders Flashcards

1
Q

Symptoms of Depression (9)

A
  1. daily low mood
  2. diminished interested in activities (anhedonia)
  3. changes in apetite/weight (more than 5% body weight)
  4. sleep disturance (insominia and hypersomnia)
  5. agitation/retardatdation (activity change; slowing down/speeding up)
  6. fatigue and energy less
  7. concentration/decision making issue
  8. guilt/wortheless ness
  9. sucididality
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2
Q

DSM Diagnosis if Major Mood Disorder

A

Symptoms must last for at least 2 weeks
Patients must have more than 5 symptoms (including 1 and 2)

1 and 2 are; depressed daily mood + anhedonia

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3
Q

Types of Mood Disorders

A

depressive disorder

bipolar disorder

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4
Q

What is a Mood DIstorder

A

a pyschological disorder chractersized by distrubances in the mood

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5
Q

Pre-History Concept of Depression

A

hippocratus coins ‘melancholia’

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6
Q

17 Century Concept of Depression

A

Robert Burton tries to estalish ‘science’ behind depression and identify strategies to treat it

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7
Q

18-19 Century Concept of Depression

A

Johann Heinroth; associates depression with spiritualism; i.e. a distrubance of the soul

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8
Q

Early 20 Century Concept of Depression

A

Kraeplin: sees ‘endogenous’ and ‘exogeneous’ types where internal and external driven personalities exist

Freud= mourning and melancholia foster this

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9
Q

Mid 20 Century Concept of Depression

A

DMS first established & developed as antidepresseds and depresssed neurons studied

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10
Q

21st Century Concept of Depression

A

DMS-V 5 at the moment

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11
Q

Prevalance of Depression?

A
  • common (4.4% of the population)
  • 1 in 5 people have it at one point in their lives
  • it afffects women more than men
  • it affects adolscents and old people
  • its high in conflict countries
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12
Q

Depressive Disorder is compose dof…

A

major mood disorder (MDD)

dysthymia (mild depression)

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13
Q

Biloplar Disorder is composed of…

A

severe bipolar disorder (mania and dperessive cycle)

cyclothymia (mild)

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14
Q

What is a comorbidity

A

symptoms overlapping/asssociating with depression

the presence of one or more additional conditions co-occurring with a primary condition

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15
Q

what commorbidities are there

A

anxiety

substance abuse

schrizophenia

medical issues; depression, cancer, hypertension, anorexia nervosa

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16
Q

Prognosis( treatement) for depression: how succesful?

A
  • usually depressive peisodes last 3-6 months and most people recover within 12
  • however high reccurence risk
  • 27% end up with chronic depressive disorder + don’t recover
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17
Q

Effects of Mood Disorders on an Individual Level

A

physical health
quality of life

higher risk for other medical conditions

higher mortality rate (suicide)

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18
Q

Effects of Mood Disorders on Collective Level

A

society and economy= depressed people x7 more likely to be unemployed (hard to function/work)

leading cause of diability with economic impacts

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19
Q

What is pathophysiology

A

The branch of science dealing with mental processes, particularly as manifested by abnormal cognitive, perceptual, and intellectual functioning, during the course of mental disorders

(Looking at potential causes)

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20
Q

public perception of depression

A

71% link it to emotional weakness

65% link it to bad parenting

35% link it to sin

10% attribute it to chemical imblanace in brain

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21
Q

list the possible causes of depression (8)

A
  1. genetic causes
  2. monoamine hypothesis
  3. neuroplasticity theory
  4. brain changes
  5. cortisol levels
  6. inflammation
  7. personality
  8. environment
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22
Q

Genetic Causes of Depression: Explain

A

(Genes= predispotiion to depression)

  1. FAMILSTU DIES
    family studies show MDD is moderatly heritable:

1st degree kin are 3 times more likely to develop it if in family history

  1. TWIN STUDIES (KENDLER)
    identitical twins= if one has it the other is 46% likely to also have it

fraternal twins= only 20%

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23
Q

Monoamine Hypothesis: Explan

A

‘depression is caused by reduced monoamine (Neurotransmitter) levels such as seratonin, nonadrenaline and dopamine that play a role in mood, cognition and anxiety levels

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24
Q

Evidence for Monoamine Hypothesis

A

–> DRUGS that treat MDD such as seratonint reuptake inhibitotrs (SSRi) or tricyclic antidepressants elevant monoamines

  • in 1950; reserpine (a hypertension drug): lowered monoamine and triggered depression
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25
Q

Critique of Monamine Hypothesis

A
  1. not all anti-depressants are effective in all patients
  2. depression is complex (not just because of monamine imblanace
  3. monoamine levels increase after treatment but it might take several weeks for mood to actually improve (prolonged effective-ness= means its hard to be accurate)
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26
Q

what does nonadrenaline do

A

for:

  • alertness
  • concentration
  • energy
  • mood
  • cognition
  • sex drive
  • anxiety + irritability
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27
Q

what does dopomaine do

A

for:
- - pleasure and reward
- appetitie
- drive and motivation
- sex drive
- mood
- cognition

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28
Q

What does seratonin do

A

for:

  • obessesions
  • anixety
  • compulsions
  • irribabilitiy
  • memory
  • appeite
  • mood
  • cognition
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29
Q

Neuroplasticity Theory of Depression

A

Our brain is plastic= so neurogensis is maybe impairted in depressed patients

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30
Q

ontogenesis of depression

A

low in childhood (1-2%)

rises in adoscelence (>4%): hormones

high in later life (15%) as eldery peopel more isolated/deterioriating

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31
Q

financial costs of depression

A
  • $210.5 Billion per year in US
  • $1.7 Billion in UK

(costs of services, treatment and lost employment)

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32
Q

examples of anti-depressants

A
  • seratonin reuptake inhibitors (SSris)
  • tricyclic anti-depressants
  • neurotrophic factor increasing drugs
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33
Q

how do SSRi’s work int eh brain

A

Healthy patient:
- monoamines are released and bind to receptors in posty-synpatic neuron and are then reabosrbed into the presynpatic neuron

Depressed patient:
- fewer monamines are availalbe in the synapse

Treatment:
- SSRis block the reuptake of monoamines in the synapse to increase seratonin level s

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34
Q

evidence for neuroplasticity theory of depression

A
  • reduced levels of neurotrophic factors (nerve growth factors, BDNF) in depressed patients that regulate brain plasticitiy
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35
Q

how to antidepresseants treat reduce neuroplasticity

A

facilitaite neurogensis by increasing neurotrophic factors such as BDNF

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36
Q

Brain Changes theory of Depression

A

the volume/structure/function of the brain is impaired;

1. reduced hippocampus in depressed patients (where nueorgensis occurs)

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37
Q

examples of anti-depressants

A
  • seratonin reuptake inhibitors (SSris)
  • tricyclic anti-depressants
  • neurotrophic factor increasing drugs
  • atypical anti depressants
  • monoamine oxidase inhibitors (MADIS)
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38
Q

what does the reduced hippocampus demonstrate as a symptom

A

reduced memory in depressed patients

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39
Q

what is the DLPFC and what is it important for

A

dorsolateral prefrontal cortex;

important for cognitive control tasks and emotional tasks like dealing with frustraiton

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40
Q

Corsitol Theory of Depression

A

depressed people are ‘chronically stressed’:

50 % of depressed patients have increased cotristol levels

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41
Q

what is cortisol

A

stress hormone released by the hypothalamic pituitary adrenal axis (HPA)

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42
Q

issues with cortisol theory

A
  • stress is also high in other disorders (aniety, hypertension, obseit)
  • no reliable evidence exists that lowering cortisol reduces depression
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43
Q

Inflammation THeory of Depression

A

similarities between sick people/depressed people, such as anhedonie, lethargy and fatigue

= depressed patients have increased inflmmation

results in compromised immuned system (mind-body dualism)

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44
Q

Cytokine Administration; a drug exmaple

A

e.g. “Interferon” treats hepatitis; might cause depression in some patients

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45
Q

Anti-Inflammatory Treatments

A

polycristatlized fatty acids and monocyclines might help

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46
Q

Cytokine Levels: how does depression effect it

A

increased cytokine levels in the peripheray and central lobe of brain; are responsible for dealing with inflammation

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47
Q

Personality Theory of Depression

A

personality traits predispose people to depression as a negative self/perception and biases inflate it.

e.g. pessismism, perfectionism, low self esteem, etc.

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48
Q

Environment Theory of Depression

A

stressful life events (divorce, death, trauma) precede it

maltreatment and childhood abuse

lack of social support (systemic issues)

environment can activate genes (epigentics) to make u more susceptible to depression

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49
Q

list the 3 pyschological theories of pathopyschology

A
  1. Becks Cognitive Theory of Depression
  2. Diathesis Stress Theory
  3. the Biopyschosocial Model

(arent mutually exclusive)

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50
Q

issues with Personality Theory of Depression

A

hard to investiage methologolicially e.g. biases in self reports

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51
Q

pyschological theories of pathopyschology say..

A

depression is heterogenous as multipel factors cause it

more research is needed to see how factors interact

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52
Q

list the 3 pyschological theories of pathopyschology

A
  1. Becks Cognitive Theory of Depression
  2. Diathesis Stress Theory
  3. the Biopyschosocial Model

(arent mutually exclusive)

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53
Q

issues with Personality Theory of Depression

A

hard to investiage methologolicially e.g. biases in self reports

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54
Q

pyschological theories of pathopyschology say..

A

depression is heterogenous as multipel factors cause it

more research is needed to see how factors interact

55
Q

What is Becks Cognitive Theory of Depression

A

Aaron Beck: looked at the tendencies of negative self-perception in depressed patients= as they are more likely to think about events/interactions/self negatively which reinforces low mood

Identified:

  1. The cognitive triad (of negative automatic thinking)
  2. Negative self schemas/cognitive disortions
  3. Errors in Logic (i.e. faulty information processing)
56
Q

What is Diathesis Stress Theory

A

some people INHERENTLY are more suscptible to develop depression so the threshold minimum to develop it is lower

An individualds diasthethesi MUST interact with stress/trigger= the greater the ‘diasththesies’ the LESS STRESS is needed to cause depression

57
Q

What is Becks Cognitive Theory of Depression

A

Aaron Beck: looked at the tendencies of negative self-perception in depressed patients= as they are more likely to think about events/interactions/self negatively which reinforces low mood

(view of world–> infleucnce emotions–> creates maldataptive/unsocial behaviour—> fewer rewarding events exist)

Identified:

  1. The cognitive triad (of negative automatic thinking)
  2. Negative self schemas/cognitive disortions
  3. Errors in Logic (i.e. faulty information processing)
58
Q

what are the cognitive distortions beck identified

A
  1. FILTERING: focusing on negative and ignoring positive
  2. B/W THINKING: percieving events all or nothing
  3. JUMPTING TO CONCLUSIONS= not examinining evidence
  4. OVERGENERALIZATION
59
Q

Becks Cognitive Triad

A

The cognitive triad are three forms of negative (i.e. helpless and critical) thinking that are typical of individuals with depression: namely negative thoughts:

  1. about the self
  2. the world
  3. the future.

These thoughts tended to be automatic in depressed people as they occurred spontaneously.

60
Q

what is diasthethesis

A

sucepbility/risk

61
Q

Diasthesis examples

A

Diasthtesis:

  • biological factors (genes, brain, etc)
  • social factor (upbrining, chornic stress, unemployment)
  • pyschological factor (unconscious conflicts, poor skills, maladaptive cognition)
62
Q

Stress examples in Diasthesis Theory

A
  • biological triggers (disease, toxin exposure)
  • social triggers (trauma, loss)
  • pscyhological triggers (trust violations, percieved loss of control, etc)
63
Q

who proposed the biopyschosocial model

A

engel in 1977

64
Q

biopyschosocial model; example of interacting factors

A

Biological: disability, physical health, Iq, drugs

Pyschological: iq, self-esteemn, social skills, family tension, trauma

social; drugs, family tension, trauma, lack of family/friends or school environment

65
Q

what are the two ways to treat depression

A
  1. pyschosocial therapy

2. anti-depressants

66
Q

what is CBT

A

cognitive bheavioural therapy; aims to ‘change how a person thinks’ (cogntiive) and acts (‘behaviour’) to improve mood over time

67
Q

cognitive approaches of CBT (4)

A
  1. Identify thought patterns in response to situation
  2. develop balanced thinking by looking at evidence and reinforcing positive thinking/rationalization
  3. learn new skills
  4. think of alternative/helpful/positive thoughts
68
Q

behaviour approaches of CBT (5)

A
  1. schedule positive activities
  2. become more active (excersize)
  3. break tasks into small and achievabl steps
  4. gradual exposure to feareful situation
  5. implement relaxation techniques
69
Q

Iproniadid

A

1958; a drug first used to treat tubercelosis that improved mood in the patients (MAOIS example)

70
Q

Impipramine

A

1958: a tricylic drug used to treat schrizophenia that elevated moods and energy levels (TCA)

71
Q

Iproniazid

A

1958; a drug first used to treat tubercelosis that improved mood in the patients (MAOIS example)

—> it increaes monoamine by inhibitidy monoamine oxidase (enzyme breaking down NT)

side effects: stokes, elevated blood pressure

72
Q

Impipramine

A

1958: a tricylic drug used to treat schrizophenia that elevated moods and energy levels (TCA)

73
Q

What are Randomised Clinical Trials (RCT)

A

studies on humans that test therpetuic effiecnecy of untested drugs that split populations into ‘control ‘and ‘invervention’ groups

divided into:

  1. preclinical stage
  2. clinical stage (with three phases)
  3. post-clinical stage
74
Q

what are the 3 clinical phases in RCTs

A

Phase 1: health people studied (establish dosage, safety and side effects)= around 50 people

Phease 2: Diseased people studied (treatment eefficenty, placebos and side effects) = around 500 people

Phase 4: large rpopulation study (treatment effiecnecy, global/temporal variance, compare to other treatments)= around 1000+ poeple

75
Q

what happens in the pre-clinical phase in RCT

A

lab tests
animal tests
resaearch

76
Q

what are the 3 clinical phases in RCTs

A

Phase 1: healthy, paid people studied (establish dosage, screening for safety/tolerance and side effects)= around 50 people

Phease 2: Diseased people studied (treatment eefficenty, placebos, test conditions, placebo/double glind groups and side effects) = around 500 people

Phase 4: large rpopulation study (treatment effiecnecy, global/temporal variance, compare to other treatments)= around 1000+ poeple

77
Q

RCT: important components

A
  1. use of control group and placevos
  2. clearly define the symptoms and side effects
  3. ensure all patients to through the same processed/measured by same outcomes
  4. blind studies: to avoid bias
78
Q

List two examples of clinical treatment testings

A
  1. Bupropion (drug): increaes dopamine levels and thought to improve pleasure experiences
  2. CBT (Pyschological)
79
Q

Bupropion; efficency testing

A

Jefferson 2006 conducted a double blind/randomized trials:
8 week study comparing placebo and bupropion treatment

270 patient sample with MDD

results= higher response rates to bupropion group

80
Q

CBT: Efficiency Testing

A

Luty 2007:
16 week comparison study of CBT and INTERPERSONAL PYSCHO THERAPY

sample size= 177 patients

results= CBT more effective for SEVERELY depressed

81
Q

how to measure the size of treatment effects

A

effect size=

(mean of experimental group)-(mean of control group)/standard deviation [variance]

82
Q

how can we interpret the results of different studies

A

conduct multiple studies and combine interventions

  1. systematic review; exhasutiive search of literatuare
  2. meta-analysis; statistical analysis of all combined results
83
Q

triangle of ‘drug process’

A

from bottom to top:
1. animal/lab studies

  1. case-controleld studies
  2. cohort studies
  3. randomized control trials
  4. systematic review
  5. meta anlyisis
  6. clinical/practical guidelines for presecription
  7. customer ‘reviews’
84
Q

Meta-analysis of Tricyli vs SSRI

A

no signitifact differences (cochrane review)

slight more side/effects in tricylic drugs however

85
Q

Meta-analysis of Antidepressants vs Active Placebo

A

active placebo= sugar pills with similar side effects

results= superiority of antidepressants only a little

86
Q

Meta-analysis of Antidepressants vs Normal Placebo

A

normal placebo= no side effects

results= both tricyclic/ssri superior 4 weeks after tratement

87
Q

Meta-analysis of CBT vs other talking therapies

A

cbt weakly superior

88
Q

Meta-analysis of CBT v Antidepressants

A

CBT equal or slightly more effective

89
Q

Meta-analysis of CBT v no treatment

A

CBT more effective (measured by placebos or putting patients on waiting lists)

90
Q

relapse rates; CBT vs anti-depressants

A

1 year after treatment:

CBT has 29% relapse rate

Anti-depressants have 60% relapse rate

91
Q

relapse rates; CBT vs anti-depressants

A

1 year after treatment:

CBT has 29% relapse rate

Anti-depressants have 60% relapse rate

92
Q

Limitations of RCTS

A
  • ethical issues of using placebos (half of patients dont get treament)
  • placebo effect= creates biases of results
  • length of time required (delays to treatment)
  • financial issues (funding)
  • does not investigate mechanisms and only symptoms
93
Q

Limitations of RCTS

A
  • ethical issues of using placebos (half of patients dont get treament)
  • placebo effect= creates biases of results or active placebos might cause other issues
  • length of time required (delays to treatment)
  • financial issues (funding, partiality and ethics, drug companies, confidentality)
  • ‘orphan’ or ‘illegal’ drugs
  • government needs to do clinical trials with soild foundation in comparitive translational research
  • does not investigate mechanisms and only symptoms
94
Q

benefits of experimental medicine

A
  • elucidates mechanisms of drug
  • can detect early only how patients might respond to a given tratment by detecting biomarkers
  • does not replace but ASISTS RCTS= speeds up process/decision making
95
Q

recent developments of treatment?

A

experimental medicine!

96
Q

where does epxerimental medicine fit in during RCT

A

during phase i and ii

97
Q

Methods of Experimental Medicine

A

–> it uses different methods to test efficency of treatments (neuroimaging, pyshcological) such as:

  1. emotional processing tasks
  2. fMRI
  3. population studies
98
Q

emotional processing tasksg

A
  • facial expression recognition and memory for faces
  • emotional memory
  • fear processining
99
Q

fMRI in experimental medicine

A

amygdala activity or hypothalmus activity studied

100
Q

population studies in experimental medicine

A
  • deseasd patients
  • individuals at risk for depression
  • healthy volunteers
101
Q

future directions for experimental medicine

A
  • research on pathopyschology of depression and interacting elements
  • refine methods to reliably predict who responds to different treatments
  • new treamtens; ketamine + neurostimulation
102
Q

example of a face proccesining task used in experimental medicine

A

FACES= ask depressed patient to recognize diffent faces and determine the facial expression; identifies negative bias perceptions and memory

103
Q

ketamine

A

an anaesthetic and analgesic (pain killer)
used to treat SEVERE depression: blocking glutamate receptors

Ketamine acts on depression by rebalancing a different set of neurotransmitters and receptors (the NMDA/glutamate receptors and GABA receptors) than the old-school Selective Serotonin Reuptake Inhibitor

104
Q

EXPERIMENTAL MEDICINE: testing antidepressants

A

Depression Effects (Studied)

  1. negative affective bias
  2. attention and memory issues (tendency to percieve efaces as sad or only reacll negative words)
  3. brain function (inrease amygadla response to negative faces)
Antidepressant effects (studied)
1. attention and memory; antidepressants increaes recall of positive words (i.e. cheerful, optimism)
  1. brain function: antidepressants reduce amygdalda activity to negative faces
105
Q

EXPERIMENTAL MEDICINE: testing CBT

A

Depression effects:
-reduced activity of PFC an DLPFC in regulating emotions

CBT effects:

  • brain function
  • shows CBT inceases activity in DLPFC
106
Q

why does CBT increase activity in the DLPFC

A

because CBT stimulates the ‘thinking part of the brain’ found there

107
Q

sigfnifance of experimental medicine predict clinical response in antidepressants

A

—> reduced amygdala neural activit yo negative faces one week after treatment with antidepressants;
patients scanned 0-1 weeks in 2016 on antidepressants showed reduced amygalda activity early one=

means that treatment adjustments can be made QUICKLY

108
Q

sigfnifance of experimental medicine predict clinical response in antidepressants

A

—> reduced amygdala neural activit yo negative faces one week after treatment with antidepressants;
patients scanned 0-1 weeks in 2016 on antidepressants showed reduced amygalda activity early one=

means that treatment adjustments can be made QUICKLY

109
Q

ICD-10

A

by WHO; another assetment of mental health;

tries to provide an ‘objective diagnosis’

110
Q

DMS-5 controversy

A

but is controversal and flawed; used to classify homosxuality as a disorder

111
Q

physical manifestations of depression

A

pain (headaches, sleep, backaches)

112
Q

NIMH STUDY 1980

A

showed US prevalance of depression is 5.2%

113
Q

DIS study

A

1970s; in tawain depression is 1.5% of popultation whereas in lebaonon is 19%

114
Q

health seeking statistics

A

only 80 out of 1000 people report depression

115
Q

process of getting help

A
  1. rough screening questions
  2. checking DSM criteria
  3. asses suicie risk/substance abuse or comorbidities
  4. discuss treatment options + decide careplan
  5. minitor progress and reasses diagnosi
116
Q

CES-D

A

Ccenter for Epidimiological Studies Depression Scale:

questions regarding social/functional impact on your life and frequency of symstpoms

117
Q

HADS

A

Hosptital Anxiety and Depression Scale:

118
Q

ways of measuring depression

A

CES-D

HADS

119
Q

how does having a family history of depression preidspose you

A

-reduced volume in anterior cingulate and amygdalda
- hypersensitive amygalda is known to be associate with negative cognitive biases/genetic polymorphisis
= this increase the risk in next generaiton

120
Q

post-natal depression

A

demonstrates that hormonal imbalances (progestero/estradiol) after birth

121
Q

Hirschefeld Premorbid Personality Assetment

A

evaluates people before they test MD to get ‘idea of their personality’ not influenced by depressed patients (i.e. patients self-rpoert personality different when depressed and when recovered)

122
Q

Hirschefeld Premorbid Personality Assetment Results

A

– decreased emotional strength and increased intepersonal depdency in ages 31-41 and not in 17-30:
suggests pyschosocial factors more important later in depression whereas genetic oens important early on

123
Q

indreict support for diasthesis theory

A

depressed people release more stress hormones; but not convincing

124
Q

Patient P.S.

A

a widow who became tagiued, less cheerful and more anhedonious after husband died;

  • ate less
  • became hospitalized
125
Q

affective disorder

A

a psychotic disorder of emotion

126
Q

DEPRESSION types

A
  1. reactive depression (triggered_

2. endogenous deprsesion (no apparent cause)

127
Q

SAD

A

seasonal affective disorder= an aeffective disorder where attacks od depression result due to reduction of sunlight

128
Q

Tricyclic Antidepressants

A

3 ring of atoms:

  1. lock reuptake of seratonon-norepinephrise
  2. increase levles in brain
  3. safter alternatives to MAO inhibitiors
129
Q

Lithuium

A

a moot stabalizer; drug that blocks the rapdi transtion between depression and mania rather than treating depression

130
Q

how does excersize help

A

increases neurogensis in hippocampus and release endorphins

131
Q

anxiety

A

a chronic fear that presists in absense of direct threat

132
Q

translational research

A

research designed to translate basic scientific discoveries into efective clinical treatments

133
Q

Beck (1967) logical errors or faulty thinking.

A

Arbitrary Inference. Drawing a negative conclusion in the absence of supporting data.

Selective Abstraction. Focusing on the worst aspects of any situation.

Magnification and Minimisation. If they have a problem they make it appear bigger than it is. If they have a solution they make it smaller.

Personalization. Negative events are interpreted as their fault.

Dichotomous Thinking. Everything is seen as black and white. There is no in between.

134
Q

Pyschodynamic theory of Depression

A

by freud: (1960s)

inwardly directed anger (Freud, 1917),
introjection of love object loss,

severe super-ego demands (Freud, 1917),

excessive narcissistic, oral and/or anal personality need (Chodoff, 1972),

loss of self-esteem (Bibring, 1953; Fenichel, 1968)

deprivation in the mother child relationship during the first year (Kleine, 1934).

Pyschology (13 decks)

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