Mood Disorders Flashcards
1
Q
Symptoms of Depression (9)
A
- daily low mood
- diminished interested in activities (anhedonia)
- changes in apetite/weight (more than 5% body weight)
- sleep disturance (insominia and hypersomnia)
- agitation/retardatdation (activity change; slowing down/speeding up)
- fatigue and energy less
- concentration/decision making issue
- guilt/wortheless ness
- sucididality
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
3
Q
Types of Mood Disorders
A
depressive disorder
bipolar disorder
4
Q
What is a Mood DIstorder
A
a pyschological disorder chractersized by distrubances in the mood
5
Q
Pre-History Concept of Depression
A
hippocratus coins ‘melancholia’
6
Q
17 Century Concept of Depression
A
Robert Burton tries to estalish ‘science’ behind depression and identify strategies to treat it
7
Q
18-19 Century Concept of Depression
A
Johann Heinroth; associates depression with spiritualism; i.e. a distrubance of the soul
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
9
Q
Mid 20 Century Concept of Depression
A
DMS first established & developed as antidepresseds and depresssed neurons studied
10
Q
21st Century Concept of Depression
A
DMS-V 5 at the moment
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
12
Q
Depressive Disorder is compose dof…
A
major mood disorder (MDD)
dysthymia (mild depression)
13
Q
Biloplar Disorder is composed of…
A
severe bipolar disorder (mania and dperessive cycle)
cyclothymia (mild)
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
15
Q
what commorbidities are there
A
anxiety
substance abuse
schrizophenia
medical issues; depression, cancer, hypertension, anorexia nervosa
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
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)
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
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)
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
21
Q
list the possible causes of depression (8)
A
- genetic causes
- monoamine hypothesis
- neuroplasticity theory
- brain changes
- cortisol levels
- inflammation
- personality
- environment
22
Q
Genetic Causes of Depression: Explain
A
(Genes= predispotiion to depression)
- FAMILSTU DIES
family studies show MDD is moderatly heritable:
1st degree kin are 3 times more likely to develop it if in family history
- TWIN STUDIES (KENDLER)
identitical twins= if one has it the other is 46% likely to also have it
fraternal twins= only 20%
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
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
25
Critique of Monamine Hypothesis
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)
26
what does nonadrenaline do
for:
- alertness
- concentration
- energy
- mood
- cognition
- sex drive
- anxiety + irritability
27
what does dopomaine do
for:
- - pleasure and reward
- appetitie
- drive and motivation
- sex drive
- mood
- cognition
28
What does seratonin do
for:
- obessesions
- anixety
- compulsions
- irribabilitiy
- memory
- appeite
- mood
- cognition
29
Neuroplasticity Theory of Depression
Our brain is plastic= so neurogensis is maybe impairted in depressed patients
30
ontogenesis of depression
low in childhood (1-2%)
rises in adoscelence (>4%): hormones
high in later life (15%) as eldery peopel more isolated/deterioriating
31
financial costs of depression
- $210.5 Billion per year in US
- $1.7 Billion in UK
(costs of services, treatment and lost employment)
32
examples of anti-depressants
- seratonin reuptake inhibitors (SSris)
- tricyclic anti-depressants
- neurotrophic factor increasing drugs
33
how do SSRi's work int eh brain
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
34
evidence for neuroplasticity theory of depression
- reduced levels of neurotrophic factors (nerve growth factors, BDNF) in depressed patients that regulate brain plasticitiy
35
how to antidepresseants treat reduce neuroplasticity
facilitaite neurogensis by increasing neurotrophic factors such as BDNF
36
Brain Changes theory of Depression
the volume/structure/function of the brain is impaired;
| 1. reduced hippocampus in depressed patients (where nueorgensis occurs)
37
examples of anti-depressants
- seratonin reuptake inhibitors (SSris)
- tricyclic anti-depressants
- neurotrophic factor increasing drugs
- atypical anti depressants
- monoamine oxidase inhibitors (MADIS)
38
what does the reduced hippocampus demonstrate as a symptom
reduced memory in depressed patients
39
what is the DLPFC and what is it important for
dorsolateral prefrontal cortex;
important for cognitive control tasks and emotional tasks like dealing with frustraiton
40
Corsitol Theory of Depression
depressed people are 'chronically stressed':
| 50 % of depressed patients have increased cotristol levels
41
what is cortisol
stress hormone released by the hypothalamic pituitary adrenal axis (HPA)
42
issues with cortisol theory
- stress is also high in other disorders (aniety, hypertension, obseit)
- no reliable evidence exists that lowering cortisol reduces depression
43
Inflammation THeory of Depression
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)
44
Cytokine Administration; a drug exmaple
e.g. "Interferon" treats hepatitis; might cause depression in some patients
45
Anti-Inflammatory Treatments
polycristatlized fatty acids and monocyclines might help
46
Cytokine Levels: how does depression effect it
increased cytokine levels in the peripheray and central lobe of brain; are responsible for dealing with inflammation
47
Personality Theory of Depression
personality traits predispose people to depression as a negative self/perception and biases inflate it.
e.g. pessismism, perfectionism, low self esteem, etc.
48
Environment Theory of Depression
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
49
list the 3 pyschological theories of pathopyschology
1. Becks Cognitive Theory of Depression
2. Diathesis Stress Theory
3. the Biopyschosocial Model
(arent mutually exclusive)
50
issues with Personality Theory of Depression
hard to investiage methologolicially e.g. biases in self reports
51
pyschological theories of pathopyschology say..
depression is heterogenous as multipel factors cause it
more research is needed to see how factors interact
52
list the 3 pyschological theories of pathopyschology
1. Becks Cognitive Theory of Depression
2. Diathesis Stress Theory
3. the Biopyschosocial Model
(arent mutually exclusive)
53
issues with Personality Theory of Depression
hard to investiage methologolicially e.g. biases in self reports
54
pyschological theories of pathopyschology say..
depression is heterogenous as multipel factors cause it
more research is needed to see how factors interact
55
What is Becks Cognitive Theory of Depression
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
What is Diathesis Stress Theory
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
What is Becks Cognitive Theory of Depression
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
what are the cognitive distortions beck identified
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
Becks Cognitive Triad
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
what is diasthethesis
sucepbility/risk
61
Diasthesis examples
Diasthtesis:
- biological factors (genes, brain, etc)
- social factor (upbrining, chornic stress, unemployment)
- pyschological factor (unconscious conflicts, poor skills, maladaptive cognition)
62
Stress examples in Diasthesis Theory
- biological triggers (disease, toxin exposure)
- social triggers (trauma, loss)
- pscyhological triggers (trust violations, percieved loss of control, etc)
63
who proposed the biopyschosocial model
engel in 1977
64
biopyschosocial model; example of interacting factors
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
what are the two ways to treat depression
1. pyschosocial therapy
| 2. anti-depressants
66
what is CBT
cognitive bheavioural therapy; aims to 'change how a person thinks' (cogntiive) and acts ('behaviour') to improve mood over time
67
cognitive approaches of CBT (4)
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
behaviour approaches of CBT (5)
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
Iproniadid
1958; a drug first used to treat tubercelosis that improved mood in the patients (MAOIS example)
70
Impipramine
1958: a tricylic drug used to treat schrizophenia that elevated moods and energy levels (TCA)
71
Iproniazid
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
Impipramine
1958: a tricylic drug used to treat schrizophenia that elevated moods and energy levels (TCA)
73
What are Randomised Clinical Trials (RCT)
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
what are the 3 clinical phases in RCTs
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
what happens in the pre-clinical phase in RCT
lab tests
animal tests
resaearch
76
what are the 3 clinical phases in RCTs
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
RCT: important components
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
List two examples of clinical treatment testings
1. Bupropion (drug): increaes dopamine levels and thought to improve pleasure experiences
2. CBT (Pyschological)
79
Bupropion; efficency testing
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
CBT: Efficiency Testing
Luty 2007:
16 week comparison study of CBT and INTERPERSONAL PYSCHO THERAPY
sample size= 177 patients
results= CBT more effective for SEVERELY depressed
81
how to measure the size of treatment effects
effect size=
| (mean of experimental group)-(mean of control group)/standard deviation [variance]
82
how can we interpret the results of different studies
conduct multiple studies and combine interventions
1. systematic review; exhasutiive search of literatuare
2. meta-analysis; statistical analysis of all combined results
83
triangle of 'drug process'
from bottom to top:
1. animal/lab studies
2. case-controleld studies
3. cohort studies
4. randomized control trials
5. systematic review
6. meta anlyisis
7. clinical/practical guidelines for presecription
8. customer 'reviews'
84
Meta-analysis of Tricyli vs SSRI
no signitifact differences (cochrane review)
| slight more side/effects in tricylic drugs however
85
Meta-analysis of Antidepressants vs Active Placebo
active placebo= sugar pills with similar side effects
results= superiority of antidepressants only a little
86
Meta-analysis of Antidepressants vs Normal Placebo
normal placebo= no side effects
results= both tricyclic/ssri superior 4 weeks after tratement
87
Meta-analysis of CBT vs other talking therapies
cbt weakly superior
88
Meta-analysis of CBT v Antidepressants
CBT equal or slightly more effective
89
Meta-analysis of CBT v no treatment
CBT more effective (measured by placebos or putting patients on waiting lists)
90
relapse rates; CBT vs anti-depressants
1 year after treatment:
CBT has 29% relapse rate
Anti-depressants have 60% relapse rate
91
relapse rates; CBT vs anti-depressants
1 year after treatment:
CBT has 29% relapse rate
Anti-depressants have 60% relapse rate
92
Limitations of RCTS
- 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
Limitations of RCTS
- 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
benefits of experimental medicine
- 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
recent developments of treatment?
experimental medicine!
96
where does epxerimental medicine fit in during RCT
during phase i and ii
97
Methods of Experimental Medicine
--> it uses different methods to test efficency of treatments (neuroimaging, pyshcological) such as:
1. emotional processing tasks
2. fMRI
3. population studies
98
emotional processing tasksg
- facial expression recognition and memory for faces
- emotional memory
- fear processining
99
fMRI in experimental medicine
amygdala activity or hypothalmus activity studied
100
population studies in experimental medicine
- deseasd patients
- individuals at risk for depression
- healthy volunteers
101
future directions for experimental medicine
- research on pathopyschology of depression and interacting elements
- refine methods to reliably predict who responds to different treatments
- new treamtens; ketamine + neurostimulation
102
example of a face proccesining task used in experimental medicine
FACES= ask depressed patient to recognize diffent faces and determine the facial expression; identifies negative bias perceptions and memory
103
ketamine
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
EXPERIMENTAL MEDICINE: testing antidepressants
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)
```
2. brain function: antidepressants reduce amygdalda activity to negative faces
105
EXPERIMENTAL MEDICINE: testing CBT
Depression effects:
-reduced activity of PFC an DLPFC in regulating emotions
CBT effects:
- brain function
- shows CBT inceases activity in DLPFC
106
why does CBT increase activity in the DLPFC
because CBT stimulates the 'thinking part of the brain' found there
107
sigfnifance of experimental medicine predict clinical response in antidepressants
---> 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
sigfnifance of experimental medicine predict clinical response in antidepressants
---> 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
ICD-10
by WHO; another assetment of mental health;
| tries to provide an 'objective diagnosis'
110
DMS-5 controversy
but is controversal and flawed; used to classify homosxuality as a disorder
111
physical manifestations of depression
pain (headaches, sleep, backaches)
112
NIMH STUDY 1980
showed US prevalance of depression is 5.2%
113
DIS study
1970s; in tawain depression is 1.5% of popultation whereas in lebaonon is 19%
114
health seeking statistics
only 80 out of 1000 people report depression
115
process of getting help
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
CES-D
Ccenter for Epidimiological Studies Depression Scale:
| questions regarding social/functional impact on your life and frequency of symstpoms
117
HADS
Hosptital Anxiety and Depression Scale:
118
ways of measuring depression
CES-D
| HADS
119
how does having a family history of depression preidspose you
-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
post-natal depression
demonstrates that hormonal imbalances (progestero/estradiol) after birth
121
Hirschefeld Premorbid Personality Assetment
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
Hirschefeld Premorbid Personality Assetment Results
-- 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
indreict support for diasthesis theory
depressed people release more stress hormones; but not convincing
124
Patient P.S.
a widow who became tagiued, less cheerful and more anhedonious after husband died;
- ate less
- became hospitalized
125
affective disorder
a psychotic disorder of emotion
126
DEPRESSION types
1. reactive depression (triggered_
| 2. endogenous deprsesion (no apparent cause)
127
SAD
seasonal affective disorder= an aeffective disorder where attacks od depression result due to reduction of sunlight
128
Tricyclic Antidepressants
3 ring of atoms:
1. lock reuptake of seratonon-norepinephrise
2. increase levles in brain
3. safter alternatives to MAO inhibitiors
129
Lithuium
a moot stabalizer; drug that blocks the rapdi transtion between depression and mania rather than treating depression
130
how does excersize help
increases neurogensis in hippocampus and release endorphins
131
anxiety
a chronic fear that presists in absense of direct threat
132
translational research
research designed to translate basic scientific discoveries into efective clinical treatments
133
Beck (1967) logical errors or faulty thinking.
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
Pyschodynamic theory of Depression
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).
