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mood disorders Flashcards

1
Q

mood disorders can be split into

A

low mood
elevated mood & low mood

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2
Q

low mood disorders divided

A

major depressive disorder
dysthymia

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3
Q

elevated & low mood disorder

A

bipolar disorder

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4
Q

major depressive disorder 2 diagnostic criteria

A

Depressed mood: For children and adolescents, this can also be an irritable mood

Diminished interest or loss of pleasure in almost all activities (anhedonia)

must have on of these for a diagnosis

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5
Q

diagnostic criteria of MDD

A

In a two week period, must have 5 of the criteria (inc. at least one of key two).
Must cause distress or impairment and do not have another cause e.g. drug abuse.

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6
Q

notable diagnostic specifiers for MDD

A

anxious distress
atypical features
melancholic features
post partum onset
seasonal pattern

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7
Q

melancholic features MDD

A

lack of joy = required
insomnia
diurnal mood variations
anorexia
psychomotor retardation or agitation
feelings of guilt

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8
Q

atypical features MDD

A

maintained ability to experience joy=required
weight gain
worse in evening
increased sleep
sensitivity to rejection
anxiety
feeling of heaviness

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9
Q

what NICE diagnostic category is not seen in DSM5

A

subthreshold depressive symptoms (fewer than 5 symptoms)

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10
Q

MDD rates in females vs males

A

2 x in females

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11
Q

prevalence MDD world population

A

5% world population

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12
Q

MDD and age

A

peak for diagnosis in 30s and 40s
age of onset decreasing- people becoming more frequently diagnosed in teens and 20s

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13
Q

prevalence bipolar world population

A

1%

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14
Q

largest cost of MDD

A

workplace cost (loss of productivity) > direct cost of care > suicide cost

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15
Q

risk factors of depression

A

age, gender, ethnicity

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16
Q

bipolar consists of

A

depressive episodes and manic episodes

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17
Q

suicide risk bipolar

A

35% attempt suicide

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18
Q

manic episode bipolar

A

Abnormally elevated, expansive or irritable mood and persistently increase activity or energy, present most of the time for at least a week. Plus three of the following (four if irritable mood):
-inflated self esteem, grandiosity
-decreased need for sleep
-more talkative than usual
-flights of ideas, racing thoughts
-distractibility
-increase in goal directed activity or psychomotor agitation
-excessive involvement in damaging activities: hypersexuality, gambling, spending, foolish business ventures

Episode causes marked impairment to functioning or has psychotic features (delusions or hallucinations)

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19
Q

mania subtypes

A

hypomania or mixed episode

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20
Q

hypomania

A

mildly elevated mood and energy level

must produce a definite change in functioning that is noticeable by others

impairment not so great: individuals can be highly productive whilst hypomanic

Tends to be underdiagnosed as often seen as a “personality trait”

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21
Q

mixed episode

A

patient has elevated energy levels, psychosis etc but is simultaneously depressed

even higher risk of suicide
-elevated energy allows you to follow through with suicidal ideations that you may not have energy to in depressive episode

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22
Q

type 1 bipolar

A

classic manic depression
-can get rapid cycling

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23
Q

type 2 bipolar

A

depressive episodes and hypomania
-can get rapid cycling

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24
Q

cyclothymia

A

mild depression + hypomania >2 years

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25
what is rapid cycling?
> 4 episodes in a year
26
what positive characteristics is bipolar suggested to be linked to
creativity and productivity
27
what 4 brain areas atrophy in MDD?
prefrontal cortex hippocampus anterior cingulate cortex amygdala
28
hippocampal atrophy in depression
Negative correlation- the longer depression is untreated the smaller the total hippocampal volume
29
glucose metabolism in depression and its implications
lower glucose metabolism un prefrontal cortex than rest of the brain - likely as result of reduced cortical volume PFC important in regulation of emotion and exerts inhibitory control over the hypothalamus hypothalamus regulates amount of cortisol cortisol may be root cause of depression
30
glucose metabolism in bipolar disorder
PFC activity decreased during depressive phase - lower metabolism PFC activity/ metabolism increased during manic episodes
31
amelioration of depression
Attempted suicide by gunshot to head Survived Afterwards it was found her depression was deeply abated The brain region that took the most damage was the ventral prefrontal cortex – shows its importance in emotion
32
the amygdala and major depressive disorder
thought to be very important in emotional regulation thought its volume is reduced in major depressive disorder amygdala activity in response to positive and negative stimuli also appears to be altered
33
mechanisms of depression
Monoamine hypothesis: dysfunction of serotonergic and noradrenergic transmission Chronic stress - dysfunction of the HPA axis, prefrontal cortex and hippocampus
34
Iproniazid
Approved as AD in 1958 Irreversible MAO inhibitor - increases monoamine concentrations 1952) developed to treat tuberculosis Patients seemed “inappropriately happy”
35
resperpine
early antihypertensive/ antipsychotic Blocks VMAT, depletes MA from the presynaptic nerve terminal Suggested to cause depression, seen as evidence for the monoamine hypothesis
36
VMAT
vesicular monoamine transporter
37
historical basis for role of monoamines in depression
iproniazid resperpine serotonin levels lowered in depressed patients tryptophan depletion lowers mood, induces relapse in sufferers of depression
38
problems with the monoamine hypothesis (antidepressants)
Almost all AD drugs act by altering serotonergic or noradrenergic transmission Effects on transmission are very quick But! AD effects delayed by 2-4 weeks MA hypothesis explains this by changes in receptor expression/desensitization
39
what is cortisol
very strong physiological regulator. It regulates the immune system and metabolism important to regulate this, so we have negative feedback systems
40
stress and cortisol
Stress can cause plasma cortisol levels to rise - useful mechanism as cortisol will help mobilise glucose works well in normal individual but seems to go wrong in depressed individuals
41
HPA activity in depressed patients
50% of depressed patients have hyperactivity of HPA axis 80% of severely depressed patients have HPA axis hyperactivity Reflected in increased cortisol levels
42
what is the dexamethasone suppression test
tests whether negative feedback systems in the HPA axis are working properly Dexamethasone is a very potent glucocorticoid and if you give someone a dose of it it will act on the glucocorticoid receptors in the anterior pituitary and the hypothalamus Result in decreased production of CRF, ACTH and therefore cortisol
43
results of dexamethasone suppression test
reduces cortisol by 85% in controls; 45% in depressed in depressed patients negative feedback loops are not working properly
44
negative feedback of HPA axis not working & depression
caused by chronic stress increased amount of cortisol and over a long period of time somehow compromises the negative feedback loops perhaps receptors become less sensitive to cortisol dramatically increase past the point stress itself would also see high levels of CRF
45
actions of CRF and cortisol on the brain
hippocampus and prefrontal cortex have receptors for cortisol and CRF Cortisol and CSF cause increased apoptosis and decreased neurogenesis of these areas leads to atrophy and depression (amygdala also has receptors for these)
46
evidence cortisol and CSF = atrophy and depression
Cushing’s syndrome (increased cortisol/long term treatment with GC) frequently -> depression
47
genetic factors of HPA hyperactivity
Polymorphisms in genes involved in the HPA axis?
48
epigenetic factors of HPA hyperactivity
Childhood trauma Deprivation May explain while early childhood problems are risk factors for depression as an adult
49
what may explain time difference between antidepressant start and effects
Drugs may influence rate of neurogenesis and apoptosis Result in restoration of structure of critical brain regions This would take time explaining 2-4 weeks If we can restore brain regions, may get HPA axis back under control
50
approaches to study mood disorders
twin studies genome wide association studies
51
genetic risk of MDD
40%?
52
genes linked to MMD (monoamine transmission)
polymorphism SERT - increase risk 20% strong association between polymorphisms in DAT and d4 receptor
53
genes linked to MMD (HPA axis dysfunction)
polymorphisms for genes involved in: the mineralocorticoid receptor corticotrophin releasing hormone receptor FKBP5, which is a protein that modulates the sensitivity of the glucocorticoid receptor strong evidence for the role of epigenetic changes
54
genes linked to MMD (other)
polymorphisms in the G protein subunit beta 3 - but the mechanism is unclear. Methylenetetrahydrofolate reductase mutations -could be that this impacts on the ability to metabolize folate and might compound environmental factors such as childhood neglect.
55
genetic contribution disease risk bipolar
as high as 80% reported
56
genes linked to bipolar
ANK3, CACNA1C and TRANK1
57
ANK3
codes for ankyrin B, which is a protein involved in neuronal myelination
58
CACNA1C
CACNA1C codes for a voltage sensitive calcium channel that is known to be expressed in the brain and which may have roles in both development and signalling
59
TRANK1
expression of its product is increased by mood stabilizers such as sodium valproate, perhaps offering clues as to the mechanism of action of these drugs in bipolar disorder also associated with schizophrenia
60
behavioural shutdown
that when it is not possible to immediately overcome a stressor, it is better to conserve energy in order to survive may also explain why there are high levels of anxiety seen in people with depression. Anxiety is essentially a state of hypervigilance and that would have an evolutionary advantage if you were sick and sheltering from danger.
61
Acceptance of subservient position
Another animal model of depression is to place young rats in a cage with a dominant adult male rat. The best way for someone in a position like this to survive, is to be subservient and accept their position
62
Psychic pain
Physical pain serves a purpose: it tells us to stop doing something that is proving damaging to us. It is possible that depression may serve a similar purpose i.e. it will make us withdraw from activities that are proving stressful
63
Rumination
that people who are depressed are actually better at solving certain kinds of problem than non-depressed individuals. By shutting down other behaviours, depression may allow us to focus on certain types of problem and find a solution. This may be particularly important in solving social dilemmas e.g. whether to stay in a relationship.
64
measures of depression
Patient health questionnaire 9 Hamilton depression rating scale

Drugs And The Brain (9 decks)

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