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Drugs And The Brain > mood disorders > Flashcards

mood disorders Flashcards

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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
Q

what is rapid cycling?

A

> 4 episodes in a year

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26
Q

what positive characteristics is bipolar suggested to be linked to

A

creativity and productivity

27
Q

what 4 brain areas atrophy in MDD?

A

prefrontal cortex
hippocampus
anterior cingulate cortex
amygdala

28
Q

hippocampal atrophy in depression

A

Negative correlation- the longer depression is untreated the smaller the total hippocampal volume

29
Q

glucose metabolism in depression and its implications

A

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
Q

glucose metabolism in bipolar disorder

A

PFC activity decreased during depressive phase - lower metabolism

PFC activity/ metabolism increased during manic episodes

31
Q

amelioration of depression

A

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
Q

the amygdala and major depressive disorder

A

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
Q

mechanisms of depression

A

Monoamine hypothesis: dysfunction of serotonergic and noradrenergic transmission

Chronic stress - dysfunction of the HPA axis, prefrontal cortex and hippocampus

34
Q

Iproniazid

A

Approved as AD in 1958
Irreversible MAO inhibitor - increases monoamine concentrations

1952) developed to treat tuberculosis
Patients seemed “inappropriately happy”

35
Q

resperpine

A

early antihypertensive/ antipsychotic

Blocks VMAT, depletes MA from the presynaptic nerve terminal

Suggested to cause depression, seen as evidence for the monoamine hypothesis

36
Q

VMAT

A

vesicular monoamine transporter

37
Q

historical basis for role of monoamines in depression

A

iproniazid
resperpine
serotonin levels lowered in depressed patients
tryptophan depletion lowers mood, induces relapse in sufferers of depression

38
Q

problems with the monoamine hypothesis (antidepressants)

A

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
Q

what is cortisol

A

very strong physiological regulator. It regulates the immune system and metabolism

important to regulate this, so we have negative feedback systems

40
Q

stress and cortisol

A

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
Q

HPA activity in depressed patients

A

50% of depressed patients have hyperactivity of HPA axis

80% of severely depressed patients have HPA axis hyperactivity

Reflected in increased cortisol levels

42
Q

what is the dexamethasone suppression test

A

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
Q

results of dexamethasone suppression test

A

reduces cortisol by 85% in controls; 45% in depressed

in depressed patients negative feedback loops are not working properly

44
Q

negative feedback of HPA axis not working & depression

A

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
Q

actions of CRF and cortisol on the brain

A

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
Q

evidence cortisol and CSF = atrophy and depression

A

Cushing’s syndrome
(increased cortisol/long term treatment with GC)
frequently -> depression

47
Q

genetic factors of HPA hyperactivity

A

Polymorphisms in genes involved in the HPA axis?

48
Q

epigenetic factors of HPA hyperactivity

A

Childhood trauma
Deprivation

May explain while early childhood problems are risk factors for depression as an adult

49
Q

what may explain time difference between antidepressant start and effects

A

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
Q

approaches to study mood disorders

A

twin studies
genome wide association studies

51
Q

genetic risk of MDD

A

40%?

52
Q

genes linked to MMD (monoamine transmission)

A

polymorphism SERT - increase risk 20%
strong association between polymorphisms in DAT and d4 receptor

53
Q

genes linked to MMD (HPA axis dysfunction)

A

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
Q

genes linked to MMD (other)

A

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
Q

genetic contribution disease risk bipolar

A

as high as 80% reported

56
Q

genes linked to bipolar

A

ANK3, CACNA1C and TRANK1

57
Q

ANK3

A

codes for ankyrin B, which is a protein involved in neuronal myelination

58
Q

CACNA1C

A

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
Q

TRANK1

A

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
Q

behavioural shutdown

A

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
Q

Acceptance of subservient position

A

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
Q

Psychic pain

A

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
Q

Rumination

A

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
Q

measures of depression

A

Patient health questionnaire 9
Hamilton depression rating scale

Drugs And The Brain (9 decks)

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