depresia Flashcards

1
Q

what is depression

A

persistent feeling of severe despondency and dejection

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2
Q

What are the 3 main elements according to the DSM 5

A

A. 5 or more symptoms present for at least a 2 week period
Symptoms result in a significant change from previous functioning
Include at least 1 of: depressed mood or loss of interest of pleasure

b. cause clinical significant distress or impairment in social, occupational or other functioning

c. should mot be direct physiological effect of a substance or a general medical condition

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3
Q

what are the major symptoms of depression

A

depressed mood most of the time - something that is obvious both to the person and others who are close to the patient

diminished interest or pleasure in vast majority of activities the person was engaged with

loss or gain in weight

changes in quality and quantity of sleep

motor changes - agitation

fatigue

feelings of wrothlessness or inappropriate guild

diminshed ability to concentrate

reccurent thorughts of death

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4
Q

what is the prevalence of depression

A

lifetime - chance of having depression at some point in life: 6-25%

high income countries have higher rate of depressed patients

annual prevalence - about 4%

more present in females

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5
Q

why might high income countries have higher prevalance

A

poor countries may lack infrastructure to collect data on depression, and are less likely to recognise it as an illness

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6
Q

what are the causes of depression

A

biological
- NT
- brain, vascular damage

genetic
-family studies
-twin studies

environmental

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7
Q

What is the role of NT in depression

A

depression related to abnormality in three main NT:
serotonin, noradrenaline and dopamine

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8
Q

What is the role of serotonin, noradrenaline and dopamine usually?

A

serotonin - calming and inhibiting action

noradrenaline - affects motivation, ability to focus, energy

dopamine - pleasure, satisfaction and reward

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9
Q

How is serotonin implicated in depression?

A

decrease in serotonin is linked to depression

Imaging studies show abnormalities in serotonin receptor density and in transporters in people with depression

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10
Q

What is evidence of serotonin involvement

A

Drugs which block serotonin re-uptake can ameliorate depression

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11
Q

what is the limitations of serotonin involvement

A

recent review suggests no consistent evidence of association between serotonin and depression

no support for the hypothesis that depression is caused by lowered serotonin activity or concentrations

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12
Q

How is noradrenaline implicated in depression?

A

regulating emotions
engaged in arousal
activities that reflect ability to concentrate

depressed mood is associated with a deficiency of noradrenaline in areas such as the brain stem and the locus coeruleus which projects to the limbic system, involved in regulating emotions

low levels of noradrenaline - emotional withdrawal, concentration and memory deficits

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13
Q

what is evidence of noradrenaline involvement

A

Drugs which block noradrenaline re-uptake can ameliorate depression

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14
Q

How is dopamine implicated in depression?

A

low dopamine levels may explain low sense of pleasure and reward in depression

inability to experience pleasure - one of the symptoms required for diagnosis

imaging studies show abnormalities in dopamine receptor density and in transporters in depressed patients

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15
Q

What are the key findings in studies of NT

A

in depression NT are involved in:

-circuits that regulate emotional arousal

-regulate a reward network (ventral striatum with orbitofrontal and media prefrontal regions)

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16
Q

what are limitations of findings

A

data makes it unclear whether NT abnormalities reflect a deficit, a consequence, a risk factor, or a compensatory mechanism in depression

the involvement of NT does not mean they cause depression

17
Q

what may cause these limitations

A

depression is a heterogeneous disorder

NT are part of a complex system that interacts with brain structure and function, genetics and the environment

18
Q

what brain regions are implicated in depression

A

hippocampus
anterior cingulate cortex
prefrontal cortex

19
Q

what is hippocampus like in depression

A

hippocapmmus is smaller in patients with depression than controls

smaller by 20%

chemical - cortisol which is released to alert the body to react to stimuli that are considered to be dangerous

when cortisol is chronically released, it would damage certain areas of the brain, one being hippocampus

that results in reduction in the ability to encode new information - hippocampus is key area for memory and encoding

20
Q

what happens to hippocampus if you leave depression untreated

A

leaving depression untreated for certain amount of time leads in consistent reduction in the volume of hippocampus

21
Q

what is the role of anterior cingulate cortex in depression

A

engaged in tasks that require resolving a conflict

engaged in memorising information

healthy controls were able to remember a short paragraph - activation in anterior cingulate and hippocampus

patients with depression were not performing well in memory task - lack of activation in these regions

22
Q

what is the role of prefrontal cortex in depression

A

patients and healthy controls viewed emotional and neutral film clips

patients with depression were less good at a task that required processing emotional stimuli

activated prefrontal cortex more than healthy controls

indicated dysfunctional use of these areas

23
Q

what are the problems with brain imaging in depression

A

despite the fact that this info is useful, it has little impact on clinical practice

because are findings contributing to the cause of depression or result of having depression

24
Q

how to address these issues

A

look at ppt longitudinally

try to test ppts before the onset of illness - recruit at risk ppts - those who might have a family history of depression and are more likely to develop depression

25
Q

what have brain images shown about studying people at risk of depression

A

3 groups:

-at risk ppts
-healthy controls
-patients with depression

Results:
1. at risk group had smaller right hippocampal and dorsolateral PFC volumes than controls

  1. at risk groups had smaller right hippocampal than patients with depression - those ppts with depression were under treatment and the treatment helped to ameliorate the symptoms and some of the brain features
26
Q

what have family studies shown about genetic influence in depression

A

children of depressed parents have 50% chance of developing a disorder of some kind

20-40% chance of developing depression

27
Q

what have twin studies showed

A

higher concordance rates among monozygotic than dizygotic twins - supports genetic influence

heritability of depression is thought to be 31-42%

28
Q

how do we measure genetic effects through molecular genetics

A

study of chromosomes and gene expressions

29
Q

genetic and environmental effects

A

study of genes involved in regulating serotonin

1,037 children assessed at ages 3,5,7,9,11,13,15,18,21,26

looked at whether genes were predicting the possibility of developing depression when this was combined to being exposed to stressful events

whether ppts had 2 short alleles which are associated with decreased serotonergic function - and therefore highest risk of developing depression

1 short and 1 long allele - some risk

2 long allele - little risk

measure the number of stressful life events

RESULTS:
group that has 2 short allele + stressful life events = increased risk of self-report depression symptoms

when there is a genetic profile combined with stress this results in higher probability of developing depression

when there are no stressful life events, the 3 groups are equal in terms of self reported depression symptoms

so allele alone do not correspond to depression. only when they are combined with stressful situations

30
Q

What is depression like in late life

A

depression common in ageing

this is typically associated with health problems

less than 1/4 of older adults with depression receive treatment

low mood is common and often undiagnosed

in late life depression, treatment is not often successful

even if mood is stabilised there are still residual cognitive deficits

31
Q

what is vascular depression

A

vascular damage that accumulates with age

vascular damage reduces integrity of white matter - some parts of the brain are less effective at communicating with each other

it disrupts the circuits that underlie emotional regulation - likely to result in late life depression