Mood Disorders Flashcards

1
Q

What does the original theories about the etiology of disorders

A

that neurotransmitters are the cause by either being upregulated or down regulated and therefore causing the disorder (it is part of the etiology, but not the whole story, it is likely a range of altered neurotransmitters)

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2
Q

what type of changes are disorders now linked to and what structures are these changes occurring in

A

permanent structural and biochemical changes in memory and behaviour systems such as the hippocampus, amygdala, dorsal striatum, and prefrontal cortex.

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3
Q

Define depression

A

a mental disorder with recurrent episodes of decreased energy, attention, and negative mood states. alterations in down regulation of serotonin is thought to be the main factor.

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4
Q

What has been used to treat depression

A

drugs that enhance serotonergic levels called SSRIs
ex. dapoxatine, fluoxetine

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5
Q

damage to what specific structure has been linked to depression

A

damage to the hippocampus
there is a strong relationship between the hippocampus, depression, and stress hormones, as stress hormones are elevated, the hippocampus becomes more vulnerable for damage

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6
Q

what levels were increased in hospitalized patients with depression and suicide victims and what does this suggest

A

corticoids and glucocorticoids which suggest a hyperactive HPA axis

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7
Q

What is the HPA axis responsible for in depression

A

responsible for daily life activities and most important is important in stressful experiences

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8
Q

what do glucocorticoids do in depression

A

they suppress the general functions from the HPA axis and upregulate the availability of energy stores to prepare for stressful situations.

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9
Q

How is the HPA axis response regulated

A

by a negative feedback system. when stressed stress hormones are released and this information gets back to the hippocampus which has glucocorticoid receptors that send signals back to the HPA axis and tells it to shut down when needed.

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10
Q

What brain region is most vulnerable to damage from prolonged exposure to glucocorticoids in depression

A

the hippocampus, mostly from chronic stress (unpredictable chronic stress)

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11
Q

Explain how the hippocampus gets damaged from chronic stress

A

elevated, long and high signal of glucocorticoids due to chronic stress, the hippocampus experiences dysfunction, less negative feedback is sent to the HPA axis so stress continues, further glucocorticoids are released and more hippocampal dysfunction and damage occurs

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12
Q

what have been found in depression in terms of neurogenesis (2)

A

down regulation of neurogenesis has been linked to depression in the adult hippocampus

serotonergic medications are commonly used to treat depression by up regulating neurogenesis in the hippocampus

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13
Q

How does the amygdala change with depression

A

the amygdala becomes more active in depressive patients, more active when specifically responding to negative situations

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14
Q

what does the increased influence of the amygdala lead to in depressive patients

A

an increase in negative attribution bias, meaning that depression takes neutral situations and make they have a bias of making them negative instead

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15
Q

define anxiety

A

mental disorder associated with inappropriate levels of fear and related physiological and behaviour responses by the situation.
(thought to be unable to differentiate between cues, environments, etc that are associated with fear and those that are not)
THEY MAKE GENERALIZATION ABOUT FEAR CAUSING

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16
Q

What nt is responsible for anxiety

A

GABA
which anxiety is treated with benzodiazepine drugs

17
Q

What structures might be weakened in individuals with anxiety

A

weaking of the systems of the hippocampus and amygdala because they support the ability to differentiate between fear responses
so damage to them would cause the generalizations
(the brainstem could also be associated)

18
Q

What is the main idea that needs to be remembered about anxiety

A

a loss of amygdala and hippocampal control over brainstem and hypothalamic regions mediates the physiological responses associated with fear and anxiety would increase generalization of fear to unrelated situations

19
Q

how is the balanced memory system altered when having anxiety

A

amygdala and hippocampus are smaller/have less control while the brainstem nuclei is much larger and gains control

20
Q

evidence that extinction learning is done by _____ for generalized anxiety

A

ventromedial-prefrontal cortex

21
Q

what is the orbital prefrontal cortex functions (3) in anxiety

A
  1. response control
  2. behavioural flexibility
  3. contingency (what happens in the future/predictions) evaluation
22
Q

what are the functions of the medial prefrontal cortex (4)

A

it includes both the infra-limbic and pre-limbic prefrontal cortex
1. extinction learning (most interested in)
2. behavioural flexibility
3. executive functions
4. higher-order attentional processes

23
Q

fear conditioning to context experiment (groups, design)

A

Groups = lesions or inactivate medial or orbital prefrontal cortex
Design = pre-exposure (to make sure no bias), training (cause painful stimulus in one context and none in the other - 8 days), extinction (no stimulus in either - 10 days)

24
Q

fear conditioning to context experiment (results)

A

Results = see on 4th day of training that conditioning is already occurring, but not in orbito prefrontal, for this group things are generalized because freezing is occurring equally in both. after more training still same generalized results for orbito. Even after 10 days of extinction, orbito damage still show huge generalization which is crazy because so much time has passed.
preference test = orbito damage can still show preference however, so they show learning and understanding but have problems controlling their physiological effects of anxiety to not generalize

25
Q

Conclusions of fear conditioning to context experiment

A

rats with orbital prefrontal cortex lesions show elevated and generalized fear responses.
preference test shows that this is not due to inability to discriminate the different contexts.
dont show normal extinction.

26
Q

GAD (generalized anxiety disorder)

A

emotional response patterns become generalized due to inability to constrain them to appropriate cues and contexts

27
Q

researches conclude that anxiety disorders are linked to what structural alterations

A

prefrontal cortex (orbito and medial), hippocampus, or amygdala
found that orbital frontal cortex play central role in expression of GAD

28
Q

Define OCD

A

characterized by re-occurring obsessions and/or compulsions that disrupt daily functions of the individual

29
Q

Define and explain the difference of obsessions and compulsions

A

obsessions = incessant intrusive thoughts or impulses
compulsions = repetitive response patterns are thought to occur in response to various obsessions

30
Q

What disorder is embedded in OCD

A

anxiety, because any attempt by an individual suffering OCD attempting to resist their compulsive behaviours results in high anxiety

31
Q

alterations in the relationships of what structures are at the core cause of OCD

A

between the dorso-lateral striatum, prefrontal cortex (orbito prefrontal is probably involved), and the amygdala/hippocampus axis
(the habit system of the dorsolateral striatum is important for compulsive behaviours)

32
Q

amygdala/hippocampal dysfunction results in what in OCD

A

heightened anxiety levels

33
Q

dampening of the prefrontal function can lead to what in OCD

A

reduction in inhibitory control of thoughts and behaviours

34
Q

What structure increases dominance in OCD

A

dorso-lateral striatum (habit system), responsible for compulsions