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PMCOL 412 > Mood Disorders I > Flashcards

Mood Disorders I Flashcards

1
Q

Physiological correlates of fear (feelings)

A 
Heart and respiratory rate
Cortisol and adrenaline
Blood flow
Analgesia
Facial muscles
Attention focused on perceived threat
Emotions
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2
Q

Feelings are…

A

mental experiences that accompany a change in body state

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3
Q

Feelings allows…

A

a glimpse into ongoing homeostatic regulation

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4
Q

Feelings directly portray…

A

the advantageous or disadvantageous nature of a psychological situation, and facilitate learning of the conditions causing the imbalance and respective corrections

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5
Q

Emotions

A

An action programme triggered by external stimuli

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6
Q

Example of emotions

A

joy, fear, etc.

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7
Q

Drive

A

action programme to satisfy an instinctual physiological need

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8
Q

Drive examples

A

hunger or thirst

ex. high osmolarity –> dry mouth –> thirst

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9
Q

2 action programs

A

drive and emotion

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10
Q

Interoception

A

notice change in internal enviro

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11
Q

Exteroception

A

notice change in external enviro

e. by 5 senses

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12
Q

Nuclei involved in generating feelings

A

internal mileu –> lamina 1 pathway to homeostatic centres (NTS, PBN, PAG) –> thalamus –> cortex (esp. insula)
Viscera –> Vagus nerve –> NTS –> PBN, PAG, hypothalamus –> insula

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13
Q

Pathway for feelings–from viscera

A

Viscera –> Vagus nerve –> NTS –> PBN, PAG, hypothalamus –> insula

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14
Q

Pathway for feelings–for internal stimuli

A

internal mileu –> lamina 1 pathway to homeostatic centres (NTS, PBN, PAG) –> thalamus –> cortex (esp. insula)

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15
Q

Mood

A

stable and constant, not linked to speicific circumstances

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16
Q

Feelings

A

Reactive, breif, intense and circumscribed to a specific environmental event

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17
Q

Difference b/t feelings and mood

A 
feeling = short term, event-related
mood= long term, un-related to events
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18
Q

Dysregualtion of feeligs leads to

A

emotional arousal and exaggerated effects

ex. fear becomes anxiety (disregulated fear)

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19
Q

Dyregulation of mood leads to

A

chornic, sustained negative mood

pervasive sadness and anhedonia

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20
Q

Depression (defintion)

A

Unpleasant or dysphoric mood present most of the day, most days

  • anhedonia
  • more prevalent in women
  • in response to life events but also has genetic and other factors
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21
Q

Depression is a mood disorder comprised of….

A 
• Sadness
• Loss of interest
• Anhedonia
• Lack of appetite
• Feelings of guilt
• Low self-esteem
• Sleep disturbances
• Feelings of tiredness
• Poor concentration
Transient and mild conditions of low mood to
severe psychiatric disorder
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22
Q

DSM criteria for depression

A 
Both of: 
• Depressed mood 
• Loss of interest
Plus 4 of the following: 
- Altered Appetite
- Altered Weight
- Altered Sleep
- Altered Psychomotor activity
- Decreased energy
- feeling Worthlessness
- feeling Guilty
- Difficulty Thinking
- Difficulty Concentrating
- Difficulty Making decisiones
- Recurrent thoughts of death
- Suicidal ideation
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23
Q

Etiology of depression

A
  1. Biogenic amine hypothesis
  2. Endocrine factors
  3. Environmental factor
  4. Immunologic factors
  5. Genetic factors
  6. Neurogenesis
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24
Q

What started the biogenic amine hypothesis

A

in 50s Noted that:
Drugs that depleted catecholamines –> depression like effects (reserpine)
Drugs that inhibited MAO and therefore increase catecholamines –> increased mood

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25
Q

NE (receptor numbers and types)

A

9 receptors
2 classes: alpha and beta
Coupled to G protein

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26
Q

NE roles

A
  • Modulates PFC function
  • Working memory processing
  • Behaviour and attention
  • Acquisition of emotionallyarousing memories
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27
Q

NE cell bodies and projection

A

cell bodies in LC or lateral trigeminal area

Project to : thalamus, hypothalamus, and cortex

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28
Q

5HT (receptors numbers and types)

A

14 5-HT receptors
classified in 7 types
mostly coupled to G-proteins

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29
Q

Altered binding potentional of ____ and distrubition of ___ in _________ in depression

A

5HT1a; 5HT1b; in cingulate, PFC, hippocampus

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30
Q

5HT involved in

A

stress repsonse

involved in everything but responsible for nothing

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31
Q

5HT cell bodies and projection locations

A

Bodies in rostral raphe nuclei or caudal raphe nuceli

project to amygdala, hippocampus, NAc, etc.

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32
Q

DA receptor numbers and classes

A

5 DA receptors
classified in 2 types
mostly coupled to G-proteins

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33
Q

DA has roles in

A
  • Reward and motivation
  • Working memory
  • Attention
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34
Q

DA cell bodies in the

A

VTA and substantia nigra

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35
Q

Substantia nigra and DA

A

degeneration of substantia nigra –> PD

important for voluntary action

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36
Q

VTA and DA

A

axons to NAc and PFC

reward, motication, working memory and attention

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37
Q

Monoamines in depression

A

want to increase MAs in depression b/c there is increased MAO activity in depression
therefore there is low bioavailability of biogenic amines and therefore low NTs

38
Q

Transporters in depression

A

Transporter-reuptake of NTS to allow for continued neurotransmission but that decreases the amount of NT in the synaptic vessicles
in depression transporeters may be upregulated causing even less NT to be in the synapse

39
Q

Receptors in depression

A

Altered levels of 5HT receptors in depressed patients (altered number and affinity)

40
Q

CRF roles

A

CRF has a regualtory role and will cause an increase in ACTH (from ant pit) –> increased cort release
CRF is also found in extrahypothalamic brain regions where it acts as a NT–coordinating behaviour, autonomic, endocrine , and immune response to stress

41
Q

HPA axis and depression

A

some depressive symptoms (ex. altered sleep, sex, eating; excessive guilt; altered psychomotor activity) are all linked to HPA activity

42
Q

When animal models are given CRF

A

they show depressive symptoms

43
Q

Depressed patients have ___ CRF and cortosol

A

increased; related to severity

44
Q

Altered HPA axis in depression

A

Increased CRF and cortisol
dysfunctional glucocorticoid feedback
impaired corticoidsteroid signalling

45
Q

___ cort in depression, ___ cort with SSRIs or ECT

A

increased with depression; decreased with therapies

46
Q

Contradictory info on depression

A

HPA axis activity is hypoactive in depression BUT also depressive patients show increased CRF and cortisol

47
Q

Thyroid hormone and depression

A

T3 and T4 associated with depression
T3/4 regaulte overall metabolism of body therefore weight loss, psychomotor dysfunction and altered sleep seen in depression may be due to altered throid hormone

48
Q

T3 supplementation

A

helpful adjunct therapy
T3/4 may act as co-transporter to NE
t3/4 increase cortical 5HT secretion

49
Q

Enviromental factors

A

Adverse life events can increase the probability of depression relapse
Environment can be + or -
Stress and depression share mediators and circuitries
Studies of monozygotic twins have shown role of environment
i.e. Depression isn’t solely genetic

50
Q

Immunological factors in depression

A

chronic stress is associated with altered immune function

“sickness behaviour”

51
Q

Anti-inflammatory drugs in depression

A

ineffective

52
Q

cytokines involved in depression include:

A

IL-1B, IL-2, IL-4, IL-8, IL-10
Interferon gamma (IFN-γ)
TNF

53
Q

Cytokine effects on monoamine metabolism (pathway)

A

Pro-inflam syotkines produced by microglia and macrophages (incl. IFNs, IL-beta and TNF) –> decrease MA availability by activating MAPK –> increase SERT, DAT, NET
AND decreasing cofactors necessary for MA synthesis

54
Q

Cyotkine effects on glutamate metabolism

A

cytokines (IFNs, IL-beta, TNF) –> increase IDO –> brekadown of trypotphan (5HT precursor)
cytokines also reduce Glu rei[tkae by astrocutes –> increased glu –> NMDA activation –> decreased BDNF secretion –> decreased neurogeneis and neuronal integrity

55
Q

Sickness behaviour: definition and why

A

in infections pro-inflammatory cytokines released cause hypothermia, nausea, loss of appetite
advantage: social withdrawal (prevent spread), tired (energy used to cope with infection)

56
Q

Sickness behaviour in depression

A

sickness behaviour may be enoigh to confer depressive behaviour
in animals: cytokine admin –> depressive symptoms BUT anti-inflam are ineffective for depression

57
Q

Genetic factors–sex differences

A

Higher prevalence in women

Higher heritability in women

58
Q

Genetic factors: polymorphisms

A 
Only a few genetic polymorphisms associated to MDD:
APOE
SLC6A3
SLC6A4
DRD4
59
Q

APOEε2 vs. 4

A 
APOEε4 = significant association with reduced brain anatomical structure and decreased function in depressed patients 
APOEε2 = protective against depression
60
Q

DRD4

A

increased in individuals with major depressive disorders

61
Q

Carriers of SLC6A4

A

increased amygdala activity and higher repsonsivity to social, emotional stress (compared to non-carriers)

62
Q

Neurogenesis in depression

A

Reduced neurogenesis capacity causes depression but… no conclusive evidence

63
Q

Antidepressants and neurogenesis

A

Antidepressants decrease ceramides, which in turn increases neurogenesis
b/c ceramides block cell growth

64
Q

Animal neurogensis–> structural differnces

A

Studies in animals suggest that neurogenesis can restore structuralchanges in hippocampus
new hippocampal connections –> associated with memory formation
NOT necessarily follow by depressive symptoms

65
Q

MAO role

A

MAO catalyze the oxidative deamination of MAs–produces peroxide,, aldehyde and ammonia

66
Q

3 treatment modalities for depression

A
  1. Antidepressant drugs
  2. Cognitive-behavioural therapy
  3. Electroconvulsive therapy
67
Q

2 types of MAO

A

A and B
differniated by their affinity for 5HT
note: type A is found in liver and gut

68
Q

Role of MAOI

A

protect neurons from exogenous amines
terminate actions of amine NTs
regulate actions of intracellular amine stores

69
Q

In neurons and glia differential MAOA and MAOB concentrations

A

low MAOA –> glia cells have role in gradient of 5HT (used to breakdown 5HT)
MAOB –> main role to minimize foreign amines (limit their access to vesicles)

70
Q

MAOIs

A

Inhibit MAO –> less degradation of MAs –> more MA in cleft

71
Q

MAOA inhibitors and non-selctive A/B inhibits are good for

A 
phobic anxiety
atypical depressions:
• hysterical traits hypersomnia
• bulimia
• tiredness
• impression of rejection
MAOIs are better than uptake inhibitors (SSRIs, SNRIs, TCAs) for these
72
Q

Phenelzine show to ___ corticosteroin levels

A

increase

the HPA axis is hypoactive in depresiion, this may help give it a boost

73
Q

Orginial MAOIs

A

Iproniazis and phenelzine–original and irreversible
side effects: liver toxicity, hemorrage, hypotensive crisis, death
withdrawn from use

74
Q

MAOA also found in ____ where they catalyze ____. Inhibition causes the _____

A

gut and liver; catalyze bioactive amines from food

cheese effect

75
Q

Cheese effect

A

When MAOA in gut/liver is inibited allows tyramine to enter blood and be taken up by sympathetic nerves –> displaced endogenous MA –> massive release of EPI and NE –> increased BP

76
Q

Reversible MAOIs

A

lozabemide and moclobemide

Block MAOA sufficiently in brain while gut can displace it –> less cheese effect

77
Q

Selegiline

A

selective for MAOB BUT at proper doses for AD loses this selectivity

78
Q

TCAs

A

ex. amitryptyline (1st), imipramine (2nd)

inhibit wither NET or SERT or both (both by newer drugs)

79
Q

chlorpromazine

A

first widely used psychiatric drug (also an antipsychotic)

80
Q

Downsides of TCAs

A

DIRTY drug
also block mACHRs, H1, α1 receptor
ANti-cholinergic side effects = dry mouth, urinary retention, hypertension
Drowsiness

81
Q

Clomipramine

A

TCA with high addintity for SERT

effective for OCD

82
Q

Iproniazid

A

Irreversible inhibitor of MAO A and B

83
Q

Lazabemide

A

Reversible MAOB inhibitor

84
Q

Moclobemide

A

Reversible MAOA inhib

85
Q

Phenelzine

A

Irreversible MAOA and MAOB inhibitor

86
Q

Tranylcypromine

A

Irreversible MAOA and MAOB inhib

87
Q

MAOA breaks down

A

DA, NE, 5HT

88
Q

MAOB breaks down

A

Mainly DA

89
Q

Irreversible MAOA inhibition causes

A

the cheese effect through increased serum tyramine levels –> hypertensive symptoms
Occurs with irreversible MAOA/B combined inhibitors

90
Q

TCA examples

A

Amitriptyline (1st), Imipramine (2nd), Clomipramine

PMCOL 412 (35 decks)

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