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Med School Yr 2 > 6 - Depression > Flashcards

6 - Depression Flashcards

1
Q

what is the correct term for a sustained period of depression?

A

major depressive episode

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2
Q

MDEs are seen principally in what 3 psychiatric diagnoses?

A
  • major depressive disorder
  • bipolar disorder
  • schizophrenia
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3
Q

what questionnaire can help diagnose MDE?

A

patient health questionnaire (PHQ-9)

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4
Q

what are the diagnostic criteria for MDE?

A

5 or more in same 2 week period that represent change from normal:
* anhedonia or depressed mood - MUST
* causes significant distress/impairment of function
* not part of bipolar
* not due to direct physiological effects of substances
* not better acocunted for by bereavement

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5
Q

what are somatic delusions?

A

fixed false beleifs about pts body, eg. “my body is rotting/hollow/empty”

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6
Q

depression is the leading cause of disability in both males and females. who is the burden of depression higher in?

A
  • burden of depression is 50% higher in females than males
  • leading cause of burden in females in high-, middle-, and low-income contries
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7
Q

what are the two types of monoamines relevant in depression?

A
  • Noadrenaline - catecholamine
  • serotonin - indoleamines
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8
Q

what is the general structure of catecholamines?

A
  • benzene ring
  • 2 hydroxyl side groups
  • amine chain
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9
Q

what is the general structure of indoleamines?

A
  • bicyclic ring of benzene
  • fused with pyrrole
  • amine side chain
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10
Q

how is noradrenaline synthesised?

A
  • tyrosine
  • hydolysed by tyrosine hydroxylase (TH) into dopamine
  • decarboxylysed by DBH (dopamine beta-hydroxylase) into noradrenaline

methyl group added = adrenaline

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11
Q

how is serotonin synthesised?

A
  • tryptophan
  • hydryolysed by tyrptophan hydroylase into 5-hydroxytryptophan
  • converted into 5-HT by L-AADC
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12
Q

what is tyrosine?

A

non-essential large neutral amino acid (LNAA)

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13
Q

how is tyrosine transported across the blood brain barrier?

A

active transport

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14
Q

where is tyrosine converted into NAdr?

A
  • neuronal cell bodies in pons
  • particularly locus ceruleus
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15
Q

what is tryptophan?

A

dietary essential, large neutral amino acid (LNAA)

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16
Q

where is tryptophan converted into 5-HT?

A
  • neuronal cell bodies in raphe nuclei (chain of brainstem nuclei)
  • particularly dorsal and medial raphe
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17
Q

how are the signals of 5-HT terminated?

A
  • 5-HT reuptake transporter (SERT)
  • monoamine oxidase (MAO-A) degrades 5-HT in synapse and also some that has been reuptaken
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18
Q

how are NAdr signals terminated?

A
  • NAdr reuptake transporter
  • MAO-A
  • COMT (catechol-O-methyl transferase
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18
Q

describe the enzymatic degradation of 5HT?

A
  • broken down by monoamine oxidase
  • into 5-HIAA (hydroxyindole acetic acid)
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19
Q

describe the enzymatic degradation of NAdr?

A
  • MAO and COMT degrade it
  • into vanillylmandelic acid and 3-methoxy-4-hydroxy-phenylglycol
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20
Q

what are the 3 types of adrenergic receptors that NAdr acts on?

A
  • alpha1
  • M2
  • N1-3
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21
Q

which noradrenergic receptor is most relevant to depression?

A

M2

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22
Q

which 5-HT receptor in the only one that isn’t coupled with a G-protein?

A

5-HT3 - ligand gated ion channel

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23
Q

serotonin stimulate nuronal firing at all 5HT receptors, apart from which 2?

A

5HT1 and 5HT5

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24
Q

NAdr stimulation at alpha2 auto and heteroreceptors on NAdr and 5HT neurons result in what?

A
  • decreased cell firing
  • reducing serotonin release
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25
Q

NAdr stimulation at alpha1 adreno-heteroreceptors on 5HT cell bodies result in what?

A

increased 5HT cell firing

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26
Q

how does NAdr regulate serotonin?

A
  • NAdr released from cell body and binds to receptors
  • if alpha2 auto or hetero on NAdr/5HT neuron, decreases cell firing and 5HT release
  • if alpha 1 adrenoreceptor on 5HT cell body, increased 5HT release
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27
Q
A
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28
Q

drugs that deplete monoamines cause what?

A

depression

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29
Q

antidepressants increase what neurotransmitters?

A

5HT and NAdr

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30
Q

what was the first anti-depressant?

A
  • iproniazid (developed for TB)
  • monoamine oxidase inhibitor
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31
Q

give an example of a VMAT blocker that causes depression as a side effect?

A
  • reserpine
  • antihypertensive +antipsychotic in 50s
  • depletes MOA by blocking VMAT
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32
Q

what does VMAT stand for?

A

vesicular monoamine transporter

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33
Q

what does VMAT do?

A

transports free cytoplasmic NAdr, 5HT, DA in presynaptic nerve terminal into storage vesicles

34
Q

how does reserpine lead to depression?

A
  • reserpine irreversibly blocks VMAT
  • cytoplasmic monoamines cannot re-enter vesicles
  • instead degraded by MAO and COMT
  • leads to long-lasting depletion
  • takes days-weeks to replenish new VMAT
35
Q

how is rapid tryptophan depletion achieved?

A

drinking mixture of LNAAs devoid of tryptophan

36
Q

iproniazid was developed for TB - what other property does it have?

A

antidepressant as it is a monoamine oxidase inhibitor

37
Q

what type of MAOIs are used in antidepressive therapies?

A

MAOA

38
Q

what type of MAOIs are used in parkinson’s disease?

A

MAOB - increases dopamine

39
Q

how do MAOIs work?

A
  • inhibit monoamine oxidase
  • neuronal and synaptic levels of monoamines increases
40
Q

list an irreversible MAO-A inhibitor?

A

phenelzine

41
Q

name a reversible MAOAI?

A

moclobomide

42
Q

what is important about diet when taking MAOA inhibitors?

A

can’t metabolise other monoamines eg. dietary tyramine (red wine, cheese, marmite) - could result in hypertensive diet

43
Q

what is the levels of monoamine oxidase A activity in depressed pts?

A

high - leads to chronically low synaptic 5HT and NA

44
Q

how does imipramine work in depression?

A
  • reversibly blocks SERT and NAT
  • increases synaptic 5HT and NA by reducting degradation
45
Q

list 3 tricyclic ADs

A

desipramine
amitriptyline
clomipramine

46
Q

desipramine, amitryptyline, clomipramine are all what type of antidepressant?

A

tricyclic

47
Q

list 3 SSRIs

A

fluoxetine
paroxetine
flucoxamine
sertraline
citalopram

48
Q

fluoxetine, paroxetine, flucoxamine, sertraline, citalopram - what type of antidepressant are these?

A

SSRIs

49
Q

what are SNRIs?

A

serotonin and noradrenaline reuptake inhibitors

50
Q

list 2 SNRIs

A

venlafaxine
duloxetine

51
Q

venlafaxine and duloxetine are examples of what type of antidepressant?

A

SNRIs

52
Q

what does each antidepressant block?

A

tricyclics and SNRIs - SERT and NAT
SSRIs block only SERT

53
Q

what is the common outcome of all antidepressants?

A

increase synaptic 5-HT levels

54
Q

mirtazapine is a new AD that is dual acting by blocking only a single receptor type - what is its mechanism of action?

A
  • adrenergic alpha2 receptor antagonist (blocks)
  • blocks negative feedback which tends to reduce NAdr release
  • net effect is increased NAdr release
  • also blocks negative feedback that reduces 5HT release
  • net effect is increased 5HT
55
Q

what is the kindling hypothesis of depression?

A
  • depressive episodes become more easily triggered over time
56
Q

as the number of depressive episodes increases, future episodes are predicted more by what?

A

the number of prior episodes, rather than by life stress

57
Q

the ventral neural system is important for what?

A

identification of emotional significance of stimuli and production of affective states

58
Q

what is the dorsal neural system important for?

A

integration of emotional inputs and the performance of excutive functions

59
Q

how are the dorsal neural system and ventral system abnormal is MDE?

A

dorsal neural system - underactive
ventral system - overactive

60
Q

in MDE the dorsal neural system is underactive - what symptoms are associated with this?

A
  • DLPFC and dorsal ACC - apathy, deficits in attention and working memory
  • hippocampus - impaired memory consolidation
61
Q

in MDEs the ventral system is overactive - what symptoms are associated with this?

A
  • ehanced sensitivity to pain
  • ventral ACC - depressed mood
  • amygdala - preferential processing of negative stimuli compared to positive
62
Q

what functional changes happen in the amygdala in MDD?

A
  • overactive when shown sad stimuli
  • underactive when shown positive stimuli
63
Q

what is the role of the amygdala?

A
  • modulates visual and attentional processing, particularly facial expression
64
Q

what structural changes occur in the amygdala during depression?

A

enlargement

65
Q

MDD is associated with what bias?

A

negative cognitive bias

66
Q

what reverses the negative cognitive bias in depressed pts?

A

elevated 5HT

67
Q

what is the most efficient treatment for MDD?

A

combined antidepressants and CBT

68
Q

longer durations in which depressive episodes go untreated is associated with what? what can be the result of this?

A
  • reductions in hippocampal volumes
  • associated with treatment resistance
69
Q

what stress hormone is consistently high in pts with MDD?

A

cortisol

70
Q

consistently high cortisol cannot be supressed by dexamethasone in pts with MDD - what does this suggest?

A
  • their is dysfunction in the HPA axis
  • drive is coming from hypothalamus
71
Q

how does chronic stress alter the HPA axis, leading to increased physical illness symptoms and increased risk of inflammatory disorders?

A
  • hypothalamus releases CRH
  • pituitary releases excessive ACTH (adrenocorticotrophic)
  • adrenal cortex = excessive glucocorticoid release
  • increased glucocorticoids dysregulates amygdala function
  • increased adrenal activity = increased sympathetic tone = increased release of IL 1 and IL6
  • IL1 + IL6 + glucocorticoids = increases MAO = decreases 5HT, NA, DA + neurotrophic factors
  • decreased neurotrophic factors = decreased neurogenesis and hippocampal volume
  • dysregulation - maintains abnormal levels
  • increases physical symptoms and inflammatory risk
72
Q

how does smoking relate to depression management?

A

ceasing smoking is as effective as starting AD treatment

73
Q

what is BDNF?

A

growth factor that is downregulated in depression affecting structural and functional processes within the limbic system, especially hippocampus

74
Q

what are the NICE guidelines for treatment of mild depression?

A
  • only consider antidepressants if there is history of depresison
  • offer low-intensity psychosocial intervention- CBT, group physical activity programme
75
Q

what are the NICE guidelines for management of moderate or severe depression?

A
  • combination of antidepressant medication and CBT
76
Q

what are the NICE guidelines for antidepressant step-wise appraoch?

A
  • SSRI
  • change to venlafaxine, mirtazapine, escitalopram or vortioxetine
  • add augmenting agent eg. 2nd gen antipsychotic or lithium
  • change antidepressant to tricyclic - amitriptyline or clomipramine
  • change to MAOI eg. phenelzine
77
Q

what antidepressants are more effective than others?

A

agomelatine
amitriptyline
escitalopram
mirtazapine
venlafaxine
paroxetine

78
Q

what are the least effective antidepressants?

A

fluoxetine
reboxetine
fluvoxamine
trazodone

79
Q

how long should ADs be continued after full recovery from MDE to prevent relapse?

A

9 months

80
Q

how do CBT and ADs compare for:
* acute efficacy?
* long-lasting protective effect after course ends>

A

acute efficacy - similar
long-lasting protection - CBT is better

81
Q

what are the guidelines for treatment-resistant depression?

A
  • check diagnosis + alcohol and/or drug misuse
  • antidepressant trials, bupropion
  • ECT
  • neurosurgery - bilateral cingulotomy, deep brain stimulation, vagus nerve stimulation
82
Q

what is the most effective AD treatment? what is a drawback of this?

A
  • electroconvulsive therapy
  • relapse risk is very high
83
Q
A

Med School Yr 2 (96 decks)

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