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Case 6 > Major Depressive Disorder > Flashcards

Major Depressive Disorder Flashcards

0
Q

Based on DSM 4 what symptoms needed for diagnosis of MDD

A

5 or mor symptoms present in last 2 columns (more than half the days) during the same 2 week period.
Little interest doing things, feeling down, trouble falling asleep, feeling tired, poor appetite, feeling bad about self, trouble concentrating, moving or speaking slowly.
Also add if thoughts of death are on several days

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1
Q

Whatis depression

A

State of low mood and aversion to activity that can have negative affect on persons behaviour, thoughts, feelings, world view and physical well being

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2
Q

Epidemiology of MDD

A

At least 350 million people have it
Burden for depression is 50% higher in women
Leading cause of disability worldwide

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3
Q

Monoamines types

A

Cathecolamines: dopamine, noradrenaline

Indoleamines: serotonin

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4
Q

Formation of dopamine

A

Starts with tyrosine
This is hydroxylated to form L DOPA
L DOPA undergoes decarboxylation to form dopamine

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5
Q

Formation of adrenaline

A

Starts with the dopamine
This is hydroxylated to form noradrenaline
Noradrenaline is metabolised to form adrenaline

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6
Q

Formation of serotonin

A

Starts with tryptopham
Undergoes hydroxylation to form 5-hydroxytryptopham
This then undergoes decarboxylation to form serotonin (5-Hydroxytryptamine)

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7
Q

Noradrenaline system

A

Tyrosine is dietary essential amino acid
Actively transported across BB barrier
Converted into NA in neuronal cellbodies in locus ceruleus in pons
NA packaged into vesicles and transported along axon to terminals to be released into synaptic cleft
Extends to entire brain

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8
Q

Serotonin system

A

Tryptopham is also a dietary amino acid
Active transport across BBB
Converted into 5-HT in neuronal cell bodies in the raphe nuclei in brainstem
Then packages into vesicles and travels in axons to be released at clefts

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9
Q

How is the serotonin and NA signal terminated

A

By reuptake into nerve terminal

And enzymatic degradation

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10
Q

What breaks down serotonin

A

MAO-A

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11
Q

What breaks down NA

A

MAO-A

COMT

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12
Q

What does breakdown of serotonin form

A

5-HIAA

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13
Q

What does breakdown of NA form

A

VMA

or MHPG

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14
Q

Noradrenergic receptors

A

a1 and b1-3 are all excitatory

a2 in inhibitory

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15
Q

Serotonin receptors

A

16 receptor subtypes
All Gprotein coupled receptors (adenylate cyclase)
EXCEPT 5-HT3 which is ion coupled

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16
Q

Serotonin and NA interactions

A

Both act on muscles with their specific receptor
But NA cell also projects to the 5-HT cell (which has NA a1 and a2 receptors)
NA cell has NA a2 receptor on it

17
Q

What effect does released NA have on each of these neurones

A

NA release via a1 receptor on serotonin cell causes the increased release of serotonin (cell firing)
NA release via a2 receptor on NA and serotonin neurone causes decreased cell firing

18
Q

Monoamine hypothesis of MDD

A

Decreased monoamine caused depression (reserpine drug)

WE WANT TO INCREASE SYNAPSE LEVELS OF 5-HT AND NA

19
Q

Other chemical causes of depression

A

Upregulation of 5-HT 2a receptors causes chronically reduced synaptic serotonin levels leading to depression

Rapid tryptopham depletion also caused depression

20
Q

Reserpine

A

Antipsychotic
Vesicular MonoAmine Transporter blocker
This transporter transported NA and serotonin into vesicles for release
Reserpine irreversibly blocks VMAT
The cytoplasmic MAO and COMT broke down the serotonin and NA

21
Q

MAOI antidepressants

A

Iproniazid developed for TB found to decrease depression, but toxic

Safer ones have been developed
MAO-A are antidepressants
MAO-B used to treat parkinsons (^dopamine)

22
Q

MAO-A inhibitors names

A

Irreversible: phenelzine, tranylcypromine

Reversible: moclobomide

Cant metabolise other monoamines (cheese, red wine, marmite)

23
Q

Tricyclic and SSRI antidepressant action

A

Reversibly block the SERT and NET reuptake transporters

Caused increase synaptic serotonin and NA

24
Q

Tricyclic AD names

A

Desipramine
Amitrypamine
Clomipramine

25
Q

SSRI names

A 
Fluoxetine
Paroxetine
Fluvoxamine
Sertraline
Citalopram
Escitalopram
26
Q

Mirtazapine

A

Newer antidepressant
Adrenergic a2 receptor blocker
Blocks negative feedback causing reduced NA release
Therefore increases NA and serotonin release

27
Q

5-HT 2a receptors in MDD

A

Postsynaptic on glutamate pyramidal neurones and GABA interneurones
Upregukated after chronic 5-HT depletion
MDD causes reduction in 5-HT and postmortem shows us that there sre increased 5-HT 2a receptors in MDD

28
Q

5-HT 2a blockage to treat MDD

A

Most atypical antipsychotics strongly block 5-HT 2a receptors (clozapine, risperidone)
Adding this to an AD augments antidepressant potency
Mirtazapine already blocks these receptors

29
Q

Recurrence of MDD

A

Up to 90% relapse in 3 years
Risk twice as high in first year

Kindling: more episodes you have, the more easily it will be to trigger. Lowers the threshold

30
Q

Ventral neural system

A

Identification of emotional significance of stimuli and production of affective states

31
Q

Dorsal neural system

A

Integration of emotional inputs and performance of executive functions

32
Q

Ventral neural system abnormality in MDD

A

Overactive
VO cortex3: Enhanced sens to pain, anxiety, depressive ruminations and tension
Vetral ACC: depressed mood
Amygdala: process negative stimuli more

33
Q

Dorsal neural system abnormality in MDD

A

Underactive
DLPRFC and dorsal ACC: psychomotor retardation, apathy, deficits in attention and working memory
Hippocampus: memory consolidation

34
Q

Amygdala in MDD

A

Enlargement
Modulates processing of faces. Will be overactive when shown sad face
Can be treated with CBT

35
Q

Hippocampus in MDD

A

Reduced volume with longer durations of untreated depression

36
Q

Stress hormones in MDD

Glucocorticoids

A
  • Chronic stress releases excessive glucocorticoids and CRH

- ^glucocorticoids dysregulate amygdala

37
Q

Stress hormones in MDD

Cytokines

A
  • adrenaline oroduced by stress which ^symp tone causing release of inflammatory cytokines (TNF, IL-1, IL-6)
  • cytokines and gcorticoids cause ^MAO, decreasing levels of 5-HT, NA, DA
  • cytokines and gc also decrease BDNF(brain derived neurotrophic factor) which decreases hippocampal volume
  • cytokines (inflammatory) also increase physical illness symptoms like CVD
38
Q

Genetics and MDD

A

Genetic variability in the 5-HTT gene

Short and long alleles (s/s has greatest development of MDD)

39
Q

Treatment of mild depression

A

Dont use AD routinely
But consider if history of recurrent severe or moderate depression or if persisted for more than 2 months
Offer low intensity pyschosocial treatment (computerised CBT, self help based on CBT principles, structured group physical activity)

40
Q

Treatment of moderate or sever depression

A

Combination of AD and high intensity psychological treatment like CBT

41
Q

Steps for ADs in severe or moderate depression

A

8-10 week trials

  1. SSRI
  2. Venlafaxine, mirtazapine
  3. Add atypical antipsychotic then lithium
  4. TCA
  5. MAOI (reversible then irreversible)

Case 6 (4 decks)

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