2-Drugs for Depression Flashcards

(50 cards)

1
Q

what are the numbers needed to treat

A

vary from 2-25

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2
Q

which type of depression sees the best results with antidepressants

A

Major depressive disorder

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3
Q

what are the monoamine neurotransmitters

A

serotonin, dopamine, adrenaline and noradrenaline

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4
Q

what is so special about the shape of the monoamines

A

amine group connected to a ring structure via two carbons

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5
Q

what is the monoamine theory of depression

A

that it is related to a deficiency in the amount of cortical and limbic serotonin, noradrenaline and dopamind

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6
Q

what is the role of the limbic system

A

emotion and please

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7
Q

what is the role of the cortex

A

higher cognitive functioning

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8
Q

what caused the monoamine theory to arise

A

drugs that depleted monoamines was associated to depression in some patients

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9
Q

what happens when a depressed patient who is responding to antidepressants that boosts serotonin levels is given a diet without tryptophan
and why

A

they relapse because tryptophan is a precursor of serotonin

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10
Q

what happens when a patient responding to a drug that boosts noradrenaline levels if given a noradrenaline synthesis inhibitor

A

relapse

cant make noradrenaline so then they can be boosted

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11
Q

which antidepressants boost the monoamine system

A

all currently available antidepressants

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12
Q

what is the neurotrophic factor theory

A

that a lack of nerve growth factors are responsible for depression

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13
Q

what are neurotrophic factors

A

nerve growth factors

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14
Q

what is BDNF

A

Brain-derived neurotrophic factor

a growth factor protein that is involved in regulation of neural plasticity and neurogenesis

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15
Q

what happens to BDNF levels when you are depressed and what does this cause

A

levels lower causes a decrease in dendritic connectivity and decreased neurogenesis

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16
Q

how do antidepressants raise BDNF levels

A

it was not a planned effect, it was a byproduct of the monoamine targets

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17
Q

what does CREB do

A

a protein that regulates transcription of certain genes by binding to DNA

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18
Q

What is the role of CREB in depression

A

it may mediate BDNF but we don’t really know if it is affected by antidepressants

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19
Q

what does cortisol do to BDNF levels

A

lowers BDNF levels

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20
Q

what has the biggest effect in a treated state on CREB

A

BDNF and Monoamines (causes more BDNF release)

glutamate does other things too

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21
Q

what volume of the brain is most important in neurogenesis

22
Q

where is decreased levels most found

A

cerebrospinal fluid

23
Q

what does electroconvulsive therapy do

A

increases BDNF and increases neurogenesis in the hippocampus

24
Q

what happens when you inhibit SERT or NET

A

serotonin and adrenaline accumulate in the synapse

25
what are autoreceptors/ what do they do/ where are they
on the presynaptic neuron, negative feedback, prevents further release
26
what do SERT and NET do
pump 5HT and NE back into the presynaptic inhibitor, reuptake
27
which drug was the first blockbuster SSRI
prozac/fluoxetine
28
what is fluoxetine/prozac more selective for
serotonin transporters than noradrenaline transporters
29
what enzyme metabolizes fluoxetine/prozac
CYP2D6
30
what is fluoxetine/prozac metabolized into
norfluoxetine
31
what is the half life of fluoxetine/prozac and why
super long because norfluoxetine has a super long half life, 180h
32
what is the issue with fluoxetine/prozac and norfluexitine what does this cause
they are potent inhibitors of CYP2D6 increases half life over time
33
what kind of drug is fluoxetine/prozac
SSRI
34
what kind of drug is venlafaxine(effexor)
SNRI
35
how is SNRI different than SSRI
it is more selective towards NET than SERT (however still more SERT than NET, just less extreme, more balanced)`
36
what metabolizes venlafaxine(effexor)
CYP2D6
37
what does venlafaxine(effexor) become after metabolism
desvenlafaxine
38
half life of venlafaxine(effexor)
8-11 hours (just know its less than fluoxetine/prozac)
39
what do MAOIs do and how do they work
boost monoamine neurotransmitter levels by inhibiting MAO, the enzyme that metabolises them
40
what do TCAs do and how do they work
inhibit SERT and NET
41
which has the most potentially lethal overdose
TCAs, also MAOIs
42
What are some TCA side effects
antimuscarinic and drowziness because they antagonize H1 receptors (prevents ACh binding)
43
what is MAO / what does it do
an enzyme that metabolizes monoamine neurotransmitters
44
do MAOI work pre or post synaptically
PRE
45
what is the reason that antidepressants take awhile to work? (2 words)
receptor desensitization
46
what causes receptor desensitization
chronic elevation of serotonin levels desensitizes the autoreceptors, thereby there will be more synaptic levels this happens with both alpha2 for noradrenaline neuron receptors too
47
how does BDNF work
changes the expression of genes, thus changing the relative abundance of proteins in various brain regions
48
why does it take awhile for BDNF to work
because new neurons still need to form and migrate, and BDNF is a protein and can take time to work
49
which drugs directly target the BDNF system
none
50
what macromolecule is BDNF
protein