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Pharmacology 200 > 2-Drugs for Depression > Flashcards

2-Drugs for Depression Flashcards

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

A

hippocampus

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
Q

what are autoreceptors/ what do they do/ where are they

A

on the presynaptic neuron, negative feedback, prevents further release

26
Q

what do SERT and NET do

A

pump 5HT and NE back into the presynaptic inhibitor, reuptake

27
Q

which drug was the first blockbuster SSRI

A

prozac/fluoxetine

28
Q

what is fluoxetine/prozac more selective for

A

serotonin transporters than noradrenaline transporters

29
Q

what enzyme metabolizes fluoxetine/prozac

A

CYP2D6

30
Q

what is fluoxetine/prozac metabolized into

A

norfluoxetine

31
Q

what is the half life of fluoxetine/prozac and why

A

super long because norfluoxetine has a super long half life, 180h

32
Q

what is the issue with fluoxetine/prozac and norfluexitine

what does this cause

A

they are potent inhibitors of CYP2D6

increases half life over time

33
Q

what kind of drug is fluoxetine/prozac

A

SSRI

34
Q

what kind of drug is venlafaxine(effexor)

A

SNRI

35
Q

how is SNRI different than SSRI

A

it is more selective towards NET than SERT (however still more SERT than NET, just less extreme, more balanced)`

36
Q

what metabolizes venlafaxine(effexor)

A

CYP2D6

37
Q

what does venlafaxine(effexor) become after metabolism

A

desvenlafaxine

38
Q

half life of venlafaxine(effexor)

A

8-11 hours (just know its less than fluoxetine/prozac)

39
Q

what do MAOIs do and how do they work

A

boost monoamine neurotransmitter levels by inhibiting MAO, the enzyme that metabolises them

40
Q

what do TCAs do and how do they work

A

inhibit SERT and NET

41
Q

which has the most potentially lethal overdose

A

TCAs, also MAOIs

42
Q

What are some TCA side effects

A

antimuscarinic and drowziness because they antagonize H1 receptors (prevents ACh binding)

43
Q

what is MAO / what does it do

A

an enzyme that metabolizes monoamine neurotransmitters

44
Q

do MAOI work pre or post synaptically

A

PRE

45
Q

what is the reason that antidepressants take awhile to work? (2 words)

A

receptor desensitization

46
Q

what causes receptor desensitization

A

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
Q

how does BDNF work

A

changes the expression of genes, thus changing the relative abundance of proteins in various brain regions

48
Q

why does it take awhile for BDNF to work

A

because new neurons still need to form and migrate, and BDNF is a protein and can take time to work

49
Q

which drugs directly target the BDNF system

A

none

50
Q

what macromolecule is BDNF

A

protein

Pharmacology 200 (29 decks)

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