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Therapeutics III > Exam 5 (final) - Watts Antidepressants > Flashcards

Exam 5 (final) - Watts Antidepressants Flashcards

1
Q

brain-derived neurotrophic factor (BDNF) effect on depression (neurotrophic hypothesis)

A

stress and pain decrease BDNF levels in animals
-has antidepressant activities in animals
-depressed pts have less BDNF
-antidepressant meds increase BDNF
-some drugs cause decreased BDNF levels (glucocorticoids)

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2
Q

targets of fluoxetine and trazodone

A

5HT-2 reuptake receptors

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3
Q

targets of desipramine and maprotiline

A

NE reuptake receptors

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4
Q

targets of MAOi

A

MAO (block conversion to metabolites?)

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5
Q

Why is there a delay in clinical effect for some antidepressants?
-reason that therapy takes about 2-3 weeks before effectiveness

A

reason is not really known for sure

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6
Q

mechanism of MAOis

A

inhibit Monoamine Oxydase in presynaptic neuron
-importance of this is NE and 5HT is normally degraded by MAO
-now more 5HT and NE is released from vesicles into synapse

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7
Q

MAO inhibitors “severe” SE

A

HA
drowsiness
dry mouth
weight gain
orthostatic hypotension
sexual dysfxn

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8
Q

MAOi clinical pearls

A

avoid foods with tyramine (many but some examples are cheeses, sour cream, liver, lots of meats like pepperoni, beer, red wine, avocados, bananas)

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9
Q

tricyclic antidepressants (tertiary amines) MOA

A

inhibit both NE and 5HT reuptake via NET and SERT

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10
Q

tricyclic antidepressants (tertiary amines) SE

A

sedation (most of any class for depression)
weight gain (most of any class for depression)
heart conduction disturbances

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11
Q

tricyclic antidepressants (tertiary amines) options

A

imipramine (Tofranil)
amitriptyline (Elavil)
trimipramine (Surmontil)
clomipramine (Anafranil)
doxepin (Adapin, Sinequan)

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12
Q

tricyclic antidepressants (secondary amines) options

A

desipramine (Norpramin)
nortriptyline (Pamelor)
pretriptyline (Vivactil)
maprotiline (Ludiomil)

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13
Q

tricyclic antidepressants (secondary amines) SE

A

less but still some of:
sedation
weight gain
anticholinergic effects
autonomic effects
cardiovascular effects

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14
Q

general all TCA SE

A

weight gain
anticholinergic effects
neuro
CV (in elderly)

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15
Q

SSRIs MOA

A

inhibit 5HT presynaptic neuron receptors
-increases amount of 5HT in synapse
-5HT in synapse stays there longer and remains active longer

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16
Q

SSRIs options

A

fluoxetine (Prozac)
fluvoxamine (Luvox)
paroxetine (Paxil)
sertraline (Zoloft)
citalopram (Celexa)
escitalopram oxalate (Lexapro)

17
Q

which SSRI has less autonomic SE and no sedation compared to other SSRIs

A

fluoxetine

18
Q

SSRI SE

A

NV
HA
sexual dysfxn
anxiety
insomnia
tremor

19
Q

abrupt SSRI d/c can lead to

A

withdrawal sx:
brain zaps
dizziness
sweating
N
insomnia
tremor
confusion
vertigo

20
Q

drugs when used in combo may cause serotonin syndrome

A

SSRIs
MAOis
TCAs
metoclopramide
tramadol
triptans
St. John’s Wort

21
Q

SSRI + 5HT1A partial agonists options

A

vilazodone (Viibryd)
vortioxetine (Brintellex)

22
Q

tetracyclic TCA

A

mirtazapine (Remeron)
-alpha2 antagonist
-5HT2 and 3 antagonist
-H1 antagonist

23
Q

unicyclic TCA

A

bupropion (Wellbutrin)
-DAT inhibitor
-NET and SERT inhibitor

24
Q

5HT2 antagonist/SERT inhibitor

A

trazodone (Dyserel)
-5HT2a antagonist
-weak SERT inhibitor

25
Q

SNRIs options

A

venlafaxine (Effexor)
desvenlafaxine (Pristiq)
duloxetine (Cymbalta)
milnacipran (Ixel)
levomilnacipran (Fetzima)
reboxetine (Vestra, Edronax)
atomoxetine (Straterra)

26
Q

more rapid acting antidepressants include what class

A

NMDA antagonists

27
Q

NMDA antagonists options

A

ketamine (subanesthetic doses)
eskatamine (expensive)

28
Q

tx for postpartum depression (PPD)

A

SSRIs: fluoxetine, paroxetine
SNRIs: venlafaxine
GABA-A modulators: brexanolone (Zulresso)
CBT

29
Q

brexanolone (Zulresso) MOA

A

-allopregnanolone levels increase during pregnancy
-GABA-A receptors become desensitized
-allopregnanolone levels return to normal postpartum
-brexanolone resensitizes GABA-A receptors

30
Q

brexanolone (Zulresso) clinical pearls

A

REMS drug
60hr infusion
$20,000-30,000 + hospital costs

31
Q

flibanserin (Addyi)

A

-developed as antidepressant but now use for hypoactive sexual desire disorder
-agonist at 5HT1A
-antagonist at 5HT2A/C

32
Q

how does reserpine cause depression (“biogenic amine” hypothesis)

A

depletes NE and 5HT from vesicles

33
Q

describe 3 steps of neuroendocrine hypothesis

A

changes in hypothalamic-pituitary-adrenal (HPA) axis
-stress causes hypothalamus to release corticotropin releasing factor (CRF)
-CRF promotes release of ACTH from pituitary
-ACTH promotes release of cortisol from adrenal

just know elevated CRF causes depression

34
Q

CRF acts on CRF1 receptors to cause:

A

arousal
anxiety
disruption of sexual behaviors
disruption of sleep

Therapeutics III (22 decks)

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