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Psychopharmacology > Chapter 7: treating mood disorders > Flashcards

Chapter 7: treating mood disorders Flashcards

1
Q

what is classified as a “response”

A

at least 50% reduction in symptoms

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2
Q

what are the 6 SSRIs

A

fluoxetine (Prozac)
Sertraline (Zoloft)
Paroxetine (Paxil)
Fluvoxamine (Luvox)
citalopram (Celexa)
escitalopram (Lexapro)

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3
Q

what is the SPARI used in clinical practice

A

Vilazodone (Viibryd)

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4
Q

what does SPARI stand for

A

serotonin partial agonist reuptake inhibitor

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5
Q

what are the 5 SNRIs

A

venlafaxine (Effexor)
desvenlafaxine (Pristiq)
duloxetine (Cymbalta)
milnacipran (Toledomen)
levomilnacipran (Fetzima)

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6
Q

what does NDRI stand-for and what is the NDRI used in clinical practice

A

Norepinephrine-dopamine reuptake inhibitor
Buproprion (Wellbutrin)

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7
Q

what is agomelatine (Valdoxen) used for

A

exerts antidepressant effect by correcting circadian rhythm by acting as a substitute melatonin

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8
Q

mechanism of action for agomelatine (Valdoxen)

A

agonist at melatonin 1 (MT1) and 2 (MT2)
antagonist at 5HT2C

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9
Q

4 principle mechanisms of action for mirtazapine

A

antagonism of 5HT2A, 5HT2C, a2-adrenergic, H1 receptors

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10
Q

what does SARI stand for and what are the SARIs used in clinical practice

A

serotonin antagonist reuptake inhibitors
nefazodone (Dutonin)
trazadone (Deseryl)

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11
Q

5 mechanisms of action for vortioxetine

A

inhibits SERT
antagonist ar 5HT3 and 5HT7
agonist at 5HT1A
weak partial agonism at 5HT1B/1D

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12
Q

name of the neuroactive steroid used in clinical practice

A

brexanolone

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13
Q

drugs most often used as augmentation agents in treatment-resistant unipolar depression

A

olanzapine/fluoxetine combo
quetiapine (seroquel)
aripiprazole (abilify)
brexpiprazole (rexulti)
cariprazine (Vraylar)

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14
Q

second line monotherapies for treatment-resistant depression

A

tricyclics
MAOIs

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15
Q

what is 1st line treatment for bipolar disorder

A

serotonin/dopamine blocker rather than monoamine inhibitor

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16
Q

drugs typically prescribed as 1st line treatment for bipolar disorder

A

olanzapine-fluoxetine combo
quetiapine (seroquel)
lurasidone (Latuda)
cariprazine (Vraylar)

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17
Q

what is the “classic” mood stabilizer

A

Lithium

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18
Q

how are anticonvulsants categorized as mood stabilizers

A

“mania minded” (tx/stabilize from above)
“depression minded” tx/stabilize from below

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19
Q

anticonvulsants proven effective in bipolar disorder

A

valproic acid (Depakote)
carbamazepine (Tegretol)
lamotrigine (Lamictal)

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20
Q

is monotherapy or combination therapy the standard for treating bipolar disorder

A

combination therapy

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21
Q

what % of SERTs need to be occupied to achieve antidepressant effect with SSRIs

A

80-90%

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22
Q

how do SSRIs work in general (common to all 6)

A

serotonin levels rise d/t SERT blockade.
There is an immediate increase of serotonin in the somatodendritic area which causes stimulation of 5HT1A autoreceptors. 5HT1A receptors downregulate (desensitized) after prolonged exposure to increased 5HT levels (correlates with time to therapeutic effect). Once autoreceptors are desensitized the neuron is disinhibited and releases 5HT at the axon terminal. Eventually, postsynaptic 5HT receptors desensitize which reduces side effects as tolerance develops

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23
Q

what is the only SSRI approved for treatment of eating disorders

A

fluoxetine (Prozac)

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24
Q

what is the mechanism of action of fluoxetine (Prozac) other than SERT inhibition

A

5HT2C antagonism

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25
Q

what neurotransmitters are increased by 5HT and 5HT2C antagonism

A

norepinephrine and dopamine

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26
Q

is 5HT2C antagonism generally activating or sedating

A

activating (energizing for increased concentration/attention)

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27
Q

half-life and available dosing options for fluoxetine

A

2-3 days
once daily or once weekly (active metabolite has a half-life of 2-3 weeks

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28
Q

binding profile of sertraline (Zoloft)

A

SERT inhibition with weaker DAT inhibition and σ1binding

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29
Q

binding porperties of stimulants like cocaine and meth

A

high-impact DAT inhibition

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30
Q

“well-oft”

A

adds weak DAT inhibition of wellbutrin and zoloft together

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31
Q

binding profile of paroxetine

A

NET and muscarinic inhibition and enzyme nitric oxide synthase

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32
Q

withdrawal rxns for paroxetine (Paxil)

A

akathisia, restlessness, GI symptoms, dizziness, tingling

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33
Q

binding properties of fluvoxemine (Luvox)

A

5HT inhibition and σ1binding properties (agonist)

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34
Q

what is Fluvoxamine approved for

A

OCD, not depression

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35
Q

available dosing options for fluvoxemine

A

IR (BID)
ER (QD)

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36
Q

one of the better tolerated SSRIs that are favorable for the elderly

A

Citalopram (Celexa)

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37
Q

enantiomers of citalopram

A

S and R

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38
Q

function of R enantiomer in citalopram

A

mild antihistaminic properties
activity may interfere with S enantiomer’s ability to inhibit SERT

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39
Q

whats important to remember about dosing citalopram

A

high doses can cause QTc prolongation

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40
Q

advantages of escitalopram over citalopram

A

only contains S enantiomer
no high dose restriction
removes antihistaminic properties

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41
Q

BEST tolerated SSRI

A

escitalopram

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42
Q

drugs typically used to augment SSRIs/SNRIs to add 5HT1A partial agonism

A

buspirone
aripiprazole/brexpiprazole/cariprazine
quetiapine

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43
Q

SPARI binding of buspirone

A

5HT1A partial agonist

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44
Q

SPARI binding profile of aripiprazole, brexpiprazole, cariprazine

A

5HT1A/D2 partial agonist

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45
Q

SPARI binding profile of quetiapine

A

5HT/D2 antagonist w/ 5HT1A partial agonist properties

46
Q

how does wellbutrin work

A

occupation of SERT and 5HT1A receptors increase 5HT in somatodendritic area. This causes 5HT1A autoreceptors to downregulate/desensitize after prolonged exposure to increased levels of 5HT. downregulated autoreceptors to increased neuronal firing and 5HT release at axon terminal

47
Q
A
48
Q

binding profile of vilazodone

A

SERT inhibition with 5HT1A partial agonism

49
Q

what is an advantage of SNRIs over SSRIs

A

ability to treat pain

50
Q

where do SNRIs increase dopamine levels and how do they do it

A

in the PFC
NET inhibition increases the diffusion radius of NET. There are not very many DATs in the PFC so dopamine uses NET for reuptake. When NET is inhibited it increases dopamine levels in PFC

51
Q

which SNRI is approved for fibromyalgia but not depression

A

milnacipran

52
Q

which enzyme converts venlafaxine to its active metabolite desvenlafaxine

A

2D6

53
Q

Is venlafaxine more potent for SERT or NET

A

SERT. Dose-dependent NET inhibition

54
Q

which enzyme is desvenlafaxine a substrate for

A

2D6

55
Q

Is desvenlafaxine more potent for SERT or NET

A

SERT

56
Q

Is duloxetine more potent for SERT or NET

A

SERT (slightly)

57
Q

Should duloxetine be dosed daily or BID

A

BID at first then transition to daily once patient is tolerant of dose

58
Q

which of mirtazapine’s mechanisms of action increases the downstream release of dopamine in the PFC

A

antagonism of 5HT2A
also improves sleep

59
Q

what is the result of mirtazapine’s 5HT2C antagonism

A

enhanced release of norepinephrine and dopamine

60
Q

what is the MAIN mechanism of action for mirtazapine

A

a2-adrenergic antagonism

61
Q

how does mirtazapine’s a-2 adrenergic antagonism work

A

a2 are norepinephrine auto receptors so when they are blocked, norepinephrine can’t shut itself off and release is increased

62
Q

which SNRI is approved for fibromyalgia but not depression

A

milnacipran

63
Q

which of mirtazapine’s mechanisms of action enhances the release of norepinephrine and dopamine in the PFC

A

antagonism of 5HT2C

64
Q

what is the main mechanism of action of mirtazapine

A

antagonism of a2 adrenergic receptors
this makes it so norepinephrine cannot turn itself off at its autoreceptors on noradrenergic neurons

65
Q

where are 5HT3 receptors usually located

A

on GABA interneurons

66
Q

how doe 5HT3 antagonist action work

A

when serotonin stimulates it it causes GABA to inhibit whatever neuron is downstream from it

67
Q

Is 5HT3 antagonism activating or sedating

A

always activating

68
Q

mechanism of action for nefazadone

A

5HT2A antagonism (robust)
5HT2C antagonism (weaker)
SERT inhibition

69
Q

why is nefazadone not really used anymore

A

liver toxicity

70
Q

what is the difference between high and low doses of trazodone

A

hypnotic at low doses (5HT2A blockade), antidepressant at higher doses

71
Q

Is 5HT2A action generally activating or sedating

A

sedating

72
Q

Mechanism of action of vortioxetine

A

SERT inhibition
5HT3 and 5HT7 antagonism
5HT1A antagonism

73
Q

cognitive domains treated by vortioxetine

A

attention
executive function
memory
processing speed

74
Q

what happens with SERT inhibition and 5HT1B/D (vortioxetine)

A

5HT1B/D autoreceptors typically turn off 5HT, when they are not inhibited it increases 5HT more than just SERT inhibition alone

75
Q

SERT inhibition and 5HT3 antagonism (vortioxetine)

A

Removes GABAs inhibition of dopamine and acetylcholine neurons causing increased neurotransmitter release

76
Q

SERT inhibition and 5HT7 antagonism

A

Prevents GABA from inhibiting downstream neurotransmitters resulting in increased serotonin in the PFC

77
Q

what does brexanolone typically treat

A

postpartum depression (60-hour continuous infusion)

78
Q

what are the typical augmenting agents for treatment-resistant unipolar depression

A

olanzapine-fluoxetine combo
quetiapine
aripiprazole
brexpiprazole
cariprazine

79
Q

What binding property of brexpiprazole contributes to efficacy for agitation in dementia

A

a1 antagonism

80
Q

How does brexpiprazole enhance dopamine release in the PFC

A

simultaneous a1 and 5HT2A blockade (antagonism)

81
Q

what is California rocket fuel

A

NRI with mirtazapine

82
Q

how does California rocket fuel work

A

blocks serotonin/norepinephrine reuptake
disinhibits serotonin and norepinephrine release

83
Q

How do you achieve triple monoamine action with an attention to dopamine

A

stimulant/modafinil (DAT inhibitor)
with SNRI

84
Q

2nd line therapy for treatment-resistant depression

A

TCAs
MAOIs

85
Q

Lethal dose of a TCA

A

1 month supply

86
Q

TCAs are very effective for depression. What is their downfall

A

side effects

87
Q

what are TCA side effects caused by

A

blockade of:
muscarinic cholinergic receptors
H1 histamine receptors
a1 adrenergic receptors
VSSCs

88
Q

Class of medication for MAOIs

A

irreversible enzyme inhibitors
enzyme activity only returns when another one is synthesized in 2-3 weeks

89
Q

MAOA

A

enzyme that preferentially metabolizes monoamines associated with depression (5HT/NE)

90
Q

MAOI and tyramine

A

may develop HTN crisis after ingesting tyramine (especially cheese) since tyramine causes NE release that is destroyed by MAOA. When that is inhibited NE is not destroyed and BP rises

91
Q

5HT/DA blockers used for bipolar

A

olanzapine-fluoxetine combo
quetiapine
lurasidone
cariprazine

92
Q

1st line treatment for bipolar

A

5HT/DA blocker

93
Q

what is olanzapine-fluoxetine combo approved for

A

schizophrenia
bipolar mania
treatment-resistant unipolar depression
bipolar depression

94
Q

how does olanzapine-fluoxetine combo work in bipolar

A

antagonism of 5HT2A/5HT2C responsible for antidepressant action
D2 antagonism keeps antidepression from spilling over into mania

95
Q

what is quetiapine approved for

A

schizophrenia
bipolar mania
bipolar depression
augmenting SSRI/SNRI for tx-resistant depression

96
Q

how does quetiapine work in bipolar

A

antagonist at 5HT2A. 5HT2C, and a2
agonism at 5HT1A
D2 antagonism keeps it from spilling over into mania

97
Q

what is Lurasidone NOT approved for

A

bipolar mania

98
Q

what med is most often prescribed for bipolar depression

A

lurasidone

99
Q

what is cariprazine approved for

A

bipolar mania and depression

100
Q

what receptors does cariprazine work at

A

partial agonist at D3, D2, 5HT1A

101
Q

what sets cariprazine apart from other D2/5HT blockers used for bipolar

A

highly potent action at D3 as a partial agonist

102
Q

how potent is cariprazine’s action at D3

A

more potent than dopamine itself

103
Q

anticonvulsants used in bipolar disorder

A

valproic acid (depakote)
carbamazepine (tegretol)
lamotrigine (Lamictal)

104
Q

what are the three hypotheses for valproic acid’s mechanism of action

A

-inhibits VSSCs
boost action of neurotransmitter GABA
-regulating downstream signal transduction cascades

105
Q

typical side effects of valproic acid

A

hair loss, weight gain, sedation, metabolic disturbance, tremor

106
Q

what warnings does valproic acid have

A

bone marrow suppression, liver, pancreatic, and fetal toxicities

107
Q

what risks does valproic acid pose to women of childbearing age

A

amenorrhea, polycystic ovaries, hyperandrogenism, obesity, insulin-resistance

108
Q

what tests should you order when starting valproic acid

A

pregnancy test, LFTs, platelet count

109
Q

What enzyme is induced by carbamazepine

A

3A4

110
Q

What additional indication is carbamazepine useful for

A

neuropathic pain

Psychopharmacology (13 decks)

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