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nmsp exam 3 > Antidepressants and Mood stabilizers > Flashcards

Antidepressants and Mood stabilizers Flashcards

1
Q

Most antidepressants are also for other ?

A

mental health conditions

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2
Q

what medication is used as an antidepressant but also for nicotine withdrawal

A

bupropion

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3
Q

what medication is used as an antidepressant but also for Enuresis

A

imipramine

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4
Q

what medication is used as an antidepressant but also for diabetic peripheral neuropathy, fibromyalgia, and chronic musculoskeletal pain

A

duloxetine

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5
Q

what medication is used as an antidepressant and also for stress incontience

A

duloxetine

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6
Q

what is enuresis

A

urinary incontience (loss of bladder control)

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7
Q

what is the first line treatment non-pharmacologic for depression

A

psychotherapy

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8
Q

what is the monoamine depression hypothesis ?

A

Norepinephrine, serotonin, dopamine, glutamate, and GABA are all dysregulated and out of wack

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9
Q

what is the neurotrophic depression hypothesis

A

there is a decrease in brain derived neurotrophic factor and neuronal plasticity

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10
Q

what is the steroid depression hypothesis

A

this is when glucocorticoids, thyroid hormones and sex hormones ( estrogen/testosterone) are out of wack causing depression

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11
Q

what are the 5 R’s in general antidepressant efficacy

A

Response
Remission
Recovery
Relapse
Recurrence

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12
Q

what is response

A

there is greater than or equal to 50% reduction in symptoms from baseline (not well, not the end goal)

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13
Q

what is remission

A

this is very low to no symptoms at all, better and well with a healthy state of functioning

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14
Q

what is recovery

A

6-12 months of ongoing remission (not cured)

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15
Q

what is relapse

A

return of symptoms after remission

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16
Q

what is recurrence

A

return of symptoms after recovery

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17
Q

how long does it take for antidepressants to kick in?

A

3-8 weeks depending on many factors

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18
Q

goal of antidepressant therapy is ?

A

remission/recovery

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19
Q

What are the classes of drugs used to treat depression

A

SSRis
SNRis
NDRis
NMDA antagonists
SARAs
Neurosteroids/Gaba modulator
MAOIs

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20
Q

what drugs are in the drug class SSRIs?

A

Citalopram
Escitalopram
FLuoxetine
Paroxetine
Sertraline
Vilazodone (2)
Vortioxetine (2)

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21
Q

what does SSRI mean

A

serotonin selective reuptake inhibitor (pre-synaptically)

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22
Q

MOA of SSRIs?

A

selectively inhibitor the presynaptic reuptake of serotonin via SERT

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23
Q

as a class, SSRIs are more _ than other classes of antidepressants

A

specific

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24
Q

Vilazodone and Vortioxetine are both SSRis but what is their 2nd mechanism of action

A

that are partial or full agonists at 5HT1 (which is an inhibitory G protein )

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25
Q

SSRIs as a class have much less impact on _ , _, and _ receptors

A

histamine, muscarinic, adrenergic

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26
Q

which SSRi has the most anticholinergic side effect ?

A

paroxetine

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27
Q

side effects of SSRIs

A

CNS depression (sedation or insomnia)
sexual dysfunction (due to serotonin)
weight gain/loss
hyponatremia
QT prolongation
serotonin syndrome

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28
Q

what is serotonin syndrome

A

this is dose dependent disorder due to an increased level of serotonin often when given concurrently with multiple serotonin affecting drugs

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29
Q

symptoms of serotonin syndrome

A

abdominal pain/diarrhea
flushing
hyperreflexia
mental status changes
shivering
rhabdomyolysis/renal failure
cardiovascular shock/death

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30
Q

all antidepressants either are known to or can be associated with a withdrawal syndrome known as?

A

FINISH

flu-like symptoms
insomnia
nausea
imbalance
sensory disturbances
hyperarousal

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31
Q

all antidepressants have a black block warning of?

A

suidical ideations, behaviors, and actions (not completions)

**highest risk in less than 24 years old

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32
Q

what is the strongest CYP450 drug inhibitor in the SSRI class (dont prescribe if they are on a shit ton of medicines already)

A

fluoxetine

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33
Q

_ (SSRI) is a potent 2D6 inhibitor

A

Paroxetine

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34
Q

what are the mild/low drug inhibitors in the SSRi class

A

citalopram, escitalopram, sertraline, vilazodone, vortioxetine

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35
Q

which 2 SSRIs have active metabolites

A

fluoxetine (long half life)

sertraline (short half life)

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36
Q

what are the SNRIs used to treat depression and what do they do

A

All the TCA’s and Desvenlafaxine, duloxetine, venlafaxine, levomilnacipran, amoxapine

they work by selectively inhabiting the reuptake of both serotonin and norepinephrine

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37
Q

what’s the difference between 3 amine and 2 amine in the SNRI class (TCA)

A

3 amine have relatively equal impact on both serotonin and norepinephrine

2 amine has more impact on norephinephrine

**most other SNRIs have more impact on serotonin than NE

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38
Q

which SNRI (serotonin and norephinephrine) also has dopamine antagonism

A

amoxapine

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39
Q

which SNRI (serotonin and norephinephrine) also has dopamine antagonism

A

amoxapine

D2 antagonist

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40
Q

what are the 3-amine TCAs

A

(have more serotonin activity)

amitriptyline
clomipramine
doxepin
imipramine
trimipramine

41
Q

what are the 2 amine TCAS

A

amoxapine, nortiptyline, desipramine, protryptyline

42
Q

TCAs also block other receptors like

A

histamine (H1), muscarinic (cholinergic) and A1 (adrenergic)

-3 amines more often

43
Q

alpha (adrenergic) stimulation from TCAs can cause

A

tachycardias, orthostatic hypotension, dysrhythmias

44
Q

muscarine stimulation from TCAs can cause? (anti cholinergic)

A

dry moth, urinary mention, constipation, blurred vision, increased IOP

45
Q

histamine stimulation from TCAs can cause

A

sedation, fatigue, seizures

46
Q

overdose of TCA 3 c’s (in the ER)

A

coma, cardiotoxicity (conduction abnormalities), convulsions

(quinidine like effect)

47
Q

non TCA SNRIs have side effects similar to SSRIs with generally less risk of _

A

sexual dysfunction

48
Q

SNRIs due to NE can cause

A

HTN, agitation, nervousness

49
Q

what are SARAs used to treat depression

A

Serotonin Adrenergic (NE) receptor antagonsits

trazodone and nefazodone and mitrazapine

50
Q

SARAs trazadone and nefazadone block the A _ receptors on the adrenergic neurons leading to _ and the post synaptic _ receptors providing efficacy

A

1

side effects

5-HT2

51
Q

trazodone is typically used when?

A

to provide H1 blockade and cause sleep

it is a weak SERT blockade

52
Q

nefazadone has _ toxicity and is usually used for what

A

hepatic

sleep (H1 blockade)

53
Q

which SARA will block presynaptic a2 receptors and Serotonergic receptors and block post synaptic 5HT 2/3 receptors

A

Mitrazapine (great add on)

**does not have SERT.NET activity

causes H1 blockade

54
Q

what are the side effects of SARAs

A

sedation
weight gain- mitrazapine
orthostatic hypotension- trazodone
hepatotoxicity- nefazodone

55
Q

what are NDRIs

A

Noreepineprhine Dopamine Reuptake inhibitors

  • inhibit presynaptic reuptake of NE and dopamine

they also work to enhance presynaptic release of NE and DE though its effects on VMAT2

56
Q

what drug is considered a NDRI

A

Busproprion (destromethopran too)

57
Q

side effects of busproprion ( NDRI)

A

stimulating! (wake up)

agitation , insomnia, hypertension, tachycardias, tremors
weight loss
seizures

58
Q

what is the mechanism of action of MAOIs

A

irreversible block monoamine oxidase inhibitors which increases the levels of monoamines in the neuronal vesicles leading to increased amounts of NE, 5-HT, and dopamine

all oral expect segeline (B selective)

59
Q

what is a MAOI that is B selective and given in a patch form for depression

A

selegiline

60
Q

what are the drugs in the MAOi class

A

Isocarbaxazid
Phenelzine
Selgeline
tranylcypromine

61
Q

which MAOIs have a stimulant like effect (2)

A

tranycypromine and selegiline

62
Q

what is the most side effect of MAOIs (broad spectrum increase in neurotransmitters)

A

hypertensive crisis

dont forget serotonin syndrome**

63
Q

symptoms of hypertensive crisis

A

severe headache, anxiety, sweating, nosebleeds, tachycardia, chest pain, changes in vision and breath, confusion, N/V

64
Q

how does MAOIs cause hypertensive crisis

A

they inhibit MAO-A which is necessary for tyramine metabolism in the GI tract

tyramine containing substances (foods) in our stomach and tyramine can induce significant catecholamine release leading to hypertensive crisis

  • need dietary counseling***
65
Q

NMDA antagonists for depression MOA

  • drug in the class?

when do you use the inhalation type?

A

NMDA is an ionotropic channel ; prevents Na+ from coming in and depolarization (glutamate)

Esketamine
Dextromethrorphan

-treatment resistant depression in conjunction with ongoing antidepressant therapy with acute suicidal ideations/behaviors

(nasally administered)

66
Q

if you are going to give esketamine the patient is observed _ hours post dose looking at blood pressure and cognitive impairment

A

2

67
Q

what is the MOA of the Neurolosteroids/GABA modulator

what drug is this?

A

they are GABA a receptor positive allosteric modulators that are identical to endogenous alloprehnalolne (these levels drop in postpartum period)- increases neuronal GABA inhibition

Brexanolone

68
Q

when and how do we use Brexanolone (Neurosteroid/GABA modulators)

A

for post-partum depression

60 hour IV administration with lots of monitoring

69
Q

what are the mood stabilizer families that are used to treat Bipolar I and Bipolar II

A

Anti-seizure agents

miscellaneous

70
Q

what are the anti seizure agents that are used as mood stabilizers in Bipolar disorder

A

carbamazepine
lamotrigine
Divalproex/Valproate
Valproic acid

71
Q

what is the miscellaneous mood stabilizer used to treat bipolar disorder

A

lithium

72
Q

BIPOLAR PATIENTS MUST BE ON?

A

mood stabilizer!!!!!!! not antidepressant (only treating one pole)

73
Q

what are the 3 MOA in lithium (broad)

A

brain structure, neurotransmitter modulator, intracellular changes

74
Q

lithium inhibits and stimulates what receptors

A

dopamine receptor (D2) GI and Gs (inhibits)

NMDA blocker

stimulates GABA

75
Q

intracellular changes due to lithium

A

blocks IPPase and IMPase which depletes MI-myoinositol (too much of this in the manic state) (decrease PIP2 pathway)

inhibits PKC, GSK-3 and MARCKS

76
Q

decreased PKC facilitates _ release

A

5HT

77
Q

decreased GSK-3 increases _ which is neuroprotective

A

B catenin

78
Q

lithium facilitates production of _ and _ which are both neuroprotective

A

CREB/BDNF and BCl-2

79
Q

side effects of lithium

A

monovalent ion and competes with Na+ for reabsorption

leads to decreased aldosterone and vasopressin effects along with RESISTANCE to ADH

leads to polyuria/polydipsia (nephrogenic diabetes insipidus)

tremor

confusion

leukocytosis

80
Q

what other drugs can interact with lithium

A

anything that impacts Na/K

ace inhibitors, diuretics. NSAIDS

81
Q

what is the therapeutic window of lithium

A

its narrow

0.6-1.5

82
Q

when do we use lithium

A

acute and maintenance of mania/bipolar I disorder

reduce risk suicide

83
Q

what are the 3 mood stabilizer initially developed as anti seizure agents utilized to treat bipolar disorder

A

valproic acid/divalproex/valproate

lamotrigine

carbamazepine

84
Q

MOA of valproid acid/divalproex

A

decreases myo-inositol-1, PKC< GSK-3, MARCKS

85
Q

therapeutic range for valproic acid

A

60-120mcg/ml

86
Q

pharmacokinestics of valproic ACID-

inhibits _ isozyme and _ glycoprotein and induces a few different _ isozymes

it _ hepatic enzyme uridine glucuronotransylferases (UGT)

A

CYP450

P

CYP450

inhibits

87
Q

side effects of valproic acid

A

thrombocytopenia, dizziness, agitation, pancreatitis, increased ammonia levels

88
Q

valproid acid indications

A

acute and maintenance of mania/bipolar disease

89
Q

MOA of carbamazepine

A

decrease inositol (MI)

90
Q

therapeutic window of carbamazepine

A

6-12 mcg

91
Q

carbamezapine is a broad _ of CYP450

A

inducer

92
Q

carbamazepine _ hepatic enzyme UGT

A

induces

93
Q

side effects of carbamazepine

A

leukopenia, neutropenia, thrombocytopenia

hypocalcemia and osteoporosis

94
Q

indications for carbamazepine use

A

acute and maintenance treatment of mania/mixed bipolar disorder

95
Q

MOA of lamotrigine

(4)

A

blocks NMDA

decreases GSK-3 and increases BDNF

5HT1a agonist down regulating SET (serotonin reuptake)

5-HT2a agonists increasing NET blockade (NE reuptake )

96
Q

metabolism of lamotrigine is reduced my

A

valproic acid

97
Q

metabolism of lamotrigine is increased by

A

carbamazepine

98
Q

side effects of lamotrigine

A

conduction abnormalities, dizziness/vertigo

99
Q

indications for lamotrigine use

A

maintenance of bipolar I disorder (esp .with mostly depressive symptoms )

nmsp exam 3 (11 decks)

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