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IDT Fall > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

what are the statistics of suicide rates in people who are depressed

A

10-15%

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2
Q

T/F depression can cause “pain in the brain” that feels the same as physical pain

A

True

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3
Q

what emotion is a potential symptom from depression that is more common in men?

A

anger

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4
Q

Define anhedonia

A

nothing gives pleasure

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5
Q

define apathy

A

inability to think there are good things in life

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6
Q

Why does bipolar depressive disorder have a higher risk of suicide?

A

their extreme swings of happiness can be followed by even more extreme depression

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7
Q

T/F men are twice as likely to suffer from depression

A

False, 2-3 times more common in women

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8
Q

what role do genetics play in depression?

A

40% of depression patients have a genetic disposition to it

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9
Q

When are antidepressants used prophylactically?

A

after a patient has had depression and is no longer depressed, they can be prescribed to take antidepressants to prevent recurrent depression

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10
Q

define reactive depression

A

a normal response to circumstances (such as grief)

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11
Q

define agitated depression

A

fear, insomnia, extreme irritability, and restlessness

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12
Q

define dysthmia

A

low level, long term (>2yr) melancholy

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13
Q

define premenstrual dysphoric disorder

A

depression or anxiety the week or two before your period starts and usually goes away a couple days from starting period

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14
Q

define post-partum depression

A

depression after giving birth, can last up to a year after delivery

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15
Q

define psychotic depression

A

perception of reality becomes altered

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16
Q

what are treatments we use for depression?

A

talk therapy
light therapy
antidepressants (ADMs)
exercise to reduce relapse
electroconvulsive therapy

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17
Q

what are potential diagnoses we should rule out before diagnosing depression?

A

hypothyroidism or adverse drug rxns

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18
Q

when do we use electroconvulsive therapy on depression patients?

A

when meds aren’t working or not working quick enough for the situation

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19
Q

what are the advantages to electroconvulsive therapy?

A

rapidly effective and useful in resistant depression

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20
Q

what are the disadvantages to electroconvulsive therapy?

A

typically causes confusion and memory

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21
Q

what are the statistics for successful treatment with antidepressants?

A

70-80% effectiveness

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22
Q

what do antidepressants improve for patients?

A

improve appetite, sleep, mood, and their behavior perceived by others (affect)

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23
Q

what are other uses for antidepressants?

A

neuropathic pain, fibromyalgia, anxiety, or OCD

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24
Q

what is the simple biogenic amine hypothesis?

A

extending the duration of biogenic amines (NE, serotonin, maybe dopamine) either through blockade or reuptake or inhibition of metabolism, elevates moods

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25
Q

what are symptoms caused by drugs that target 5-HT?

A

agitation, appetite disturbance, sleep disturbance, anxiety, loss of libido

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26
Q

what are symptoms caused by drugs that target NE?

A

attention deficit, poor working memory, reduced alertness, low energy, social withdrawal

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27
Q

what two classes of antidepressants are consider “older agents”
what are the disadvantages of the older agents?

A

tricyclic antidepressants and MAOIs
more side effects

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28
Q

what do tricyclic antidepressants block?

A

serotonin and NE reuptake

29
Q

SNRIs also block serotonin and NE reuptake, why do they not cause the same side effects as tricyclic antidepressants?

A

they act at less receptors

30
Q

what is a natural product/herbal remedy used to help with depression?

A

St. John’s Wort

31
Q

explain the hypothesis: antidepressant action requires changes in brain structure

A

this hypothesis aims to explain why antidepressants take weeks to months to become effective. Ultimately, increased 5-HT transmission over a long term will lead to structural changes in the brain
Essentially, they increase neurotrophic agents leading to structural changes, especially on the hippocampus that improve mood

32
Q

which two transporters to tricyclic antidepressants block?
what are they also useful for?

A

NE and 5-HT
treating neuropathic pain

33
Q

list the tricyclic antidepressants

A

Imipramine
Amitriptyline
Desipramine
Doxepin
Maprotiline

34
Q

why do we see cardiovascular side effects from tricyclic antidepressants?
what side effect in specific?

A

antagonism of a1 receptors -> low bp
antagonism of muscarinic cholinergic receptors -> tachycardia
NE activation of cardiac B receptors

35
Q

why do tricyclic antidepressants cause drowsiness and weight gain?

A

antagonism of histamine H1 receptors

36
Q

what do MAOIs block breakdown of?

A

NE and 5-HT

37
Q

what are three medications that are MAOIs?

A

Phenelzine
Tranylcypromine
Isocarboxazid

38
Q

what line of treatment do we consider MAOIs for depression? (first line? second line?…..)

A

last resort treatment

39
Q

what are other conditions MAOIs are useful for treating?

A

anxiety, phobias, hypersomnia, hyperphagia (extreme unsatisfied drive to consume food)

40
Q

what are some side effects of MAOIs?

A

insomnia followed by daytime sleepiness
dry mouth
loss of libido
hepatotoxicity (phenelzine)

41
Q

what drug class should MAOIs not be mixed with due to risk of oversympathetic stimulation?

A

adrenergic stimulants

42
Q

why is serotonin syndrome a concern with pts using MAOIs?

A

since they are usually add-on therapies, other drugs pt is on likely also increase serotonin in synaptic cleft, so the risk increases with more drugs used

43
Q

foods high in ______ have toxic interactions with MAOIs

A

tyramine

44
Q

what are the symptoms of serotonin syndrome?

A

causes hyperthermia, muscle rigidity, and mental disorientation

45
Q

what are the first line agents for depression and anxiety?

A

SSRIs

46
Q

why do SSRIs not have the same side effects as TCAs despite acting at the same receptors to treat depression?

A

they have no affinity for alpha, muscarinic, histamine, or dopamine receptors

47
Q

which SSRI should we avoid in elderly or bulimic patients and why?

A

Fluoxetine b/c it causes sodium inbalances

48
Q

which SSRI is the most stimulating?

A

Fluoxetine

49
Q

Why should Sertraline be less considered for teenagers?

A

it may cause increases suicidal ideation

50
Q

which two SSRIs have the largest selectivity for SERT over NET?

A

Citalopram and Escitalopram

51
Q

what are the side effects of SSRIs?

A

nausea
headaches
nervousness
insomnia
sexual dysfunction
suicidal ideation

52
Q

what is discontinuation syndrome from SSRIs?
how long does it last?

A

if pt abruptly stops taking they can experience nightmares, insomnia, cofusion and/or virtigo. increased irritability and agitation
can experience “brain zaps”, “brain shivers”

usually resolves after a few weeks

53
Q

what would happen if a pt were to OD on SSRIs?

A

seizures leading to death

54
Q

list the 4 SNRIs

A

Venlafaxine
Duloxetine
Desvenlafaxine
Levomilnacipran

55
Q

T/F SNRIs have greater efficacy than SSRIs and are 1st line use for anxiety

A

false, same efficacy, but yes they are 1st line for anxiety

56
Q

in addition to having similar SEs to SSRIs, what other side effects do SNRIs have and why?

A

due to increasing NE at synapse may cause mild hypertension, dry mouth, increased HR, and dilated pupils

57
Q

list the serotonin antagonists and modulators

A

Vilazodone, Vortioxetine, Trazodone

58
Q

what is Vortioxetine classified as?

A

a 5HT1A/B partial agonist

59
Q

What is Trazodone classified as?

A

SERT blocker, H1 histamine and a1 antagonist

60
Q

what is a natural supplement that may have similar efficacy to SSRIs in treating depression?

A

St. John’s Wort

61
Q

what metabolic pathway does St. John’s Wort induce?

A

Cyp3A

62
Q

what are the atypical antidepressants that treat depression but don’t target SERT/NET?

A

mirtazapine
bupropion
esketamine nasal spray
dextrometorphan + bupropion
brexanolone

63
Q

what makes mirtazapine a good drug of choice for anxiety with depression?
when do we use it?

A

it has H1 antagonism
for treatment resistant depression

64
Q

why is bupropion used to treat depression?

A

we currently do not know

65
Q

when do we use esketamine nasal spray?
how long does it take to have an effect? how long does it last? how often is it given?

A

for treatment resistant depression
hours. about 5 days. 2x weekly dosing

66
Q

what are the SEs of esketamine nasal spray?

A

sedation, dissociation, visual disturbances, trouble speaking, confusion, numbness, dizziness

67
Q

what drug class is esketamine nasal spray?

A

NMDA receptor antagonist

68
Q

how long does it take for dextromethorphan + bupropion to have benefits?
what is the reasoning why this combo might work for depression?

A

2 weeks
bupropion inhibits rapid metabolism of dextromethorphan to dextrorphan
dextromethorphan is a weak NMDA antagonist, sigma agonist, weak NET and SERT reuptake inhibitor, and mu opioid agonist

69
Q

when do we use Brexanolone?
drug class?
time for effect?
length of effect?
how is it given?
how long does it take to give?
cost?

A

for post-partum depression
positive allosteric modulator of GABA A-receptor
within days
persist for at least a month
clinical administration only due to sedation and loss of consciousness
IV infusion for 60 hours
costs $34,000

IDT Fall (29 decks)

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