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Spring 2024 Therapeutics 3 > Final-Antidepressants > Flashcards

Final-Antidepressants Flashcards

1
Q

What is the goal of antidepressant therapy?

A

Alleviate signs and symptoms

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2
Q

What are the 3 types of depression?

A

-Reactive
-Major Depressive Disorder
-Bipolar Affective

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3
Q

What is the most common type of depression?

A

Reactive

(reaction to an event)

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4
Q

What are the 3 categories of the symptoms of depression?

A

-Physiological
-Psychological
-Cognitive

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5
Q

What are the physiological features of depression?

A

-Decreased sleep
-Appetite changes
-Fatigue
-Psychomotor dysfunction (clumsiness, etc)

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6
Q

What are the psychological features of depression?

A

-Dysphoric mood
-Worthlessness
-Excessive guilt
-Loss of interest/pleasure in all or most activities

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7
Q

What are the cognitive features of depression?

A

-Decreased concentration
-Suicidal ideation

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8
Q

What needs to be ruled out in a diagnosis of depression?

A

That it is not caused by:
-Drugs
-Medical condition
-Bereavement

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9
Q

Which antihypertensive/cardiovascular drugs can induce depression?

A

-Reserpine
-Methyldopa
-Propranolol + Metoprolol
-Prazosin
-Clonidine
-Digitalis

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10
Q

Which sedative-hypnotic drugs can induce depression?

A

-Alcohol
-Benzodiazepines
-Barbiturates
-Meprobamate

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11
Q

Which anti-inflammatory/analgesic drugs can induce depression?

A

-Indomethacin
-Phenylbutazone
-Opiates
-Pentazocine

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12
Q

Which steroid drugs can induce depression?

A

-Corticosteroids
-Oral contraceptives
-Estrogen withdrawal

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13
Q

What other drugs can induce depression?

A

-Anti-parkinson
-Anti-neoplastic
-Neuroleptics

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14
Q

What is the Biogenic Amine hypothesis of depression?

A

Reserpine depletes NE and 5HT from vesicles which causes depression

-Therefore, agents that increase NE and 5HT are effective for treating depression

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15
Q

How does Reserpine (BP drug) cause depression?

A

Depletes NE and 5HT from vesicles

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16
Q

What is the Neuroendocrine Hypothesis of depression?

A

There are changes in the Hypothalamic-Pituitary-Adrenal Axis (HPA) that cause it to be overactive

-Stress causes hypothalamus to release CRF
-CRF promotes release of ACTH from pituitary
-This promotes release of cortisol from adrenal glands

*Overactive HPA and elevated CRF is found in almost all depressed patients

*Overactive HPA may desensitize feedback response in hypothalamus and pituitary

*Antidepressants and Electroconvulsive therapy (ECT) lower CRF levels

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17
Q

What does elevated CRF cause?

A

-Insomnia
-Anxiety
-Decreased appetite
-Decreased libido

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18
Q

How does the Neuroendocrine Hypothesis relate to depression treatment?

A

Antidepressants and Electroconvulsive therapy (ECT) reduce CRF levels

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19
Q

What is the Neurotrophic Hypothesis of depression?

A

Brain-derived neurotrophic factor (BDNF) is critical in: neural plasticity, resilience, neurogenesis

*Stress and pain decrease BDNF

*Decreased BDNF causes depression

*Antidepressants increase BDNF levels

Brain Chemistry:
-dendritic sprouts disappear due to loss of BDNF
-this loss of sprouts leads to a depressed state

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20
Q

How does the Neurotrophic Hypothesis relate to depression treatment?

A

Antidepressants increase BDNF levels

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21
Q

How do the depression hypotheses integrate together?

A

HPA and steroid abnormalities regulate BDNF

Cortisol activates hippocampal glucocorticoid receptors, decreasing BDNF

Chronic monoamine receptor activation increases BDNF signaling and downregulates the HPA axis

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22
Q

True or False: The effects of antidepressants take days to weeks to occur but the body’s biochemistry immediately changes

A

True

-antidepressants cause an immediate change in serotonin levels and body chemistry

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23
Q

How long does antidepressant therapy take to work?

A

2-3 weeks

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24
Q

Why does antidepressant therapy take so long to work?

A

NO ONE REALLY KNOWS

Neuroadaptive responses?
-Antidepressants increase the amount of neurotransmitter in the intrasynaptic space
–Could cause delay due to pre/postsynaptic adaptation or activation of receptors

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25
Q

What is the MOA of MAOIs?

A

-MAO normally degrades norepinephrine (NE) and serotonin (5HT)

-When MAO is inhibited, more NE and 5HT is packaged into vesicles

-This results in more NE and 5HT being released into the synapse

(increase NE and 5HT)

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26
Q

What are the non-selective MAO inhibitors?

A

Phenelzine (Nardil)

Tranylcypromine (Parnate)

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27
Q

What are the MAO-B selective inhibitors?

A

Selegiline (Eldepryl/Ensam)*

Safinamide (Xadago)

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28
Q

What is the MAO-A selective inhibitor?

A

Moclobemide (Manerix)

*only in Europe

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29
Q

When are non-selective MAO inhibitors reserved for?

A

Drug treatment resistant depression

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30
Q

Whis MAO inhibitors are reversible and which are irreversible?

A

Non-Selective: Irreversible

MAO-B Selective: Reversible

MAO-A Selective: Reversible, only Europe

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31
Q

Which MAOI is only used in Europe?

A

Moclobemide (Manerix)

-MAO-A Selective

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32
Q

What are the side effects of MAO inhibitors?

A

-Headache
-Drowsiness
-Dry mouth
-Weight gain
-Orthostatic hypotension
-Sexual dysfunction

Hypertensive Crisis

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33
Q

What drugs do MAOI interact with?

A

OTC:
-Cold preparations
-Diet pills

Rx:
-TCA’s
-SSRI’s
-L-DOPA

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34
Q

Foods with what amino acid should be avoided when taking MAOI’s?

A

Tyramine

-Cheese, sour cream, sausage, bologna, salamis, red wine, avocado, banana, soy sauce, etc (any good foods)

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35
Q

What herbal product may be effective in depression due to its MAOI activity?

A

St. John’s Wort

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36
Q

For antidepressants that function as reuptake blockers, what site do they bind?

A

Allosteric site

(do not bind the active site, bind elsewhere)

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37
Q

What is the MOA of Antidepressants that work as Reuptake Blockers?

A

-Antidepressants bind the allosteric site and are not transported
-They block transport of NE and serotonin into the synapse which increased their levels in the extracellular space

*Note: do not bind the orthosteric site (where serotonin binds)

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38
Q

What are the indications for Tricyclic Antidepressants (TCAs)?

A

-Depression
-Panic Disorder
-Chronic Pain
-Enuresis

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39
Q

What is an important point to remember about Tricyclic Antidepressant Overdose/Toxicity?

A

DANGEROUS

-Depressed patients are more likely to be suicidal
—More likely to commit self-harm or suicide 2 weeks into treatment

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40
Q

At what point in Tricyclic Antidepressant therapy are patients more likely to commit self-harm or suicide and why?

A

2 weeks into treatment

-when people are depressed they do not have enough energy to take their own life, but the medication can give them more energy before the antidepressant effects start so they commit suicide before they start actually feeling better

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41
Q

What are the tertiary amines TCA’s?

A

Imipramine (Tofranil)
Amitriptyline (Elavil)
Clomipramine (Anafranil)
Doxepin (Adapin, Sinequan)

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42
Q

What is the function of the tertiary amine TCA’s?

A

Inhibit BOTH NE and 5HT reuptake via NET and SERT

Also act as receptor antagonists:
-Antihistamine (H1)
-Antimuscarinic
-Antiadrenergic (a1)

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43
Q

What side effects are associated with the tertiary amine TCAs?

A

These cause THE MOST:
-Sedation
-Weight gain
-Autonomic SE

-Conduction disturbances of the heart

*many, not great

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44
Q

Which tertiary amine can also be used for Enuresis and ADHD?

A

Imipramine (Tofranil)

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45
Q

Which tertiary amines get metabolized to secondary amines?

A

Imipramine (Tofranil)

Amitriptyline (Elavil)

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46
Q

What is Impramine (Tofranil) metabolized to?

A

Desipramine

(*secondary amine)

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47
Q

What is Amitriptyline (Elavil) metabolized to?

A

Nortriptyline

(*secondary amine)

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48
Q

Which tertiary amine can also be used for OCD?

A

Clomipramine (Anafranil)

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49
Q

True or False: Secondary Amines cause more side effects than Tertiary Amines

A

FALSE
-secondary amines cause many less side effects

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50
Q

Secondary amines inhibit which transporters?

A

Better NET inhibitors than SERT

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51
Q

What are the secondary amine drugs?

A

Desipramine (Norpramin)

Nortiptyline (Pamelor)

Maprotiline (Ludiomil) -NET inhibitor

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52
Q

Which secondary amine TCA is a NET inhibitor only?

A

Maprotiline (Ludiomil)

*tetracyclic reduced side effects

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53
Q

What are the SE of ALL TCA’s?

A

-Anticholinergic
-CV (elderly)
-Neurological
-Weight Gain
-Suicidal ideation

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54
Q

What is the MOA of SSRI’s?

A

Block serotonin transporter pumps presynaptically

-Increase serotonin in the synapse

(14 serotonin receptors: 13 G-coupled, 1 inotropic)

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55
Q

What are the SSRI drugs?

A

-Fluoxetine (Prozac)
-Fluvoxamine (Luvox)
-Paroxetine (Paxil)
-Sertraline (Zoloft)
-Citalopram (Celexa)
-Escitalopram oxalate (Lexapro)

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56
Q

Which SSRI is associated with little autonomic SE and no sedation?

A

Fluoxetine (Prozac)

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57
Q

Which SSRI is an Isomer of citalopram?

A

Escitalopram oxalate

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58
Q

What are uses of SSRIs?

A

Depression
Alcoholism
OCD
Enuresis
PTSD
Eating Disorder
Social Phobias
Panic Anxiety
PMDD
GAD

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59
Q

What are the SE of SSRIs?

A

Not many, widely used

Nausea+ Vomiting/ Headache/ Sexual Dysfunction/ ANXIETY/Insomnia/ Tremor

SSRI Discontinuation Syndrome

Serotonin Syndrome

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60
Q

What are the signs of SSRI discontinuation syndrome?

A

“Brain Zaps”
Dizziness
Sweating
Nausea
Insomnia
Tremor
Confusion
Vertigo

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61
Q

Use of SSRIs with what drugs can cause serotonin syndrome?

A

MAOIs
TCAs
Metoclopramide
Tramadol
Triptans
St. John’s Wort

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62
Q

What are the symptoms of serotonin syndrome?

A

Hyperthermia/ sweating
Muscle Rigidity
Restlessness
Myoclonus
Hyperreflexia
Shivering
Seizures
Coma

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63
Q

If Serotonin Syndrome occurs with use of SSRIs, how do we treat it?

A

Discontinue medication

Manage symptoms

Administer serotonin antagonists and benzodiazepines to control myoclonus

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64
Q

What are the two SSRI + 5HT partial agonists?

A

Vilazodone (Viibryd)

Vortioxetine (Brintellex)

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65
Q

What are the Tetracyclic and Unicyclic antidepressants?

A

-Maprotiline (Ludiomil)
-Mirtazapine (Remeron)
-Bupropion (Wellbutrin)

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66
Q

What is the only 5HT2 Antagonist/ SERT Inhibitor?

A

Trazodone (Dyserel)

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67
Q

What is an important side effect to remember for trazodone?

A

Sedating
-used for sleep!

Off-label-hypnotic (a1, H1, 5HT2)

68
Q

What are the SNRI drugs?

A

Venlafaxine (Effexor)
Desvenlafaxine (Pristiq)
Duloxetine (Cymbalta)
Milnacipran (Ixel)
Levomilnacipran (Fetzima)

69
Q

All of the SNRIs are inhibitors of what?

A

NET + SERT

70
Q

What are the Norepinephrine Selective Reuptake Inhibitor Drugs (NSRIs)?

A

Reboxetine (Vestra, Edronax)

Atomoxetine (Straterra)

71
Q

Which NSRI is not approved for use in the US?

A

Reboxetine

72
Q

Which NSRI is used for ADHD?

A

Atomoxetine

*not found to be useful in depression

73
Q

When examining a selectivity ratio for a drug, does a high or low number indicate MORE selectivity?

A

Low numbers indicate that the drug is more selective for that substance

Ex:
NE/ 5HT
1/3

=more selective for NE

74
Q

What is an example of a Serotonin-Norepinephirne-Dopamine reuptake Inhibitor (SNDRI) or “Triple Blocker”?

A

Cocaine

75
Q

What are the NMDA antagonists?

A

Ketamine

Esketamine (Spravato)

76
Q

What are some considerations to make when using NMDA antagonists?

A

-Very expensive
-Only available through REMS restricted program

*Esketamine must be used in conjunction with an oral antidepressant

77
Q

What treatment option are available for Postpartum Depression (PPD)?

A

SSRIs (fluoxetine, paroxetine)

SNRI (venlafaxine)

**Brexanolone (Zulresso)

CBT and counseling

78
Q

What is the MOA of Brexanolone (Zulresso)?

A

Allopregnanolone levels increase during pregnancy

GABA-A receptors desensitize

Allopregnanolone levels return to normal postpartum

Brexanolone resensitizes GABA-A receptors

79
Q

What are the non-pharmacological treatment options for depression?

A

-Electroconvulsive therapy
-Psychotherapy
-Hospitalization

80
Q

Which drug originally developed as an antidepressant is now being used for hypoactive sexual desire disorder in females?

A

Filbanserin (Addyi)

“female viagra”

81
Q

What is the % risk of a depressive episode reoccurring after 1 episode?

A

50-60%

82
Q

What is the % risk of a depressive episode reoccurring after 2 episodes?

A

70%

83
Q

What is the % risk of a depressive episode reoccurring after 3 episodes?

A

90%

84
Q

Why is the % risk of recurrence of a depressive episode important to consider?

A

Determines the dose and duration of medication a person will receive

85
Q

True or False: The risk of depression relapses becomes lower over time as duration of remission increases

A

True

86
Q

What is a predictor of recurrence of depressive episodes?

A

Persistent mild symptoms during remission

87
Q

True or False: Function deteriorates during a depressive episode and can never go back to baseline even upon remission

A

False, function will go back to baseline upon remission

88
Q

To meet the DSM-5 diagnostic criteria for depression, patients must show at least 5 symptoms and at least ONE of them must be what?

A

Depressed Mood
or
Loss of Interest/Pleasure in Doing Things

89
Q

Besides the main 2 symptoms of depression what are the others?

A

Sleep (insomnia/hypersomnia)
Interest (decreased)
Guilt (or worthlessness)
Energy (loss/fatigue)
Concentration (difficulties)
Appetite (changes; increase or decrease)
Psychomotor (agitation/retardation)
Suicidal (ideation)

SIGE CAPS

90
Q

What are the 2 self-administered rating scales used for depression?

A

Patient Health Questionnaire (PHQ-9)
–determines efficacy of treatment

Mood Disorder Questionnaire (MDQ)
–rules out bipolar disorder

91
Q

What are the 4 goals of depression treatment?

A
  1. Reduce or eliminate signs and symptoms of depression
  2. Restore occupational and psychosocial functioning to baseline
  3. Reduce the risk of relapse and recurrence
  4. Reduce the risk of harmful consequences (suicidal ideation)
92
Q

How do we decide which depression pharmacotherapy to choose?

A

Efficacy is generally comparable between classes

-Patient preference
-Prior medication response
-Safety, Tolerability, Side Effects
-Co-occurring psychiatric and medical conditions
-Pharmacologic properties
-Cost

93
Q

What are the 3 phases of depression treatment?

A

Acute
Continuation
Maintenance

94
Q

How long does the acute phase of depression treatment last and what is its goal?

A

6-12 weeks or until remission of symptoms

Goal: Induce Remission

95
Q

How long does the continuation phase of depression treatment last and what is its goal?

A

4-9 additional months (after acute phase)

Goal: Prevent Relapse

96
Q

What patients should have the continuation of their depression treatment?

A

Recommended for all patients

97
Q

How long does the maintenance phase of depression treatment last and what is its goal?

A

*Patient-specific duration

*Normally indefinite treatment if => 3 major depressive episodes

Goal: Prevent Recurrence

note: often 1 year, if recurrence 5 years, if 3rd recurrence then long term

98
Q

What antidepressants have a boxed warning for suicidality?

A

ALL ANTIDEPRESSANT MEDICATIONS

99
Q

What is the caveat to the boxed warning for suicidality associated with antidepressants?

A

Only refers to patients < or = 24 years of age

100
Q

At what age do antidepressants actually show a decreased risk of suicidality?

A

> or = 65 years old

101
Q

Which SSRI causes QTc prolongation?

A

Citalopram (Celexa)

102
Q

What is citalopram a substrate of?

A

2C19

3A4

103
Q

Which SSRI is the longest acting (longest half-life)?

A

Fluoxetine (Prozac)

Half-life (96-144 hours)
*Only SSRI not requiring a taper

104
Q

Which SSRI does not require the dose to be tapered off?

A

Fluoxetine (Prozac)

-because of its long half-life

105
Q

Which SSRI has an activating potential?

A

Fluoxetine (Prozac)

-has an active metabolite (norfluoxetine)

106
Q

Fluoxetine inhibits two things, what are they?

A

2D6 inhibitor

3A4 inhibitor

*these are inhibited by its active metabolite (norfluoxetine)

107
Q

What is the active metabolite of Fluoxetine (Prozac)?

A

Norfluoxetine

108
Q

Which SSRI is only indicated for OCD treatment?

A

Fluvoxamine (Luvox)

109
Q

Fluvoxamine is an inhibitor of two things, what are they?

A

1A2 inhibitor*

2C19 inhibitor

110
Q

Which SSRI has anticholinergic effects making it one of the hardest to stop with an excessive taper?

A

Paroxetine (Paxil)

*not used much

111
Q

Which SSRI is the only one with a teratogenic effect and what is the effect?

A

Paroxetine (Paxil)

-causes septal wall defect to the fetus

112
Q

What are the two main side effects associated with Paroxetine?

A

Weight Gain

Sedation

113
Q

What time of day should Paroxetine be taken?

A

Bedtime

-because of sedation side effect

114
Q

Paroxetine is an inhibitor of two things, what are they?

A

2D6 inhibitor

2B6 inhibitor

115
Q

Which SSRI causes more GI upset (nausea) than any others?

A

Sertraline (Zoloft)

116
Q

Which SSRI is the best for nonadherent patients?

A

Fluoxetine (Prozac)

-because of long half-life and lack of taper

117
Q

Which SSRI causes weight gain?

A

Paroxetine

118
Q

Which SSRI causes weight loss?

A

Fluoxetine

119
Q

What are the 3 side effects that every single SSRI can cause?

A

-Increased bleeding risk (platelet inhibition)
-Hyponatremia (elderly)
-Sexual dysfunction

120
Q

What are the two most commonly used SNRIs?

A

Duloxetine

Venlafaxine

121
Q

Which SNRI is the active metabolite of venlafaxine?

A

Desvenlafaxine

122
Q

What is the biggest side effect associated with Desvenlafaxine?

A

Nausea

*major limiting factor of this drug

123
Q

Which SNRI has no CYP interactions?

A

Desvenlafaxine

124
Q

Which SNRI has an FDA warning for hepatotoxicity?

A

Duloxetine (Cymbalta)

125
Q

What is Duloxetine an inhibitor of?

A

2D6
(good for pain too)

126
Q

When must the dosing of Levomilnacipran (Fetzima) be adjusted?

A

Renal impairment or with strong 3A4 inhibitors

*note: this drug is a 3A4 substrate

127
Q

What is an important dosing consideration with Venlafaxine?

A

Must be >150 mg/day to have norepinephrine effects

(Basically an SSRI before this)

128
Q

At higher doses, venlafaxine has what activity?

A

2D6 inhibitor

129
Q

What are the two most common side effects with SNRIs?

A

-BP elevation

-Nausea

130
Q

What other conditions are SNRIs useful in?

A

-Pain syndrome
-Musculoskeletal Pain
-Fibromyalgia
-Neuropathic Pain

131
Q

What is an important monitoring parameter with Duloxetine?

A

Need to obtain LFTs at baseline and when symptomatic or every 6 months

132
Q

What is the most important tricyclic antidepressant to remember?

A

Amitriptyline (Elavil)

133
Q

True or False: Tricyclic Antidepressants have a lot of side effects

A

True

134
Q

What are the side effects associated with TCAs?

A

CNS: sedation, reduces seizure threshold, confusion

Anticholinergic: Blurred vision, urinary retention, constipation

Cardiovascular: orthostatic hypotension, tachycardia

Other: weight gain, sexual dysfunction

135
Q

What is an important dosing consideration with TCAs?

A

Narrow therapeutic index drugs

Fatal in overdose as low as 1000mg (4-10 tablets) due to cardiac arrhythmias or seizures

136
Q

What are the important pearls for MAO inhibitors?

A

Need 2 week washout period before switching antidepressants (5 weeks if switching from fluoxetine)

All require a tyramine diet except the selegiline 6mg/24 hr patch

Caution due to hypertensive crisis and serotonin syndrome

137
Q

How long must we wait before switching from another antidepressant to an MAO inhibitor?

A

2 week washout period

(if switching from fluoxetine then a 5 week washout)

138
Q

What are the two most concerning side effects with MAO inhibitors?

A

Hypertensive crisis

Serotonin syndrome

139
Q

True or False: We cannot use combo therapy with MAO inhibitors

A

True

140
Q

What is the only MAOi that does not require the Tyramine diet?

A

Selegiline 6mg patch

Note: 9mg and 12 mg DO require the diet

141
Q

What is the MOA of bupropion (Wellbutrin)?

A

Dopamine and Norepinephrine reuptake inhibitor

142
Q

What are the side effects associated with bupropion (Wellbutrin)?

A

*Stimulating: Insomnia + Appetite Suppression

143
Q

What is an important dosing consideration with bupropion?

A

Only use the XL dosing!

-SR dosing has large fluctuations in peaks and troughs that increase the risk for seizures

144
Q

When is bupropion (Wellbutrin) contraindicated?

A

Active seizure disorder

Eating disorders

145
Q

What is bupropion an inhibitor of?

A

2D6

146
Q

True of False: Bupropion is a combination product

A

True, can be used in combination with SSRIs and SNRIs

147
Q

What is an important dosing consideration with Mirtazapine (Remeron)?

A

Sedation and increased appetite occur with doses < or = 15 mg/day

148
Q

What warnings are associated with Mirtazapine (Remeron)?

A

Agranulocytosis
Increased cholesterol

149
Q

True or False: Mirtazapine (Remeron) is a combination product

A

True -can be used with SSRI/SNRIs

150
Q

What is an important dosing consideration with Trazodone (Desyrel)?

A

Higher doses are needed for depression

151
Q

What are the side effects of trazodone?

A

-Orthostatic hypotension

-Priapism risk *emergency

152
Q

What is the MOA of Vilazodone (Viibryd)?

A

Primarily SSRI, may have some 5HT1a agonism which can provide anxiolytic effects

153
Q

True or False: Vilazodone (Viibryd) is a combination product

A

False!

-Do not use in combo with SSRI/SNRIs because it is an SSRI

154
Q

What are the clinical pearls associated with Vilazodone (Viibryd)?

A

Take with food
-significant nausea
bioavailability increases with food

155
Q

What is Vilazodone (Viibryd) a substrate of?

A

3A4

156
Q

What is the MOA of Vortioxetine (Trintellix)?

A

SSRI + 5HT1A agonist + 5HT3 antagonist

157
Q

True or False: Vortioxetine is a combination product

A

False!

-Do not use in combo with SSRIs or SNRIs because it is one

158
Q

What side effect is caused less by Vortioxetine?

A

Less sexual dysfunction

159
Q

What is Vortioxetine (Trintellix) a substrate of?

A

2D6

160
Q

True or False: Serotonin Syndrome is a medical emergency

A

TRUE

161
Q

How do we treat serotonin syndrome?

A

Stop offending agent

Can potentially use serotonin blocking agents (Cyproheptadine)

162
Q

Which antidepressant is antidepressant withdrawal syndrome not common in?

A

Fluoxetine

163
Q

True or False: Antidepressants with anticholinergic activity should be tapered no matter what

A

True

164
Q

True or False: Antidepressant withdrawal syndrome is not life-threatening

A

TRUE

-not life-threatening but extremely uncomfortable

165
Q

What are the FDA-approved augementation agents?

A

Aripiprazole
Brexpiprazole
Cariprazine
Quetiapine

166
Q

What are the drugs that can be used for post-partum depression?

A

Brexanolone
Zuranolone

167
Q

What is one of the most effective treatments for treatment-resistant depression?

A

Electroconvulsive Therapy (ECT)

Spring 2024 Therapeutics 3 (24 decks)

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