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Neurology > Major Depressive Disorder (MDD) > Flashcards

Major Depressive Disorder (MDD) Flashcards

1
Q

What are the types of depressive disorder?

A
  • Major Depressive Disorder
  • Persistent Depressive Disorder
  • Substance/Medication-Induced Depressive Disorder
  • Premenstrual Dysphoric Disorder
  • Depressive Disorder due to another medical condition
  • Other specified depressive disorder
  • Unspecified depressive disorder
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2
Q

What are the DSM-5 Criteria for Major Depressive Disorder?

A

Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning

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3
Q

What are the symptoms of Major Depressive Disorder?

A
  • Depressed mood
  • Sleep
  • Interest
  • Guilt
  • Decreased energy
  • Decreased concentration
  • Appetite (weight loss or weight gain)
  • Psychomotor changes
  • Suicidal thoughts
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4
Q

What are medications that can induce major depressive disorder?

A
  • Acyclovir
  • Alcohol
  • Antiepileptic medication
  • Antiretrovirals
  • Barbiturates
  • BB/CCB
  • Corticosteroids
  • Interferon-a & b
  • Isotretinoin
  • Levonorgestrel implants
  • Montelukast
  • Opioids
  • Varenicline
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5
Q

What is the onset of MDD?

A
  • Late 20’s but first episode can develop at any age
  • Can develop over days to weeks or suddenly
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6
Q

What is the duration of MDD?

A
  • Median time to recovery is 20 weeks with adequate treatment
  • 15% of patients never achieve remission (chronic depression)
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7
Q

What is the recurrence of MDD?

A
  • 50% with a single episode will recover without recurrence
  • Risk of recurrence increases with number of episodes
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8
Q

Remission

A

Absence of depressive symptoms or only 1 or 2 symptoms to a mild degree of > 2 months

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9
Q

Monoamine Hypothesis

A

Depressive symptoms related to deficiencies in serotonin (5-HT), Norepinephrine (NE), and Dopamine (DA)

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10
Q

Dysregulation Hyopthesis

A

Depression results from dysregulation of neurotransmitters that leads to alteration in pre & post receptors

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11
Q

Neuroendocrine Hypothesis

A

Dysregulation of thyroid and HPA axis results in sustained in sustained depression

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12
Q

What is the mechanism of action SSRIs?

A

Inhibit the reuptake of serotonin (5HT) in the presynaptic neuron of the CNS–> increased serotonin in the synaptic cleft

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13
Q

SSRI

A
  • First line treatment for MDD
  • Well tolerated
  • Low risk of toxicity
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14
Q

What is the CYP450 metabolism of fluoxetine?

A

2D6

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15
Q

What is the CYP450 Metabolism of fluvoxamine?

A
  • 1A2
  • 2C19
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16
Q

What is the CYP450 metabolism of paroxetine?

A

2D6

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17
Q

What is the longest half-life SSRI?

A

Fluoxetine (norfluoxetine: ~4-6 days)

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18
Q

What are the adverse effects of SSRIs?

A

Common:
* Nausea and/or vomiting
* Headache
* Sleep changes
* Increased in anxiety/agitation or sedation

Serious:
* Hyponatremia
* Increased bleeding/bruising
* Serotonin syndrome

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19
Q

List the SSRIs from most actvivating to most sedation

A
  • Fluoxetine
  • Setraline
  • Escitalopram & citalopram
  • Fluvoxamine
  • Paroxetine
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20
Q

What are some clinical pearls of citalopram?

A
  • Max daily dose not to exceed 40 mg (QTc prolongation)
  • Lower max dose of 20 mg is recommended for elderly (> 60 years), significant hepatic impairment, interacting medications
  • Sedating
  • Starting dose can also be maintenance dose
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21
Q

What is the clinical pearl of escitalopram?

A
  • Also has a risk of QTc prolongation, but no boxed warning
  • Starting dose can also be maintenance dose
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22
Q

What are the clinical pearls of fluoxetine?

A

Longest half life (1-3 days) with longer half life for metabolite (4-16 days)

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23
Q

What are the clinical pearls of setraline?

A

Non-selective–> can affect serotonin in gut and cause more diarrhea and nausea

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24
Q

What are the clinical pearls of fluvoxamine?

A
  • OCD, NO FDA approval in depression
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25
Q

What are the clinical pearls of Paroxetine?

A
  • “Dirtiest SSRI” (anticholinergic & histaminic, more sexual dysfunction)
  • Most weight gain
  • Short half-life–> withdrawal
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26
Q

What are the clinical pearls of vortioxetine?

A

Brand only

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27
Q

What is the mechanism of action of Serotonin & Norepinephrine Reuptake Inhibitors (SNRIs)?

A

Inhibits the reuptake of serotonin and norepinephrine presynaptically

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28
Q

SNRIs

A
  • Well tolerated
  • Low risk of toxicity
  • Additional mechanism (norepinephrine)
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29
Q

What is the CYP metabolism Duloxetine (Cymbalta)?

A

CYP1A2
-Inactive: CYP2D6

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30
Q

What is the CYP450 metabolism of Levomilnacipran (Fetzima)?

A

CYP3A4

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31
Q

What are the common side effects of SNRIs?

A
  • Nausea and/or vomiting
  • Sleep changes
  • Increased agitation/anxiety
  • Sexual dysfunction
  • Dose-dependent blood pressure elevation
  • Constipation
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32
Q

What are the serious adverse effect of SNRIs?

A
  • Hyponatremia
  • Increased bleed/bruising
  • Serotonin Syndrome
33
Q

What are the clinical pearls of Venlafaxine?

A
  • Doses > 225 mg/day needed for NE activity, but this dose is also very nauseating
  • Also inhibits dopamine reuptake at higher doses (>300 mg)
  • Withdrawal risk high due to half-life, do not use IR formulation
34
Q

What are the clinical pearls of Desvenlafaxine?

A
  • Active metabolite of venlafaxine
  • Renal dose adjustment needed for CrCl < 50 mL/min
  • $$$
35
Q

What are the clinical pearls of Duloxetine?

A
  • Contraindicated in hepatic disease
  • FDA approved for diabetic peripheral neuropathy, musculoskeletal pain, fibromyalgia
36
Q

What are the clinical pearl of Levomilnacipran?

A
  • Brand only, $$$
  • Renal adjustment needed for CrCl < 60 mL/min
37
Q

What are the mechanism of action of Serotonin 2 Antagonist/Reuptake Inhibitors (SARIs)?

A
  • 5-HT2A and 5-HT2C receptor antagonist (post-synaptic)
  • Inhibits serotonin reuptake
38
Q

What are the adverse effects of SARIs?

A
  • Sedation
  • Dizziness
  • Orthostatic hypotension
  • Priapism (rare)
39
Q

What are the clinical pearls of trazodone?

A
  • More commonly used for insomnia than MDD
  • Doses > 200 mg/day required for treatment of MDD
  • Doses for insomnia are subtherapeutic for the treatment of MDD
40
Q

What are the clinical pearls of Nefazodone?

A
  • Boxed warning: may cause liver failure
  • Not first line due to toxicity
  • Can be used in PTSD
41
Q

What are the mechanism of action of Norepinephrine & Dopamine Reuptake Inhibitor (NDRI)?

A

Inhibits the reuptake of norepineprhine and dopamine

42
Q

NDRIs

A
  • First or second line treatment of MDD
43
Q

What are the adverse effects of NDRIs?

A
  • Activation (insomnia, agitation, tremor)
  • Weight loss
  • Headache
  • Nausea/vomiting/constipation
44
Q

What are the clinical pearls of NDRIs?

A
  • Beneficial: Fatigue, poor concentration, smoking cessation interest
  • Contraindicated: Bulimia, anorexia, seizure disorder
  • Appetite suppression
  • Lowers the seizure threshold
  • Activating
45
Q

What is the mechanism of action of the Noradrenergic & Specific Serotonergic Antidepressant (NaSSa)

A
  • Primary–> alpha 2 agonist
  • Secondary–> 5-HT2A, 5-HT2C, and 5-HT-3 antagonist, antihistamine
46
Q

NaSSa

A
  • Considered as a second line agent
47
Q

What are the clinical pearls of NaSSa?

A
  • Less sexual dysfunction
  • Weight gain/sedation are worse at lower dose (7.5-15 mg)
48
Q

What are the mechanism of action of Serotonin modulator?

A
  • Serotonin reuptake inhibitor, 5-HT1A partial agonist
  • Similar to SSRI and buspirone
49
Q

What are the clinical pearls of serotonin modulator?

A
  • Dose adjust with CYP3A4 inhibitor
  • Must take with food to increase bioavailability
  • Lowest incidence of sexual dysfunction
50
Q

What is the mechanism of action of tricylic antidepressant?

A
  • Presynaptic inhibition of norepinephrine and serotonin reuptake–> increase NE and 5-HT in the synaptic cleft
  • Varying affinities for H1, alpha adrenergic, and muscarinic antagonist
51
Q

What are the common adverse effects of tricyclic antidepressants?

A
  • Anticholinergic
  • Antihistaminergic
  • Orthostasis
  • Photosensitivity
52
Q

What are the serious adverse events of tricyclic antidepressants?

A
  • Cardiotoxicity (QTc prolongation and risk of MI)
  • Decreased seizure threshold
53
Q

What are the clinical pearls of amitriptyline?

A
  • Most cholinergic and alphalytic
  • More often used for chronic pain and migraine
54
Q

What are the clinical pearls of clompramine?

A
  • Most serotonergic
  • FDA approved for OCD
55
Q

What are the clinical pearls of desipramine?

A
  • Most noradrenergic
  • Low anticholinergic properties
56
Q

What are the clinical pearls of doxepin?

A

Most antihistamine

57
Q

What are the clinical pearls of imipramine?

A
  • Used for GAD
  • Best for panic disorder with agoraphobia
58
Q

What are the clinical pearls of nortriptyline?

A
  • Low anticholinergic properties
  • Best tolerated TCA
59
Q

What is the mechanism of action of Monoamine Oxidase Inhibitor (MAO-Is)?

A

Inhibition of monoamine oxidase enzymes (MAO-A & MAO-B) resulting in increased concentrations of norepinephrine, serotonin & dopamine in synapse

60
Q

What are the adverse effects of MAOIs?

A

Common:
* Hypotension
* Dizziness
* Urinary retention, constipation, and xerostomia

Serious:
* Hypertensive crisis–> drug-food interactions
* Serotonin syndrome–> drug-drug interaction

61
Q

Hypertensive Crisis

A

Diastolic blood pressure > 120 mm Hg

62
Q

What are some presentations of Hypertensive crisis?

A
  • Occipital headache
  • Palpitations
  • Neck stiffnes/soreness
  • Nausea and/or vomiting
  • Dilated pupils, photophobia
  • Tachycardia or bradycardia
  • Chest pain
63
Q

What is the dietary modifications of hypertensive crisis?

A

Avoid tyramine

64
Q

How do you treat hypertensive crisis?

A

Phentolamine (also nifedipine and chlorpromazine)

65
Q

Which antidepressants should you avoid if you have hypertensive crisis?

A
  • TCAs
  • NRIs
  • SNRIs
  • NDRIs
66
Q

What are some clinical pearls of Phenelzine?

A
  • Increased weight gain
  • May cause hepatoxicity (rare)
67
Q

What are some clinical pearls of selegiline?

A
  • Low doses selective for MAO-B (increases dopamine)
  • No need for dietary restriction with 6 mg/24hr patch
  • Drug-drug interactions are still a concern
68
Q

What are some clinical pearls of Tranylcypromine?

A
  • Structurally similar to amphetamine–> stimulating
  • Can cause insomnia
  • Transient hypertension
69
Q

What is the Hunter’s Criteria of Serotonin Syndrome?

A
  • Spontaneous clonus
  • Inducible clonus + agitation or diaphoresis
  • Ocular clonus + agitation or diaphoresis
  • Tremor + hyperreflexia
  • Hypertonia + temperature > 35 C + ocular clonus or inducible clonus
70
Q

What are some drug interactions of antidepressants for Serotonin Syndrome?

A
  • SSRIs
  • TCAs
  • SNRIs
  • Mirtazapine
  • MAO-Is
71
Q

What is the drug interaction of Antibiotics for Serotonin Syndrome?

A

Linezolid

72
Q

What are some drug interactions of appetite suppressants for Serotonin Syndrome?

A

Sibutramine

73
Q

What are some drug interactions of opioids for Serotonin Syndrome?

A
  • Dextromethorphan
  • Meperidine
  • Methadone
  • Tramadol
  • Fentanyl
74
Q

What are the washout periods to prevent Serotonin Syndrome with MAOIs?

A

MAO-I–> non-MAO-I antidepressant
* Allow for 2-week washout period
Non-MAO-I antidepressant–> MAO-I
* Allow for 2-week washout period
* Allow for 5-week washout period after fluoxetine
MAO-I–> MAO-I
* Allow for 2-week washout period

75
Q

What is the boxed warning on ALL antidepressants?

A
  • Seen in children/adolescents up to 24 years old
  • Notify family/caregiver to monitor
  • Balance benefits vs risk
76
Q

What is the symptoms of Discontinuation Syndrome?

A
  • Flu-like, paresthesia
  • Most severe: venlfaxine > SSRIs
77
Q

What is the onset and duration of Discontinuation Syndrome?

A
  • Onset: 1-2 days after discontinuation
  • Duration: 1-2 weeks depending on medication half-life
78
Q

What medication do you avoid in pregnant patients?

A

Paroxetine

79
Q

What is the empiric therapy selection based on?

A
  • History of antidepressant response
  • Family history of antidepressant response
  • Concurrent with diseaes states and drug therapy
  • Drug interactions
  • Adverse effect profile
  • Cost

Neurology (21 decks)

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