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PHAR 253 > Depression > Flashcards

Depression Flashcards

1
Q

define a mental health disorder

A

*psychiatric diagnosis, mental illness
- results in significant changes in a persons thinking, emotional state and behaviour, and ability to function in social and occupational settings

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2
Q

define mental health problem

A

*poor mental health, minimal mental well-being
- broad term that includes mental health disorders and less severe mentak health symptoms that do not meet diagnostic criteria but may disrupt personal, social, and occupational functioning

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3
Q

history of psychiatry

A

divine punishment & demonic processes
bodily fluid imbalance
natural physical causes
psychological and social stress
*now = biological causes +/- psychological and social stressors

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4
Q

how can culture influence mental illness?

A

racial and ethnic minorities are less likely to seek mental health treatment than caucasians
influence treatment decisions and coping
it impacts the way people describe their symptoms

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5
Q

what is the purpose of the mental health services act?

A

assist people from serious mental illness in receiving treatment

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6
Q

what are the three mental health practitioners?

A

psychiatrist
psychologist
therapist

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7
Q

what is done for a clinical assessment in psychiatry?

A

physical exam & clinical interview
- use diagnostic statistical manual of mental disorders (DSM-5)

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8
Q

pros of the DSM-5

A

provides criteria for standardizing diagnoses
designs to produce reliable diagnosis
helps guide research in mental health

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9
Q

cons of DSM-5

A

defines illness to close to “normal” leading to overdiagnoses
largely based on expert opinion
risk of misdiagnoses
stigmatization

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10
Q

what is looked at during mental status exam (MSE)?

A

general observations
thinking
emotion
cognition

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11
Q

what is the difference between mood and affect?

A

mood is subjective - it is the inner feeling of emotion
affect is objective - its the external expression of emotional responsiveness

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12
Q

what is the purpose of a physical exam?

A

rule out medical and/or medication-induced causes

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13
Q

what is measurement-based care?

A

refers to the systematic use of measurement tools, such as validated scales, to monitor outcomes and support clinical decision-making (such as diagnosis and treatment)

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14
Q

what are some measurement-based scales for depression?

A

HAM-D
PHQ-9
BDI

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15
Q

what are some measurement-based scales for anxiety?

A

HAM-A
GAD-7

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16
Q

how can we remember what is measured in the PHQ-9 for depression?

A

SIG E CAPS
Sleep decreased
Interest decreased in activities
Guilt or worthlessness
Energy decreased
Concentration difficulties
Appetite disturbance or weight loss
Psychomotor retardation / agitation
Suicidal thoughts

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17
Q

what are the limitations of current psychotropic nomenclature?

A

outdated
does not support clinical decision-making
inconsistent with other areas of medicine
may confuse patients & exacerbate non-adherance
negatively contributes to stigma

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18
Q

what are the goals of the neuroscience-based nomenclature(NbN)?

A
  • based on contemporary scientific knowledge
  • help clinicians make informed choices when working out the next ‘pharmacological step’
  • system of naming that does not conflict with the actual use of the medications
  • be future-proof to accommodate new compounds
  • help patients understand and accept a prescribed treatment for a condition
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19
Q

what are the 4 distinct components of stigma?

A

labeling someone with a condition
stereotyping people who have that condition
creating a division
discriminating against someone on the basis of their label(s)

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20
Q

what should you say instead of mental illness?

A

mental illnesses or a mental illness

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21
Q

what is the mental health first aid’s 5-step action plan?

A

A - assess for risk of suicide or harm
L - listen nonjudgmentally
G - give reassurance and information
E - encourage appropriate professional help
E - encourage self-help and other support strategies

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22
Q

what is the definition of major depressive disorder?

A

persistently and abnormally low mood, characterized by feelings of sadness, emptiness or irritability, and accompanied by other somatic or cognitive changes that significantly affect the individual’s capacity to function

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23
Q

T or F: depression is the leading cause of disability worldwide

A

False, its the 2nd leading cause

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24
Q

etiology of depression

A

complex, multifactoral (developmental, biologic, environmental)
can be genetic

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25
Q

what are the proposed pathophysiology theories for the cause of depression?

A

monoamine hypothesis
neuroplasticity hypothesis
endocrine and immune system abnormalities
structural and functional alterations

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26
Q

what is the monoamine hypothesis?

A

5HT, NE, DA
dysfunction in monoamine production (low 5HT - serotonin)
dysregulation in monoamine activity (decreased 5HT activity in presynaptic areas = upregulated autoreceptors = less 5HT in synapse)

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27
Q

what is the neuroplasticity hypothesis?

A

downstream effects -> altered cell growth and adaptation
low levels of brain-derived neurotrophic factor (BDNF) ??

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28
Q

what is the endocrine and immune system abnormalities theory?

A

increased plasma cortisol, increased peripheral cytokine concentrations
chronic stress model - involves hypothalamic-pituitary-axis(stress long term)

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29
Q

what is the structural and functional alterations theory?

A

alterations identified in brain regions involving emotional processing
- reduced volume or hyperactivity in prefrontal cortex, cingulate cortex, hippocampus, amygdala

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30
Q

risk factors for MDD

A

genetics - blood relatives
life experiences - traumatic or stressful events
personality disorders
substance use
medical comorbidities

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31
Q

what is DSM-5?

A

psychiatry diagnostic criteria
- diagnostic and statistical manual of mental disorders

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32
Q

what are the diagnostic criteria for MDD?

A
  • at least 5 symptoms
  • at least 1 symptom must be depressed mood or anhedonia (lack of interest)
  • present nearly every day for at least a 2 week period
    – symptoms cause significant distress
    – episode is not attributable to direct physiological effects of a substance of another medication
    – MDD is not better explained by a different mental illness
    – there has never been a manic or hypomanic episode
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33
Q

what is considered mild MDD?

A

5 or 6 symptoms, minimal functional impairment

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34
Q

what is considered severe MDD?

A

nearly all symptoms, significant functional impairment or motor impairment

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35
Q

what are the symptoms of depression?

A

*depressed mood
*anhedonia
- feelings of worthlessness or guilt
- suicidal ideation, plan, or attempt
- fatigue or loss of energy
- sleep changes
- weight or appetite changes
- decreased ability to think or concentrate, or indecisiveness
- psychomotor retardation or agitation
(this is SIG E CAPS)

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36
Q

what are the descriptive factors for MDD?

A

MDD with…
- anxious distress
- mixed features
- catatonic features
- melancholic features
- atypical features
- peripartum onset
- seasonal pattern
- psychotic symptoms

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37
Q

what medications may be associated with MDD?

A

CV agents - reserpine
anticonvulsants - phenobarbital
hormonal agents - GnRH agonists
immunologic - interferon alpha

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38
Q

based on the PHQ-9 scale what number corresponds with the severity of depression?

A

<5 = no symptoms
5-9 = minimal
10-14 = moderate
15-19 = moderately severe
20-27 = severe

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39
Q

what are the risk factors for suicide?

A

I - ideation
S - substance use

P - purposelessness
A - anxiety
T - trapped
H - hopelessness

W - withdrawal
A - anger
R - recklessnes
M - mood changes

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40
Q

what is the prognosis for MDD?

A

40% recover in 3 months
60% within 6 months
80% within 12 months
15% never achieve remission

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41
Q

response to antidepressants

A

40-60% response rate
- response rate decreases with each subsequent treatment trial

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42
Q

what are the predictors of remission?

A

female sex
white race
employment
higher level of education
higher income

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43
Q

what is the overall goal of therapy for acute treatment of MDD?

A

symptom remission and restoration of premorbid functioning within 8-12 weeks

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44
Q

what is the overall goal for maintenance treatment of MDD?

A

prevent recurrence of mood episode

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45
Q

general goals of therapy for MDD?

A

minimize adverse drug effects
maximize adherence
provide education to patients and family
identify and manage risk factors for comorbid conditions

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46
Q

non-pharmacological treatment for MDD?

A

positive lifestyle changes
natural products
psychological treatment - counseling
neurostimulation

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47
Q

what are the pharmacological treatments?

A

antidepressants
adjunct drugs

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48
Q

what are the natural products for treatment?

A

st. johns wort
s-adenosyl methionine
omega-3 fatty acids
folate L-methylfolate

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49
Q

when is psychological treatment indicated?

A

for moderate to severe depression or if the patient prefers

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50
Q

what are the psychological treatments?

A

cognitive behaviuoral therapy (CBT)
behavioural activation (BA)
interpersonal psychotherapy (IPT)
mindfulness-based cognitive therapy (MBCT)

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51
Q

what are the neurostimulation treatments?

A

transcranial magnetic stimulation (TMS)
electroconvulsive therapy (ECT)

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52
Q

what is TMS?

A

used for refractory depression
magnetic fields are used to stimulate nerve cells in regions of the brain involved in mood regulation and depression

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53
Q

how long is TMS course?

A

4-6 weeks

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54
Q

adverse effects of TMS

A

headache
scalp discomfort

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55
Q

what is ECT?

A

used for severe depression, depression with psychosis or catatonic features
electrodes placed on various scalp regions
electrical charge is applied to stimulate the brain and produce a seizure while patient under general anesthetic
seizure lasts 1 minute

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56
Q

efficacy of ECT

A

80-90% effective for MDD

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57
Q

how many ECT treatments required?

A

usually 6-12

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58
Q

adverse effects of ECT

A

confusion during post-ictal period
impaired memory after procedure
headache
muscle ache

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59
Q

what were the conclusions from the cipriani trial?

A

no strong evidence to conclude that any antidepressant is superior in efficacy
new medications not better than old ones
individualize therapy

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60
Q

which antidepressants might have the best balance of efficacy and tolerability from meta-analyses?

A

sertraline
escitalopram
vortioxetine
venlafaxine
mirtazapine

61
Q

what did the STAR*D trial find?

A

no difference in remission rates or times to remission

62
Q

what are the CANMAT first-line options?

A

SSRI
SNRI
bupropion
mirtazapine

63
Q

what is our role in MDD

A

provide patient centred care
- education
- empathy
ensure optimal efficacy and safety of medication use

64
Q

what are the 1st line SSRIs

A

sertraline
escitalopram
citalopram
fluoxetine
paroxetine

65
Q

what are the 1st line SNRIs

A

duloxetine
venlafaxine

66
Q

what is the MOA of SSRIs

A

inhibition of presynaptic 5-HT reuptake by inhibition of the 5-HT transporter CNS neurons
- increased 5HT in synaptic cleft

67
Q

what is the onset of action of SSRIs?

A

1st few days: decreased agitation and anxiety, improved sleep and appetite
1-3 weeks: increased activity and sex drive, improved self-care, concentration, memory, thinking and movements
2-4 weeks: relief of depressed mood
*monitor for signs of suicide within first 3 weeks

68
Q

adverse effects of SSRIs

A

HANDS
headache
anxiety
nausea
diarrheas & other GI upset
sleep disturbances
- also anticholinergic
- sexual dysfunction
- emotional blunting/detachment

69
Q

what can cause SIADH?

A

SSRIs
SNRIs
NSAIDs
mirtazapine
opioids
carbamazepine
pain
vomitting
inflammation

70
Q

warnings for SSRI

A

increased risk of suicide
increased fracture risk
citalopram and escitalopram have a does-dependent risk of QTc prolongation

71
Q

which SSRI is most sedating?

A

paroxetine
sert, and cita have mild sedation

72
Q

which SSRI has a higher probability of weight gain and sweating?

A

paroxetine

73
Q

which SSRI is the most stimulating?

A

fluoxetine

74
Q

which SSRIs have higher rates of nausea/diarrhea?

A

fluvoxamine and sertraline

75
Q

which SSRIs have best tolerability?

A

escitalopram
sertraline

76
Q

what are the potent drug CYP450 drug interactions for SSRIs?

A

fluvoxamine - IA2 (clozapine, warfarin, methylxanthines)
fluoxetine and paroxetine - 2D6 (metoprolol, desipramine)

77
Q

other drug interactions of SSRIs

A

NSAIDs, antiplatelets, anticoagulants
serotonergic agents

78
Q

which SSRI has increased bioavailability with food?

A

sertraline

79
Q

where are SSRIs metabolized?

A

liver - hepatically and only fluoxetine, citalopram and sertraline form active metabolites

80
Q

what is the MOA of vortioxetine?

A

serotonin reuptake inhibitor
serotonin receptor agonist
serotonin receptor partial agonist
serotonin receptor antagonist

81
Q

adverse effects of vortioxetine

A

HA
nausea
vomiting
diarrhea
sexual dysfunction

82
Q

what is the MOA of SNRIs

A

inhibit presynaptic 5-HT and NE reuptake by inhibiting 5-HT and NE transporters in CNS neurons

83
Q

at what doses will venlafaxine act like what?

A

binds 5-HT @ doses < 150mg/day (SSRI)
binds to NE and 5-HT @ doses >150mg/day (SNRI)
weekly inhibits dopamine @ doses >450mg/day

84
Q

which SNRIs have higher overall NET inhibition and therefore higher incidence of dry mouth and constipation?

A

duloxetine and desvenlafaxine

85
Q

which SNRI is hardest to taper off of with the most withdrawl?

A

venlafaxine

86
Q

what is the onset of action for SNRIs?

A

similar to SSRIs but possibly more agitation in 1s few days

87
Q

adverse effects of SNRIs

A

HANDS
- anticholinergic-like effects
- sexual dysfunction
- SIADH (especially venlafaxine)
- risk serotonin syndrome
- increase BP/HR and sweating

88
Q

what side effect with SNRI might be less than SSRIs?

A

less emotional blunting than with SSRIs

89
Q

PK relevance with SNRIs

A

dose adjustment for renal impairment
venlafaxine and duloxetine are hepatically metabolized

90
Q

drug interactions of SNRIs

A

duloxetine - moderate inhibitor & substrate of CYP2D6
venlafaxine - weak inhibitor & substrate of CYP2D6
NSAIDs, antiplatelets, anticoagulants (caution only)
serotonergic agents

91
Q

warnings with SNRIs

A

avoid abrupt withdrawal
duloxetine contraindicated in narrow angle glaucoma

92
Q

what is the MOA of bupropion?

A

inhibits NE and DA transporters increasing concentrations in the synpases
- NO 5-HT effects

93
Q

what is bupropion place in therapy?

A

useful for patients with psychomotor retardation, hypersomnia, ADHD type symptoms - its is stimulating/activating
can be used to augment SSRI or SNRI in treatment resistant cases
much less risk of sexual dysfunction

94
Q

adverse effects of bupropion

A

agitation, insomnia, tremor and ANXIETY
sweating
reduced appetite/weight loss
GI upset
psychosis
seizures
less sexual dysfunction than SSRI and SNRI

95
Q

how is bupropion metabolized?

A

in the liver by CYP2B6
eliminated primarily by the kidneys
- renal dosing adjustments may be needed

96
Q

drug interactions for bupropion

A

Zyban - same drug but for tobacco cessation
concurrent MAOI therapy
potent CYP2D6 inhibitor

97
Q

what is the dosing for bupropion?

A

usual daily dose: 100-300mg
SR formulation - OD or BID
XL formulation - OD

98
Q

contraindications of bupropion

A

seizure disorder
eating disorders
abrupt discontinuation of alcohol or sedatives

99
Q

warnings for bupropion

A

dependence on opioids, cocaine, stimulants
concurrent use of seizure lowering drugs
head trauma
HTN
unstable CVD/CAD
psychosis
anxiety
insomnia
overdose lethality

100
Q

which treatment for MDD should you not go with if the patient has a history of overdose?

A

bupropion

101
Q

what is the MOA of mirtazapine?

A

increased serotonin and NE

102
Q

what is mirtazapines place in therapy?

A

useful as monotherapy and adjunctive treatment with SSRI or SNRI
consider in patients with insomnia, anxiety, reduced appetite

103
Q

adverse affects of mirtazapine

A

sedation - feeling hungover the next morning
increased TGs & weight gain due to increased appetite
significantly less sexual dysfunction than SSRI/SNRI

104
Q

where is mirtazapine metabolized?

A

hepatically
75% renally excreted

105
Q

drug interactions with mirtazapine

A

serotonergic agents
other CNS depressants - benzodiazepines

106
Q

what is the dosing for mirtazapine?

A

initial: 15mg PO HS
may increase q1-2 weeks up to a max of 45mg PO HS

107
Q

at what dose of mirtazapine is the sedation effect typically lost?

A

30mg or higher

108
Q

what are the second line agents for MDD?

A

TCAs
SNRI - levomilnacipran
MAOI - moclobemide
trazodone
atypical antipsychotic - quetiapine
vilazodone

109
Q

what are the TCAs available in Canada?

A

tertiary amines
- amitriptyline
- clomipramine
- doxepin
- imipramine
secondary amines
- nortriptyline
- desipramine

110
Q

MOA of TCAs

A

inhibit presynaptic 5-HT and NE reuptake by inhibiting 5-HT and NE transporters in CNS neurons
tertiary = more 5-HT activity
secondary - more NE activity, better tolerated

111
Q

why are TCAs the “dirty” antidepressants?

A

have varying affinity for other receptors
- adrenergic
- histamine
- muscarinic
- sodium channels

112
Q

where are TCAs place in therapy?

A

MDD with:
- insomnia
- anxiety
- chronic, non-cancer pain
- migraines/headaches
- OCD (clomipramine)

113
Q

contraindications of TCAs

A

acute MI, heart block, CHF
severe liver impairment

114
Q

cautions with TCAs

A

any CVD
suicidal ideation
QT prolongation
seizure history/risk
elderly
bipolar disorder

115
Q

adverse effects of TCAs

A

sedation, anticholinergic effects, CV
- tachycardia
- QT prolongation
weight gain
tremors
sexual dysfunction

116
Q

what is the lethal overdose amount for TCAs?

A

only ~3x max therapeutic dose

117
Q

MOA of trazodone

A

weak inhibition of SERT and NET (doses >200mg)

118
Q

adverse effects of trazodone

A

dizziness, sedation, headache, akathisia, myalgia, tremor
prolonged QT interval
nausea, constipation, dry mouth
sexual dysfunction (but less than SSRI/SNRI)

119
Q

what kind of drug is quetiapine?

A

atypical antipsychotic

120
Q

does MAO-A or MOA-B have more impact on serotonin and NE?

A

MAO-A

121
Q

what is important to check before starting moclobemide (MAOI)?

A

*check for drug interactions
- stop serotonergic drugs 2 weeks before starting
-> Stop fluoxetine 5 weeks prior to starting
- if stopping, wait 2 weeks before starting another antidepressant
- stop at least 2 days prior to local or general anesthesia

122
Q

what are the thrid line options?

A

irreversible MOAI
- phenelzine
- tranylcypromine
noradrenaline reuptake inhibitor
- reboxetine

123
Q

where does ketamine work in the body?

A

NMDA receptors - inhibits sensory perception
opioid receptors (activation) - potential euphoric effects
AMPA receptors (activation) - rapid antidepressant effects

124
Q

MOA of ketamine

A

upregulates neurotrophic signaling -> increased protein synthesis and restoration of synaptic connectivity in the prefrontal cortex
*“reset” the brain by restoring brain pathways

125
Q

which type of ketamine is commercially available in Canada?

A

racemic ketamine - for anaesthesia

126
Q

which type of ketamine is approved for depression in Canada?

A

s-ketamine - nasal spray

127
Q

how fast does ketamine work?

A

within 1-2 days

128
Q

adverse effects of ketamine

A

most common:
- dissociation
- dizziness, feeling drunk
- sedation
- increased blood pressure
nausea

129
Q

Which medications are most likely to cause nausea and stomach upset?

A

Venlafaxine > SSRIs > bupropion > moclobemide > mirtazapine

130
Q

What drugs is constipation common with?

A

TCAs
And paroxetine is associated with highest rates out of SSRIs

131
Q

What should be done for those who develop suicidality during treatment?

A

Lower dose
Switch drug
Discontinue

132
Q

Which drugs have the greatest risk of sexual dysfunction?

A

SSRIs > TCAs > SNRIs
Bupropion has lowest risk

133
Q

Which drugs are lower risk for QT prolongation?

A

SSRIs (except cital and escital)
Bupropion
Moclobemide

134
Q

How can serotonin syndrome be described?

A

Mental status changes
Autonomic hyperactivity
Neuromuscular abnormalities

135
Q

Which drugs have worst discontinuation syndrome?

A

Venlafaxine and paroxetine

136
Q

What is the mnemonic for symptoms of discontinuation syndrome?

A

FINISH
Flu-like symptoms
Insomnia
Nausea
Imbalance
Sensory disturbances
Hyperarousal

137
Q

Which drug may you be able to stop without a taper and why?

A

Fluoxetine due to long half-life

138
Q

When might we augment/combine medication?

A

Partial response
Faster or synergistic response

139
Q

When might we switch drugs?

A

No response
Less pill/cost burden
Fewer adverse effects

140
Q

What can be added as combo therapy for TRD?

A

SSRI/SNRI + mirtazapine
SSRI/SNRI + bupropion
SSRI + TCA

141
Q

When is cross-tapering recommended?

A

Between drugs with different MOAs

142
Q

What are the first line options for augmentation?

A

2nd gen antipsychotics
- aripiprazole*
- quetiapine *
- risperidone *
- olanzapine

143
Q

What are the second line options for augmentation?

A

Bupropion
Mirtazapine
Lithium

144
Q

Which drugs are on BEERS list?

A

SSRIs, SNRIs, mirtazapine

145
Q

Which drugs are better choices for elderly?

A

Duloxetine
Bupropion
Sertraline

146
Q

Are any antidepressants approved for use in <18 years?

A

No

147
Q

Can pregnant women take antidepressants?

A

If they are already taking them, they should continue because the benefit often outweighs the risk of stopping

148
Q

What drugs are first-line in pregnancy?

A

SSRIs

PHAR 253 (8 decks)

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