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660 exam 2 Flashcards

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1
Q

Medications with the strongest evidence of efficacy in bipolar depression with mania:

A

Quetiapine, olanzapine-fluoxetine, lurasidone

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2
Q

Gina is a 24-year-old patient with no psychiatric history. She gave birth to her first child 2 weeks ago and now presents with symptoms of depression. She scores a 20 on the Edinburgh Postnatal Depression Scale (EPDS; possible depression). Which of the following courses of action should be the next step?

A

Administer a (hypo)mania screening tool such as the Mood Disorders Questionnaire (MDQ)

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3
Q

MADRS Scoring

A

0-6 Normal
7-19 Mild depression
20-34 Moderate Depression
>/= 35 severe depression

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4
Q

Bipolar presentation

A

– + family Hx
– Early onset of first depressive episode (<25)
– Post partum depression x
– Rapid onset of depressive episodes
– Antidepressant induced hypomania
- -Psychotic features
– Impulsivity
– Aggression
– Hostility
– Comorbid substance use disorder

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5
Q

Which drugs would theoretically reduce glutamate release by blocking voltage-sensitive sodium channels?

A

Valproate and lamotrigine

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6
Q

Lithium MOA

A

DOWNSTREAM
Inhibition of glycogen synthase kinase 3ß (GSK-3ß) and inositol monophosphatase (IMPase)

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7
Q

Jimmy is a 20-year-old man recently diagnosed with major depressive disorder (MDD) with mixed features. Approximately what percentage of patients with MDD exhibit subthreshold symptoms of (hypo)mania during a major depressive episode?

A

26%

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8
Q

A 24-year-old man with bipolar disorder is being initiated on lithium, with monitoring of his levels until a therapeutic serum concentration is achieved. Once the patient is stabilized, how often should his serum lithium levels be monitored (excluding one-off situations such as dose or illness change)?

A

Every 6-12 months.

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9
Q

Blockade of which two receptors was most likely responsible for this weight gain induced by quetiapine?

A

Serotonin 2C and H1

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10
Q

According to data from the Stanley Foundation Bipolar Network, how many patients with bipolar disorder exhibit subsyndromal hypomanic symptoms during a major depressive episode in at least one single visit?

A

65%

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11
Q

Fluoxetine/Prozac MOA

A

5HT2C antagonism (only SSRI that does)

  • enhances release of NE and DA
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12
Q

Halflife of Fluoxetine/prozac

A

Very long - 5 weeks

good for non compliant patients

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13
Q

Sertraline MOA

A

Sigma 1 receptor and DA transporter binding:

– Sigma 1 may help with anxiety and delusional/psychotic depression

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14
Q

Sertraline dosing above 150mg causes what?

A

Moderate CYP2D6

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15
Q

Which antidepressant for pregnancy

A

Sertraline

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16
Q

Paroxetine/Paxil MOA

A

Weak NET inhibition

Inhibits nitric oxide: Weight gain, sexual SE

Anticholinergic (M1):
calming, sedation

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17
Q

Which SSRI is notorious for withdrawal reactions?

A

Paroxetine/Paxil

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18
Q

Which SSRI is a potent CYP2D6 inhibitor

A

Paroxetine/Paxil

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19
Q

Fluvoxamine MOA

A

Sigma 1 receptor - more potent than sertraline

  • good for anxiety and psychotic/delusion depression
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20
Q

Fluvoxamine Indications

A

OCD, social anxiety

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21
Q

Fluvoxamine CYP activity

A

1A2 & 3A4

decreases metabolism of caffeine

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22
Q

Citalopram/Celexa MOA

A

2 enantiomer: two molecules that are mirror images of each other (R&S)

Mild histamine (H1) - a little sedating

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23
Q

Citalopram BB Warning

A

higher doses (40mg) associated with QTc prolongation

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24
Q

Escitalopram MOA

A

S enantiomer of citalopram

PURELY ON SERT

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25
Q

Which SSRI is usually best tolerated

A

Escitalopram

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26
Q

Medication Names - serotonin partial agonist/reuptake inhibitor (SPARI)

A

Vilazodone (Vibrid)

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27
Q

Vilazodone MOA

A

Blocks SERT

5HT1A partial agonism is unique to vilazodone
– 5HT1A action can be achieved by adding buspirone or aripiprazole to SSRI/SNRI

Theoretically helps speed up the process because it helps down regulate the 5HT1A receptors faster

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28
Q

Vilazodone SE compared to SSRI

A

Lower incidence of wt gain

Lower incidence of sexual SE

Tends to have more GI SE due to rapid elevation of 5HT

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29
Q

Medication names: SNRIs

A

Venlafaxine
Desvenlafaxine
Duloxetine
Levomilnacipran

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30
Q

SNRI MOA

A

Block SERT

Blocks NET

Increases DA in PFC without blocking DAT

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31
Q

SSRI MOA

A

blocks SERT

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32
Q

Venlafaxine SERT vs NET dosing

A

low dosing - SERT (<200mg)
high dosing - NET (>200)

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33
Q

which SNRI is notorious for withdrawal reactions?

A

Venlafaxine

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34
Q

Desvenlafaxine MOA

A

More NET vs SERT

active metabolite of venlafaxine

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35
Q

Duloxetine MOA

A

Slightly more SERT vs NET

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36
Q

Levomilnacipran MOA

A

S enantiomer of milnacipran

NET>SERT

May be better for cognitive symptoms, fatigue, anergia, anhedonia

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37
Q

Levomilnacipran SE

A

sweating, urinary hesitancy, hypertension

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38
Q

Which SNRI should you avoid with liver issues?

A

Duloxetine

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39
Q

Trazodone
Serotonin antagonist and reuptake inhibitors (SARIs) - MOA

A

Block 5HT2A & 5HT2C

Behaves differently depending on dose

Higher doses (150-600) - antidepressant

Lower doses (25-150) - Sedative/Hypnotic
– 5HT2a antagonism, H1, alpha 1/2

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40
Q

Trazodone SE

A

PRIAPISM

too sedating to use as an antidepressant

NO wt gain or sexual SE

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41
Q

Nefazodone MOA

A

Blocks 5HT2A, HT2C, and SERT

also works on NET – differentiates from Trazadone

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42
Q

Nefazodone SE

A

Less sedating than Trazadone

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43
Q

1 concern with Nefazodone

A

Rare: Spontaneous liver failure

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44
Q

Medication names: Serotonin antagonist and reuptake inhibitors (SARIs) are

A

Trazadone
Nefazodone

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45
Q

Mirtazapine MOA

A

A2 antagonism
– increases NE release by blocking its ability to turn itself off

– enhances serotonin release by blocking norepinephrine’s ability to block serotonins release

Stimulates serotonin release via a2 receptor
– Essentially a2 antagonism cuts the breaks and steps on the gas

DOES NOT BLOCK ANY TRANSPORTER

5HT2C activity - increase NE and DA
H1 activity - sedating
5HT2C antagonism +H1 action = weight gain

5HT2C on suprachiasmatic nucleus in hypothalamus (brains pacemaker - helps manage sleep/wake cycle) - interact with melatonin receptors there. Can resync circadian rhythms

5HT3 localized in the chemoreceptor trigger zone (don’t see N/V/D)

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46
Q

Why might you give mirtazapine with an SSRI or an SNRI

A

When given with SNRI or SSRI it enhances the 5HT receptor response

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47
Q

Norepinephrine and dopamine reuptake inhibitors (NDRIs): Med name and MOA

A

Wellbutrin

Inhibits both NE and DA

Lacks SERT activity

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48
Q

BB Warning for Bupropion

A

BLACK BW: Increased seizure risk - especially with IR formulation)
– IR has higher risk
– increased risk with – pts going through drug withdrawal, bulimia/anorexia due to electrolyte imbalance

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49
Q

MAOI drug names

A

Nardil

Parnate

Marplan

(No Popular Meds)

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50
Q

MAOI MOA

A

Inhibit both MAO-A and MAO-B IRREVERSIBLY
→ increase in all three monamines (5HT, NE, DA)

(only antidepressant that directly increase neurotrasmission of all three)

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51
Q

MOAI SE

A

OH WISE:
- Orthostatic Hypotension
- Weight gain
- Insomnia
- Sexual Dysfunction
- Edema

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52
Q

MAOI drug interactions

A

Barbiturates
Tricyclic Antidepressants
Antihistamines
CNS Depressants
Antihypertensives
OTC Cold meds

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53
Q

MAOI - avoid what

A

No foods with tyramine: If it’s stinky or old.
- dried, aged, smoked, fermented, spoiled meat

  • Aged cheese
  • Tap & unpasteurized beer
  • Marmite
  • Sauerkrout, kimchee, soy
  • Banana peel
54
Q

TCA MOA

A

H1 blockade:
Sedation and wt gain

M1 blockade:
anticholiergic SEs -
dry mouth/blurred vision/urinary retention, constipation

Alpha1 blockade:
orthostatic hypotension and dizziness

Voltage-sensitive Na+ channel blockade:
coma, seizure, cardiac arrhythmias, cardiac arrest/death

TERTIARY AMINES:
block serotonin reuptake more potently than norepinephrine

SECONDARY AMINES:
block nerepinephrine more than serotonin reuptake

Some secondary amines metabolize into secondary amines so they have strong 5HT and NE

55
Q

TCAs SE

A

Tertiary:
more anticholinergic SE and are more sedating

Hypotension, tachy, cardiac arrhythmias, cardiac arrest, death

dizziness, lethargy, confusion, agitation

coma, seizures

sedtaion, wt gain

dry mouth, burred vision, urinary retention, constipation

WIDENING QRS - hallmark, diagnostic value for seizures and ventricular arrhythmias

56
Q

TCA initial monitoring

A

ECG if >50 yo

BMI, fasting glucose, A1C, Triglycerides, LDL

K+ and Mag+ if on diuretics

57
Q

Nortriptyline (TCA): drug level and when to monitor

A

Drug lvl: 50-100

Check when you get to 100mg around 5-7 days

58
Q

Glutamate receptor modulator medication names

A

Ketamine, Esketamine, Auvelity

59
Q

Ketamine MOA

A

R&S ketamine
- binding on NMDA for glutamate (on GABA neuron)

Mu opiod receptor activity - if on naloxone it won’t work

Increases growth factors

Immediate glutamate burst – increased dendridic spine density and neuroplasticity
- stimulates AMPA, blocks NMDA

60
Q

Esketamine MOA

A

S (only)

Inhibits NDMA on GABA – decreased stimulation of GABA neuron

61
Q

Dextromethorphan/buproprion MOA

A

NMDA antagonist – reduces glutamate transmission
— increases glutamate

Blocks SERT - increases serotonin

Sigma 1 agonist - increases serotonin

Dextromethorphan is rapidly metabolized by CYP2D6
Buproprion inhibits CYP2D6
–Maintains dextromethorphan concentrations

62
Q

Esketamine contraindications

A

Aneurysm, brain bleed, risk for stroke, uncontrolled HTN

Driving after treatments

Pregnancy

63
Q

Esketamine SE

A

HTN, tachycardia

temporary cognitive impairment: attention, judgement, reactions

Dissociative, dizzy, sedation

64
Q

Esketamine - what do we monitor

A

BP

65
Q

Esketamine BB Warning

A

BLACK BW: risk of sedation and dissociation
MUST MONITOR FOR 2 HRS

all providers/patients have to enroll in program

66
Q

Ketamine r/t suicide

A

suicide protective for a few days

67
Q

When is ketamine given

A

treatment resistant depression or persistent suicidal thoughts

68
Q

Lithium SE

A

Tremor

increased urination

acne, psoriasis, hair loss

decreased thyroid function

Stomach upset

69
Q

Lithium initial labs

A

Serum Creatinine, UA
– to screen for renal function
– to avoid lithium toxicity
– chronic use can affect kidney fx

T4, TSH
– attacks thyroid

Pregnancy test
– teratogenic

ECG
- if >40 or clinically indicated

Electrolytes
– because lithium is a salt
– Na+ competes for reabsorption in renal tubule

CBC
– if indicated by patient’s risk factors
– lithium increases WBC

70
Q

Lithium toxicity S/S

A

Lithium toxicity
– Early:
N/V/D
Dry Mouth
Ataxia, Dizziness, Slurred Speech, Nystagmus, Muscle weekness

Moderate - severe:
Anorexia, n/v/d
muscle fasiculations, clonic limb movements
hyperactive deep tendon reflexes
convulsions
delirium
syncope
stupor, coma
circulatory failure: low BP, arrhythmias

71
Q

Lithium drug interactions

A

Renally excreted so minial dru-drug interactions

Diuretics:
Loop: increase or decrease lithium lvl
Thiazide: Increase lithium lvl - reduce lithium by 50%

NSAIDS
Reduces kidney’s ability to clear lithium: Lithium lvl increases

Carbamazepine
Inhances neurological effects of lithium even without incresaed lithium lvls
dizziness, tremor, confusion, hyperreflexia

SSRIs
Increases serotonergic SEs = incresed chance of serotonin syndrome

ACE I
Increases risk of lithium toxicity and may increase lithium lvls
- possibly due to increased Na+ and H2O excretion

Iodides
Increse in the hypothyroid properties of lithium

72
Q

Valproate MOA

A

Voltage sensitive sodium channels

73
Q

Lithium and pregnancy -

A

Teratogenic - Ebstein’s anomaly

74
Q

3 antisuicidal medications

A

Clozapine, Ketamine, Lithium

75
Q

Therapeutic Lvl of Lithium

A

0.6-1.2

76
Q

How often to get lithium level

A

Lithium LVL every 3-6 months or if clinical indicated

Checking to make sure patient isn’t toxic

77
Q

Lithium ongoing monitoring

A

Lithium LVL every 3-6 months or if clinical indicated

Checking to make sure patient isn’t toxic

BUN/Creatinine & TSH every 3 months intially then every 6-12 months

78
Q

Valproate and pregnancy

A

BIG contraindication –

Teratogenic: neural tube defects = cleft palate, cleft lip
CONTRAINDICATED IN PREGO

79
Q

Valproate lvl monitoring

A

Depakote:
3 days after initial dose
12 hrs after last dose

Depakote ER:
8-9 days after initial dose
15 hrs after last dose

80
Q

Valproate lvls

A

Acute Mania: 45-125
Maintenance: 75-100

81
Q

Initial monitoring for Valproate

A

Pregnancy Test

LFT:
hepatically clear - can dmg

CBC:
can affect decrease platelets/RBCs

82
Q

Valproate r/t Lamictal

A

Increases lamictal levels by 50%

83
Q

Valproate SE

A

N/V, tremor, hair loss, sedation

wt gain

84
Q

Carbamazepine/Tegratol MOA

A

Blocks voltage sensitive sodium channels

85
Q

Carbamazepine/Tegratol Indications

A

Bipolar
– better for mania - less so for depressive phase

86
Q

Carbamazepine/Tegratol SE

A

Tremor

Confusion, Ataxia, Rash

Blurred vision, aplastic anemia, bone marrow suppression

eosinophelia

Agranulocytosis, ADH release

Neutropenia

87
Q

Carbamazepine/Tegratol Drug interactions

A

POTENT CYP3A4 inducer
– increases metabolizer

Lamictal: Will decrease the lamictal lvl by 1/2

88
Q

Carbamazepine/Tegratol Serious ADR

A

SJS & TEN - certain Asian population higher risk

89
Q

Carbamazepine/Tegratol Initial Labs

A

CBC
- can cause neutropenia, decreased RBCs, and agranulocytosis

LFT
- Hepatic clearance

Na+ level

90
Q

Carbamazepine/Tegratol: Continued Labs

A

Carbamazepine lvl:
Two lvls to establish dose – 4 weeks apart to account for autoinduction

CBC, LFT, Electrolytes, BUN/Creat monthly for 3 months then annually

91
Q

Carbamazepine/Tegratol: Important Testing for specific group of people

A

Genetic testing for Asian decent - HLA - B 1502

BEFORE YOU START THEM ON TEGRATOL

92
Q

Lamictal MOA

A

Blocks Na+ channels

Reduces the release of glutamate

93
Q

Lamictal MOA

A

Blocks Na+ channels

Reduces the release of glutamate

94
Q

Lamictal Indications

A

Prevent recurrence of manic and depressive bipolar

Good for depressive phase - not for acute

95
Q

Lamictal SE

A

infection

HA, Nausea, dry mouth

96
Q

Lamictal Drug interactions

A

Carbamazepine, Phenytoin, Phenobarbital, Primidone, Rifampin, Rifampin
– DECREASES LAMICTAL

Oral estrogen BC
– DECREASES LAMICTAL and possibly BC efficacy

Valproic Acid
– INCREASES VALPROIC ACID

97
Q

Major ADR r/t Lamictal

A

SJS

98
Q

Lamictal Standard Dosing

A

SLOW TITRATION
Start at 25mg for 2 weeks
50mg for 2 weeks
100mg for 2 weeks
Then 200mg

99
Q

Lamictal Dosing with Depakote

A

Half the dose

100
Q

Lamictal dosing with Tegratol/Carbamazapine

A

Double the dose

101
Q

Which psychotropic treatment(s) can be considered as ALTERNATIVE maintenance treatments to antidepressants?

A

Atypical antipsychotic such as quietiapine and mood stabilizers such as Lamictal

Both atypical antipsychotics with mood stabilizing properties and mood stabilizers have shown some efficacy in the treatment of major depressive episodes with mixed features and are therefore recommended as first- or second-line treatments.

102
Q

How long does it take for withdrawal dyskinesias to resolve?

A

Weeks to months

103
Q

Of the following, the agent with the lowest risk of cardiometabolic side effects is:
– Lithium
– Lumateperone
– Olanzapine
– Valproate

A

Lumateperone

Both lithium and valproate are associated with a relatively high risk of significant weight gain. Among the atypical antipsychotics, olanzapine carries with it one of the highest risks for cardiometabolic side effects, including weight gain.

Lumateperone has been shown to be neutral for weight gain in long-term studies and in early clinical practice, and has a favorable metabolic profile that is similar to placebo for changes in triglycerides, fasting glucose, and cholesterol.

104
Q

Patricia is a 31-year-old patient with bipolar I disorder who frequently exhibits impulsive symptoms of mania, including risk taking and pressured speech, during her manic episodes. Compared to a healthy brain, neuroimaging of this patient’s brain during a no-go task (designed to test response inhibition) would likely show:

– Increased activity in the orbitofrontal cortex

– Decreased activity in the orbitofrontal cortex

– Increased activity in the dorsolateral prefrontal cortex

A

Decreased activity in the orbitofrontal cortex

Neuroimaging of the orbitofrontal cortex of manic patients during a no-go task (a task that required the patient to suppress a response) shows that they fail to appropriately activate this brain region. This neuroimaging anomaly suggests that patients with bipolar disorder have problems with impulsivity associated with mania and with the orbitofrontal cortex.

105
Q

Katherine is a 24-year-old patient who presents with symptoms of depression (including sadness, feelings of worthlessness, and suicidal ideation) occurring every day for the past month. Clinical interview with Katherine reveals that she has a maternal aunt with bipolar disorder I. Further assessment reveals that this patient also feels distracted and as though her thoughts are racing. Upon speaking with the patient’s mother, it is discovered that Katherine has been, at times, more talkative than usual and irritable with her friends and family. Which class of medication would NOT be recommended as monotherapy for this patient?

– A mood stabilizer

– An antipsychotic

– An antidepressant

– All of the above would be recommended as monotherapy

A

Antidepressant

Expert consensus and published guidelines recommend that antidepressant monotherapy NOT be used (and is contraindicated) in patients with depression who exhibit mixed features and a positive family history of bipolar disorder.

106
Q

Of the following symptoms, which is the most common subsyndromal mania symptom in patients during a major depressive episode with mixed features?

– Decreased need for sleep

– Inflated self-esteem

– Psychomotor agitation

– Elevated mood

– High-risk behavior

A

Psychomotor agitation

During a major depressive episode with mixed features (concomitant subthreshold levels of mania or hypomania), the most common manic/hypomanic symptom exhibited is psychomotor agitation.

107
Q

Approximately what percentage of patients with bipolar disorder have comorbid ADHD?

A

20-25%

108
Q

A 26-year-old woman began treatment for a major depressive episode 8 months ago. Two months into her treatment she began to experience noticeable symptom improvement, and for the last 5 months she has been mostly symptom free, except for persistent cognitive dysfunction. Which of the following statements regarding cognitive dysfunction in depression is most accurate?

  • Cognitive dysfunction is one of the most common residual symptoms following recovery
  • Cognitive dysfunction can be treated with serotonergic modulation of glutamate transmission
  • Both
A

BOTH

Cognitive dysfunction is one of the most common residual symptoms of major depressive disorder and can endure longer than mood symptoms following recovery. Moreover, cognitive dysfunction is strongly correlated with physical, mental, and functional disability. Pharmacotherapies used to treat depression that have action on glutamate signaling via serotonergic modulation also show pro-cognitive effects. The prime example is vortioxetine, which has agonist action at 5HT1A, weak partial agonist action at 5HT1B/D, and antagonist action at 5HT3, 5HT1D, 5HT7, and the serotonin transporter. Antagonism of 5HT3 disinhibits glutamate release, while antagonism of 5HT7 enhances release of glutamate release in the prefrontal cortex. In addition, agonism of 5HT1A (full) and 5HT1B (partial) may enhance or suppress glutamate transmission based on neuronal localization.

109
Q

Theoretically, what is the therapeutic advantage of a SNRI over a SSRI?

– Increased norepinephrine via norepinephrine transporter inhibition

– Increased dopamine via norepinephrine transporter inhibition

– Increased norepinephrine and dopamine via norepinephrine transporter inhibition

A

Increased norepinephrine and dopamine via norepinephrine transporter inhibition

In addition to boosting serotonin like SSRIs (via inhibition of serotonin reuptake by the serotonin transporter [SERT]), SNRIs can boost norepinephrine by inhibiting reuptake by the norepinephrine transporter (NET). Additionally, in the prefrontal cortex, SNRIs can boost dopamine levels. In prefrontal cortex, SERTs and NETs are present in abundance on serotonin and norepinephrine nerve terminals, respectively, but there are very few dopamine transporters (DATs) on dopamine nerve terminals. Therefore, dopamine action is terminated either by enzymatic degradation or NET. If NET is inhibited by an SNRI then it cannot terminate the action of dopamine and dopamine levels increase in this brain region.

110
Q

A 36-year-old man with major depressive disorder is having lab work done to assess his levels of inflammatory markers. Based on the current evidence regarding inflammation in depression, which of the following results would you most likely suspect for this patient?

– Elevated lvls of tumor necrosis factor-alpha

– Reduced levels of interleukin 6 (IL-6)

– Reduced C-reactive protein (CRP)

– Elevated interferon gamma (IFN?)

A

Elevated levels of tumor necrosis factor-alpha (TNF-alpha)

There is growing evidence that inflammation may play an important role in the pathophysiology of major depression. Clinical studies have shown that depressed patients have significantly higher concentrations of several inflammatory central and peripheral markers, including the pro-inflammatory cytokines TNF-alpha and interleukin-6. Patients with depression also have higher concentrations of C-reactive protein, which is synthesized by the liver in response to pro-inflammatory cytokines, and reduced interferon gamma, which is a pro-inflammatory cytokine. Furthermore, both cytokines and cytokine inducers can cause symptoms of depression. For example, as many as 50% of patients receiving chronic therapy with the cytokine interferon develop symptoms consistent with idiopathic depression.

111
Q

A 28-year-old man with moderate depression achieves remission after 16 weeks on a therapeutic dose of an antidepressant. According to the neurotrophic hypothesis of depression, what is most likely true of his brain-derived neurotrophic (BDNF) expression before and after his successful treatment?

A

BDNF expression was abnormally low while he was depressed, and increased during antidepressant treatment

The neurotrophic hypothesis of depression posits that depression results from decreased neurotrophic support, leading to neuronal atrophy, decreased hippocampal neurogenesis, and that antidepressant treatment blocks or reverses this deficit, thereby reversing atrophy and cell loss. Several meta-analyses have reported deficient BDNF levels in patients with major depressive disorder and an elevation in BDNF following antidepressant treatment.

112
Q

Which of the following antidepressant treatments is associated with the greatest risk of weight gain?

– Escitalopram

– Fluoxetine

– Mirtazapine

– Vilazodone

A

Mirtazapine

113
Q

Which of the patient’s current medications MUST you discontinue BEFORE initiating tranylcypromine?

– Duloxetine

– Trazodone for insomnia

– Both

– Neither

A

Duloxetine

Although trazodone does have serotonin reuptake inhibition at antidepressant doses (150 mg or higher), this property is not clinically relevant at the low doses used for insomnia. In fact, because there is a required gap in antidepressant treatment when switching to or from an MAO inhibitor, low-dose trazodone can be useful as a bridging agent when switching.

114
Q

A 56-year-old male patient with major depression is brought to the ER with cardiac arrhythmia and possible cardiac arrest. While at the hospital, he suffers a seizure. His wife states that he may have ingested an increased dose of his medication. Which of the following is most likely responsible for this apparent overdose reaction?

– Atomoxetine
– Clomipramine
– Fluvoxamine
– Venlafaxine

A

Clomipramine

lomipramine, a tricyclic antidepressant (TCA), may be most likely to cause these effects in overdose. TCAs block voltage-sensitive sodium channels (VSSCs) in both the brain and the heart. This action is weak at therapeutic doses, but in overdose may lead to coma, seizures, and cardiac arrhythmia, and may even prove fatal.

115
Q

A 65-year-old patient on theophylline for chronic obstructive pulmonary disease (COPD) and fluvoxamine for recurring depressive episodes required a decreased dose of theophylline due to increased blood levels of the drug. Which of the following pharmacokinetic properties may be responsible for this?

A

Inhibition of CYP450 1A2 by fluvoxamine

Fluvoxamine is a strong inhibitor of CYP450 1A2. Theophylline is metabolized in part by CYP450 1A2, and thus strong inhibition of this enzyme by fluvoxamine may require a dose reduction of theophylline if the two are given concomitantly, so as to avoid increased blood levels of the drug.

116
Q

Mike is a 31-year-old patient with major depressive disorder (MDD) has experienced some response with the serotonin and norepinephrine reuptake inhibitor (SNRI) venlafaxine XR (150 mg/day). However, the patient acknowledges that he and his wife have been having relationship problems because of his poor libido. The patient experienced this problem prior to being diagnosed and treated for MDD, but he has found that the venlafaxine has worsened this troubling symptom despite the fact that his mood has improved. He asks if there is a way to both prevent worsening of his mood and avoid this side effect. Which class of depressant should he be switched to?

A

Switch to a norepinephrine and dopamine reuptake inhibitor (NDRI) – Wellbutrin

Pharmacological agents that increase dopaminergic neurotransmission and/or decrease serotonergic neurotransmission (e.g., serotonin 1A agonists or serotonin 2 antagonists) are often effective in ameliorating sexual dysfunction. Switching to an NDRI such as bupropion would be expected to increase dopaminergic neurotransmission and improve sexual function. Given that the patient experienced libido problems prior to treatment with the SNRI, and that the problem has worsened on treatment with the SNRI, it makes sense to switch to bupropion. Augmentation with bupropion to address sexual dysfunction, although commonly done in clinical practice, is not actually supported by randomized controlled studies.

117
Q

In addition to treating depressed mood, preclinical data indicate that serotonin 5HT3 receptor antagonists may have clinical utility as adjunct treatment for which symptoms?

A

Cognitive symptoms

Serotonergic neurons synapse with noradrenergic neurons, cholinergic neurons, and GABAergic interneurons, all of which contain serotonin 5HT3 receptors. When serotonin is released, it binds to 5HT3 receptors on GABAergic neurons, which release GABA onto noradrenergic, glutamatergic, and cholinergic neurons, thus reducing release of norepinephrine, glutamate, and acetylcholine, respectively. In addition, serotonin may bind to 5HT3 receptors on noradrenergic and cholinergic neurons, further reducing release of those neurotransmitters. This may theoretically contribute to symptoms of depressed mood and impaired cognition. Therefore, treatment with 5HT3 receptor antagonists improve depressed mood and cognitive problems.

118
Q

A 36-year-old patient has only partially responded to his second monotherapy with a first-line antidepressant. Which of the following has the best evidence of efficacy for augmenting antidepressants in patients with inadequate response?

– atypical antipsychotic

– buspirone

– stimulant

A

atypical antipsychotic

Atypical antipsychotics have been studied as adjuncts to selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitor (SNRIs), with approvals for aripiprazole, brexpiprazole, quetiapine XR, and olanzapine (in combination with fluoxetine). Overall, most studies of atypical antipsychotics show a benefit of combination treatment over monotherapy, although effect sizes have been modest. Although atypical antipsychotics have the best evidence of efficacy for augmenting antidepressants in patients with inadequate response, their adverse event profiles may still put them later in the treatment algorithm.

119
Q

Miryam is a 24-year-old woman with a major depressive episode that is only partially responding to treatment with a selective serotonin reuptake inhibitor. In particular, she continues to display reduced positive affect. She is prescribed adjunctive bupropion to manage this symptom. Through which mechanism(s) does bupropion theoretically ameliorate reduced positive affect?

A

Inhibition of dopamine and norepinephrine transporters

120
Q

Which of the following statements about ketamine treatment is true?

– The strongest evidence for the efficacy of ketamine is in bipolar depression

– Repeated dosing extends the duration of ketamine effects

– High frequency ketamine administration is recommended

– A history of antidepressant treatment is NOTnecessary to start ketamine treatment

A

Repeated dosing extends the duration of ketamine effects

Studies suggest that repeated dosing may extend the duration of ketamine effects. Ketamine administration of 2–3 times per week over 2–3 weeks, followed by a taper period and/or continued treatments, may be most effective.

121
Q

A patient with depression is prescribed mirtazapine as adjunctive treatment to venlafaxine, a serotonin-norepinephrine reuptake inhibitor. Mirtazapine acts on alpha 2 receptors to produce what effect?

A

Disinhibition of norepinephrine and serotonin release via alpha 2 antagonism

Norepinephrine turns off its own release via alpha 2 presynaptic receptors; therefore, alpha 2 antagonism with mirtazapine facilitates disinhibition of norepinephrine. Furthermore, norepinephrine migrating from a norepinephrine terminal can also turn off serotonin release via alpha 2 presynaptic heteroreceptors on serotonin neurons. Therefore, alpha 2 antagonists like mirtazapine can have a dual effect on facilitating the release of both norepinephrine and serotonin.

122
Q

A 34-year-old man with depression characterized by depressed mood, sleep difficulties, and concentration problems has not responded well to a selective serotonin reuptake inhibitor (SSRI) or a serotonin norepinephrine reuptake inhibitor (SNRI). His clinician elects to switch him to vortioxetine, which has prominent 5HT7 antagonism. What may be a primary function of these receptors?

A

Regulation of serotonin-glutamate interactions 68%

5HT7 receptors are postsynaptic G protein-linked receptors. They are localized in the cortex, hippocampus, hypothalamus, thalamus, and brainstem raphe nuclei, where they regulate mood, circadian rhythms, sleep, learning, and memory. A major function of these receptors may be to regulate serotonin-glutamate interactions.

Serotonin can both activate and inhibit glutamate release from cortical pyramidal neurons. Serotonin released from neurons in the raphe nucleus can bind to 5HT2A receptors on pyramidal glutamate neurons in the prefrontal cortex, activating glutamate release. However, serotonin also binds to 5HT1A receptors on pyramidal glutamate neurons, an action that inhibits glutamate release. Additionally, serotonin binds to 5HT7 receptors on GABA interneurons in the prefrontal cortex. This stimulates GABA release, which in turn inhibits glutamate release.

Serotonin binding at 5HT7 receptors can also inhibit its own release. That is, when serotonergic neurons in the raphe nucleus are stimulated, they release serotonin throughout the brain, including not only in the prefrontal cortex but also in the raphe itself. Serotonin can then bind to 5HT7 receptors on GABA interneurons in the raphe nucleus. This stimulates GABA release, which then turns off serotonin release.

Serotonin binding at 5HT7 receptors in the raphe inhibits serotonin release; therefore, an antagonist at this receptor would be expected to enhance serotonin release. Specifically, by blocking serotonin from binding to the 5HT7 receptor on GABA interneurons, a 5HT7 antagonist would prevent the release of GABA onto serotonin neurons, thus allowing the continued release of serotonin in the prefrontal cortex.

123
Q

A 32-year-old woman with major depressive disorder has been taking a selective serotonin reuptake inhibitor (SSRI) with good response for months. She presents now with complaints that she feels numb, and that even when she’s sad she can’t cry. Her clinician is considering reducing the dose of her SSRI in an effort to alleviate this problem. Is this a reasonable option?

A

Yes, data suggest that SSRI-induced indifference is dose-dependent and can be alleviated by reducing the dose

Apathy and emotional blunting can be symptoms of depression, but they are also side effects associated with selective serotonin reuptake inhibitors (SSRIs). These symptoms—termed “SSRI-induced indifference”—are under-recognized but can be very distressing for patients. They are theoretically due to an increase in serotonin levels and a consequent reduction of dopamine release. The first recommended strategy for addressing SSRI-induced indifference is to lower the SSRI dose, if feasible. Additional options include adding an augmenting agent or switching to an antidepressant in another class.

124
Q

Theoretically, individuals with depression may display a lack of normal GABAergic tonic inhibition via:

A

Extrasynaptic benzodiazepine-insensitive GABA-A receptor

125
Q

A 27-year-old patient who has been taking a selective serotonin reuptake inhibitor (SSRI) for depression for the last 2 years has just found out that she is 12 weeks pregnant. Cumulative data for SSRI use in pregnancy have established a small but clinically significant increase in absolute risk of:

– Cardiovascular malformations

– Persistent Pulmonary HTN

– Autism spectrum disorder

– None of the above

A

None of the above

126
Q

Sasha is a 58-year-old patient with a history of depression who has been prescribed agomelatine. At present, she is relatively free of depressive symptoms, likely due in part to binding of agomelatine to what receptors in the suprachiasmatic nucleus?

– Melatonin receptors

– 5HT2C receptors

– Both

A

Both

Agomelatine is both a melatonin M1 and M2 receptor agonist and a serotonin 5HT2C receptor antagonist. This unique receptor profile gives agomelatine the ability to address impairments in neurotransmission as well as circadian rhythm dysfunction.

127
Q

April is a 14-year-old patient recently diagnosed with moderate-to-severe major depressive disorder (MDD). She endorses passive suicidal ideation, but no specific plan or intention for suicide attempt. She denies any suicidal ideation or attempts prior to her current depressive episode. In addition to beginning cognitive behavioral therapy (CBT), which pharmacotherapy option would be best suited for treating her depressive episode?

– Imipramine

– Bupropion

– Fluoxetine

– No pharmacotherapy

A

Fluoxetine

Fluoxetine, a selective serotonin reuptake inhibitor (SSRI), has a good evidence base for efficacy treating pediatric MDD and is one of only two antidepressants with FDA approval for pediatric MDD. Escitalopram, also an SSRI, is the second antidepressant approved for treating pediatric MDD. There is no strong evidence to suggest that any particular SSRI is more effective than any other for pediatric MDD. However, both the National Institute of Clinical Excellence (NICE) and the American Academy of Child and Adolescent Psychiatry (AACAP) recommend evidence-based psychotherapy, such as CBT, and/or fluoxetine to treat moderate-to-severe depression in adolescence.

128
Q

The hypothesis that the therapeutic effects of antidepressants are due to downstream changes in neuroplasticity is consistent with the fact that clinical improvement with antidepressants is typically delayed by several weeks. The downstream effects of monoamine antidepressants include:

r/t AMPA, NMDA, and glutamate

A

Increased AMPA receptor expression, decreased NMDA receptor expression, decreased glutamate

There is increasing evidence, the underlying mechanism of antidepressant treatment may not be alterations in the levels of monoamines themselves, but rather changes in the downstream molecular events and neuroplasticity triggered by those monoamines. Monoaminergic antidepressants likely exert their therapeutic effects by influencing downstream signaling, such as increased a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, or AMPA receptor expression, decreased N-Methyl-D-aspartate, or NMDA receptor expression, and decreased glutamate, suggesting agents with direct activity at these downstream targets may lead to faster treatment response. Antidepressant treatments may modify the AMPA:NMDA receptor ratio, resulting in downregulated NMDA receptors, and increased AMPA receptors.

129
Q

Vortioxetine/Trintellix MOA

A

Blocks SERT

Multiple serotonin pathways in unique ways

May have a procognitive effect

130
Q

Vortioxetine/Trintellix max dose with Wellbutrin

A

10mg

131
Q

Vortioxetine/Trintellix SE

A

Wt neutral
Lower incidence of sexual SE

Nausea

132
Q
A

Psych 660 (6 decks)

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