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PHAR 358 - Therapeutics (Dr. K. Halpape) > Mental Health Review / Bipolar > Flashcards

Mental Health Review / Bipolar Flashcards

1
Q

What are the primary differences between “Mental Health Disorders” & “Mental Health Problems”?

A

MHD: Significant impairments to emotional state, behaviors that hinder one’s ability to function; meets diagnostic criteria.

MHP: Disruptions to function but person can still function; does not meet diagnostic criteria.

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2
Q

T or F: Non mental health medications can be authorized by attending physicians for those whom are admitted as involuntary patients.

A

False… Only mental health drugs can be forcibly administered to involuntary patients (they can refuse other meds).

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3
Q

What defines “involuntary admission criteria”?

A

1) Mental disorder & requires inpatient care

2) Not capable of making admission / treatment decisions

3) Likely to harm self or others

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4
Q

What are some issues with the current psychotropic drug nomenclature system?

A

-Confuses patients
-Stigma contributions
-1st indication descriptors

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5
Q

Define “dysthymia”.

A

A persistent depressive mood

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6
Q

Define “cyclothymia”.

A

Mood swings between short periods of mild depression and hypomania

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7
Q

What is Bipolar I Disorder?

A

Period of one or more weeks with a full manic episode (abnormally & persistently elevated mood / energy)

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8
Q

What is Bipolar II Disorder?

A

Current or past hypomanic episode INCLUDING a current or past major depressive episode

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9
Q

Who does Bipolar affect more: Men or Women?

A

Equal

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10
Q

How does Bipolar presentation differ between men and women?

A

Men: More manic episodes

Women: More depressive or mixed

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11
Q

Is Bipolar curable?

A

No… Realistic goal is to halt disease progression or put somebody into a maintenance state where disease is well managed.

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12
Q

What are the risk factors for developing Bipolar?

A

-1st degree relative
-Drug / alc abuse
-High stress
-Traumatic events

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13
Q

What medical conditions can serve as risk factors for Bipolar development?

A

-Hyperthyroid
-Hormonal changes
-CNS disorders
-Endocrine dysregulation
-CVD

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14
Q

What pharmacologic drug classes can induce mania?

A

-Antidepressants
-Dopamine Augmenting Agents (ie. Amphetamines, Cocaine)
-Thyroid Preps
-Steroids
-Alc / Marijuana / Caffeine

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15
Q

How does the taper strategy for antidepressants differ in bipolar management as opposed to MDD management?

A

Abrupt stoppage (rather than a gradual taper in MDD) in cases of extreme mania.

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16
Q

What pneumonic is used to remember the antidepressant withdrawal symptoms?

A

FINISH

F - Flu-Like Sx
I - Insomnia
N - Nausea
I - Imbalances
S - Sensory Disturbances
H - Hyperarousal

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17
Q

What is the average age of onset for a new bipolar diagnosis?

A

20 - 25yrs

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18
Q

What is a bipolar patient’s best predictor of functionality levels?

A

Medication Adherence!!!

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19
Q

Approximately ___ % of bipolar patients discontinue their medications due to adverse effects.

A

50%

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20
Q

What types of medical conditions may worsen existing bipolar or make it more challenging to treat?

A

-Anxiety Disorders
-Substance Use Disorders
-ADHD
-PTSD

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21
Q

Death via suicide is up to ___ x higher in bipolar patients than it is other patient subtypes.

A

20x

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22
Q

What sorts of deviations from normal behavior would indicate somebody is going through a manic episode?

A

-Inflated self esteem
-Reduced need for sleep
-Racing thoughts
-Increased agitation & pressured speech
-Distractable
-Risky behavior partaking

At least three of these!

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23
Q

Pneumonic to remember manic symptoms?

A

DIGFAST

D - Distracted
I - Irritable
G - Grandiosity
F - Flight of ideas
A - Activity increases
S - Sleep decreases
T - Talkative

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24
Q

Manic symptoms in Bipolar I last >/= __ days, whereas symptoms in Bipolar II last </= __ days.

A

BDI: >/= 7 days
BDII: </= 4 days

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25
Q

Are there severe functional impairments in BDI? BDII?

A

BDI: Yes
BDII: No

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26
Q

Is psychosis present in BDI? BDII?

A

BDI: Yes
BDII: No

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27
Q

Does BDI warrant hospitalization? BDII?

A

BDI: Yes
BDII: No

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28
Q

Does one require a history of depression to be diagnosed with BDI? BDII?

A

BDI: No (can have previous history of it, but not necessary for diagnosis).

BDII: Yes (needed for diagnosis).

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29
Q

Which antidepressant class do we see the highest rates of manic episode development with?

A

SNRIs (then TCAs, then SSRIs)

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30
Q

Symptomatic improvements during a manic episode should be seen within __ - __ weeks being on therapies, whereas full benefits are often seen within __ - __ weeks.

A

Improvement: 1-2 wks
Full Benefit: 3-4 wks

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31
Q

What other adjunctive non-pharmacologic interventions should be incorporated into the care plans of bipolar patients?

A

-Exercise
-Sleep
-Balanced Diet
-Reduced or Eliminate Substance Use
-Reduced Nicotine / Caffeine Intake

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32
Q

What are the most commonly used mood stabilizers in bipolar management?

A

Lithium

Valproic Acid / Divalproex

Lamotrigine

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33
Q

What important PK parameters should be noted with Lithium?

A

1) Even Vd within total body water spaces… Reduced Vd in elderly = Increased concentrations.

2) t1/2 = 12-27hrs… Longer in elderly (30-36hrs) due to declining renal function as we age.

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34
Q

Which organ is extensively involved with Lithium elimination?

A

Kidneys (95%)
Perspiration (4%)

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35
Q

What percentage of Lithium is reabsorbed at the Proximal Tubules?

A

80%

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36
Q

Is Lithium highly plasma protein bound?

A

Nope (freely filtered by glomerulus similar to other cations such as K+ and Na+).

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37
Q

What factors may reduce the clearance of Lithium?

A

-Low Na+
-Dehydration
-Kidney Failure
-Reduced Renal Perfusion

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38
Q

What are the target serum concentrations that we want to aim for with bipolar Lithium treatments?

A

0.8 - 1.2mmol/L (very narrow TI drug)

0.6 - 0.8mmol/L in elderly

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39
Q

What are the signs of Lithium toxicity?

A

Drowsiness
Ataxia
Tremors
Slurred Speech
Hypertonia

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40
Q

When should Lithium levels be sampled?

A

12hrs post-dose (usually AM after an evening dose)

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41
Q

How often should Lithium levels be sampled?

A

1) 5-7d after starting

2) OW once on stable dose x 2wks

3) Monthly x 3mths

4) q6mths thereafter

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42
Q

How do the therapeutic ranges for Lithium differ for treating an acute manic episode vs. maintenance?

A

Acute: 1.0 - 1.2mmol / L

Maintenance: 0.6 - 1.0 mmol / L

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43
Q

What advantage does dosing Lithium once daily as opposed to twice daily have?

A

-Increased compliance
-Decreased renal toxicity
-Slowed renal dysfunction progression

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44
Q

How would you elect to adjust maintenance doses of Lithium if a patient had a reported CrCl of </= 50mL / min?

A

50 - 75% of normal maintenance dose

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45
Q

If a patient is on a BID Lithium dosing regimen, what must we ensure happens before taking serum levels?

A

HOLD THE MORNING DOSE!!! Skews serum concentrations…

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46
Q

How might pregnancy or severe burns influence Lithium levels?

A

Increased Vd (fluid levels increase, which dilutes Lithium concentrations).

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47
Q

How does increased caffeine consumption reduce Lithium levels?

A

Increases renal activity

48
Q

What pharmacologic agents might reduce serum concentrations of Lithium?

A

Theophylline
Acetazolamide
NaHCO3

49
Q

What pharmacologic agents would increase serum concentrations of Lithium?

A

NSAIDs
Diuretics
ACEi / ARBs

50
Q

Primary side effects of Lithium?

A

Polydipsia / Polyuria
Tremors
GI Upset
Acne Development
Alopecia
Wt Gain

51
Q

Serious signs of Lithium toxicity?

A

Arrythmias
Seizures
Myocarditis
Acute Tubular Necrosis
Hypothyroidism
Coma
Death

52
Q

Which of the following is cleaved into its active drug form within the stomach?

Divalproex
Valproic Acid

A

Divalproex

53
Q

What percentage of Valproic Acid is bound to plasma proteins?

A

85 - 90%

54
Q

Valproic Acid is extensively eliminated by what organ?

A

Liver (> 95% hepatically metabolized)

55
Q

What’s the major metabolic pathway responsible for eliminating Valproic Acid?

A

UDP-mediated glucuronidation / beta oxidation

56
Q

Describe Valproic Acid’s potential mechanisms of action.

A

1) Inhibit Voltage-Gated Na+ Channels

2) Increase GABA actions

3) Modulate signal cascades

4) Effects neuron excitation (mediated by NMDA subtype Glutamate receptors)

5) Serotonin / Dopamine / Aspartate / T-Type Ca2+ Channels

57
Q

What is the therapeutic range for Valproic Acid?

A

350 - 700umol / L (total)

-However, range is extrapolated from Seizure treatments (often may need to strive higher, individualized levels).

58
Q

When should steady state trough levels of Valproic Acid be taken?

A

3 - 4d after starting therapy

59
Q

What is the general principle for dose adjusting Valproic Acid in hepatic disease?

A

Avoid altogether (reduced protein binding & clearance of drug).

60
Q

Do renally impaired patients require Valproic Acid dose adjustments?

A

Nope

61
Q

What enzymes do Valproic Acid inhibit?

A

CYP2C9
Epoxide Hydroxylase
UDPGT

62
Q

What important drug classes increase Valproic Acid levels?

A

Macrolide ABs (ie. Clarithromycin, Erythromycin)

Salicylates (ie. Aspirin, Na+ Salicylate)

63
Q

What drug classes reduce Valproic Acid levels?

A

Carbapenem ABs (ie. Meropenem, Ertapenem)

Anti-Convulsants (ie. Phenytoin, Carbamazepine, Phenobarbital)

64
Q

What drugs show concentration increases when on-board with Valproic Acid?

A

Lamotrigine (cut dose 1/2 & double the titration period)

Warfarin

TCAs

Anti-Convulsants

65
Q

Adverse effects of Valproic Acid?

A

Dose-Related: NVD, Anorexia, Constipation (< Divalproex), Tremor, Sedation, Ataxia, Dizziness, Thrombocytopenia

Chronic: Wt Gain, Balding, Menstrual Disturbances

66
Q

Should Valproic Acid & derivates be avoided in pregnancy?

A

Yes… Highly teratogenic (strongly encourage contraception use).

67
Q

JB is a Bipolar patient on Valproic Acid & comes in for a refill. He complains of unexplained fits of fatigue, confusion & vomiting. What test should he get done?

A

Ammonia

68
Q

When should CBCs, Platelets, & LFTs be assessed in a patient starting Valproic Acid?

A

Baseline
qmthly x 3mths
q4 - 6mths

69
Q

What are some counseling points you can provide a patient on Valproic Acid with to combat common GI & sedative side effects?

A

TWF, switch to Divalproex (less upsetting to stomach), H2RAs such as Ranitidine.

Taking higher of the two doses at bedtime.

70
Q

What indications do Lamotrigine have in treating Bipolar?

A

Maintenance therapy, acute depressive episodes… NOT (!!!) recommended for acute manic episodes.

71
Q

Describe Lamotrigine’s MOA.

A

Binds open conformation of Voltage-Gated Na+ Channels, reduces Glutamate release.

Somewhat of an inhibitory effect on Serotonin Receptor.

72
Q

What is t1/2 of Lamotrigine? When do peak plasma levels occur?

A

t1/2: 25 - 33hrs
Peak: 1 - 5hrs

73
Q

Are dose adjustments of Lamotrigine needed in hepatic impairment? Renal impairment?

A

Yep to both.

74
Q

After what length of time (in days of missed doses) must Lamotrigine titrations be restarted from scratch?

A

5d (as concentrations will be totally eliminated from the body by this point).

75
Q

Why must Lamotrigine be titrated up slowly?

A

Risk of SJS Rash (1-2% kids, 0.1% adults but more prevalent in first 8wks of starting)

76
Q

What are the most common side effects of Lamotrigine?

A

Sedation, Headaches, Dizziness, GI (to lesser extent)

77
Q

Is it necessary to obtain serum concentrations of Lamotrigine?

A

Nope… Routine blood work you do with everything else should still be done though.

78
Q

What sorts of drugs decrease Lamotrigine levels?

A

ACs (ie. CBZ, Phenytoin, Phenobarbital, Topiramate)

Oral Contraceptives (primarily the estrogen component)

79
Q

What drug increases Lamotrigine two-fold (you’ve seen this already don’t get this wrong).

A

Valproic Acid / Divalproex

80
Q

Chronic use of what OTC medication induces Lamotrigine metabolism & thus decreases its levels?

A

Tylenol (4g / day)

81
Q

Why is it important to taper all of the anti-seizure agents used in Bipolar?

A

Sudden withdrawal / stoppage can trigger seizures (even in those with no prior history).

82
Q

Describe Carbamazepine’s MOA.

A

Blocks Voltage-Dependent Na+ Channels

Blocks NMDA Glutamate Receptor, reduces Ca2+

Modulates Aspartate, Glutamate release

83
Q

What side effect secondary to increased fluid retention is something to worry about with CBZ?

A

Hyponatremia… Drug stimulates ADH release, promotes increased water reabsorption.

84
Q

Primary route of elimination of CBZ?

A

Hepatic (> 99%, primarily CYP3A4)

85
Q

Why is it so hard to get CBZ to target therapeutic ranges?

A

Autoinduction (induces its own metabolism via Epoxide-Diol Pathway)

86
Q

When does autoinduction of CBZ usually stabilize?

A

1 - 5wks

87
Q

Trough concentrations of CBZ should be taken within ___ hr(s) prior to next dose.

A

1hr

88
Q

In what disease state would we not recommend using CBZ?

A

Decompensated Liver Disease (not outright CI but dose decrease with Stable Liver Disease)

89
Q

Does CBZ require renal dose adjustments?

A

Nope

90
Q

A bipolar patient is on a CYP3A4 metabolized drug and the physician elects to discontinue their Carbamazepine. What you expect would happen to the other CYP3A4 metabolized drug’s serum concentrations?

A

Would go up (as CBZ is a potent CYP Enzyme Inducer)

91
Q

What highlighted drug class increases CBZ levels?

A

-Macrolide ABs (ie. Erythromycin, Clarithromycin, Telithromycin)

-“Azole” Antifungals (ie. Ketoconazole)

-Cardiovascular Ca2+ Channel Blockers (ie. Diltiazem, Verapamil)

-Cimetidine & Grapefruit Juice

92
Q

What highlighted drug classes decrease CBZ levels?

A

-Other ACs (ie. Phenytoin, Phenobarbital)

-Warfarin

-Other Antipsychotics (ie. Lurasidone, Risperidone, Quetiapine…)

-Antidepressants (ie. Citalopram)

-Methadone

-Antiretrovirals (ie. NNRTIs)

93
Q

Side effects of CBZ?

A

-GI
-Dizzy / Sedation / Ataxia (same as others)
-Tremors
-HR increase
-Low BP
-SIADH & Hyponatremia
-“Penias”
-Rash & Hypersensitivity Rxns

94
Q

Asian patients with a positive test for HLA-B____ & Caucasian patients with a positive HLA-A____ are at an increased risk of suffering from hypersensitivity reactions while on Carbamazepine.

A

Asian: HLA-B1502
White: HLA-A3101

95
Q

What conditions are outright CIs to CBZ use?

A

-Hepatic Disease
-CVD
-Blood Dyscrasias
-Bone Marrow Depression
-Concurrent Clozapine use (due to potential WBC Ct drops)

96
Q

What monitoring parameters for those on CBZ should be assessed?

A

-CNS, ongoing

-Ocular Exam, baseline & yearly (due to blurred vision / diplopia)

-ECG, baseline

-CBC / LFT / Renal Function, baseline, mthly x 3mths, then q6-12mths

-Bone Mineral Density (if taking CBZ > 5yrs or risk factors of osteopenia)

-Rash, ongoing

97
Q

Important counseling point for females on CBZ who are sexually active & on hormonal birth control?

A

Use of alternative contraception (as CBZ reduced efficacy of contraceptive forms on board).

98
Q

What is the primary MOA of atypical antipsychotics?

A

Dopamine Blockade

99
Q

Of the following antipsychotics, which one(s) would you predict to have higher rates of EPS & hyperprolactinemia symptoms?

Quetiapine
Risperidone
Haloperidol
Aripiprazole
Chlorpromazine

A

Haloperidol, Chlorpromazine (FGAs)

100
Q

What are the general adverse effects of atypical antipsychotics?

A

-EPS (ie. Stiffness, Tremor, Shuffling Gait)

-Sexual Dysfunction

-Wt Gain / Dyslipidemia / Diabetes / CVD (Metabolic Conditions)

-AC (ie. Sedation, Constipation, Dry Mouth, Blurry Vision)

-QT Prolongation

-Seizures

101
Q

What is the current consensus around using antidepressant monotherapies in the management of Bipolar?

A

Avoid without antimanic agents onboard!!!

102
Q

Rank the following ADs from best to worst in terms of safety in treating BDII:

Bupropion
Sertraline
Other SSRIs
Venlafaxine

A

Same order as shown on other side of the card!

103
Q

Which of the following SSRIs is NOT recommended for BDII management?

Escitalopram
Citalopram
Fluoxetine
Paroxetine

A

Paroxetine

104
Q

Ideally, when should antidepressant use be tapered off in managing bipolar?

A

Short courses of 3 - 4mths, with a taper good to initiate once asymptomatic for 6 - 12wks.

105
Q

Which antidepressant classes possess the highest risk of switching a bipolar patient over from a depressive episode to a manic one?

A

TCAs (number one)
SNRIs (number two)

106
Q

When would combination therapy for bipolar management be recommended?

A

-Faster response needed

-Those at risk for harming self or others

-Hx partial response to monotherapy

-Those with severe manic episodes

107
Q

What are 1st line CANMAT guideline bipolar treatments for acute mania?

A

Monotherapies: Lithium, DVP, Quetiapine, Aripiprazole, Paliperidone, Risperidone

Combo: Lithium or DVP + Quetiapine, Risperidone, or Asenapine

108
Q

In cases of mixed feature bipolar, what combination of medications is preferred?

A

Antipsychotic & DVP

109
Q

What are considered to be the second line options for acute mania?

A

Monotherapy: Olanzapine, CBZ, Ziprasidone, Haloperidol

Combo: Lithium or DVP + Olanzapine

110
Q

What agents suck at treating acute mania?

A

-Gabapentin
-Lamotrigine
-Omega 3 FAs
-Topiramate

111
Q

1st line options for treating Bipolar I Depression (according to CANMAT)?

A

Quetiapine, Lamotrigine, Lithium, Lurasidone, Lurasidone + Li/DVP

112
Q

The Young et al study in 2010 showed that Lithium was no more effective than placebo in treating acute bipolar depression… What was the study’s caveat?

A

Mean Lithium levels were only 0.61 mEq/L (needed to be higher to see true effects).

113
Q

Early improvement within ___ wks is a reasonable predictor of overall response to a treatment in BDI Depression.

A

2wks (however, may take up to 4 - 6wks to see response)

114
Q

What should be considered the only 1st line BD maintenance therapy that we recommend to all patients?

A

Psychoeducation

115
Q

In cases of mixed episode bipolar, should antidepressants be continued or discontinued?

A

Discontinued (because of worsening potential)

116
Q

Which medications should be avoided in pregnancy?

A

DVP / VPA
CBZ
Lithium (Trimester 1)

117
Q

Which agent appears to be the least risky for managing bipolar in pregnancy?

A

Lamotrigine

PHAR 358 - Therapeutics (Dr. K. Halpape) (8 decks)

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