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PHAR 358 > Bipolar > Flashcards

Bipolar Flashcards

1
Q

Define bipolar I disorder (BDI)

A

A distinct period of at least one week of full manic episode: abnormally and persistently elevated mood and increased energy

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2
Q

Define bipolar II disorder (BDII)

A

A current or past hypomanic episode and a current or past major depressive episode

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3
Q

How do men and women compare in terms of prevalence of bipolar disoder?

A

Men = Women, but:
- Men have more manic episodes, women more depressive or mixed

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4
Q

True or False? There is a cure to bipolar disorder

A

False, but full recovery/maintenance is possible

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5
Q

The exact cause of bipolar is _______

A

unknown

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6
Q

What are 5 risk factors for developing bipolar disorder?

A
  1. Drug or alcohol abuse
  2. Having a first-degree relative
  3. Period of high stress
  4. Medical conditions (hyperthyroidism, hormonal changes, CNS disoders, endocrine dysregulation, CVD)
  5. Major life changes, such as the death of a loved one or other traumatic experiences
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7
Q

Describe the clinical presentation of bipolar

A

Mood can fluctuate from euthymia where everything is normal, to hypomania –> mania then down to subthreshold depression –> major depression, and back and forth, sometimes achieving a mixed state.

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8
Q

What is kindling theory of bipolar disorder? (2)

A
  1. Abnormalities lead to more abnormalities
  2. Syndromal episodes increase vulnerability to more episodes
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9
Q

What is neurodegeneration?

A

Persistent neurocognitive deficits, increasing impairment, delayed functional recovery

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10
Q

What is the best predictor of level of functioning in bipolar?

A

Medication adherence
- ~50% of pts ds/c meds due to adverse effects

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11
Q

What are some comorbid conditions that may worsen existing bipolar or make treatment challenging? (5)

A
  1. Anxiety disorders
  2. Substance use disorder (alcohol is most common)
  3. ADHD
  4. PTSD
  5. Medical comorbidities (e.g., diabetes, dyslipidemia, obesity, CVD)
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12
Q

One of the leading causes of death in bipolar is _______

A

suicide
(20x higher than the general population)

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13
Q

What are some factors that are associated with suicide attempts in bipolar? (8)

A
  1. Female sex
  2. Younger age of illness onset
  3. Depressive polarity of 1st illness episode
  4. Comorbid anxiety
  5. Comorbid SUD
  6. Comorbid cluster B personality disorder
  7. 1st degree family history of suicide
  8. Previous attempt
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14
Q

True or False? Comprehensive assessment for suicide risk for a bipolar patient should only be done after the initial diagnosis

A

False - should occur during all BD patient interactions

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15
Q

From the DSM-5, mania is classified as persistently and abnormally elevated mood (irritable or expansive) and energy, with at least 3 of the following changes from usual behaviour: (7)

A
  1. Grandiosity or inflated self-esteem
  2. Decreased need for sleep
  3. Racing thoughts
  4. Increased talking/pressured speech
  5. Distractibility
  6. Increased goal-directed or psychomotor agitation
  7. Excessive engagement in high risk behaviours
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16
Q

In the DSM-5 for bipolar, not only do patients need the 3+ specific symptoms they ALSO need to have these 3 things alongside it

A
  1. Symptoms occur nearly every day for at least 1 week
  2. Leads to significant functional impairment OR includes psychotic features OR necessitates hospitalization
  3. Episode is not due to physiological effects of a substance or another medical condition
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17
Q

What is the DIGFAST mnemonic to help remember the mania symptoms?

A

Distractibility
Irritability or indiscretion
Grandiosity
Flight of ideas (racing thoughts)
Activity (or energy) increased
Sleep decreased
Talkativeness

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18
Q

True or False? Both manic and hypomanic episodes are required for a diagnosis of BDI in the DSM-5

A

False
Manic episode is required
Hypomanic or major depressive episodes may occur before or after manic episode but are NOT required for diagnosis

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19
Q

Essentially a hypomanic episode is the same as a manic episode but it is a shorter time period and less severe. What are the diagnostic criteria of one of these episodes? (4)

A
  1. Same symptom criteria as manic episode, but only lasting up to 4 days
  2. Unequivocal change in functioning or mood that is uncharacteristic of the individual and/or observable by others
  3. Impairment in social or occupational functioning is not severe. Hospitalization not required. No psychosis
  4. The episode is not due to physiological effects of a substance or another medical condition
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20
Q

What is the main diagnostic criteria of BDII?

A

Hypomanic episode AND major depressive episode (current or past episodes)

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21
Q

Compare and contrast: BDI vs. BDII - Duration of manic symptoms

A

BDI ≥7 days
BDII ≤ 4 days

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22
Q

Compare and contrast: BDI vs. BDII - Functional impairment

A

BDI: necessary
BDII: not necessary

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23
Q

Compare and contrast: BDI vs. BDII - Psychotic features

A

BDI: necessary
BDII: not necessary

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24
Q

Compare and contrast: BDI vs. BDII - Requires hospitalization

A

BDI: necessary
BDII: not necessary

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25
Q

Compare and contrast: BDI vs. BDII - History of depression

A

BDI: - nil
BDII: necessary

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26
Q

What type of scale is the Montgomery-Asberg Depression Rating Scale (MARDS)?

A

Clinican-rated to assess severity of depression

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27
Q

What type of scale is the Hamilton Depression Rating Scale (HDRS)(HAM-D)?

A

Clinician-rated to assess severity of depression - gold standard for clinical research

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28
Q

What type of scale is the Young Mania Rating Scale (YMRS)?

A

Clinician-rated - used in research for screening and assessing severity of mania

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29
Q

What type of scale is the Mood Disorders Questionnaire?

A

Patient-rated. Used to screen for possible BD. Most specific for identifying BDI

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30
Q

What are 3 challenges in BD diagnosis and treatment?

A
  1. Delay to diagnosis
  2. Misdiagnosis
  3. Limited clinical trials
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31
Q

Why might there be a delay in diagnosis of BD? (3)

A
  1. Average delay 8-12 years
  2. Often patients do not recall hypomanic symptoms
  3. More likely to seek help for depression vs. mania
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32
Q

Why might there be misdiagnosis of BD? (3)

A
  1. Survey found that 73% of BD pts are initially misdiagnosed
  2. In 2000 ~30% of pts waiting 10 years for correct dx
  3. Most often misdiagnosis = depression - consequences include developing hypo/manic episodes and rapid cycling
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33
Q

Why are there limited clinical trials involving BD? (4)

A
  1. Heterogenous illness
  2. Co-morbidities
  3. Manic symptoms –> impaired judgement –> impaired adherence
  4. Require longitudinal assessment
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34
Q

ZZ is a 25yo female that presents to the emergency room today. With increased energy, no need for sleep for the past 4 days, pressured speech. Diagnosed with mania. What med on her BPMH is of concern?
a. Pregabalin
b. Prednisone
c. Pindolol
d. Pantoprazole

A

B

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35
Q

What are 8 goals of therapy for BD?

A
  1. Eliminate mood episode with complete remission of symptoms, ongoing. “Acute treatment”
  2. Prevent recurrences or relapses of mood episodes, ongoing. “Maintenance treatment”
  3. Improve quality of life and optimize psychosocial functioning, ongoing
  4. Minimize harm to self and others (including prevent suicide, ongoing
  5. Maximize adherence and minimize adverse effects of pharmacotherapy, ongoing
  6. Identify and minimize risk factors for mood episodes, ongoing
  7. Provide care for comorbid psychiatric, substance use or, medical condition, ongoing
  8. Provide education to patient and family members, ongoing
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36
Q

For mania, what is the timeline in which we see improvement from medication (response and full benefit)?

A
  1. Response = 1-2 weeks
  2. Full clinical benefit = 3-4 weeks
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37
Q

For depression, what is the timeline in which we see improvement from medication (response and full benefit)?

A
  1. Response = 2-4 weeks
  2. Full clinical benefit = 6-12 weeks
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38
Q

What are some easyish lifestyle changes to recommend a patient (non-pharm therapy) with BD? (5)

A
  1. Exercise
  2. Adequate sleep
  3. Healthy diet
  4. Decreased/abstinent substance use
  5. Decreased caffeine/nicotine/alcohol
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39
Q

What are some other non-pharm options to potentially try for BD patients? (7)

A
  1. Bright light - more for depression
  2. Relapse prevention plan
  3. Psychoeducation, supportive counselling, biosocial rhythm normalization, psychotherapy (CBT, interpersonal therapy)
  4. ECT
  5. Collaborative care
  6. Case management
  7. Medication adherence
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40
Q

What are the 3 most commonly used mood stabilizer medications used for BD?

A
  1. Lithium
  2. Valproic Acid/Divalproex
  3. Lamotrigine
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41
Q

What are the anticonvulsant drugs that can be used for BD? (6). Only 2 of them are really used, so why not use the other 4?

A
  1. VPA/Divalproex
  2. Lamotrigine
  3. Carbamazepine
  4. Oxcarbazepine (3 and 4 use is limited by ADEs and drug interactions)
  5. Topiramate
  6. Gabapentin (5 and 6 rare used as mood stabilizers due to lack of efficacy & poor tolerability)
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42
Q

What are the indications for lithium? (3)

A
  1. BD
    - Acute mania treatment
    - Prophylaxis/maintenance
  2. Schizoaffective disorder
  3. Unipolar depression
    - Antidepressant augmentation
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43
Q

While the exact mechanism of action of lithium is not fully understood, what are some examples of the multiple effects on cellular functioning it might have? (4)

A
  1. Interaction with downstream signaling cascades
  2. Enhances GABA activity
  3. Alters Ca-mediated intracellular functions
  4. Decreases CNS adrenergic activity
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44
Q

Is bioavailability of oral lithium high, medium, or low?

A

High

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45
Q

True or False? Lithium is almost completely absorbed from the small intestine

A

True

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46
Q

What is the potential issue with time to peak onset of IR lithium?

A

Can lead to tremors or nausea, can switch to XR if that’s the case

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47
Q

True or False? Lithium is bound to plasma proteins

A

False - not bound to plasma proteins

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48
Q

What should you know about lithium’s volume of distribution in the body?

A

It distributes evenly in the total body water space

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49
Q

What is the t1/2 of lithium in normal renal function?

A

12-27 hours (typically call it 24 hours for the sake of calculations)

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50
Q

How is lithium eliminated?

A

95% renally
It’s freely filtered by the glomerulus like Na and K, 80% reabsorbed in the proximal tubules (with sodium)

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51
Q

True or False? Lithium follows non-proportional dose pharmacokinetics?

A

False - follows linear, dose-proportional PK

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52
Q

What are some causes for decreased clearance of lithium in the body? (4)

A
  1. Hyponatremia
  2. Dehydration
  3. Renal failure or dysfunction
  4. Decreased renal blood flow
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53
Q

Should know the therapeutic range of lithium (in mmol/L) in the following populations:
1. Acute mania
2. Maintenance therapy
3. Elderly

A
  1. Acute mania = 1.0-1.2 mmol/L
  2. Maintenance therapy = 0.6-1.0 mmol/L
  3. Elderly = 0.6-0.8 mmol/L
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54
Q

When are lithium levels taken when doing bloodwork for it?
In what situation would that be different?

A
  1. 12 hour post dose level
  2. Take is STAT if toxicity or non-adherence is suspected
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55
Q

How frequent are lithium levels checked starting from initiation of therapy?

A
  1. 5-7 days after starting or changing dose, then q weekly until at stabilized dose for 2 weeks, then q monthly for up to 3 months, then at least q 6 months.
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56
Q

With acute mania, how often is lithium typically dosed?

A

Initial is 1-2 times per day then try to go with BID

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57
Q

With BD maintenance, once the person is stabilized on lithium they can be given once daily dosing (if able to tolerate it). What are some of the benefits/things to look out for? (4)

A
  1. Usually given at night to improve compliance
  2. Some trials show decrease in urine volume and decreased renal toxicity with once daily dosing
  3. Pts sensitive to peak related side effects may respond to XR formulations
  4. When Li changes from multiple daily dosing to once daily dosing, can expect ~10-25% increase in 12h Li level
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58
Q

When CrCl is below __, we have to adjust Li dosing

A

50mL/min

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59
Q

Can we use Li in acute renal failure?
How about dialysis?

A

No.
Pts undergoing dialysis should have dose after dialysis

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60
Q

What are 3 things that should be done if Li is at a toxic level?

A
  1. Hold dose
  2. Repeat plasma level next day
  3. Restart therapy when within target range
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61
Q

Assuming the pt has stable renal function and they are on 900mg of lithium/day and at 0.6mmol/L blood levels, what dosing regimen would we want in order to achieve 1mmol/L?

A

Because Li PK is linear can do cross multiplication
900mg/0.6mmol/L = Xmg/1.0mmol/L
X = 1500mg

62
Q

What are some important factors that can decrease lithium levels in the body? (6)

A
  1. Pregnancy (contraindicated in 1st trimester anyways)
  2. Sodium supplement
  3. Hemodialysis
  4. Peritoneal dialysis
  5. Burns
  6. Caffeine
63
Q

What are some important factors that can increase Li level in the body? (4)

A
  1. Sodium loss
  2. NSAIDs
  3. Thiazide diuretics
  4. ACEis/ARBs
64
Q

What are some drug interactions to look out for with lithium? (5)

A
  1. Diuretics (e.g., furosemide, chlorthalidone)
    - Potentially mixed effects
  2. NSAIDS
    - Decrease Li clearance, increasing concentration
  3. ACEis
  4. Antipsychotics
    - Risk of additive neurotoxicity
  5. Antidepressants
    - Theoretical risk of serotonin syndrome
65
Q

What are some common side effects of Li to be aware of? (7)

A
  1. Increased thirst and urinary frequency (dose-related)
  2. Fine tremors to hands/arms (usually symmetric and at high frequency and worse with fine motor activity; dose-related)
  3. Headache, sedation, weakness (dose-related)
  4. GI upset (nausea, diarrhea) (dose-related)
  5. Skin changes (acne, psoriasis)
  6. Alopecia
  7. Weight gain (avg 4-6 kg in first 2 years)
66
Q

What are some serious side effects of Li to be aware of? (5)

A
  1. Hypothyroidism
  2. Renal injury: interstitial nephritis, renal failure, end stage renal disease
  3. Blood dyscrasias (i.e., leukocytosis)
  4. Bradycardia or conduction abnormalities
  5. Nephrogenic diabetes insipidus
    - Cannot concentrate urine –> polydipsia, polyuria
    - Secondary to Li accumulation in collecting tubule
    - Li interferes with antidiuretic hormone
    - Volume depletion = Li reabsorption = toxicity
67
Q

Severe Li poisoning may also result in: (10)

A
  1. Coma with hyper-reflexia
  2. Muscle tremor
  3. Hyperextension of limbs
  4. Pulse irregularities
  5. HTN or hypotension
  6. ECG changes (T wave depression or inversion)
  7. Peripheral circulatory failure
  8. Neuroleptic malignant syndrome
  9. Epileptic seizures
  10. Acute tubular necrosis (renal failure) can occur
68
Q

How will the following factors affect Li levels
1. Eating a lot of pretzels after being on a low sodium diet
2. Hot yoga
3. Giving up caffeine after previously drinking 3-4 cups coffee/day
4. Starting naproxen 500mg BID for gout flare
5. 2nd trimester of pregnancy
6. Increasing fluid intake to 15 cups of water/day to help with overall health

A
  1. Decrease
  2. Increase
  3. Increase
  4. Increase
  5. Decrease
  6. Decrease
69
Q

What are some counselling points about common side effect manangement of Li?
1. Thirst
2. Nausea
3. Sedation
4. Acne
5. Tremors

A
  1. Drink water, hard candies (should subside)
  2. Take with food; can consider ER formulation if doesn’t subside
  3. Take at bedtime; don’t drive
  4. Talk to pharmacist or physician for treatment
  5. Talk to physician if doesn’t subside
70
Q

What are 2 indications for valproic acid?

A
  1. Seizures
    - Generalized tonic-clonic (grand mal), partial onset, absence
    - Has broad-spectrum anti-epileptic activity
  2. Bipolar disorder
    - Acute mania treatment
    - Maintenance (prophylaxis)
71
Q

The exact mechanism of action of valproic acid (VPA) is unknown, but what are 5 possible mechanisms to know of?

A
  1. Inhibition of voltage-gated Na channels
  2. Increasing action of GABA
  3. Modulates signal transduction cascades and gene expression
  4. May effect neuronal excitation mediated by the NMDA subtype of glutamate receptors
  5. Also effects serotonin, dopamine, aspartate, and T-type Ca channels
72
Q

True or False? VPA is not very protein bound?

A

False, it is bound 85-90% to serum albumin

73
Q

How is VPA metabolized?

A

Hepatically

74
Q

4-ene-valproic acid metabolite can cause _____ ________

A

liver toxicity

75
Q

What is the t1/2 of VPA?

A

12-18 hours

76
Q

What is the therapeutic range for VPA (In umol/L)?

A

350-700 umol/L

77
Q

When is VPA sampled and what is the frequency?

A

Steady state trough level 3-4 days after initial therapy

78
Q

How does hepatic disease and renal impairment impact VPA dosing?
How about being elderly?

A
  1. Hepatic disease - decreased protein binding and clearance. Avoid in hepatic disease b/c unbound conc goes up
  2. Renal impairment - no dosage adjustment necessary.
  3. Elderly have decreased protein binding and clearance, use lower initial doses
79
Q

Is valproic acid and enzyme inhibitor or inducer?

A

Inhibitor

80
Q

What antibiotic class can increase VPA levels (drug-drug interaction)?

A

Macrolides
- Clarithromycin
- Erythromycin
- Telithromycin

81
Q

What antibiotic class can decrease VPA levels (DDI)?

A

Carbapenems
- Ertapenem
- Imipenem
- Meropenem

82
Q

What OTC drug can increase VPA levels?

A

ASA/salicylates

83
Q

What is the MOST MAJOR drug-drug interaction to be aware of when it comes to VPA?

A

Lamotrigine

84
Q

What are the dose-related side effects of VPA? (5)

A

GI
1. NVD
CNS
1. Tremors
2. Sedation
3. Ataxia
4. Dizziness

85
Q

What are the serious (idiosyncratic) side effects of VPA? (3)

A
  1. Increased transaminases and LDH
  2. Hepatotoxicity
  3. Pancreatitis
86
Q

What are 3 chronic side effects of VPA?

A
  1. Weight gain
  2. Menstrual disturbances
  3. Alopecia
87
Q

True or False? VPA can be used in pregnancy

A

False - it is teratogenic

88
Q

What are the 2 indications for lamotrigine?

A
  1. Seizures
    - Partial seizures (adjunct), absence seizures (monotherapy), generalized tonic-clonic (monotherapy)
  2. BD
    - Acute bipolar depression
    - Maintenance in BDI or II
89
Q

What is the MOA of lamotrigine? (2)

A
  1. Alters signal transduction via:
    - Binding to the open channel conformation of the voltage-gated Na channels
    - Reducing release of glutamate (which may be a secondary result of blocking Na channels, rather than an independent effect)
  2. Weak 5-HT3 receptor inhibitory effects
90
Q

What is the t1/2 of lamotrigine?

A

25-33h

91
Q

What are 3 drugs that can induce metabolism of lamotrigine?

A
  1. Phenytoin
  2. Carbamazepine
  3. Oral contraceptives
92
Q

What drug can inhibit metabolism of lamotrigine?

A

VPA

93
Q

What is the most important dosing principle you need to know regarding lamotrigine? Why?

A

Slow titration is very very important.
Faster titration can lead to SEVERE skin rashes, such as SJS or necrolysis (leading to end organ failure)

94
Q

What are the common side effects of lamotrigine? (4)

A
  1. Sedation
  2. Headaches
  3. Nausea
  4. Dizziness
95
Q

What are the less common side effects of lamotrigine? (3)

A
  1. Dyspepsia
  2. Dysmenorrhea
  3. Anxiety or emotional lability
96
Q

What are the rare/serious side effects of lamotrigine? (3)

A
  1. Risk of SJS (if titrated too quickly)
  2. Aseptic meningitis
  3. Hepatotoxicity
97
Q

What is the MOST MAJOR drug-drug interaction to remember for lamotrigine?

A

VPA/DVP - can increase lamotrigine level two-fold or more

98
Q

What is the most important self-monitoring tip to tell a patient regarding lamotrigine?

A

Self-monitoring for rash. If any signs of skin abnormalities, STOP taking, and seek medical attention. Don’t start any new lotions or creams when starting this med.

99
Q

Carbamazepine is structurally similar to ____

A

TCAs

100
Q

What are 4 indications for carbamazepine?

A
  1. Seizures
    - Generalized tonic-clonic (grand mal), partial-onset
  2. BD
    - Acute mania treatment
    - Maintenance
  3. Neuropathic pain (off-label)
  4. Trigeminal neuralgia
101
Q

What is the MOA of carbamazepine?

A

Signal transduction modulation (decrease repetitive action potential firing) and anti-kindling properties
- Blocks voltage-dependent Na channels (at a different recpetor/subunit than VPA)
- Blocks NMDA glutamate receptor and decreases [Ca2+]
- May depress activity in the nucleus ventralis of the thalamus or decrease synaptic transmission

102
Q

Carbamazepine and ADH. What happens here?

A

Carbamazepine stimulates the release of ADH and potentiates its action in promoting reabsorption of water

103
Q

How is carbamazepine metabolized?

A

Hepatically via CYP enzymes (CYP3A4)

104
Q

Carbamazepine-10,11-epoxide is the major metabolite of carbamazepine. Why is it important and how is that metabolized?

A

It is active and has therapeutic and toxic effects.
Is hydrolyzed by CYP1A2

105
Q

What is the unique thing to remember about carbamazepine metabolism?

A

It induces its own metabolism via the epoxide-diol pathway (AUTOINDUCTION)

106
Q

What is the clearance and t1/2 of carbamazepine?

A

Both are variable due to autoinduction

107
Q

What is the time of sampling of carbamazepine levels?

A

Trough within 1 hour prior to dose

108
Q

What is the frequency of sampling of carbamazepine levels? (2)

A
  1. During auto-induction (every 1-2 weeks until on stable regimen)
  2. Steady state trough (after 5 weeks)
109
Q

How does hepatic disease and renal impairment impact carbamazepine dosing?
How about being elderly?

A
  1. Hepatic disease - not recommended in pts with decompensated liver disease, dose reduction may be needed in pts with stable liver disease
  2. Renal impairment - no dosage adjustment necessary
  3. Elderly have decreased hepatic clearance, use initial lower doses and smaller dose increases
110
Q

What are 4 dosing principles of carbamazepine?

A
  1. Initiate slowly due to early long half-life in order to minimize side effects
  2. Can initiate with any dosage form
  3. Best to give in divided doses, usually Q12H or Q8H, instead of a single dose
  4. Dosing best at mealtime
111
Q

Any time carbamazepine is started or stopped, what must be done?
Why?

A

Do a drug interaction check.
- Co-administration of CYP3A4 inhibitors and inducers increase and decrease CBZ levels respectively with initiation or dose increase
- CBZ induces multiple enzyme systems too

112
Q

What are the drug classes that can increase CBZ levels? (3)

A
  1. Macrolides (clarithromycin, erythromycin, telithromycin)
  2. Azoles (itraconazole, fluconazole, ketoconazole)
  3. CCBs (diltiazem, verapamil)
113
Q

What are some “other” substances that can increase CBZ levels (3 are drugs, one is non drug)

A
  1. Cimetidine
  2. Grapefruit juice
  3. Propoxyphene
  4. Quinine
114
Q

What is an important class of medications that can be decreased by CBZ?

A

Anticoagulants - warfarin and DOACs

115
Q

What are some dose-related side effects of CBZ? (3)

A
  1. GI - NV
  2. CNS - sedation
  3. CV - tachycardia
116
Q

What are 3 important serious (idiosyncratic) side effects of CBZ?

A
  1. SIADH/hyponatremia
  2. Blood dyscrasias: leukopenia, thrombocytopenia, eosinophilia
  3. Rash (10% morbilliform) and hypersensitivity reactions.
117
Q

What are the contraindications for using CBZ? (5)

A

1. Concurrent use with clozapine
2. History of hepatic disease
3. CVD
4. Blood dyscrasias
5. Bone-marrow depression

118
Q

Should be able to list the atypical antipsychotics (6)
(Real Quests Only After Leveling Alts)

A
  1. Risperidone
  2. Quetiapine
  3. Olanzapine
  4. Aripiprazole
  5. Lurasidone
  6. Asenapine
119
Q

Atypical vs. typical antipsychotic use in bipolar disorder. Which is used more?

A

Atypicals - generally have a lower risk of EPS and hyperprolactinemia.
Typicals rarely used in BD

120
Q

Doses of antipsychotics are lower for BD than for psychosis. Why?

A

BD patients are more likely to show EPS when treated with comparable doses of antipsychotics compared to patients with psychosis (more likely to go into depression)

121
Q

What is the consensus to using antidepressants in bipolar as of right now? (4)

A
  1. Avoid AD monotherapy without antimanic agent
  2. Use with caution in people with history of AD-induced mania, mixed features, or rapid cycling
  3. Ds/c during acute manic episode (taper or abrupt discontinuation if severe mania)
  4. Consider tapering off once depression symptoms eliminated for 3-4 months
122
Q

IF going to use an antidepressant in bipolar, then what should be done? (3)

A
  1. Avoid TCAs > Avoid SNRIs (higher risk of switching)
  2. Safest in BDII
    - Bupropion > sertraline, then fluoxetine or other SSRIs > venlafaxine
  3. Paroxetine NOT recommended due to level 2 negative evidence in BDII
123
Q

Following the CANMAT guidelines, what is being assessed if the person has acute mania? (8)

A
  1. Risk of aggressive behaviour or violence to others
  2. Risk of suicide
  3. Degree of insight
  4. Ability to adhere to treatment
  5. Co-morbidities
  6. Substance use
  7. Physical conditions & lab tests
  8. Most appropriate treatment setting (inpatient vs. outpatient)
124
Q

Following the CANMAT guidelines, what substances should be discontinued if the person is experiencing acute mania? (4)

A
  1. Antidepressants
  2. Stimulants (caffeine, amphetamines)
  3. Alcohol
  4. Nicotine (gradual discontinuation)
125
Q

Following the CANMAT guidelines, what needs to be ruled out before stating the person is experiencing acute mania? (4)

A
  1. Prescribed medication
  2. Illicit-drug use/abuse (treat if present)
  3. Endocrine disorder
  4. Neurological disorder
126
Q

What are 1st line monotherapies for acute mania?
(Just know the meds) (6)

A
  1. Lithium
  2. Quetiapine
  3. Divalproex
  4. Aripiprazole
  5. Paliperidone (dose >6mg)
  6. Risperidone
127
Q

What are the 1st line combination therapies for acute mania? (4)

A
  1. Quetiapine + Li/DVP
  2. Aripiprazole + Li/DVP
  3. Risperidone + Li/DVP
  4. Asenapine + Li/DVP
128
Q

What are the patient specific factors for giving a manic patient lithium?

A

Lithium is preferred over DVP for individuals who display classical euphoric grandiose mania (elated mood in the absence of depressive symptoms), few prior episodes of illness, a mania-depression- euthymia course, and/or those with a family history of BD, especially family history of lithium response

129
Q

What is the patient specific factors for giving a manic patient DVP?

A

DVP is equally effective in those with classical and dysphoric mania. It is recommended for those with multiple prior episodes, predominant irritable or dysphoric mood and/or comorbid substance abuse or those with a history of head trauma

130
Q

When might you add on or switch therapy for a patient with acute mania?

A

Some therapeutic response is expected within 1-2 weeks after starting a 1st line agent. If no response is observed within 2 weeks with therapeutic doses of antimanic agents, and other contributing factors are excluded, then switch or add-on strategies should be considered

131
Q

What are some agents that are NOT recommended to use in acute mania? (4)

A
  1. Gabapentin
  2. Lamotrigine
  3. Omega 3 fatty acids
  4. Topiramate
132
Q

What things should be assessed in a patient with BDI depression? (7)

A
  1. Severity of depression
  2. Risk of suicide/self-harm behaviour
  3. Ability to adhere to treatment
  4. Psychosocial support network
  5. Ability to function
  6. Previous treatments
  7. Decided appropriate treatment setting:
    - Hospital
    - Outpatient
133
Q

What substances should be discontinued if a patient has BDI depression? (5)

A
  1. Stimulants
  2. Nicotine
  3. Caffeine
  4. Drugs
  5. Alcohol
134
Q

What should be ruled out if a patient is presenting with BDI depression? (2)

A
  1. Symptoms due to alcohol/drug use, medications, other treatments
  2. General medical conditions
135
Q

What are the first line treatments for BDI depression? (6)

A
  1. Quetiapine
  2. Lurasidone + Li/DVP
  3. Lithium
  4. Lamotrigine
  5. Lurasidone (monotherapy)
  6. Lamotrigine (adjunct)
136
Q

What agents are NOT recommended for acute bipolar depression?

A

Antidepressant monotherapy
- Available trials do not support their efficacy
- Safety concern = mood switching

137
Q

What is the importance of effective bipolar maintenance treatment early in illness, even after first episode? (3)

A
  1. Reverse cognitive impairment
  2. Preserve brain plasticity
  3. May lead to improved prognosis and minimization of illness progression
138
Q

Pharmacotherapy is the foundation to BD maintenance therapy but alone is often ineffective to prevent recurrence. What then should also be done 1st line?

A

Psychoeducation is the only 1st line psychosocial intervention for maintenance therapy that should be offered to all patients

139
Q

What should be assessed in a patient on BDI maintenance? (5)

A
  1. Medications effective in acute phase (usually effective in maintenance phase)
    - Controversial if antidepressants should be continued
  2. History (clinical course, response to previous medications, family history)
  3. Psychiatric comorbidities
  4. Predominant illness polarity
  5. Polarity of most recent illness
140
Q

What substances should be discontinued if a patient is on BDI maintenance therapy? (5)

A
  1. Stimulants
  2. Nicotine
  3. Caffeine
  4. Drugs
  5. Alcohol use
141
Q

What should be ruled out when patient present in BDI maintenace? (2)

A
  1. Symptoms due to alcohol/drug use, other treatments
  2. General medical condition
142
Q

What are the first-line treatment options in BDI maintenance? (9)

A
  1. Li
  2. Quetiapine
  3. DVP
  4. Lamotrigine
  5. Asenapine
  6. Quetiapine + Li/DVP
  7. Aripiprazole + Li/DVP
  8. Aripiprazole
  9. Aripiprazole OM
143
Q

When might you add on or switch therapies in BDI maintenance?

A

If therapy requires adjustment and no acute mania or depression

144
Q

What is the recommended pharmacotherapy in a BD patient with mixed episodes? (3)

A
  1. Discontinue antidepressants
  2. Monotherapy –> atypical antipsychotic
  3. Combination therapy –> Li/DVP + atypical antipsychotic
145
Q

What BD meds should be avoided in pregnancy? (3)

A

Avoid: DVP/VPA, CBZ
Small increased risk in 1st trimester: lithium

146
Q

Which BD agent has the least risk/appears to be safe in pregnancy?

A

Lamotrigine

147
Q

Can antipsychotics be used in pregnancy?

A

Least studied, but risk appears neutral for quetiapine, risperidone, aripiprazole, olanzapine

148
Q

Which BD medication has the most evidence for reducing the risk of suicide in a BD patient? How?

A

Lithium
Reduces risk of depressive relapse, serotonin-mediated reduction in impulsivity or aggressive behaviour (e.g., toward triggers) and a non-specific benefit from long-term monitoring provided during therapy with lithium

149
Q

In general, what important roles do we as pharmacists have in treating a BDI patient? (5)

A
  1. Screening for presence or history of mania
  2. Avoiding antidepressant monotherapy
  3. Patient education
  4. Appropriate dosing
  5. Supporting adherence
150
Q

Secondary Causes of Mania:
What are some medical conditions that can induce mania? (4)

A
  1. CNS disorders (brain tumor, strokes, head injuries, etc.)
  2. Infections (encephalitis, sepsis, HIV, etc.)
  3. Electrolyte or metabolic abnormalities (Ca or Na fluctuations)
  4. Endocrine or hormonal dysregulation (Addison’s disesase, Cushing’s, etc.)
151
Q

Secondary Causes of Mania:
What are some medications/drugs that can induce mania? (7)

A
  1. Alcohol intoxication
  2. Drug withdrawal states
    3.Antidepressants (MAOIs, TCAs, etc.)
  3. DA-augmenting agents (CNS stimulants: amphetamine, cocaine; DA agonists)
  4. Marijuana intoxication
  5. NE-augmenting agents
  6. Steroids (anabolic, cortico, etc.)
152
Q

Secondary Causes of Mania:
What are some somatic therapies that can potentially induce mania? (3)

A
  1. Bright light therapy
  2. Deep brain stimulation
  3. Sleep deprivation

PHAR 358 (16 decks)

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