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PHAR 358 > Bipolar Disorder > Flashcards

Bipolar Disorder Flashcards

1
Q

What is dysthymia?

A

persistent depressive disorder

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2
Q

What is cyclothymia?

A

mood swings between short periods of mild depression and hypomania

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3
Q

What is the bipolar I disorder?

A

a distinct period of at least one week of full manic episode

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4
Q

what is bipolar II disorder?

A

a current or past hypomanic episode AND a current or past major depressive episode

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5
Q

T or F
a depressive episode is required for a bipolar I disorder diagnosis?

A

false

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6
Q

what are some risk factors for bipolar disorder?

A

drug or alcohol abuse
having a first degree relative
period of high stress
major life changes
medical conditions

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7
Q

what medical conditions can induce mania?

A

hyperthyroidism, hormonal changes, CNS disorders, endocrine dysregulation, CVD

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8
Q

what drugs can induce mania?

A

alcohol
drug withdrawal states
antidepressants
DA-augmenting agents – stimulants, sympathomimetics
NE-augmenting agents
steroids
thyroid preparations
herbal products (St. John’s Wort)

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9
Q

what is the average age of onset of bipolar?

A

20-25 years

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10
Q

what type of symptoms of bipolar do people typically develop before age 18?

A

depressive symptoms

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11
Q

what are the consequences of early onset bipolar?

A

longer delay to treatment
greater depressive symptom severity
higher levels of comorbid anxiety/substance use

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12
Q

what is a mixed episode of bipolar?

A

depressive and hypomanic symptoms occurring at the same time

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13
Q

what is the kindling theory of bipolar disorder?

A

abnormalities lead to more abnormalities
syndromal episodes increase vulnerability to more episodes
leads to neurodegeneration

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14
Q

and is neurodegeneration?

A

persistent neurocognitive deficits, increasing impairment, delayed functional recovery

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15
Q

what is the best predictor of functioning in bipolar disorder?

A

medication adherence

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16
Q

what percentage of bipolar patients discontinue their medications?

A

50%
usually due to adverse effects

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17
Q

what are some common comorbid conditions with bipolar disorder?

A

anxiety disorders (50-60%)
substance use disorder (60%)
ADHD 920%)
PTSD
medical comorbidities: diabetes, dyslipidemia, obesity, CVD

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18
Q

what is the most commonly abused substance in BD?

A

alcohol

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19
Q

what is the leading cause of death in BD?

A

suicide

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20
Q

what is the diagnostic criteria for mania?

A

persistently and abnormally elevated mood (irritable or expansive) and energy, with at least 3 of the following changes from unusual behaviour:
1. grandiosity
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
symptoms occur nearly every day for at least 1 week
leads to significant functional impairment OR includes psychotic features OR necessitates hospitalisation
episode is not due to physiological effects of a substance or another medical condition

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21
Q

what are the symptoms of mania?

A

DIGFAST
D: distractibility
I: irritability or indiscretion
G: grandiosity
F: flight of ideas (racing thoughts)
A: activity (or energy) increased
S: sleep decreased
T: talkativeness

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22
Q

what is the diagnostic criteria for a hypomanic episode?

A

same symptoms of a manic episode but only lasting up to 4 days
unequivocal change in functioning or mood that is uncharacteristic of the individual and/or observable by others
impairment in social or occupational functioning is not severe. hospitalisation not required. no psychosis
the episode is not due to physiological effects of a substances or another medical condition

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23
Q

what is the diagnostic criteria for a major depressive episode?

A

5+ symptoms must be present nearly every day during the same 2-week period and result in change in functioning (SIG E CAPS):
S: changes in sleep pattern
I: changes in interests or activity
G: feelings of guilt or increased worry
E: changes in energy
C: changes in concentration
A: changes in appetite
P: psychomotor disturbances
S: suicidal ideation
must include one or both of the following:
1. depressed mood most of the day, nearly every day
2. diminished interest or pleasure in all or most activities

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24
Q

what does the MADRS measure?

A

clinician rated severity of depression

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24
Q

what does the HAM-D measure?

A

clinician rated severity of depression

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25
Q

what does the YMRS rate?

A

clinician rated screening and assessing severity of mania

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26
Q

what does the MDQ measure?

A

patient rated screening for possible BD

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27
Q

what is a positive MDQ screen?

A

yes to 7/13 items in question 1
yes to question 2
moderate to severe in question 3

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28
Q

what are some challenges in BD diagnosis and treatment?

A

delay to diagnosis
misdiagnosis
limited clinical trials

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29
Q

what is the most common misdiagnosis of BD?

A

depression

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30
Q

what is the average delay to treatment of BD?

A

8-12 years

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31
Q

how long does it take for bipolar mania to respond to medication?

A

response: 1-2 weeks
full clinical benefit: 3-4 week

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32
Q

how long does is take for bipolar depression take to respond to medication?

A

response: 2-4 weeks
full clinical benefit: 6-12 weeks

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33
Q

T or F
bipolar depression takes longer to respond to medication than bipolar mania

A

True

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34
Q

T or F
bipolar depression responds to medication faster than unipolar depression

A

false

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35
Q

what is a WRAP?

A

wellness recovery action plan

lists early warning signs
tools they can use when the threat of a crisis starts to come
what they have to do to stay well
what they will do and who they will entrust to do things for them - help take care of them - when they are in crisis
a list of people they can call when in a crisis
what their triggers are
post-crisis plan

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36
Q

what are the medical indications of lithium?

A

bipolar:
- acute mania treatment
- prophylaxis/maintenance

schizoaffective disorder

unipolar depression adjunct

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37
Q

T or F
lithium is highly protein bound

A

false

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38
Q

what is the half life of lithium?

A

12-27 hours
longer in elderly

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39
Q

how is lithium eliminated

A

95% renal
4% perspiration

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40
Q

what causes decreased clearance of lithium?

A

hyponatremia, dehydration, renal failure or dysfunction, decreased renal blood flow

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41
Q

what is chronokinetics?

A

varies with circadian rhythm

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42
Q

what are the lithium concentration therapeutic range for acute mania?

A

1.0 to 1.2 mmol/L

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43
Q

what are the lithium concentration therapeutic range in maintenance therapy?

A

0.6 to 1.0 mmol/L
0.6 to 0.8 mmol/L in elderly

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44
Q

when is time of sampling for lithium?

A

12 hours post dose level
stat if toxicity or non-adherence is suspected

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45
Q

when should lithium levels be taken?

A

5-7 days after starting therapy or changing doses, then once weekly until at a stabilized dose for 2 weeks, then monthly for up to 3 months, then at least every 6 months

during times of infection, debilitation, changes in diet, recurrences of symptoms, noncompliance, signs of toxicity

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46
Q

why is it best to give lithium once daily in maintenance therapy?

A

improves compliance
decrease in urine volume and decrease in renal toxicity

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47
Q

what should be done when lithium toxicity is suspected?

A

hold dose
repeat plasma level next day
restart therapy when within target range

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48
Q

T or F
lithium syrup contains lithium carbonate

A

False
syrup contains lithium citrate; caps and XR tabs contain lithium carbonate

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49
Q

what are some factors that can decrease lithium levels?

A

pregnancy
sodium supplementation
hemodialysis
peritoneal dialysis
burns
theophylline/aminophylline
caffeine
acetazolamide
sodium bicarb

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50
Q

what are some factors than can increase lithium levels?

A

dehydration
renal impairment
sodium loss
increased age
strenuous exercise
cirrhosis
NSAIDs
thiazide diuretics
ACEi/ARBs
SSRIs/SNRIs
chronic lithium use

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51
Q

what is the interaction between lithium and NSAIDs?

A

decreased lithium clearance = increased lithium concentrations

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52
Q

what is the interaction between lithium and ACEi/ARBs?

A

angiotensin II and decreased aldosterone levels = sodium depletion/lithium retention
vasoconstriction results in decreased renal perfusion, decrease lithium clearance = increased lithium level

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53
Q

what are some common AEs with lithium?

A

increased thirst and urinary frequency
fine tremors to hands/arms
headache, sedation, weakness
GI upset
skin changes
alopecia
weight gain

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54
Q

what is usually the first sign of lithium toxicity?

A

GI upset

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55
Q

what are some serious AEs of lithium?

A

hypothyroidism
renal injury
blood dyscrasias
bradycardia or conduction abnormalities
nephrogenic diabetes insipidus

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56
Q

what is nephrogenic diabetes insipidus?

A

cannot concentrate urine = polydipsia, polyuria

57
Q

how can lithium cause nephrogenic diabetes insipidus?

A

lithium accumulation in collecting tubule
lithium interferes with antidiuretic hormone
volume depletion = lithium reabsorption = toxicity

58
Q

what are the signs and symptoms of lithium toxicity?

A

mild: ataxia, fine tremors of the limbs, GI disturbances, muscle weakness, fatigue

moderate: sedation, lethargy, ataxia, dysarthria, headaches, increased reflexes, hyperthermia, coarse tremors, impaired sensorium, nystagmus

severe: coarse tremors, delirium, seizures, coma, respiratory complications, death

59
Q

what concentration of lithium is toxic?

A

1.5 mmol/L +
toxicity can occur at doses close to therapeutic levels

60
Q

what are the monitoring parameters for lithium?

A

manic symptoms
depressive symptoms
CBC with differential
weight
electrolytes
thyroid function
renal function
ECG
plasma lithium concentrations
lithium adherence
lithium side effects
suicide risk

61
Q

T or F
lithium is safe in pregnancy

A

false
causes heart anomallys

62
Q

what are the clinical indications of valproic acid?

A

seizures: generalised tonic clonic (grand mal), partial-onset, absense

bipolar disorder
- acute mania treatment
- maintenance

63
Q

T or F
Vaproic acid is highly protein bound

A

TRUE

64
Q

how is valproic acid eliminated?

A

> 95% hepatic metabolism via glucuronidation, B-oxidation, alpha-hydroxylation
major metabolism via UDGT-catalysed glucuronidation and B-oxidation

65
Q

which metabolite of vaproic acid can cause liver toxicity?

A

4-ene-valproic acid

66
Q

what is the half life of valproic acid?

A

12-18 hours

67
Q

what is the therapeutic level of valproic acid?

A

350-700 umol/L
(total valproate levles)

68
Q

what is the time of sampling of valproic acid?

A

trough

69
Q

when are valproic acid levels taken?

A

steady state trough level – 3-4 days after initial therapy
seizure activity
suspected signs and symptoms of valproic acid toxicity
addition or withdrawal of other enzyme inducing drugs
suspected non-adherence

70
Q

does lithium need to be adjusted for hepatic or renal impairment?

A

hepatic: no
renal: yes

71
Q

does valproic acid need to be dose adjusted for hepatic or renal impairment?

A

hepatic: yes
renal: no

72
Q

which enzymes are key to valproic acid drug interactions?

A

CYP2C9
epoxide hydroxylase
UDPGT

73
Q

which drugs can increase valproate levels?

A

macrolides
topiramate
isoniazid
ASA/salicylates

74
Q

which drugs can decrease valproate levels

A

carbapenems
anticonvulsants: carbamazepine, phenytoin, phenobarbital
rifampin

75
Q

which drugs are increased by valproate?

A

anticonvulsants: carbamazepine, phenytoin, phenobarbital, lamotrigine
warfarin
TCAs

76
Q

what is the interaction between valproate and lamotrigine?

A

valproate increases lamotrigine levels by 50%
enhances AEs of lamotrigine

labeling recommends 50% dose reduction when used with valproate

77
Q

what are the AEs of valproate?

A

dose related
- GI: N/V/D/C, anorexia
- CNS: tremor, sedation, ataxia, dizziness

idiosyncratic
- increased transaminases and LDH
- hepatotoxicity
- hyperammonemia
- leukopenia
- skin rash (SJS, TENS, DRESS)
- hyponatremia

chronic
- weight pain
- menstrual disturbances, polycystic ovaries
- alopecia

78
Q

is valproic acid safe in pregnancy?

A

no
causes neural tube defects

79
Q

what are the monitoring parameters of valproic acid?

A

sedation
CBC with diff and platelets
LFTs
ammonia
rash
valproate levels

80
Q

what are the clinical indications of lamotrigine?

A

seizures: partial onset (Adj), absence seizures, generalised tonic-clonic

bipolar disorder
- acute bipolar depression
- maintenance

81
Q

what is the MOA of lamotrigine?

A

alters signal transduction via:
- binding to the open channel conformation of the voltage gated sodium channels
- reducing release of glutamate

weak 5-HT3 receptor inhibitory effects

82
Q

what is the half life of lamotrigine?

A

25-33 hours

83
Q

how is lamotrigine metabolised?

A

hepatic and renal
metabolised by glucuronidation and UGT enzymes

84
Q

why is a slow titration so important with lamotrigine?

A

risk of SJS

85
Q

what are the AEs of lamotrigine?

A

common: sedation, headache, N, dizziness

less common: dyspepsia, anxiety or emotional lability, chest pain, peripheral edema, dysmenorrhea, ataxia, rash (non serious)

rare/serious: risk of SJS, aseptic meningitis, blood dyscrasias, hepatotoxicity

86
Q

what monitoring parameters are there for lamotrigine?

A

baseline: hepatic and renal function
ongoing: rash

no serum levels or lab monitoring required

87
Q

what are the important DIs of lamotrigine?

A

VPA/DVP: increase lamotrigine 2-fold

carbamazepine, phenytoin, phenobarb, topiramate

oral contraceptives: decrease lamotrigine levels by 50%

88
Q

what are the clinical indications of carbamazepine?

A

seizures: generalised tonic-clonic, partial onset

bipolar disorder
- acute mania treatment
- maintenance

neuropathic pain

trigeminal neuralgia

89
Q

what is the MOA of carbamazepine?

A

signal transduction modulation (decrease repetitive action potential firing) and anti-kindling properties

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

90
Q

how is carbamazepine eliminated?

A

> 99% hepatic metabolism via CYP enzymes

91
Q

what is the major metabolite of carbamazepine and is it active?

A

carbamazepine-10,11-epoxide
active and has therapeutic and toxic effects

92
Q

what is unique about carbamazepines metabolism?

A

it induces its own metabolism via the epoxide-diol pathway (autoinduction)

93
Q

why is carbamazepines clearance and half life variable depending on dosing?

A

due to autoinduction

94
Q

what is the therapeutic range of carbamazepine?

A

17-51 umol/L

95
Q

what is the time of sampling of carbamazepine?

A

trough within 1 hour prior to dose

96
Q

when is carbamazepine levels taken?

A

until stabilised at target dose
- during autoinduction (every 1-2 weeks until on stable regimen)
- steady state through (after 5 weeks)

routine monitoring
- suspected non-adherence
- suspected s/sx of carbamazepine toxicity
- potential DIs or altered PK
- conversion between carbamazepine dosage forms
- to establish what concentration resulted in mood stability

97
Q

how long does autoinduction of carbamazepine last?

A

around 5 weeks

98
Q

is dosing adjustments of carbamazepine needed in renal or hepatic impairment?

A

renal: no
hepatic: yes
- not recommended in pts with decompensated liver disease

99
Q

T or F
there is an IV formulation of carbamazepine

A

False

100
Q

what is the primary mechanism of DIs in carbamazepine?

A

CYP3A4 inhibitors and inducers
CYP450 isoenzymes

101
Q

which drugs increase carbamazepine levels?

A

macrolides
anticonvulsants: valproate acid, lamotrigine
antidepressants: fluoxetine, fluvoxamine, trazodone
- MAOIs: CI within 2 weeks of use
azoles
- voriconazole: CI
isoniazid
calcium channel blockers (esp. non-DHP)
cimetidine
grapefruit juice
propoxyphene
quinine

102
Q

which drugs decrease carbamazepine levels?

A

anticonvulsants: phenytoin, phenobarbital, primidone
rifampin
theophylline
isotretinoin

103
Q

which drugs are decreased by carbamazepine?

A

doxycycline
anticoagulants
- warfarin: monitor INR
- DOACs: use not recommended
anticonvulsants: phenytoin, valproic acid, lamotrigine, topiramate
antipsychotics
- lurasidone: CI
antiretroviral – NNRTIs: CI
estrogen OR progesterone contraceptives
methadone

104
Q

what are the AEs of carbamazepine?

A

dose related
- GI: N/V, anorexia, dry mouth, constipation
- CNS: lethargy, dizziness, sedation, headache, incoordination, ataxia, blurred vision, diplopia, tremor
- CV: tachycardia, hypotension, cardiac conduction abnormalities (rare)

idiosyncratic
- SIADH/hyponatremia
- blood dyscrasias
- hepatic: increased GGT, hepatitis
- abnormal thyroid function tests: decreases free T3/T4
- diplopia, nystagmus
- menstrual disturbances
- weight gain
- photosensitivity
- rash (10% morbiliform) and hypersensitivity reactions

chronic: osteomalacia, vitD deficiency

105
Q

what level of WBC warrants d/c of carbamazepine?

A

< 2x10^9/L

106
Q

which genetic test should be done in Asian individuals before carbamazepine use and why?

A

HLA-B*1502
if positive at increased risk for SJS

107
Q

what are the CI of carbamazepine?

A

hx of hepatic disease, CVD, blood dyscrasias, bone marrow depletion
concurrent use with clozapine

108
Q

what are the monitoring parameters of carbamazepine?

A

sedation, tremor, cognitive changes
ocular exams
ECG
CBC with diff and platelets
electrolytes
LFTs
renal function
TSH, free T3/T4
BMD
rash
baseline pregnancy or allele testing if applicable

109
Q

which contraception method is preferred with carbamazepine?

A

copper IUD, condoms (non hormonal)
decreases efficacy of hormonal methods of contraception

110
Q

what is the primary mode of action of antipsychotics?

A

DA blockade

111
Q

which antipsychotics are used in BD?

A

atypicals

112
Q

which symptoms of antipsychotics are pts with BD at an increased risk of?

A

EPS

113
Q

what are some AEs of antipsychotics?

A

EPS
hyperprolactinemia, sexual dysfunction
metabolic disturbances (weight gain, dyslipidemia, DM, CVD)
anticholinergic: sedation, constipation, dry mouth, blurred vision, confusion
antihistaminergic: sedation
alpha1 blockade: hypotension, reflex tachycardia, dizziness, sedation
QT prolongation
seizures

114
Q

what are the monitoring parameters for antipsychotics?

A

BMI, vitals
A1C/FBG, lipids
ECG
liver function, renal function, electrolytes, CBC
prolactin

115
Q

what was the objective of the STEP-BD study?

A

to determine if adjunctive antidepressant therapy reduces symptoms of bipolar depression without increasing risk of mania

116
Q

what is the consensus with antidepressants in bipolar?

A

avoid AD monotherapy without an antimanic agent
use with caution in people with a hx of AD-induced mania, mixed features or rapid cycling
d/c use during acute manic episode
consider tapering off once depression symptoms eliminated for 3-4 mo.

117
Q

which antidepressants seem to be the safest in BD?

A

bupropion > sertraline, then fluoxetine and other SSRIs (NOT paroxetine)

118
Q

which antidepressants have the highest risk of switch in bipolar depression?

A

TCAs&raquo_space; SNRIs
paroxetine also not recommended

119
Q

what is the first line treatment for acute mania?

A

monotherapy:
- lithium
- quetiapine
- divalproex
- aripiprazole
- paliperidone (>6mg)
- risperidone

combination: lithium or divalproex + quetiapine, risperidone or asenapine

120
Q

when is it recommended to start acute mania treatment off as combination therapy over monotherapy?

A

a response is needed faster, history of partial acute or prophylactic response to monotherapy or in those with more severe manic episodes

121
Q

when is lithium preferred over divalproex?

A

in individuals who display classical euphoric grandiose mania, few prior episodes of illness, a mania-depression-euthymia course, and/or those with a family history of BD, especially with a family hx of lithium response

122
Q

when is divalproex recommended?

A

those with multiple prior episodes, predominant irritable or dysphoric mood and/or comorbid SUD or those with a hx of head trauma

123
Q

which medication regimens are recommended in BD with mixed features?

A

DVP or APs, especially AP + DVP

124
Q

when should an add on or switch strategy be considered in acute mania treatment?

A

if not response within 2 weeks of starting a first line agent

125
Q

what is second line treatment of acute mania?

A

2nd line monotherapy:
- olanzapine
- carbamazepine
- ziprasidone
- haloperidol

2nd line combination: olanzapine + lithium or divalproex

ECT

126
Q

which agents are NOT recommended for acute mania?

A

gabapentin
lamotrigine
omega 3 fatty acids
topiramate

127
Q

what is first line treatment of BD I depression?

A

quetiapine
lurasidone + Li/DVP
lithium
lamotrigine monotherapy or adj
lurasidone

128
Q

what is the 2nd line treatment of bipolar I depression?

A

2nd line monotherapy: divalproex

2nd line add on therapy
- adj SSRI or bupropion (added to Li/DVP or AAP)
- olanzapine-fluoxetine

ECT

129
Q

when is ECT considered in bipolar I depression?

A

refractory pts and if rapid response in needed (imminent suicide risk, catatonia, psychotic depression, medical stabilization)

130
Q

which agents are not recommended in bipolar I depression?

A

antidepressant monotherapy
aripiprazole monotherapy
ziprasidone mono/adjunctive therapy
lamotrigine with folic acid
mifepristone adj

131
Q

why is it important for maintenance treatment early in disorder?

A
  • reverse cognitive impairment
  • preserve brain plasticity
  • may lead to improved prognosis and minimisation of illness progression
132
Q

what are some risk factors for recurrence of episodes?

A

younger age at onset
psychotic features
rapid cycling
more previous episodes
comorbid anxiety
comorbid SUD

133
Q

which psychosocial treatment is 1st line in bipolar I maintenance?

A

psychoeducation

134
Q

what are the first line agents for BDI maintenance therapy?

A

lithium
quetiapine
divalproex
lamotrigine
asenapine or aripiprazole
quetiapine or aripiprazole + Li/DVP

135
Q

what is 2nd line therapy for BDI maintenance therapy?

A

2nd line monotherapy
- olanzapine
- risperidone injectable
- carbamazepine
- paliperidone injectable

2nd line add on therapy: risperidone injectable adj

136
Q

which agents are not recommended for BDI maintenance?

A

perphenazine
TCAs

137
Q

which bipolar agents should be absolutely avoided in pregnancy?

A

DVP/VPA, CBZ

138
Q

which agent has the least risk in pregnancy?

A

lamotrigine

139
Q

which bipolar agent has evidence that it reduces suicide risk?

A

lithium

140
Q
A

PHAR 358 (10 decks)

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