Mood D/O Flashcards

1
Q

MDD characterization

A

depressed mood
lack of interest in usual acitivities
marked wt loss or gain
sleep distrubances, agitation, fatigue or loss of energy
feelings of worthlessness or inappropriate guilt
difficulty concentrating or making decisions
thoughts of death or suicide

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2
Q

MDD epidemiology

A
  • after age of 13 the rate doubles for girls
  • age of onset is early adulthood; late 20s with average age 27 y/o
  • onset after 50 y/o frequently associated with brain lesions or strokes
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3
Q

MDD risk fx

A

female gender; personality traits of hypersensitivity to negative stimuli; prior episodes of anxiety or depression; fx hx; hx of SI and attempts; post-partum period; co-morbid medical px; substance abuse; lack of social support; widowed or divorced; lower socioeconomic and education; stressful life events

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4
Q

MDD etiology

A

genetic influence accounts for 37%; multiple genes operate in conjunction with environmental fx;

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5
Q

MDD theories

A
  1. kindling model: events or expereinces have long lasting effects on brain chemistry, structure, and fx; so it may begin with a life stressor but subsequent episodes don’t necessarily have to be precipitated by stressor
  2. dysregulation of neurotransmitters model: impairment of ability of neurons involved in emtion and cognitive circuitry to tolerate abnormal levels of certain neurotransmitters; decreased levels of SE associated with sx of depression and behavior; decreased NE associated with fatigue, apathy, cognitive disturbances, slowness in info processing and poor memory; DA may be involved in psychomotor retardation and lack of pleasure; neuropeptides are also thought to be involved
  3. psychosocial theories: having negative view of oneself, their life situations and future; one’s automatic assumptions determine feelings/associated with depression and negative self view elicits negative response from others;
    - interpersonal theory: depression is viewed as result of distrubance in interpersonal relationships that impairs ability to cope with difficult situations and leads to depression
    - learned helplessness theory proposes that individuals learn in inescapable, painful, and auncontrollable situaitons that they can not escape the stressor with any action of their own and they generalize this learning to other situations
  4. attachment theory: failure of mother to sooth and provide security; results in lack of cortisol modulation in infnats brain development; this in turn could result in hypersensitivity of circuitry involved in emotions and cognition
    - development theory: belief that early adverse expereinces lay foundation for lateral mental d/o like depression; buffereing provided by responsive cregivers may decreases reisk
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6
Q

biological theory of MDD

A
  • abnormalities in brain dvelopment; enlargement of ventricles and sulcal prominence and decreased volumes of PFC, amygdala, hippocampus; fewer neurons in PFC triggers depression and mania and amy act as a brake for emotional responses; decreased density of glial cells in areas support hypothesis of dysfx of specific neurotransmitter systems NE, SE, glutamate, GABA
  • those w/out depression have increased blood flow to frontal cortex, left amygdala, and decreased flow to right amygdala when sad mood occurs
  • those w/ depression have reduced blood flow to frontal cortx in basal ganglia indicating less brain activity in area; have increased blood flow in amygdala, orbital cortex and thalamus
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7
Q

brain chemistry in MDD

A
  • believed that cascades of NE, SE, dopamine, glutamate, GABA, acetylcholine, and cortisol play role in regulation of stress and depression
  • SE modulates dopamine in limbic areas and plays role in maintaining synapses; low levels of SE associated w/ aggression, impassivity, and suicide
  • stress depletes NE, SE, ACETYL, and increased cortisol; acute stress, chronic stress, anticpated stress or imagines losses may precipatiate incrased cotisol activity and may produce abnormal chemistry
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8
Q

SAD description

A
  • sx appear in fall or winter and improve in spring
  • onset and remission of episode must have occured during last 2 years w/out any non-seasonal episodes occuring during this period
  • onset in early 20s
  • rate is higher among women of childbearing age
  • sx include overeating, carbohydrate cravings, wt gain, lethrgy, oversleeping, feelings of sadness, anxiety, irritability
  • physical sx often appear first
  • genetic finluence believed to be related to three areas of alteration (dysregulation in SE, circadian rhythms, and abnormal processing of environmental light by eyes)
  • light serves as a time cue to help establish and reset underlying biological rhythms including circadian rhythm of various hormones sleep/wave and rest/activity rhythms
  • comorbidities include anxiety d/o, personality d/o
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9
Q

MDD catatonic fx

A
  • immobility
  • mutism
  • echolalia (repeating words or phrases of someone else)
  • posturing
  • negativism (resistance to passive movement or repeatedly turning away from examiner)
  • mannerisms (repeated movements that have no purpose)
  • stereotypies (repeated movements of behaviors that are not goal directed)
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10
Q

MDD melancholic fx

A
  • loss of pleasure in all or almost all activities
  • lack of reactivity to a pleasurable event
  • diurnal variation (depression is worse in morning)
  • early morning awakening
  • slowed motor acitivty or agitation
  • loss of appetite and wt loss
  • expression of inappropriate guilt
  • melancholic depression is more likely to occur w/ severe MDD epidosdes and w/ + sx
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11
Q

MDD atypical fx

A
  • mood reactivity (mood improves when something good or pleasure occurs)
  • an unusually excessive need to sleep
  • feeling that arms or legs are heavy
  • overeating b/c of carbohydrate ans sweets cravings
  • inability to anticipate pleasure, but no loss of actual ability to experience pleasure once involved in an activity
  • anxiety
  • rejection sensitivity
  • changes of relationships d/t percieved rejection
  • fluctutating course in response to events -impairment of fx (missed work, school, social)
  • atypical depression is often co-morbid with bipolar d/o, substance abuse, axis II personality d/o like avoidant, histrionic, and BPD; pt w/ early onset before 20 tend to have lower levels of cortisol, more chronic course and poor response to TCAs; late onset after 20 tend to be more similar to those with depressive d/o w/ melancholic fx, elevated cortisol, and less chronic depression
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12
Q

MDD postpartum onset

A
  • onset occurs in first 3 months after delivery
  • risks: low levels of social suppor; conflicted marriages; being ambivalent about pregnancy; insecure attachment patterns; feel baby blues first 10 days after delivery; prior episodes of postpartum; prior hx of mood d/o; fx history; hx of drug/alcohol use; childhood separation or abuse from parents; single parenting
  • w/o + sx: depression, lack of interest in baby; thoughts to hurt baby; anxiety; agitation; sleep px; thoughts of death or suicide
  • w/ + sx: severe ruminations, delusional thoughts about infnat that are associated with increased risk of infnaticide or paranoia, grandiose or bizarre delusions and disorganized behaviors present a risk to mother and child
  • can be cause by bipolar d/o in depression stage
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13
Q

medical conditions associated with MDD

A
  • nutritional deficits; lack of exercise
  • infections
  • cancers
  • lupus, RA, MS
  • diabetes, lung disease
  • fibroyalgia, PD
  • chronic pain
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14
Q

Lab tests for MDD

A

CBC, liver and renal fx; TSH, rapid plasma regain (syphilis); VA, urine toxicology; alcohol level; pregnancy test; HIV serology

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15
Q

recovery definition

A

-an extended period of time where minimal or no sx are present for atleast 2months

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16
Q

recurrence definition

A

-appearance of a new episode of MDD during recovery

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17
Q

relapse definition

A

-return to a fully symptomatic state during remission

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18
Q

psychotherapy in MDD

A
  • CBT and IPT found to be effective as medicaitons in treating MDD w/ exception of severe MDD
  • chronic may respond better to combo (reserved for chronic because mild does not have increased response)
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19
Q

Pharmacology and MDD

A
  • Venlafaxine and mirtazepine are recommended for severe
  • ECT has been effective in severe and those with + sx
  • those with + sx have good response rate with antidepressant and antipsychotic
  • MDD w/ catatonic: may use ECT, lithium in combo with antidepressant; acute tx inclucdes BZD; if + sx may use atypical
  • melancholic: mirtazepine, reboxetine; ECT, TCAs MAOIs have been more effective than SSRI’s
  • postpartum: lithium, SSRIs
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20
Q

Switching atidepressants

A
  • SSRI to another SSRI: first med tapered off over 1-2 weeks
  • TCA to SSRI no wash out required but first med sould be tapered at time of intitation of second
  • switching to MAOI requires wash out time
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21
Q

how long should antidepressant/pharmacotherapy continue for MDD tx?

A
  • combined tx should continue for at least 6 months before tapering off one of the drugs
  • to prevent relapse medications should continue for 2 years after remission of MDD sx
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22
Q

clinical presentation in children with MDD

A

Until the age of three, signs of depression include: feeding problems, tantrums, and lack of playfulness.
From 3-5 years of age, children may be accident prone, have many fears, blame themselves for things, and be apologetic for small mistakes.
From 6-8 years, they may show vague physical symptoms, aggressive behavior, or cling to their parents.
At 9-12 years, they may worry about school work and blame themselves for disappointing their parents.
Symptoms include: sadness, anhedonia (lack of pleasure in usual activities), lack of energy, irritability, anger, hostility, poor school performance, low self-esteem, fear of death, feelings of worthlessness, and somatic complaints.
In comparison to children who are not depressed, children with depression have more school related problems with behavior, attitude, and academic achievement, lower levels of social skills, and more problems with family and peer relationships.
Children tend to have fewer melancholic symptoms, delusions and suicide attempts than adults.

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23
Q

clinical presentation in adolescents with MDD

A

Symptoms include: depressed mood, self-deprecatory ideation, anger, restlessness, grouchiness, aggression, sulkiness, reluctance to participate in family activities, and hypersensitivity to criticism rather than sadness, anxiety, and guilt.
They may be uncommunicative and annoying to others.
They may show poor academic achievement, drop out of school, have problems with relationships with others, and exhibit delinquent behavior.
Individuals who experience clinical depression during adolescence are at increased risk for other psychiatric disorders, impairments of functioning in adulthood, and suicide.

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24
Q

comorbid illnesses in adolescents and children with MDD

A

MDD and dysthmia in children are frequently accompanied by other psychiatric disorders: anxiety disorders, disruptive behaviors, ADHD.
Anxiety disorders are nine times more frequent in depressed children than in those without depression.
Conduct disorder and oppositional defiant disorder are six times more frequent and attention deficit hyperactivity disorder is five times more frequent.
High rates of comorbid medical conditions: diabetes mellitus, asthma and epilepsy.
Substance abuse is comorbid in 25% to 48% of adolescent and tends to follow the onset of depression.
Suicide ideation, suicide attempts, and suicide are comorbid conditions among depressed children and adolescents.

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25
Q

Treatment of older adults with MDD

A

Laboratory tests include complete blood count with differential, chemistries, electrolytes, urinalysis, BUN, creatinine clearance, renal and liver panels, thyroid function test (T3, T4), vitamin B12, thiamine and folate, syphilis screening, drug levels when indicated, ECG, and toxicology screen.

  • SSRIs cause less orthostatid hypotension; fewer anticholinergic effects; are associated with increased risk of px with balance and falls
  • citaolpram and sertraline are well tolerated and seem to produce fewer drug to drug interactions
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26
Q

dysthymic d/o main characteristics

A

Dysthymic disorder is a chronic unipolar depressive disorder with depressive symptoms present most of the day, for two years.
Symptoms include: poor appetite or overeating, insomnia or hypersomnia, fatigue, lack of energy, low self-esteem, difficulty concentrating and making decisions, and feelings of hopelessness.
It is characterized by a relatively mild level of symptoms, a chronic course, and disability.
essential features of dysthymic disorder are: gloom, brooding, lack of joy in life, and preoccupation with their own inadequacy; patients may be chronically complaining, demanding, brooding, sarcastic, introverted, morose and self-deprecating.
A major depressive episode may occur after the onset of dysthymia and that occurrence is called double depression
Patients with dysthymic disorder have been found to have a greater severity of depressive symptoms, more suicide attempts, and more hospitalization than patients with MDD.

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27
Q

dysthymic d/o in older adults

A

-often chronic with increased risk for cardiovascular and cerebrovascular morbidity, mortality, and suicide.
Clinicians often take a “pseudoempathic approach” in which they consider the depression to be a normal reaction to aging or illnesses associated with aging. As a result, older adults with dysthymic disorder often do not receive treatment.

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28
Q

dysthymic d/o in children and adolescents

A
Irritability 
Pessimism
Depression
Low self-esteem 
Poor social skills
Impairment of school performance and social interactions
Changes in appetite
Sleep problems
Fatigue
Problems with making decisions
Feelings of hopelessness  
More than two-thirds of children with dysthymic disorder develop MDD.
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29
Q

treatment in dysthymic d/o

A

IPT and CBT have been found to be effective in the treatment
SSRI’s, bupropion (Wellbutrin)
Sertaline (Zolft) was found to be more effective than interpersonal psychotherapy for adults with dysthymic disorder and sertraline (Zoloft) has been found to be effective in treating dysthymic disorder among adolescents
good response to mirtazapine (Remeron) and bupropion SR.
For double depression, dysthymia and coexisting major depression, sertraline (Zolft) has been found to be effective.
-older adults: nothing proven efficient at this time

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30
Q

characteristics of bipolar I

A

-occurrence of one or more manic episodes or a mixed episode or episodes w/ or w/ out depressive episode

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31
Q

characteristics of bipolar 2

A
  • at least one hypomanic episode
  • occurrence of MDD episode or episodes
  • absence of hx of a manic episode and significant distress or impairment of social, vocational, or important areas of fx
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32
Q

characteristic of cyclothymic d/o

A
  • recurrent hypomanic episodes without full MDD
  • fluctuating mood disturbances w/ presence of numerous periods of hypomanic sx and numerous periods of depressive sx
  • hypomanic sx must be present for at least two years for adults and 1 year for children
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33
Q

bipolar nos characteristics

A

-used to describe rapid alterations of mood that do not meet duration criteria for manic, hypomanic, or MDD or hypomanic episodes without depressive episodes

34
Q

epidemiology of bipolar d/o

A
  • chronic recurrent
  • depressive or mixed sx most common
  • high rates of morbidity and disability
  • high risk for SI
  • age of onset 15-19
  • one-third developed d/o in childhood
  • earlier onset, greater severity; more frequent occurrence among those with relatives
  • earlier onset is associated with fx hx
35
Q

Late onset bipolar d/o

A
  • occuring after age 50
  • common in females
  • more depressive sx
  • late onset mania is d/t medical d/o like trauma, tumors, MS, strokes hyperthyroidism, AIDS, lupus
  • can be caused by stimulants like cocaine; alcohol; psych meds; steriods
36
Q

gender and bipolar d/o

A

-men are more likely to be manic and women likely to have depressive sx
-women who have d/o are increased risk for postpartum mood episodes
-rapid cycling often more in women
women likely to experience manic switches when receiving treatment with antidepressant meds and are more likely to have comorbid med and psych d/o

37
Q

etiology of bipolar d/o

A

-genetic vulnerabilities; abnormal brain development; stressful life events; mutant genes; genetic influences mold develop0ment of temperament or early personality; personality modulates individuals selection of life experiences and environments that have potential for encountering stressors (aka genes influence decisions we make that put us in harms way as well as predisposition of d/o)

38
Q

theories of bipolar d/o

A

1kindling theory; stress theory; stressful life events theory; goal dysregulation theory; dysruption of social rhythms theory; family expressed emotions theory
2 biological basis: structure changes in ventricles, PFC, subgenual cingulate, medial temporal lobe, cerebellum (involved in mood regulation neuronal circuits)
-gray matter decreased density
-subgenual PFC (defects with this demonstrate abnormal autonomic responses to emotional experiences; decreased ability to experience emotions r/t concepts that usually evoke emotion; and have inability to adjust their social behavior based on likelihood that their behavior will result in punishment or reward; may underly pathological guilt and mania)
-deficits in glial cells cause lack of modulation of glutamate and result in overexcitement of cells and cause cell death; decreased density of neurons and glial cells in PFC of pts with bipolar d/o

39
Q

what do glial cells and gray matter do

A
  • neurons in gray matter of brain carry and recieve messages
  • glial cells in white matter supply brain with oxygen and glucose; supply neurons with neurotoropins or nerve growth factor and brain derived neurotropic factors; this helps in neuronal survival and formation of synapsis and process of neurotransmission
  • glial cells modulate excitatory neurotransmitter glutamate
40
Q

white matter hyperintensities and bipolar d/o

A

white matter hyperintensities are small white areas in brain that are made up of glial cells and they occur in patients with d/o than in normal controls;

  • it impairs cortical fx, damage brain tissue, indicate disruptions in connections of brain areas
  • the cause of WMH is unknown but it is associated with poorer clinical outcomes; one explanation is glial vulnerability to oxidative stress
  • also found in those with HTN, CVD
41
Q

Parts of the brain that have altered fx of DA are responsible for sx in bipolar d/o. What areas and other alterations of nuerotransmitters are involved?

A
  • reduced DA in reward pathways during acute mania (seeking goals to increase pleasure results)
  • GABA decreased and level of N-acetyl aspartic acid (needed for healthy neurons) is decreased
  • neuropeptides serve as intracellular second messangers that carry messages within cell are abnormal; and those that fx as a neurotrasmitteers and influence other transmitters and neurohomones are abnormal in bipolar; (endorphins, somatostatin, vasopressin, oxyto0cin, substance P, cholecystokinin, neurotensin, and calcitonin are neuropeptides being studied)
  • decrease in thyroid and adrenal glands; (hypothyroid =depressive sx); (hyperthyroid = increased energy and euphoria); endocrine system: HPA
42
Q

hypothyroid and mood d/o

A

hypothalamus secretes TRH->stimulates pituitary to secrete TSH->stimulates thyroid to release thyroid hormones
-mod to severe mood sx in bipolar and depression have been found to have reduced TSH response to TRH; many comorbid with hypothyroidism

43
Q

hypothalamus and mood d/o

A

hypothalamus secretes CRF (corticotrophin releasing factor)->stimulates pituitary gland to release adrenocorticotropin (ACTH)->stimulates adrenal gland to release cortisol
-pts with depression and bipolar have been found to have abnormalities of this circuit

44
Q

prodromal phase of bipolar disorder

A

-changes don’t meet criteria
-usually experience unusual thoughts before manic phase and cognitive disorganization before depression
sx include: reduced sleep; increased activity and talkativeness; euphoria, irritability; sensitivity; racing thoughts; spending mondey; promiscuous sexual behavior
OR
decline in energy and interest in ppl or activities; increased need for sleep and rumination about fears and worry

45
Q

which phase usually presents first in bipolar disorder

A

usually pts have depressive episode first. with time, overall the pts with bipolar d/o will have more and longer episodes of depression than of mania;

46
Q

how does the depressive phase of bipolar d/o differ from MDD

A
  • in bipolar d/o in those with depression they are going to have a higher rate of melancholic type depression; earlier onset of mood sx; more psychotic sx;
  • bipolar d/o is less likely to be associated with anxiety, tearfulness, and initial insomnia
  • worthlessness, anhedonia, restlessness, leaden paralysis and hypersomnia are more likely to be present in bipolar d/o
47
Q

mood changes in bipolar d/o

A

may be elated, euphoric, angry or iritable, hostile or aggressive
may be easily excited, may be tearfulness and alternating humor

48
Q

cognition changes in bipolar d/o

A

could have grandiose, expansive ideas or racing thoughts, flight of ideas; lack of insite; delusions that fit the mood; it may be evidenced in distractibility, inability to concentrate and executive dysfunction

49
Q

speech changes in bipolar d/o

A

it may be increased in output or pressured; pt may describe a sense of connected to the world
manic phase: will be very rapid, circumstatial speech; express inflated view of abilities, wealth, status

50
Q

somatic sx in bipolar d/o

A

decreased need for sleep, decreased appetite; excessive energy; significant wt loss; psychomotor agitation;

51
Q

behavior changes in bipolar d/o

A

may have increased goal-directed activity (social goals, work goals, sexual activities: they want to feel pleasure/reward)
may be excessive involvement in seeking pleasure in risky behaviors

52
Q

mixed episode criteria for bipolar d/o

A
  • mixed is severe form of bipolar I d/o characterized sx that meet criteria for both manic and depressive and occur nearly every day for atleast 1 week
  • could have rapid cycling
  • depressive sx tend to be early in day and manic sx in late day
53
Q

hypomania sx

A
  • it is a marked difference than mania; does not have + sx and it does not require hospitalization; usually they carry on their normal acitivities and it does not affect work and fx impairment
  • usually carefree, unrealistic thinking, lively, happy/euphoric, joking attitude, witty, unaware or uncaring of others feelings; if you criticize their plans they will become very angry and irritable
54
Q

what comorbid personality d/o are associated with bipolar d/o

A

narcissitic, borderline, antisocial, obessive compulsive; this increases risk for suicide, impedes response to tx, and is associated with lower rates of recovery

55
Q

Tx of bipolar d/o

A
  • prodromal phase is treated with lithium or lamotrigine
  • lithium appears more effective for delaying hypomanic or mixed sx and mania or mixed
  • lamotrigine appears more effective in delaying depressive phase
  • valproate and quetiapine may improve prodromal sx
56
Q

lithium and bipolar

A
  • is a natural occuring alkali metal
  • effective for tx acute episodes of mania and hypomania; may prevent recurrances of mania and depression and decrease suicidality
  • as effective as valproate, carbgamazepine, risperdal, olanzapine
  • it is slower acting than many atypicals; takes 7-14 days for onset of action; may be less effective than atypical antipsychotics for pts with psychotic mania
  • currently it is the most effective medication in reducing suicidal behaviors
57
Q

carbamazepine and bipolar d/o

A

-effective in acute mania with onset of antimanic effect in 7-10 days; not clear that it is effective for depressive phase; used as an augmenting agent with lithium and other anticonvulsants or atypicals

58
Q

oxcarbazepine and bipolar d/o

A

similar to carbamazepine but does not induce blood dyscrasias and it does not induce CYP450 enzyme system
more likely to cause hyponatrermia than carbamazapine
lakcs sufficient evidence for use as monotherapy

59
Q

depakote and bipolar d/o

A

apporved for tx in acute mania
effeective in acute tx of manic episodes or mixed as lithium, haloperidol, and olanzapine
more effective than lithium for pts with mixed mania, irritability and hostility, or more episodes, comorbid alcoholo dependence and mania with depression
found to be effective in those who don’t respond to lithium
good with rapid cycling
found to be as effective as antipsychs for pts with psychosis
-has been found to cause PCO and has black box warning for hepatotoxicity, pancreatitis, and teratogenicity

60
Q

gabapentin and bipolar d/o

A

no reported effectiveness as monotherapy for rapid cycling or mania
frequently added to lithium or depakote for breakthrough sx; it is effective in preventing migraine HA that frequently occur with bipolar d/op

61
Q

lamotrigine and bipolar d/o

A

has both mood stabilizing and antidepressant properties; effective for rapid cycling; no demonstrated efficacy for acute mania; effective for acute or prophylactic tx of depressive episodes in both I and II d/o; approved for maintenance tx in bipolar d/o

62
Q

topiramate and bipolar d/o

A

not effective for acute mania; useful w/ comorbid wt gain, binge eating, and migraine HA; when added to lithium or depakote it is associated with a decrease of depressive sx

63
Q

antipsychotics and bipolar d/o

A
  • chlorpromazine and haldol good for agitation or psychosis during manic episodes; used less often b/c of EPS
  • olanzapine, risperdone, quetiapine, ziprasidone, aripiprazole approved by FDA for monotherapy in bipolar d/o;
  • asenapine recently approved
  • closapine used last resort
64
Q

approved combination therapies for bipolar d/o

A
  • risperidone and depakote or lithium
  • quetiapine and lithium or depakote
  • aripiprazole and lithium or depakote
65
Q

what does the american psychiatric association practice guidelines (APA) suggest for first line in depressive episode of bipolar d/o

A

-lithium or lamotrigine

66
Q

approved medications for treating depressive episode in bipolar d/o

A

olanzapine and fluoxetine and quetiapine

67
Q

antidepressants and bipolar d/o

A
  • all antidepressants have potential to induce manic or hypomanic episodes
  • increased risk for this is associated with previous antidepressant induced mania, family hx of bipolar d/o and exposure to multiple antidepressant trials
68
Q

continuation phase

A
  • usually two to 6 months

- it is time between acute phase and the achievment of response or remission and recovery

69
Q

maintenance phase

A

starts with recovery phase

70
Q

medications approved for monotherapy in bipolar d/o

A

lithium, lamotrigine, olanzapine, aripiprazole

71
Q

how long recommended to stay on meds after manic phase

A

at least one year

72
Q

what is recommended for relapse prevention in bipolar d/o

A

fluoxetine-olanzapine combination
aripiprazole
lithium and lamotrigine approved for prevention

73
Q

what meds are recommended for preventing remission for mania or mixed?

A

carbamazepine, valproic acid, lamotrigine

74
Q

Older adults with bipolar d/o

A

usually they are misdx as having schizophrenia; usually occurs in mid 70s; usually have mixed sx; likely to have more cognitive impairment than younger person;
-depressive sx may be associated with pseudodementia (can differentiate by duration; usually depression ℅ recent and longterm memory loss not just recent)
r/o medical (medical dx likely: hyperthyroid, epilepsy, stroke, head injury, uremia, vitamin B12 deficiency)
-sx: confusio0n, disorientation, irritability, distractibility
-onset of mania is most likely to be associated not with fam hx but with medical illness like CVD, trauma, MS, thyroid

75
Q

medications recommended for bipolar in older adults

A

mood stabilizers first line
valproate and lamotrigine may be effective and have fewer troublesome SE; lithium causes polydipsia, nocturia and falls
lamotrigine tolerated and delays recurrence of bipolar depression (SE is steven johnson syndrome)

76
Q

bipolar d/o in children and adolescents

A
  • dx begins before 18 is 2/3 pts
  • children and adolescents with dx have high rate of mixed, rapid cycling, and co-occurring ADHD as compared with adults
  • high familial risks
  • high risk to get if abusing drugs and alcohol; high family stress; stressful life events
  • dysfx of fronto-limbic-circuitry may be involved in exagerated emotional responses and diff regulating
77
Q

clinical presentation of children 6 -7 y/o with bipolar d/o

A

increased energy; bold or demanding behavior; cognitive px; anxious, fearful or worried mood; shyness ot imid; quick temper

78
Q

clinical presentation of children 7-12 y/oand older with bipolar d/o

A

irritable mood; quick temper; oversensitive; decreased energy and labile mood; mood distrubances; sleep px; hyperactive or giddy or agitated; panic attacks; hostile or aggressive or impulsive

79
Q

adolescent presentation with bipolar d/o

A

same as other age groups and may have silliness and oppositional behaivor;

80
Q

treatment of bipolar d/o in children and adolescents

A

lithium, monotx with risperdal, and aripiprazole; valproate
ages 10-17
-avoid beta blockers that can cause depression; caffeien, TCA’s, steroids, sudafed, ginkgo biloba and st john’s can cause increase in norepinephrine and arousal;

81
Q

antidepressants in children with bipolar d/o

A

children with unrecognized bipolar disorder who receive antidepressant medications are at risk for developing suicidal, homicidal, or psychotic behaviors

82
Q

rapid cycling in children and adolescents

A

rapid cycling: four or more episodes in 12 months
ultrarapid cycling: mood changes within a few days or weeks
ultradian cycling: four cycles per day
increased risk in pre-pubertal onset