Ancc Pmhnp Cert Review Ch 7

Front 1

Most common of all psychiatric illnesses and can manifest initially as physical health states

Back 1

Mood disorders

Front 2

It has become increasingly common for mood disorders to be treated where & why?

Back 2

In primary care setting
because often pt 1st present to primary care because of the high degree of somatic symptomatology that accompanies mood disorders

Front 3

Are mood disorders well tx in primary care?

Back 3

No, many studies have indicated that mood disorders are not well identified or treated in primary care settings if a psychiatric care provider is not involved

Front 4

How common or normal is depression?

Back 4

Depression is a very common, very normal human emotion.

PMHNP caring for pt who present for eval of depression must distinguish between normal level s of depression and pathological levels that are symptomatic of an underlying brain-based illness

Front 5

Pathological levels of depression require _______ and generally will not _______without __________

Back 5

Pathological levels of depression require TREATMENT and generally will not RESOLVE without THERAPEUTIC INTERVENTION

Front 6

Depression is one of the most common human emotions

Back 6

it consists on a continuum ranging from the absence of depression at one end to pathological levels that produce significant sx of psych disorder at the other

Front 7

Do cultural differences affect depression?

Back 7

Yes cultural differences affect the behavioral manifestations of depression

Front 8

Depression can be a normal healthy reaction to life stressors that

Back 8

that motivates the person to deal with events and emotions

Front 9

Depression can be pathological if:

Back 9

~it is disproportionate to events & sustained over a sig time period
~it sig impairs normal social fxning (occupational, social, school, relational fxning)
~it sig impairs normal somatic fxning (loss of appetite, altered sleep, altered self-care activities, altered sexual fxning)
~it is apparently unrelated to any identifiable event or situation in an individual's life

Front 10

The primary unipolar affective disorder

Back 10

Major depressive disorder

Front 11

MDD description

Back 11

~one of the most common psych d/o
~a complex brain-based illness w/ a primary characteristic of a PERSISTENT DISTURBANCE in mood
~Represents an excessive or distorted degree of sadness and manifests with BEHAVIORAL, AFFECTIVE, COGNITIVE AND SOMATIC SX.
~may have known precipitating even, situation or concern but often occurs w/o any precipitating stressor identified
~significantly interferes with daily fxning and goal attainment
~has a COMPLEX GENETIC, BIOCHEMICAL & ENVIRONMENTAL ETIOLOGICAL factors

Front 12

MDD etiology

Back 12

~multiple theories of the etiology
~theories are categorized as psychodynamic and biological

Psychodynamic theories
*object loss theory (fairbairn, winnicott, guntrip)
*aggression-turned inward theory(freud)
*Cognitive theory (beck)
*learned helplessness-hopelessness theory (seligman)

Biological Theories
*Genetic predisposition
*endocrine dysfxn
*abnormalities of NT fxn
*structural brain changes
*chronobiological theory

Front 13

Desynchronization of the circadian rhythms produce the sx constellation collectively called MDD is what theory of etiology?

Back 13

Chronobiological theory

Circadian rhythms control biological processes that are frequent problems in depressed ppl:
*interrupted sleep-rest cycle
*REM abnormalities
*frequent walking
*more intensified dreaming
*diurnal variations to circadian-related behaviors
*decreased arousal and energy levels
*decreased activity patterns
*increased cortisol secretion
*increased emotional reactivity

Front 14

Circadian rhythms control what biological processes that are frequently problems in depressed pts?

Back 14

*interrupted sleep-rest cycle
*REM abnormalities
*frequent walking
*more intensified dreaming
*diurnal variations to circadian-related behaviors
*decreased arousal and energy levels
*decreased activity patterns
*increased cortisol secretion
*increased emotional reactivity

Front 15

What consistent abnormalities has neuroimaging demonstrated in certain structures of the brain in individuals w/ chronic and severe depression?

Back 15

~Hypovolemic hippocampus
~hypovolemic PFC-limbic striatal regions

Supports biological theory of etiology of structural brain changes

MDD is a common comorbidity in ppl who have experienced brain damage, including damage from stroke and trauma

Front 16

Psychodynamic theories of depression's etiology

Back 16

*object loss theory (fairbairn, winnicott, guntrip)
*aggression-turned inward theory(freud)
*Cognitive theory (beck)
*learned helplessness-hopelessness theory (seligman)

Front 17

Biological Theories of depression's etiology

Back 17

*Genetic predisposition
*endocrine dysfxn
*abnormalities of NT fxn
*structural brain changes
*chronobiological theory

Front 18

Structural brain changes biological theory of depression

Back 18

neuroimaging has demonstrated consistent abnormalities in certain structures of the brain in individuals w/ chronic or severe depression

Hypovolemic hippocampus
Hypovolemic PFC-limbic striatal regions

MDD is a common comorbidity in individuals who have experienced brain damage including damage from stroke and trauma

Front 19

Abnormalities of NT fxn biological theory of etiology of depression

Back 19

All the following are possible NT fxn abnormalities causing depression

~deregulation of 1 or more biogenic amine NTs (DA, 5HT, NE)

~Low levels of endogenous catecholamines in specific areas of the brain

~low levels of 5HT precursor tryptophan

~Low levels of 5HT metabolite 5HTIAA

~receptor sensitivity of NT set unusually high in specific area of the brain

~Low density of receptro sites in specific areas of the brain

~hypometabolism in specific areas of the brain regulating mood, appetite and cognition

~Complexity of brain fxns imply that the etiology of complex disorders like MDD involves the relative balance of available NT and NOT JUST A LOW LEVEL OF ONE NT

Front 20

In postmortem studies on individuals who commit suicide and in ppl w/ MDD showed

Back 20

Low 5HT levels

Front 21

Deregulation of one or more biogenic amind NTs

Back 21

(specifically DA, 5HT, NE)

Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn

Front 22

Low levels of endogenous catecholamines in specific areas of the brain

Back 22

Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn

Book says 5HT levels shown to be low in dead ppl who killed themselves and had MDD. Unknown this is a postmortum change, if the violent nature of suicide caused or if there is a causal relationship

Front 23

Low levels of precursor tryptophan

Back 23

this is the precursor for 5HT

Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn

Front 24

Low levels of 5HT metabolite 5HTIAA

Back 24

Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn

Front 25

Receptor sensitivity for NTs set unusually hign in specific areas of the brain

Back 25

therefore a stronger NT receptor cascade is required to induce neuronal activity

Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn

Front 26

Low density of receptor sites in specific areas of the brain

Back 26

Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn

Front 27

Hypometabolis in specific areas of the brain regulating mood, appetite and cognition

Back 27

Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn

Front 28

MDD NOT JUST DUE TO LOW LEVEL OF 1 NT

Back 28

complexity of brain fxn impy that the etiology of complex d/o like MDD involves the realative balance of available NT and not just due to low level of one neurotransmitter

Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn

Front 29

Dexamethasone suppression test

Back 29

DST a screening test for depression which has proved to be too nonspecific and is not commonly used in clinical practice

HPA dysregulation is the rational and scientific basis for the dexamethasone suppression test (DST)

Front 30

HPA controls?

Back 30

the physiological response to stress

Front 31

HPA is composed of.....?

Back 31

interconnective feedback pathwasys between the hypothalamus, pituituary gland, and the adrenal glands

Front 32

Desregulation of hypotahalamic-pituitary-adrenal axis

Back 32

is another theory of endocrine basis of MDD (biological theory of etiology)

hyperactivity of the HPA acis has been demonstrated to be present in ppl w/ MDD & who have possible elevated cortisol levels

~elevated corisol levels over time damage the CNS by altering neurotransmission 7 electrical signal conduction

~evidence supports that cortisol over time can cause changes in size & fxn of brain tissue

Front 33

HPA cascade of rxns....

Back 33

~ HPA fxns in response to stress

~hypotahalamus releases CRH

~CRH stimulates the anterior pituitary

~anterior pituitary releases ACTH

~ACTH stimulates the adrenals

~adrenals release cortisol

Front 34

Effects of cortisol on the brain

Back 34

Elevated cortisol levels over time damage the CNS by altering neurotransmission and electrical signal conduction

~evidence supports that cortisol over time can cause changes in size and fxn of brain tissue

Front 35

High incidence of postpartum mood disturbances suggests

Back 35

endocrine dysfxn as part of the etiologic picture of MDD

Endocrine dysfxn theory of MDD etiology

Front 36

Neurovegetative sx commonly seen in MDD

Back 36

*sleep disturbances
*appetite disturbances
*libido disturbances
*lethargy
*anhedonia

are r/t fxn of the hypothalamus and pituitary and the hormones they secrete

Endocrine dysfxn theory of MDD etiology

Front 37

Genetic predisposition for MDD

Back 37

~there is a CLEAR GENETIC PREDISPOSITION to depressive d/o; one assumption is a polygenic single nucleotide polymorphism (SNP) d/o

~Having a depressed parent is the single strongest predictor of depression

~Childeren of depressed parents are 3x more likely to experience MDD in their lifetime than the general population and have a 40% chance of having a depressive episode before age 18

~the earlier the age of onset of MDD & more severe the sx the more likely it is that a person has a strong genetic load for depression

Genetic predisposition theory of etiology of MDD

Front 38

the earlier the age of onset of MDD & the more severe the sx the more likely it is that __________

Back 38

a person has a strong genetic load for depression

Front 39

The single strongest predictor of depression

Back 39

having a depressed parent

clear genetic predisposition

Front 40

*sleep disturbances
*appetite disturbances
*libido disturbances
*lethargy
*anhedonia

Back 40

are neurovegetative sx commonly seen in MDD that are r/t fxn of the hypothalamus and pituitary and the hormones they secrete

Endocrine dysfxn theory of MDD etiology

Front 41

Object loss theory

etiology of MDD

Back 41

Fairbairn, winnicott, guntrip

~early psych dev issues lay the foundation for depressive responses in later life

~1st stage of dev (able to form relationships) is normal

~2nd stage of dev kid experiences traumatic separation from significant objects of attachment (usually maternal object)

~Loss from (death, illness, emotion unavail) is unexpected and overwhelming

~responsed to loss dominated by separation anxiety, greif, mourning & dispair

~this critical object loss event predisposed the child to respond in similar ways to future losses or sig separation

Front 42

Aggression-Turned-Inward Theory

etiology of MDD

Back 42

Freud
~early psych dev issues lay the foundation for depressive responses in later life

~1st sage of dev (able to form relationships) normal

~2nd stage of dev kid experiences loss OF SIG MOTHERING INDIVIDUAL

~loss can be real or imagined; loss is unexpected and overwhellming

~loss may be r/t mom death, illness, emotional unavail, birth of new sibling, kid's perception of losing undivided attn from mom

~kid's initial rxn = anger

~kid feels unsafe to express anger at mom openly and directly

~kid uses defense mech to deal w/ conflict (desire for love object but co-occuring anger for the love object)

~instead of anger being expressed outward at maternal fig it turns inward bc it's more acceptable & safer to be angry @ self than @ the mom

~anger rationalized as kid assumes that loss of mom was r/t something bad that they did not that caregiver's actions

~Excessive guilt becomes a manifestation of the process of dealing w/ aggression experienced with the loss of mom's attn

~a similar emotional rxn (low self-esteem excessive guilt, inability to cope w/ anger, self-destructive impulses) occurs as an adult when ever a loss is experienced

Front 43

kid experiences loss of mom

and rxn is mourning, despair, grief, separation anxiety

Back 43

Object loss theory

The critical loss event predisposes the kid to respond in similar ways to future losses or significant separation

theory of etiology of MDD

Front 44

Kid experiences loss of mom

and rxn is anger

Back 44

aggression-turned inward theory

anger at mom gets turned inward and is rationalized bc kid thinks loss is r/t something they did bad

leads to low self-esteem, excessive guilt, inability to cope with anger, self-destructive impulses and a similar emotional rxn occurs as an adult whenever a loss is experienced

theory of etiology of MDD

Front 45

Learned helplessness hopelessness theory

Back 45

Seilgman

~assumes person becomes depressed r/t perceptions of lack of control over life events and experiences

~these perceptions are learned over time especially as the individual perceives others seeing him or her as inadequate

~ perceptions of lack of control lead to the individual not adapting or coping

~the individual's behavior becomes PASSIVE and NONREACTIVE because of self-perceptions of personal characteristics of being HELPLESS, HOPELESS, & POWERLESS

Front 46

Perceptions of lack of control lead to the individaual not adapting or coping and behavior become passive d/t self-perceptions of being helpless, hopeless and powerless

Back 46

Learned helplessness hopelessness theory

psychodynamic theory of etiology of MDD

Front 47

Cognitive theory

Back 47

Beck

~dev experiences sensitize a person to respond to a stressful life events in a depressed manner

~Ppl w/ a tendency to be depressed think about the world differently
*more negative
*believe bad things are going ot happen to them b/c of their own shortcomings & inadequacies

When confronted by stressful events, these ppl tent to appraise them & the potential consequences in a negative, hopeless manner and therefore are more depressed than individuals with different cognitive styles

~When confronted by stressful events, these ppl tent to appraise them & the potential consequences in a negative, hopeless manner and therefore are more depressed than individuals with different cognitive styles

Front 48

Theory that people with tendency to be depressed think differently than nondepressed

Back 48

Cognitive theory

thinking is more negative, believe that bad things are going to happen to them because of their own personal shortcomings and inadequacies

Front 49

Thinking that is more negative, believe that bad things are going to happen to them because of their own personal shortcomings and inadequacies PROMOTES

Back 49

When confronted by stressful events, these ppl tent to appraise them & the potential consequences in a negative, hopeless manner and therefore are more depressed than individuals with different cognitive styles


~When confronted by stressful events, these ppl tent to appraise them & the potential consequences in a negative, hopeless manner and therefore are more depressed than individuals with different cognitive styles

Front 50

When confronted by stressful events, these ppl tent to appraise them & the potential consequences in a negative, hopeless manner and therefore

Back 50

are more depressed than individuals with different cognitive styles

Cognitive theory as a etiology of MDD

Front 51

How common in MDD ?

Back 51

a common illness with approximately 5% of the us population 18+ in a given yr having the d/o

~this represents almost 10 million American adults

Front 52

Most common psychiatric illness seen in primary care practices

Back 52

MDD

Front 53

Leading cause of disability in the US?

Back 53

MDD

Front 54

Per of people with MDD who ever receive tx?

Back 54

50%

Front 55

Average age of onset for MDD

Back 55

MDD can occur at any age

the average age of onset is mid 20s

the earlier the age of onset of MDD & the more severe the sx the more likely it is that a person has a strong genetic load for depression

Front 56

MDD and women

Back 56

~MDD is a greater source of morbidity for women than any other illness

~During reproductive yrs the lifetime risk for MDD varies w/ gender 25% for women 12% men (risk = before puberty and after menopause)

Increased risk during the postpartum period

Front 57

MDD mortality

Back 57

~MDD is associated with high mortality

~15% ppl w/ MDD will commit suicide

~ppl w/ MDD have 4 greater risk than the normal control population

Front 58

MDD disease course

Back 58

~varible
~can involve isolated episodes separated by many years
~clusters of episodes
~severe episode w/ some remission of sx but with chronic sx persisting over time

Front 59

If left untreated an episode of sx of MDD usually lasts __________ or longer

Back 59

4 mo

Front 60

MDD tend to a _____, ______ illness

Back 60

chronic , recurrent

Front 61

One yr after initial dx of MDD sx often persist
___% of pt have sig enough sx to meet full DSM-IV criteria. ____% do not meet full DSM criteria but still have sig sx level that impairs fxn
_____% have no sx

Back 61

One yr after initial dx of MDD sx often persist 40% of pt have sig enough sx to meet full DSM-IV criteria. 20% do not meet full DSM criteria but still have sig sx level that impairs fxn 40% have no sx

Front 62

The # of prior episodes of MDD predict.....

Back 62

the likelihood of future episodes of MDD

Front 63

The is approx a ______% risk of a 2nd episode in a person w 1st episode of MDD

Back 63

There is approximately a 60% risk of a 2nd episode in a person w/ 1st episode

Front 64

There is approximately a _____%
risk of a 3rd episode after the 2nd episode of MDD

Back 64

There is approximately a 70% risk of a third episode after the 2nd episode of MDD

Front 65

There is approximately a ____% risk of a 4th episode after the 3rd episode of MDD

Back 65

There is approximately a 90% risk of a 4th episode after the 3rd episode of MDD

Front 66

Risk factors for MDD

Back 66

~genetic loading
***fam hx especially 1st degree relative
~prior episode of MDD
~postpartum period
~medical comorbidity
~single marital status
~sig environmental stressors
***especially multiple losses

Front 67

Prevention & screening of MDD

Back 67

~provide @-risk fam edu
~provide community edu to
***help reduce stigma
***convey S&S of illness
***emphasize the tx potential for control of sx

~Provide sig screening efforts to help
***recognize
***intervene
***initiate tx early
~provide HCP edu to facilitate early recognition and effective tx

~Significant & protracted prodromal sx period usually noted before full onset of illness

Front 68

Assessment
Initial presentation

Back 68

often manifests as vague somatic complaints
*bodily aches, pains
*headaches
*muscle pains
*lack of energy
*GI problems
*Sleep disturbance (almost always present)

Front 69

Women often report sx of MDD occurring>>>>

Back 69

in fixed pattern around several days before onset of menses

so assess menstrual hx

Front 70

Sleep disturbance and MDD

Back 70

Almost always present
*typically problems occur w/ middle or terminal insomnia
*hypersomnia can be present
*Diurnal variations can be present

Front 71

A prodromal episode of MDD commonly consists of

Back 71

a high level of subjective anxiety
mild depressive sx

often develops over days to weeks before onset of a full episode

Front 72

DSM-IV-TR diagnostic criteria for MDD

Back 72

At least 5 of the following:
Either depressed mood or loss of interest or pleasure (irritable mood in children)

AND:

~sig wt loss/wt gain (of more than 5% of body wt)
~insomnia/hypersomnia
~psychomotor agitation or retardation
~fatigue or loss of energy
~worthlessness/excessive or inappropriate guilt
~decreased concentration; indecisiveness
~recurrent thoughts of death

Sx @ least 2 weeks
Sig distress or impairment
Not d/t substance
Not d/t med contion
Not accounted for by bereavement

Front 73

Melancholic feature of depression

Back 73

Sx worse in the morning

Front 74

PMDD is coded as WHAT?

Back 74

Depression NOS

Front 75

NOS diagnoses does not belong where?

Back 75

In differential diagnosis

NOS means didn't have enough time or doesn't meet criteria but important psych symptomalogy

Front 76

Steps for differential diagnosis

Back 76

1) Is presenting sx real?
2) R/o substance etiology
3) r/o disorder d/t gen med condition
4) determine specific primary d/o(s)
5) differentiate adjustment d/o from NOS
6) Estab the boundary w/ no mental d/o
5)

Front 77

To be considered Pathology in psych must have

Back 77

presence of specific distress or impairment

Axis II: the practitioner gets to observe inflexible and pervasive behavior cause distress (pt doesn't see it )

Front 78

Step one of Differential diagnosis

Back 78

Is the presenting sx real?

Some patients may elect to deceive the clinician by producing or feigning sx

Front 79

Step 2 of Differential diagnosis

Back 79

R/O substance tiology

including drugs of abuse, medication, toxin exposure, environmental exposure

Front 80

Step 3 of Differential diagnosis

Back 80

R/o d/o d/t gen medical condition

refer if need be

Front 81

Step 4 of Differential diagnosis

Back 81

determine the specific primary disorder(s)

Front 82

Step 5 of differential diagnosis

Back 82

differentiate adjustment disorder from NOS

***bereavement sx w/o a loss is adjustment d/o

Front 83

Step 6 of differential diagnosis

Back 83

Establis the boundary with no mental disorder

is problem causing sig distress
pathology = presence of significant distress or impairment
Axis II practitioner gets to observe inflexible pervasive behavior cause distress (patient doesn't see it)

Front 84

Individuals with certain other disorders (e.g. _____, ____, _____, _____) have a statistically significant increased risk for MDD.

Back 84

Individuals w/ certain other disorders (e.g. diabetes, myocardial infarction, carcinomas, stroke) have a statistically significant increased risk for MDD

Front 85

Physical exam findings in MDD

Back 85

There are NO specific physical findings

Pts w/ MDD often have trouble participation w/ assessments r/t cognitive problems of the d/o
*impaired ability to report chronological timeline of illness
*Poor decision making
*slowed thought precess
* requires focus assessment

Pts w/ MDD often have psychomotor findings
* Agitation
* Retardation

Front 86

Lethality of intended suicide action
High:
Moderate:
Low:

Back 86

High lethality: jumping sig height, gun, hanging

Moderate lethality: overdose of toxic agents (e.g. aspirin, sleeping pills, BP meds)

Low Lethality: Superficial wrist cutting, breath holding

Front 87

Assessing for suicidal behavior

Back 87

~past hx for suicide attempts or completed suicide in pt or family
~negativity or morbidity
~suicidal ideation currently
~plan and intent for suicide action
~means & access to commit suicide
~perceived social supports
~lethality of intended suicide action
~ability to contract for safety
~impulsivity
~substance abuse/dependence
~Hx of psych d/o

SAD Persons scale is psychometric to measure

Front 88

Labs to run if think MDD

Back 88

~CBC
~chemistry profile
~thyroid fxn test
~B12 level
Above to r/o metabolic causes or unidentified conditions

Drug toxicity screening, if indicated by history or suspected

Front 89

Common abnormal lab findings in MDD

Back 89

No specific lab findings specific to MDD exist

the more severe the depression the more likely lab abnormalities are present

~elevated glucocoricoid levels
~Increased urinary free cortisol levels
~decreased hormonal levels
~decreased TSH levels
~decreased growth hormone levels

Front 90

Before establish MDD diagnosis obtain baseline lab studies to r/o other differential dx

Back 90

!thyroid panel
CDC w. differential
Electrolyte panel
drug screen

Front 91

Polysomnographic testing abnormalities of MDD include

Back 91

*slleep continuity disturbances (e.g. prolonged latency)
* Reduced non-rapid eye movement (NREM) stage 3-4 (i.e. slow-wave sleep which is the restorative kind of sleep)
*Decreased REM latency
*increased phasic REM activity
*increased duration of early REM

Front 92

Med w/ altered mood states as side effects

Back 92

~steroids
~estrogen compounds
~anthypertensive agents
~anti-Parkinson's agents
~Anti-neoplastic agents
~Sulphanamides
~tetracyclin
~analgesics
~opiates
~antibacterial/antifungal agents
~ampicillin
~cycloserine
~metronidazole
~streptomycin
~NSAIDs
~Indomethacin
~Ibuprofen
~beta-blockers

Front 93

Endocrine d/o to consider in differential for MDD

Back 93

~hypothyroidsm
~diabetes
~hyperaldosteronism
~Cushing's/ Addison's disease

Front 94

Infectious & inflammatory states to r/o in diff dx for MDD

Back 94

~Mononucleosis
~AIDS
~Pneumonia: Viral & bacterial
~Systemic lupus erythematosus
~Temporal arteritis
~Tuberculosis

Front 95

Cardiac d/o to r/o in diff dx for MDD

Back 95

~myocardial infarction
~Congestive heart failure
~Hypertension

Front 96

Neurological d/o to r/o in diff dx for MDD

Back 96

~Stroke
~Epilepsy
~Dementia
~Huntington's disease
~Sleep apnea
~Wilson's disease
~Neoplasms
~Head trauma
~Multiple sclerosis

Front 97

Nutritional disorders to r/o in diff dx for MDD

Back 97

~Pernicious anemia
~pellagra: is a vitamin deficiency disease most commonly caused by a chronic lack of niacin (vitamin B3) in the diet. It can be caused by decreased intake of niacin or tryptophan, and possibly by excessive intake of leucine.

Front 98

Other d/o to r/o in diff dx for MDD

Back 98

~Fibromyalgia
~Chronic fatique syndrome
~Bereavement or grief rxn (bereavement is not pathology; bereavement sx w/o loss is adjustment d/o)
~electrolyte imbalance
~uremia and other renal conditions

Front 99

Psychiatric d/o to r/o in diff dx for MDD

Back 99

~Anxiety d/o
~Eating d/o
~Bipolar affective d/o
~substance dependence-related d/o

Front 100

Reasons for brief hospitalization during acute episodes of MDD

Back 100

~to ensure pt safety
~to initiate med change
~to restabilize on med
~to monitor suicidality
~to ensure pt compliance w/ tx to reach stabilization

Front 101

The top goal in the acute phase of MDD is

Back 101

ensuring pt safety

Front 102

Inform pt that therapeutic effect of pharm mgmt may take

Back 102

at least 4-6 wks

Front 103

Once started continue antidepressants for a minimum of

Back 103

8-12 mo

If pt has more than one prior episode of MDD consider longer term use

Front 104

Research has found that the most effective intervention for MDD is

Back 104

combination of medication and counseling

Front 105

Not all sx of MDD will respond to pharm interventions how to measure response

Back 105

identify clear measurable target sx & edu pt about these sx

Common target sx:
~depressed mood
~sleep-rest disturbances
~anxiety
~irritability
~impaired concentration
~impaired memory
~appetite disturbance
~agitation
~anhedonia

Front 106

Target sx of antidepressant tx

Back 106

~Depressed mood
~sleep-rest disturbances
~anxiety
~irritability
~impaired concentration
~impaired memory
~appetite disturbance
~agitation
~anhedonia

Front 107

Classes of antidepressants

Back 107

~selective serotonin reuptake inhibitors
~tricyclic antidepressants
~monoamine oxidase inhibitors
~Serotonin norepinephrine reuptake inhibitors
~Norepinephrine dopamine reuptake inhibitors
~serotonin agonist and reuptake inhibitors

Front 108

Selective Serotonin reuptake inhibitors (SSRIs)

Back 108

~action primarly to increase serotonin levels in CNS by inhibiting their reuptake

~serious side effects typically few
~The most common side effects of SSRIs are
*GI upset
*sexual dysfxn
*nervousness
*headache
*dry mouth

Front 109

SSRI are effective in what d/o

Back 109

MDD
Panic d/o
OCD
Bulima
GAD
Social phobia
PTSD
Premenstrual dysphoric d/o (PMDD)

Front 110

Most common sx w/ SSRI

Back 110

~headache
~dry mouth
~GI upset
~sexual dysfunction
~nervousness

Front 111

Citalopram

Back 111

Brand: Celexa
Class: SSRI
Dosage: tablet/ 20-60mg/d
Side Effects:
~sedation
~sexual dysfunction
~agitation
~Yawning
~GI disturbances
~Wt gain

Front 112

Escitalopram

Back 112

Trade: Lexapro
Class: SSRI
Dose: Tablet 20-60 mg/d
SE: ~Somnolence
~Headache
~sexual dysfunction
~GI disturbances

Front 113

Fluvozamine

Back 113

Trade: Luvox
Class: SSRI
Dose: Tablet, 100-300 mg/d
SE:
~sedation
~sexual dysfunction
~agitation
~gi disturbances

*****Black Box warning for liver toxicity!!!*****

Front 114

Fluoxetine

Back 114

Trade: Prozac, Sarafem
Class: SSRI
Dose: Capsule/tablet/liquid
~5-40mg/d (child_
~10-60mg/d for depression & anxiety d/o
~60-80mg/d for bulimia
Prozac weekly: 90mg
SE:Insomnia
~Headache
~GI disturbances
~sexual dysfxn

****Long half life, is stable so pills don't go bad***

Front 115

Paroxetine

Back 115

Trade: Paxil/ CR Pexeva
Class: SSRI
Dose Tablet/ liquid
~10-40mg/d (child)
~20-60mg/d
Also paxil CR
Side Effects:
~Headache
~GI disturbances
~Sexual dysfunction

***teratogenic effect possible
***sig discontinuation syndrome

Front 116

Sertaline

Back 116

Trade: zoloft
Class: SSRI
Dose: Tablet
~25-150mg/d (child)
~50-200mg/d
SE:
~sexual dysfunction
~GI disturbances
~somnolence
~headache

******teratogenic effect possible
~~~~sig discontinuation synd

Front 117

SSRI dose for adolescents/ kids

Back 117

Adolescents often receive adult dose
~doses are slightly less for kids

Start LOW go slow for children, elderly and pts w/ anxiety d/o

Observe for activation in known or unknown bipolar d/o and/or suicidal ideation

****Inform parents or guardian of this risk so they can help observe child or adolescent for patterns

Front 118

SSRIs Start LOW and go SLOW especially for

Back 118

children
Elderly
Patients with anxiety d/o

Front 119

Indications for SSRI

Back 119

Depression,
OCD
Panic d/o
Social anxiety d/o
PTSD
Eating d/o
Borderline personality d/o

*from review course slides

Front 120

Pharmacokinetics SSRIs

Back 120

Therapeutic effects may take 3-6 wks for depression
12-16wks for OCD

Observe for activation in known or unknown bipolar d/o and/or suicidal ideation

Inform parents or guardian of this risk so they can help observe child or adolescent for patterns

Front 121

Serotonin syndrome

Back 121

Excess serotonin:
Get high fever *******HIGH FEVER IN ABSENCE OF DIPHERISIS
(HIGH FEVER AND NO SWEATING IT IS 5HT SYNDROME)
~diarrhea
~restlessness
~extreme agitation
~hyper-reflexia & automatic instability
~myoclonus
~seizures
~hyperthermia
~rigidity
~delirium
~coma
~possible death

Front 122

Common side effects of SSRI


*slides from review course

Back 122

~anziety
~agitation
~akathisia
~insomnia
~nausea
~diarrhea
~sexual dysfxn

(may see motor restlessness, behavioral inhibition and disinhibition in kiddos)

Front 123

High fever in absence of dipherisis

Back 123

It is 5HT syndrome

Front 124

To pts with side effects when starting don't fear

Back 124

~most SE will pass
~may need to add buprpion to tx sexual sE or switch to another agent

Front 125

Why should I take an SSRI for my anxiety when I take it the pill makes me MORE ANXIOUS than I was before?

Back 125

5HT has several receptors in the brain: 5HT1a, 5HT1d, 5HT2, 5HT2a, 5HT3, 5HT4

SSRI will have GI sx, headaches, incr anxiety, for 3-5 d. 5HT2a caused GI, HA, Anxiety
5HT2 causes hallucinations

when take the med you are increasing the amount of 5HT in the synapse b/c inhibiting reuptake of all receptors

therefore stimulate 5HT2A which causes the side effects as well as 5HT1 which decreases depression and anxiety.

these SE are self limiting bc after 3-5 days 5HT2 receptors desensitive to the additonal serotonin because of chronic saturation so SE go away

Front 126

Children and adolescents being tx with antidepressants

Back 126

~kiddos and adolescets DO respond well to SSRI (and perhaps to other classes of antidepressants

~Recent FDA warning regarding 2-3% greater rick of suicidal behavior in kids taking antidepressants

**REMAIN VIGILANT ABOUT SUICIDAL THOUGHT & action

Educate parents about this risk and instruct them on the patterns to watch for at home as well

~unlike adults, kiddos may NOT respond to tricyclics

Front 127

TCAs are considered ______lind drugs for tx MDD

Back 127

2nd line

Front 128

TCA dirty side effect profile promotes poor patient compliance
SE include

Back 128

Anticholinergic SE:
~dry mouth
~blurred vision
~constipation
~memory problems (from muscarinic receptor blockade)

Antiadrenergic SE:
~orthostatic hyptension (from alpha 1 receptor blockade)

~EKG changes & cardiac dysrythmias
~unsafe in many co-occuring d/o (cardiac disease)
~Known to induce hypomania in certain patients

Front 129

MANIA inducer psych meds

Back 129

SSRIs in bipolar pts

TCAs are known to induce hypomania in certain pts

Front 130

Advantages of TCAs

Back 130

~can have well-identified serum blood levels that assist in dosing strategies to reach symptom control

~Are inexpensive & available in generic forms

~slow down the gut, so good for ppl w/ sig gi problems

Front 131

REMEMBER NOT TO Rx TCAs with _________. THIS CAN CAUSE A LETHAL REACTION

Back 131

DO NOT Rx TCAs and MAOIs together can cause a lethal rxn

Front 132

Disadvantages of TCAs

Back 132

~dirty SE profile promotes poor pt compliance
~pts can use pills to kill themselves
~significant abstinence syndrome with abrupt withdrawl
~If pt on both TCA & SSRI, Careful! SSRI can possibly elevate TCA concentrations in blood

Front 133

Lethal dose of TCA

Back 133

Lethal dose is 1000mg or more
~*A weeks supply of an average dose*~

~Avoid rx to suicidal pts

~CAUTION in pt on both TCA & SSRI as the SSRI can possibly elevate TCA concetrations in the bloodstream. Monitor TCA levels

Front 134

Pt on TCA & SSRI is this okay?

Back 134

Yes but caution bc SSRI can possibly elevate TCA concentrations in the blood stream

MONITOR TCA LEVELS

Front 135

Pt on TCA and MAOI is this okay?

Back 135

NO THIS CAN CAUSE A LEATHA RXN

DON"T KILL YOU PTS DONT rx TCA & MAOI together

Front 136

Child of TCA is this okay?

Back 136

Unlike adults kiddos may NOT respond to tricyclics

Front 137

Tricyclic antidepressants indications

Back 137

~Depression
~OCD
***Clomipramine (anafranil)
~Chronic pain
***neurogenic pain
***Trigeminal neuralgia
***Diabetic neuropathy
***Sciatica: efers to pain, weakness, numbness, or tingling in the leg. It is caused by injury to or pressure on the sciatic nerve. Sciatica is a symptom of another medical problem, not a medical condition on its own.
***Fibromyalgia
~Sleep disorders
***insomnia (elivil, trazadone)

Front 138

TCA pharmacokinetics

Back 138

~Therapeutic effects within 3-4 wks
~improved Energy & sleep in 1-4 wks

Front 139

ALL ANTIDEPRESSANTS HAVE THE SAME _______ ONLY CAN WORK ON _______ & _______

Back 139

All antidepressants have the same EFFICACY only can work on SE and TOXICITY

Front 140

TCAs have a ____ theraputic index

Back 140

low theraputic index

Lethal dose is 3x highest dose

Front 141

TCAs and bezos is this okay?

Back 141

Can give but dose is much less

Front 142

TCAs and EtOH is this okay?

Back 142

Can give but does is much less

Front 143

Have anticholinergic, antiadrenergic, cardiac and antihistaminergic SE

Back 143

TCAs

Anticholinergic: dry mouth, blurred vision, constipation, memory effects

Antiadrenergic: orthostatic hypotension

Antihistaminergic: sedation & wt gain

Cardiac: ECG changes, use in pts w/ conduction defects is contraindicated. Obtain baseline and yearly EKG & vital signs

Front 144

TCAs and Beta blockers is this okay?

Back 144

NO

Cardiac side effects; changes ECG

Front 145

TCAs and benadryl is this okay?

Back 145

NO

Antihistaminergic side effects already; sedation & wt gain

Front 146

How do you stop low dose of TCAs?

Back 146

there can be abstinence syndrome so

Avoid abrupt withdrawal

Taper

Front 147

What do should PMHNP monitor in a pt on TCA?

Back 147

~Obtain baseline and yearly ECG
~monitor serum blood levels
~suicidality

Front 148

TCA in elderly is this okay?

Back 148

Nope

Because of the potential for severe side effects and even death avoid rx to elderly

(ortho hypotension--falls
Anticholinergic--confusion)

Front 149

TCA in preggo lady is this okay?

Back 149

NOPE

Because of the potential for severe side effects and even death avoid rx to Preggos

Front 150

Amitriptyline

Back 150

Brand: elavil
Class: TCA
Dose: Tablet/IM
~50-300mg/d

**also used
***chronic pain
***insomnia
***sciatica
***fibromyalgia
***trigeminal neuralogia
***diabetic neuropathy

Front 151

Clomipramine

Back 151

Trade: anafranil
Class: TCA
Dose: Capsule
~100-250mg/d ****book
~50-100mg/d (child)***slides
~50-200mg/d (child/adol)
~130-250mg (adult)

*~approved for OCD; used most for this
*~250mg/d maximum due to increased seizure risk

Front 152

TCA used most often to tx OCD

Back 152

Clomipramine (anafranil)

Pronounced Clum-IP-ra-mean

Front 153

Hard max dose of clomipramin (anafranil) is _______ because_______

Back 153

250mg/d

due to increased seizure risk

Front 154

Desipramine

Back 154

Trade: norpramin
Class: TCA
Dose: tablet, capsule
~~25-125 (child)
~~50-150mg (adol)
~~150-300mg (adult)
~~**100-300mg (adult in book)

Additional child applications: ADHD

Front 155

Most TCAs are used off label because

Back 155

pts cannot tolerate the high doses needed for antidepressant, (so used for chronic pain, diabetic neuropathy, sleep)

Front 156

Doxepin

Back 156

Trade Sinequan
Class TCA
Dose capsule, liquid
~100-3--mg/d

**also used for insomnia

Front 157

Imipramine

Back 157

Trade Tofranil
Class TCA
Dose tables, capsule
~25-150mg (child)
~50-200 mg (adol)
~150-300mg (adult)
~~100-300mg/d **book

Also used for enuresis (peeing the bed) & separation anxiety in kiddos

Front 158

Nortriptyline

Back 158

Trade Pamelor
Class TCA
Dose Capsule, liquid
~25-100mg (kid)
~50-125mg (adol)
~50-100mg (adult)
~~50-150mg (adult book**)


**Least sedating of TCAs

Also used for enuresis (bedwetting) & ADHD

Front 159

Protriptyline

Back 159

Trade Vivactil
Class TCA
Dose Table
~15-60mg/d

Front 160

Trimipramine

Back 160

Trade: Surmontil
Class: TCA
Dose: Capsule
~100-300mg/d

Front 161

gun is a ____ lethality plan of suicide

Back 161

High lethality

as is jumping from sig height & hanging

Front 162

Superficial wrist cutting is a _____ lethality plan of suicide

Back 162

low lethality

as is holding breath

Front 163

Overdose of toxic agents is a ____ lethality plan of suicide

Back 163

Moderated lethality

Front 164

Suicide risk is especially high for individuals w/ certain sx or history: 5 things

Back 164

1) presence of psychotic sx
2) hx of past attempts
3) hx of 1st degree relative who committed suicide
4) concurrent substance abuse or dependency
50 current serious health problem

Front 165

Luvox generic name and class

Back 165

Fluvoxamine (SSRI)

Front 166

zoloft generic name, class and dose range

Back 166

Sertaline

SSRI

Tablet 50-200mg/d

Front 167

Anticholingic sx

Back 167

~dry mouth
~blurred vision
~constipation
~memory problems from muscarinic receptor blockade


Seen with TCAs

Front 168

What is the lethal rxn to watch out for with TCAs?

Back 168

TCAs + MAOIs = death (can happen)

Also TCAs in suicidal pt bad! lethal does is 1000mg or more (a wks's supply of an average dose)

Front 169

Elavil

Back 169

Amitriptyline
TCA

Also used for chronic pain
insomnia
sciatica
fibromyalgia
trigeminal neuralgia
diabetic neuropathy

Front 170

Pamelor

Back 170

Nortriptyline
TCA
Capsule and Liquid
50-150mg/d

Also used for enuresis & ADHD

Front 171

hypertensive crisis

Back 171

a life threatening and irreversible until more MAO is produced by the body.

This occurs when MAOIs are taken in conjunction with foods containing tyramine a dietary precursor to norepinephrine

Front 172

Tyramine

Back 172

a dietary precursor to Norepinephrine

Exerts Strong vasopressoer effect (stim release of catecholamines, epi, NE, which can increase blood pressure & HR when MAO is inhibited

Found in:
Aged cheeses
Smoked, aged & cured meats
Smoked, aged & cured fish
Any aged & fermented beverage
Bean curd
Soy bean paste
Sauerkraut
Soy sauce
Yeast extract
CHOCOLATE
MSG
nuts
Bananas

Front 173

MAOIs are never ____ or _____ for MDD because of dangerous food & drug interactions

Back 173

MAOIs are never 1st line or 2nd line agents for MDD because of dangerous food and drug interactions

Front 174

What do PMHNP worry about with a pt on an MAOI

Back 174

Drug interxns
Food interxns (foods containing tyramine) resulting in hypertensive crisis
Dirty side effect profile

Front 175

Sx of hypertensive crisis

Back 175

~sudden, explosive-like headache, usually in occipital region
~elevated blood pressure
~facial flushing
~palpitations
~pupillary dilation
~diaphoresis
~fever

Front 176

Tx of Hypertensive crisis

Back 176

~Hold the MAOI
~Give Phentolamine (binds with NE receptor sites, blocks NE)
~stabilize fever
~reeval the pt's dies & adherence & reiterate medication guidelines as necessar

Front 177

Pts on MAOIs must be on a ______ free diet & must avoid many meds including most over the counter ___ & ____ preparations

Back 177

Patients on MAOIs must be on a tyramine-free diet & must avoid may medications including most over the counter cold and allergy preparations

Front 178

What about MAOIs promote poor pt compliance

Back 178

~ Dirty side effect profile & stringent dietary restrictions

Front 179

Clinically sig side effects of MAOIs include:

Back 179

~~insomnia
~hypertension crisis
~weight gain
~anticholinergic side effects
~light headedness & dizziness
~sexual dysfxn

Front 180

MAOIs are ____ in many co-occuring disorders

Back 180

UNSAFE

Front 181

Are MAOIs are expensive or inexpensive?

Back 181

Inexpensive & most com in generic form

Front 182

Isocarbozazid

Back 182

Marplan (Trade)
Tablet 100-60mg/d

For MDD
Also used for panic d/o selective mutism
~Caution: High tyramine diet; sympathomimetic agents
~divided dosing bid & qid

Front 183

Phenelzine

Back 183

Nardil
MAOI
Tablet 30-60mg/d

For MDD
~also used for panic d/o
phobic d/o,
selective mutism

~CAUTION: high tyramine diet: sympathomeimetic agents

~divided dosing: bid & qid

Front 184

What does MAOI stand for?

Mech of Action for MAOI?

Back 184

Monoamine Oxidase Inhibitors

Elevate serotonin and norepinephrine levels primary by inhibiting MAO the enzyme that destroys neurotranmitters (in the cytosol)

Front 185

Tranylocypromine

Back 185

Parnate
MAOI
Tablet
20-60mg/d

For MDD
~also used for panic d/o
phobic d/o,
selective mutism

~CAUTION: high tyramine diet: sympathomeimetic agents

~divided dosing: bid & qid

Front 186

Selegiline

Back 186

EMSAM, Eldepryl, Atapryl
MAOI

Also available as transdermal patch EMSAM 6 & 12 mg
NO dietary restrictions with EMSAM 6

Selegiline is also used for the tx of Parkinsonism

Front 187

EMSAM patch

Back 187

Selegiline (generic)
MAOI

Avail in 6mg & 12 mg

No dietary restritions with EMSAM 6 BUT tell pt if don't get remission of sx pt will put 2nd patch on w/o telling PMHNP and then can have problems (HYPERTENSIVE CRISIS)

Front 188

Nardil

Back 188

Phenelzine
MAOI
table 30-60mg
For MDD
~also used for panic d/o
phobic d/o,
selective mutism

~CAUTION: high tyramine diet: sympathomeimetic agents

~divided dosing: bid & qid

Front 189

MAOIs & kiddos

Back 189

not recommended for kiddos

Front 190

Marplan

Back 190

Isocarbozazid
MAOI
Tablet 100-60mg/d

For MDD
~also used for panic d/o
phobic d/o,
selective mutism

~CAUTION: high tyramine diet: sympathomeimetic agents

~divided dosing: bid & qid


For MDD
~also used for panic d/o
phobic d/o,
selective mutism

~CAUTION: high tyramine diet: sympathomeimetic agents

~divided dosing: bid & qid

Front 191

Parnate

Back 191

Tranylcypormine
MAOI
Tablet 20-60mg/d

For MDD
~also used for panic d/o
phobic d/o,
selective mutism

~CAUTION: high tyramine diet: sympathomeimetic agents

~divided dosing: bid & qid

Front 192

MAOIs efficacy?

Back 192

Have been proven most efficacious of any anti-depressant

but dirty side effect profile, dietary restrictions and medications interactions promote poor pt complience

Also because of the potential for serious adverse effects MAOIs are not commonly used in clinical practice

Front 193

MAOIs pharmacokinetics

Back 193

Antidepressant effects may take 3-6 weeks

Front 194

Most frequent adverse effect of MAOIs

Back 194

Orthostatic hypotension


Most providers worry about the possibility of Hypertensive crisis but this is RARE

Front 195

Most frequent adverse effectS of MAOIs

Back 195

~Orthostatic hypotension
~Insomnia
~Weightgain
~edema
~sexual dysfxn

Potential for severe drug-drug interactions (can caused death when mixed with SSRIs, TCAs, atypicals, decongestants, methyphenidate, asthma meds

Front 196

Rare side effect of MAOIs

Back 196

Tyramine-induced hypertensive crisis

Avoid food that are preserved, pickled or aged, caffeine, chocolate, soy

Front 197

Things NOT to mix with MAOIs

Back 197

Tyramine
co-occuring med conditions
childhood

SSRIs
TCAs
atypicals
decongestants
Methyphenidate
asthma meds

Front 198

Most MAOIs will eventually stop working in vast majority of people because

Back 198

work by elevating serotonin & norepinephrine levels primarily by inhibiting MAO, the enzyme that destroys neurotrasmitters in the cytosol.

Becausebrain circit thinks too much monoamine is deadly . Therefore the brain finds wasy to destroy monoamine (5HT & NE(by COMT in synapse) before the monoamine gets to the cytosol

Front 199

Many SSRI inhibit CDY2D6 metabolize why is this important?

Back 199

A dentist gives tylenol 3 to a pt.
Tyenol 3 is a produr meaning it is metabolized to its active metabolite after in the body
In this case tylenol 3 is metabolized by 2D6 enzyme to morphine.
Since several SSRIs inhibit 2D6 metabolize the codine isn't metabolized to morphine and therefore the Tylenol 3 does NO provide analgesia CDY2D6 enzyme

Front 200

Indications for MAOI

Back 200

May be useful in the tx of depressed pts with marked anxiety or phobic sx.

Selegiline is also used for the tx of parkinsonism

Front 201

SSRI dosed for anxiety

Back 201

Low doses at sub-theraputic level for anxiety because 5HT2 issues

Start low go slow

Front 202

SSRI dosed for depression

Back 202

Normal dose for depression

Therapeutic effects may take 3-6 weeks

Front 203

SSRI dose for OCD

Back 203

High doses for OCD

therapeutic effects may take 12-16 weeks for OCD

Front 204

Pt comes in has a sudden explosive-like headache in the occipital region

Back 204

Is the pt on an MAOI?
Sx of tyramine-induced hypertensive crisis.

Other sx to look for: elevated BP
Facial flushing
Palpitations
Pupillary dilation
Diaphoresis
fever

Front 205

Tyramine effects

Back 205

This precursor to norpinephrine exerts STRONG VASSOPRESSOR EFFECT
****does this by stimulating the release fo catecholamines, epinphrine, and norepinephrine which can increase blood pressure and heart rate

Need MAO to break these down but MAO is inhibited so must wait until more MAO is produced by the body (2 weeks)
and give PHENTOLAMINE

Front 206

Switching from SSRI to MAOI anything important?

Back 206

Must be off SSRI for at least 14 days.

SSRI + MAOI can possibly = death

Front 207

SSNRIs MOA

Back 207

~Inhibit dual reuptake
~Action very selective on NTs
~Elevate 5HT & NE levels by inhibiting their reuptake

Front 208

SSNRI drugs

Back 208

Effexor Venilafaxine
Must be at dose of 225 to be SSNRI, acts as SSRI at lower doses

cymbalta Duloxatine

Front 209

Serotonin- 2 antagonist reuptake inhibitors drugs

Back 209

SARIs

Nefazodone (serzone

Trazodone (desyrel)
Heterocyclic (between TCA & SARIs) class technically but close 1st cousin with serzone

Front 210

Venlafaxine

Back 210

Effexor
SSNRI
75-375 mg/day
Also Effexor XR 75-225mg

Monitor for HTN
Discontinuation syndrome
~Venlafaxine must be at 225mg/dose to be SSRI; acts as an SSRI at lower doses
~Prliminary studies suggest effectiveness for kids and adolescents w/ depression, anxiety d/o & ADHD

Caution with use in kids/adolescents SUICIDE

Front 211

Duloxatine

Back 211

Cymbalta
SSNRI
40-60mg/d *slides
30-120mg/d *book

Once daily dosing
~can possibly elevate BP
~Can possibly elevate liver fxn tests
~Has SIGNIFICANT discontinuation syndrome if stopped abruptly

SE: dizziness
Headace
GI disturbances

Front 212

Desyrel

Back 212

Trazodone
SARI
Tablet 200-600/d
Generally used for insomnia d/t sedative properties
~risk priapism in males
~Use caution in kids/adolescents

SE: Sedation Nausea Headache

Safer in Overdose than TCAs
~Not well tolerated at antidep dose d/t segaion

Mot commonly used at hypnotic at 50-200mg/hs

May potentially prolong QTc interval

Front 213

Venlafaxine Side effects

Back 213

Can raise BP

Diaphoresis
Headache
Dizziness

Potent inhibitor of CYP450 system

~q day for XR capsules
~bid-tid dosing for tablets
~safer in OD than TCA
~sig discontinuation syn if stopped abruptly

Front 214

Nefazodone

(pronounced NA-FAZE-A-DONE or NA-FAZ-A-DONE)

Back 214

Serzone
SARI
Tablet 300-600mg/d

SEL headache
Drowsiness
GI disturbances

MUST monitor LFTs
~Can cause Liver failure
~safer in OD than TCAs
~qhs or bid dosing

~Potent P450 3A4 inhibitor

Front 215

Trazodone

Back 215

Desyrel
SARI
Tablet 200-600 (depression)
50-200mg/hs (insomnia)

~May potentially proong QTc interval
~Priapism possible

Front 216

Cymbalta

Back 216

Duloxetine
SNRI
Capsule 30-120mg/d
~Once daily dosing
~can possibly elevate BP
~Can possibly elevate liver fxn tests
~Has significant discontinuation syndrome if stopped abruptly

Often used for fibromyalgia & chronic pain in addition to MDD & anxiety

SE: dizziness
Headache
GI disturbances

Front 217

Cymbalta big risks

Back 217

Elevated LFTs & HTN

Discontinuation syndrome

Front 218

Serzone

Back 218

Nefazodone
SARI

Front 219

SARI stands for

MOA of SARI

Back 219

Serotonin-2 antagonist/ reuptake inhibitors

~Dual action
~Agonist of 5HT-2 receptors
~Action very selective on NTs
~Elevate 5HT levels by inhibiting serotonin reuptake

Front 220

Effexor XR

Back 220

SNRI
XR 75-225 mg/d

~Potent inhibitor of CYP450
~once a day dosing
~Can raise BP
~Significant discontinuation syndrome

Front 221

Bupropion

Back 221

Wellbutrin: Zyban
NDRI
100-450mg/d
Also available in SR & XL forms
SR max 400mg
XL mac 450mg

Coomnly used as an augmenting agent w/ other anitdepressants
~no sexual side effects
~useful for smoking cessation
~has been used to tx ADHD in kids @100-250mg/d
~Seizure risk:contraindicated in individuals with seizure hx and bulima
~caution with caffeine & panic d/o
~Good in bipolar d/o & ADHD, dysthmic d/o or where the targe sx is draggin

Some say bupropion agument will help w/ sexual side effects

Front 222

Antidepressants that generally will not as a class cause sexual side effects

Back 222

Bupropion (wellbutrin, Zyban)

Mirtazapine (remeron)

Front 223

Dont give Bupropion to who

Back 223

Pts with history of seizure

Bulimics

Front 224

Wellbutrin is good in what d/o

Back 224

~bipolar
~ADHD
~dysthmic
~depression

Front 225

Mirtazapine

Back 225

Remeron
Tablet 15-45mg/d

~Inverse relationship between dosage and sedation
~WT GAIN
~increased cholesterol

Front 226

Bupropion come in what formulations ?

Back 226

Bupropion 150-450mg/d

Sustained release 150-400mg/d
MAX 400
Extended release 150-450mg/d
MAX 450

Front 227

NDRI stands for what?

NDRI MOA?

Back 227

Norepinephrine dopamine reuptake inhibitors

Inhibit dual reuptake
Action very selective on NTs
Elevate dopamine & NE levels by inhibiting their reuptake

Front 228

Classes of antidepressants that elevate 5HT

Back 228

~SSRI
~TCA
~MAOI
~SARI

Front 229

Classes of antidepressants that elevate norepinephrine

Back 229

~TCA
~MAOI
~SSNRI
~NDRI

Front 230

Classes of antidepressants the elevate dopamine

Back 230

~NDRI

Front 231

Since psychotic features can be present with MDD should

Back 231

routinely assess for the presence of psychotic sx during periods of sx exacerbation

Front 232

Psychotic features in MDD

Back 232

Are usually mood congruent
~Can be managed in short-term use of antipsychotic med

~psychosis is less common in kids before onset of puberty

Front 233

Electroconvulsive Therapy

Back 233

ECT
~Grand mal seizure induced in anesthetized individual

Usual course 6-12 treatments

Front 234

Usual # of tx in ECT

Back 234

6-12

Front 235

ECT MOA

Back 235

NT theory: increased DA, 5HT, NE
Neuroendocirne theroy: releases hormones such as prolactin, TSH, Pituitary hormones, endorphins and adrenocorticotropic hormone

Anticonvulsant theory: exerts and anticonvulsant effect, which then produces an antidepressant effect

Front 236

Similar new methods to ECT

Back 236

Transcranial magnetic stimulation
vegal nerve stimulation
Phototherapy

Front 237

Individual therapy methods in MDD

Back 237

CBT
Brief therapy (solution focused therapy)
Group therapy
Family therapy

Front 238

Goals of CBT in MDD

Back 238

~Modify perceptions
~decrease negativity
~increase sense of internal control
~enhance coping skills
~modify environmental factores contribution to illness

Front 239

Goals of brief therapy (solution focused therapy) in MDD

Back 239

~focus on precipitant stressor
~cope with immediate impact of MDD on personal life
~modify contributory environmental factors

Front 240

Goals of group therapy with MDD

Back 240

~improve decision making
~improve socializations skills
~improve assessment of individual strengths
~gain new coping skills

Front 241

Goals of family therapy with MDD

Back 241

~enhance family coping
~improve knowledge base
~plan for relapse
~gain insight into effects of MDD on family unit
~undertake psychoeducation for family members about the illness of MDD

Front 242

Clinical mgmt of suicidality

Back 242

~pay sig attn to positive assessments for suicidality
~alway assume the pt is serous when they vocalize suicidal thoughts
~Id current stressors that may be contributing to crisis
~Generally do not manage in community setting during acute suicidal ideation periods unless pt is able to make no-harm agreement
~consider hospitalization
~consider mobilizing available social resources

Front 243

Risk factors for suicide

Back 243

~age 45 or older if male
~age 55 or older if female
~divorced/single/seperated
~white
~living alone
~psych d/o
~physical illness
~substance abuse
~previous suicide attempts
~family hx of suicide
~recent loss
~male gender

Front 244

MDD sx in kiddos

Back 244

Core sx of MDD are the same
However some sx are more pronounced in kids:
~irritability
~somatic complaints
~social withdrawal

MDD often has a strong separation anxiety component in kids

Some core sx are less common in kids before onset of puberty
~psychosis
~motor retardation
~hypersomnia
~increased appetitie

Front 245

MDD often has a strong ______________ component in kids

Back 245

separation anxiety

Front 246

These core sx are less common in kids before onset of puberty

Back 246

~psychosis
~motor retardation
~hypersomnia
~increased appetite

Front 247

kids usually do not respond well to ______; however they do respond well to _______

Back 247

do not respond to TCAs

do respond to SSRIs

Monitor closely for suicidal behavior, agitation and aggression in kids taking antidepressants

Front 248

What to monitor for in kids taking antidepressants

Back 248

SUICIDAL BEHAVIOR
inform parents so they can watch for this as well

agitation
aggression

Front 249

Individuals with MDD admitted to a long-term-care facility have _________spans than normal population

Back 249

Pts with MDD admitted to long term care facility have SIGNIFICANTLY SHORTER LIFE spans than normal control population

~65% are more likely to die within the 1st year in a long term care facility

Front 250

_____ & _____ sx of MDD in the elderly population often are confused with ________-related sx

Back 250

COGNITION AND MEMORY sx of MDD in the elderly population often are confused with dementia-related sx (pseudodemntia)

Front 251

In dementia there is usually a premorbid hx of _______ declining cognition

Back 251

Slowly declining cognition

Front 252

In MDD cognitive changes ahd a relatively ____ onset and are ____when compared to premorbid functioning

Back 252

In MDD cognitive changes have a relatively ACUTE onset and are SIGNIFICANT when compared to premorbid functioning.

Front 253

It is important to complete a functional assessment for elderly pts to....

Back 253

Determine the degree to which the pt's abilities and performance match the demands of their life

Determine the impact of ilnees on the overall fxning
~skill deficit:inability to perform a fxnal skill despite the physical ability, as in dementis
~performance deficit: ability to perform a fxnal skill but lacks the motivation to do so, as in depression

Front 254

Skill deficit:

Back 254

inability to perform a functional skill despite the physical ability as in dementia

Front 255

Performance deficit:

Back 255

ability to perform a functional skill but lacks the motivation to do so as in depression

Front 256

Reasons fro performing functional assessment

Back 256

(important to complete in elderly)

to correctly dx (i.e. differentiate depression from dementia

to track pt improvement or decomp

to help families set realistic expectations

Front 257

Components of functional assessment

Back 257

ADLs; basic self care skills (bathing, dressing, eating, toileting)

IADLs (instrumental activites of daily living) complex activites needed for independent fxning (shopping, cooking, driving, housekeeping

Executive functioning: Judgement and planning: ability to maintain calendar, manage money and appts, prioritize activities

The degree of change over time and the speed of change are better observed as objective recording and when the assessment is measured in intervals such as q 6mo

Front 258

ADLs

Back 258

Component of the functional assessment which should be part of an elderly pts assessment

these are the basic self-care skills; bathing, dressing, eating, toileting

Front 259

IDLs

Back 259

A componet of the functional assesment which should be preformed for elderly pts.
(executive functioning and ADLs are the other components)

Instrumental activites of daily living are complex activities need for independent fxning such as shopping, cooking, driving and house keeping

Front 260

Executive functioning of the _______ assessment is

Back 260

part of the FUNCTIONAL ASSESSMENT especially important for elderly to differentiate dementia from depression

Judgement and planning; ability to maintain calendar, manage money and appointments and prioritize activities.

Front 261

The degree of change over time and the speed of change of the functional assessment are better observed with

Back 261

objective recording and when the assessment is measured at intervals such as q 6 mo

Front 262

Follow-up care for MDD

Back 262

~pt teaching the risks, benefits and potential side effects of medication tx

~continuously monitor pt's response to medication; the tx goal is complete remission of sx

~teach pt of sx of depression and that it is a chronic illness; establish a relapse plan for all pts

~assess for suicidality during q pt contact

~assess for the presence of psychotic sx during q pt contact

~assess & manage pt for SE of tx including sexual SE in an attempt to increase med compliance

~observe all pt treated with antidepressants for dev of serotonin syndrome (overstimulation of 5HT receptors usually caused from drug-drug interactions)

Front 263

Teach patient about

Back 263

~their diagnosis
~benefits/risks, potential SE of med tx
~sx of depression
~chronic nature of illness
~assess for suicide, psycotic sx,

Front 264

Drug combinations that may cause serotonin syndrome

Back 264

~SSRIs & MAOIs
~Drug & herbal interactions
~SSRIs & St. John's wort (a weak MAOI)

Front 265

Symptoms of 5HT syndrome

Back 265

~Fever w/o sweating
~Restlessness
~agitation
~myoclonis
~hyperreflexia
~hyperthermia
~diaphoresis
~altered sensorium
~tremor
~chills
~diarrhea & cramps
~ataxia
~headache
~insomnia

Front 266

Some SSRIs are known to increase _______ & contribute to __________ and others may elevate _____________tests.

Back 266

Some ssris are known to increase BLOOD GLUCOSE and contribute to HYPERLIPIDEMIA and others may elevate LIVER FUNCTION tests

Front 267

When discontinuing SSRIs

Back 267

discontinue SSRIs slowly to prevent discontinuation syndrome

Front 268

Sx of Discontinuation syndrome

Back 268

~Flu like sx
~fatigues & lethargy
~myalgia (muscle pain)
~decreased concentration
~N/V
~impaired memory
~irritability
~anxiety
~insomnia
~crying w/out provocation
~dizziness and vertigo

Front 269

Risk factors for discontinuation syndrome

Back 269

~medications with short half-life
~abrupt discontinuation
~non compliant, irregular use pattern
~high dose range
~long-term tx
~prior hx of discontinuation syndrome

Front 270

Discontinue TCAs slowly..

Back 270

Pts can get cholinergic rebound syndrome
~Nausea
~GI upset
~Diaphoresis
~myalgias (sore muscles) especially of neck muscles

Front 271

Expected Course of MDD

Back 271

Evidence indicates the best tx outcomes if meds are used in conjunction with appropriate therapy

~Evidence indicates that pts should take an antidepressants agent for at least 12 mo after remission of sx

~Pts who have had two or more episodes of MDD usually require lifelong meds

Front 272

Pts who have had 2 or more episodes of MDD usually require

Back 272

lifelong medications

Front 273

How long should pts take an antidepressant agent for how long after remission of sx

Back 273

for at least 12mo after remission of sx

Front 274

Evidence indicates the best tx outcomes if what tx is used?

Back 274

medications are used in conjunction with appropriate therapy.

Front 275

Pts who have ____ or more episodes of MDD require ______________

Back 275

Pts who have 2 or more episodes of MDD usually require lifelong medications

Front 276

DYSTHYMIC D/O

Back 276

A disorder similare to MDD but with less acute sx. with a more protracted chronic disease course; & w/o any manifestations of psychotic sx

Less discrete episodes of illness than MDD

Sx often go undetected and therefore untreated for yrs

Vegetative sx (sleep, appetite, wt changes) much less common in dysthymic d/o than in MDD

Front 277

Vegatative sx

Back 277

sleep disturbances
appetite disturbances
libido disturbances
lethargy
anhedonia

are r/t the functions of the hypothalamus and pituitary and the hormones they secrete (endocrine dysfunction biological theory of MDD)

Much less common in dysthymic d/o than in MDD

Front 278

Etiology of dysthymic d/o

Back 278

similar to MDD

Front 279

Incidence of dysthymic d/o

Back 279

6% of people in us will develop dysthymic d/o in their lifetime

Affects 5.4% of the population ages 18 and up or 10.9 million americans

Front 280

individuals with dysthymia have an _______ risk of developing _____

Back 280

Individuals with dysthymia have an INCREASED risk for developing MDD

Front 281

_______% of individuals diagnosed with dysthymic d/o will have a lifetime episode of MDD

Back 281

15-25% of individuals diagnosed with dysthymic d/o will have a lifetime episode of MDD

Front 282

Early onset dysthymic d/o

Back 282

dysthymic sx occur befoer age 21
~usually the type of dysthymic d/o with most sx
~Most at risk for onset of MDD

Front 283

Late onset dysthymic d/o

Back 283

Dysthymic sx occur at or after age 21

Front 284

In pts with onset of dysthymic d/o sx before age ____ there is a ____% likelihood they will have a lifetime episode of ______

Back 284

In individuals with the onset of dysthymic sx before the age of 21 there is a 75% likelihood that they will have a lifetime episode of MDD

Front 285

Women are _____x more likely than men to develop dysthymic d/o

During reproductive yrs the lifetime risk for MDD varies by gender who is at greater risk when is it = risk?

Back 285

Women are 2-3x more likely than men to develop dysthymic d/o

During reproductive yrs:
women 25% lifetime risk for MDD
12% lifetime risk for MDD

Before puberty and after menopause the risk is equal for the genders

MDD is a greater source of morbidity for women than any other illness

Front 286

2 types of dysthymic d/o

Back 286

Early onset: sx before 21
75% likelihood will have MDD episode
usually more symptoms than late onset type

Late onset dysthymic d/o
Sx at or after 21 yr of age

Front 287

Risk factors for dysthymic d/o

Back 287

~genetic loading
~1st degree relative with MDD
~1st degree relative w/ dysthymic d/o
~FEMALE gender (2-3x more likely to develop dysthymic d/p than men)

Front 288

Prevention & screening dysthymic d/o

Back 288

~at risk family edu
~community edu
~stigma reduction
~signs & sx of illness
~tx potential for control of illness
~early recognition
~early intervention
~early initiation of tx
~Because of chronic nature of d/o, sx become part of pt's day to day existence and oftern go unreported unless solicited by direct questioning
~aggressive screening procedure required

Front 289

Pts with this d/o often under report sx unless solicited by direct questioning because sx become part of pt's day to day existence

Back 289

Dysthymic d/o

Aggressive screening procedure required as sx often go unreported unless solicited by direct questioning

Front 290

Hx assessment findings for dysthymic d/o

Back 290

Chronically depressed mood that occurs for most of the day , more days than not for at least 2 yrs

Prominent presence of:
~low self-esteem
~self-criticism
~perception of general incompetence compared to others

Front 291

" other" common sx in dysthymia d/o

Back 291

~low E & fatigue
~poor concentration
~difficulty w/ decision making
~feelings of hopelessness
~feelings of inadequacy
~mild anhedonia
~Social withdrawal
~brooding about past issues
~subjective irritability of anger
~decreased productivity & activity

Front 292

Less common sx in dysthymic d/o

Back 292

vegetative sx
alteration in appetite
Alteration in sleep-rest pattern (almost always present in depression)

Front 293

Mental status exam findings in dysthymic d/o

Back 293

~Usually no vegetative findings
~Mood describes as "sad, down for all my life"
~similar to MDD
****appearance: unkept, tired looking, clothing showing little attn or care into looks, dark--colored loose fitting clothing,

Speech: underproductive, blocking, slowed response times, monotonal intonation

Affect: constricted or blunted, sad, anxious, irritable

thought Process: usually organized, slowing, distractible, rumination

Thought content
Morbid preoccupation, suicidal ideation exists on continuum of severity, despair

COgnition: usually impaired
Orientation: usually intact
Memory: usually impaired recent & short term memory
Concentration: usually sig impaired
Abstraction: abstract ability of proverb testing usually intact

Front 294

Diagnostic and lab findings in dysthymic d/o

Back 294

Nonspecific
Poly somnographic findings similar to those found in MDD
**sleep continuity distubances (e.g. prolonged latency)
**reduced NREM stages 3-4 (slow wave restorative sleep)
**decreased REM latency
**increased phasic REM activity
**increased duration of early REM

Less common in dysthymia d/o to have sx of alteration in sleep-rest pattern

Front 295

Differential dx of dysthymic d/o

Back 295

similar to MDD but includes MDD too

Front 296

Pharmacological mgmt of dysthymic d/o

Back 296

because of increased risk for dev of MDD, dysthymia is usually tx with antidepressant medications in a manner similar to MDD

Front 297

Dysthymic d/o diagnostic criteria

Back 297

~depressed mood for at least 2 yrs (**1yr is kid/adol)
~While depressed at least 2:
**poor appetite or overeating
**insomnia/hypersomnia
**low energy fatigue
**low self-esteem
**poor concentration:indecisiveness
**hopelessness
~not without s/s for more than 2 months

Front 298

Non-pharm mgmt of dysthymic disorder

Back 298

Similar to MDD
*CBT
*brief therapy (solution focused therapy)
*group therapy
*family therapy
Often good clinical outcomes w. just nonpharm tx if pt is willing

Front 299

CBT aim in dysthymic pts

Back 299

~modify perceptions
~decrease negativity
~increase sense of internal control
~enhance coping skills
~modify enviro factors contributing to illness

Front 300

Brief therapy (solution-focused therapy) aim in dysthymic pts

Back 300

~focus on precipitant stressor
~cope with immediate impact of MDD on personal life
~modify contributory enviro factors

Front 301

Group therapy aim in dysthymic pts

Back 301

~improve decision making
~improve socialization skills
~improve assessment of individual strengths
~gain new coping skills

Front 302

Family therapy aim in dysthymic pts

Back 302

~enhance family coping
~improve knowledge base
~plan for relapse
~gain insight into effect of dysthymia on family
~undertake psychoeducation for family members about the Dysthymic disorder

Front 303

Dysthymic d/o is often superimposed on ____

Back 303

MDD

Front 304

Common comorbidities of dysthymic d/o

Back 304

~dysthymic d/o is often superimposed on MDD
~the subjective worsening of sx or onset of new sx such as vegetative ones often brings pts into tx
~when dysthymia precedes MDD clinical mgmt is more complex and outcomes can be less positive
~dysthymic d/o is assoc w. personality d/o:
*borderline
*histrionic
*narcissistic
*avoidant
*dependent

Front 305

What often brings people with dysthymic d/o in for tx?

Back 305

Subjective worsening of sx or onset of new sx such as vegetative ones

Front 306

Clinical mgmt of dysthmia can be more complex and outcomes less positive when....?

Back 306

dysthymia precedes MDD

Front 307

Dysthymia and kiddos

Back 307

~In kids prevalence rates = for boys and girls

~associated w/ several childhood d/o
*ADHD
*conduct d.o
*anxiety d/o
*learning d/o
*mental retardation

Period of sx required fo dx only 1 yr for kid/adol

Mood is usually describes as irritable rather than sad but may report both irritability and sadness

Low self-esteem
poor social skills
pessimism

Front 308

period of sx required for kids/adol to be dx with dysthymic d/o

Back 308

1 yr of depressed mood

mood usually describes as irritable rather than sad in kids but may report both sadness and irritable

Front 309

Bipolar d/o descrip

Back 309

complex brain based illness with primary characteristics of disturbance in mood

mood disturbance often of both polarities:
Depressive
Expansive or manic

Represents an excessive or distorted degree of sadness or elation or both
complex genetic, biochem and enviro etiological factors

manifest with behavioral affective cognitive and somatic sx

May have precipitating event situation or concern

Front 310

This disorder is a complex brain based illness with a primary characterc of disturbance in mood

mood disturbance often of both polarities

Back 310

BIpolar disorder

mood disturbance polarities
depressive
expansive or manic

Front 311

One of 3 patterns of sx present in bipolar pts

Back 311

~single polarity sx only
~manic sx only
~cyclic sx patterns of alternating polarity, manic sx alternating with depressive sx, mixed polarity sx at the same time

Front 312

Bipolar d/o manifests with ____, _____, ______, _________ sx

Back 312

BIpolar d/o manifests with cognitive, affective, behavioral and somatic sx

Front 313

Etiology of bipolar disorder

Back 313

multiple theories ranging from psychological to neurobiological

~probable multifactorial etiological profile

*NT dysreg
*GABA dysreg
*increased noradrenergic activity
*voltage-gated ion channel abnormalitites
*abnormalities lead to abnormal balances of intracellular & extracellular levels of NT which then cause susequent disruption of electric signal transmission in brain regions
*kindling
*long lasting, epileptogenetic changes induced by daily substreshold brain stimulation
*~*~brain becomes overly sensitive to electrical stimuli
*~*~neuronal misfiring occurs
*~*~process becomes automatic, neuronal firing occurs even w/o stimuli

Front 314

long-lasting epileptogenic changes induced by daily subthreshold brain stimulation

Back 314

~*brain becomes overly sensitive to electrical stimuli
~*neuronal misfiring occurs
~*process becomes automatic, neuronal firing occurs even w/o stimuli

probable part of the multifactorial etiological profile of bipolar d/o

Front 315

Abnormalities that lead to abnormal balances of intercellular and extra cellular levels of NT which then cause

Back 315

subsequent disruption of electric signal transmission in brain regions

bipolar d/o etiology theory

Front 316

GABA dysregulation

Back 316

Bipolar d/o etiology theory

Front 317

voltage gated ion channel abnormalities

Back 317

bipolar d/o etiology theory

Front 318

kindling

Back 318

bipolar d/o etiology theory

process of neuronal membrane threshold sensitivity dysfunction

Front 319

is bipolar d/o more or less common than MDD

Back 319

less common

0.7 % of general population at risks

affects 2.3 million american adults; 1.2% of us adult population

Front 320

Mean age of onset for bipolar d/o

Back 320

early 20s

common in the adolescent yrs

Front 321

Risk factors for bipolar d/o

Back 321

~genetic loading
~family hx of 1st order relative having MDD or BP d/o

Front 322

24% increased risk of BP d/o if relative had BPd/o type____

Back 322

24% increased risk if relative has BP disorder type I

Front 323

5% increased risk if relative has BP d/o type _____

Back 323

5% increased risk if relative has BP d/o type II

Front 324

25% increased risk of BP d/o if relative has ____

Back 324

25% increased risk of BP d/o if relative has MDD

Front 325

Prevention and screening general

Back 325

At risk family edu
community edu
**stigma reduction
**s/s of illness
**tx potential for control of sx
Early recognition, intervention and initiation of tx

Front 326

Bipolar d/o does or does not have a prodromal sx period

Back 326

Significant & protracted prodromal sx period usually noted before full onset of illness

usually mild manifestations of criteria sx before full clinical syndrome apparent

Front 327

The longer time period between onset of sx and dx of bipolar d/o....

Back 327

the more difficult to interrupt cyclicity of illness

Front 328

Bipolar I diagnostic criteria

Back 328

Persistently elevated or irritable mood lasting at least 1 week
~3 of the following (if predominant mood elevated or expansive) or 4 of the following (if predominant mood is irritable)
**inflates self-esteem;grandiosity
**decreased need for sleep
**pressured speech
**flight of ideas/racing thoughts
**distractibility
*increased goal directed activity/psychomotor agitation
*impulsivity
~do not have to have had a depressive episode
~marked impairment hospitalization or psychotic features
~sx not d/t substance or medical problem

Front 329

dysthymia d/o cannot have what sx?

Back 329

Psychosis

Front 330

bipolar II d/o diagnostic criteria

Back 330

~at least 1 depressive episode
~at least 1 hypomanic episode
**persistently elevated, expansive, or irritable mood @ least 4 days
**3 ot the other s/s (if mood elevated/expansive) 4 s/s if mood irritable)
***inflated self esteem/gradiosity
***decreased need for sleep
***pressured sleep
***flight of ideas/racing thoughts
***distractibility
***increased goal directed activity/psychomotor agitation
***impulsivity
~disturbance is observable by others
~never had psychotic s/s
~has neveer been a manic episode or mixed episode
~never needed hospitalization

Front 331

time period for abnormally or persistently elevated, expansive or irritable mood in bipolar d/o

Back 331

Lasting for @ least 1 week

Front 332

Mood episode has rapid development and escalation of s over a few days

Back 332

think bipolar

Front 333

mood disturbance may result in brief psychotic sx

Back 333

Bipolar

psychotic sx also possible in MDD

Never present in dysthymic d/o

Front 334

Manic episodes last _____ to ____

Back 334

Manic episodes last DAYS to SEVERAL MONTHS

in 60% of bipolar pts major depressive episode immediately precedes or follows the manic episode

Front 335

____ episodes have a shorter duration and ending more abruptly than _______ episodes

Back 335

MANIC episodes have a shorter duration and ending more abruptly than major depressive episodes

Front 336

Persistance of suggestive sx such as _____ think Bipolar

Back 336

~decreased need for sleep
~feels rested after 3 hrs of sleep on average
~usually a marked difference from normal baseline sleep pattern
~inflated self-esteem
~grandiosity
~ increased goal-directed activities
~excessive involvement in pleasurable activities with a high potential for painful consequences
~unrestrained buying sprees
~sexual indiscretions
~unsound business ventures
~excessive substance use or abuse

Front 337

Hypomanic

Back 337

~similar to mania
~briefer in duration
~episode not a s severe as mania
~does not require hospitalization
~does not cause significant functional impairment

Front 338

Type I bipolar

Back 338

clinical hx characterized by occurrence of one or more manic OR MIXED episodes

Front 339

Type II bipolar

Back 339

Clinical hx characterized by occurrence of one or more major depressive episodes accompanied by at least one hypomanic episode

mood episodes either major depressive, manic, hypomanic or mixed

Front 340

Rapid cycling

Back 340

In a small subset of individuals with BP d/o the recurrent shifts in polarity can occure more frequently

occurrence of 4 or more mood episodes in the previous 12 months

mood episodes either major depressive, manic, hypomanic or mixed

other than occurring more frequently, mood episodes same as non-raapid cycling episodes

20% of individuals w/ BPd/o have rapid cycling

most rapid cyclers are women (90%)

Front 341

Things to consider r/t rapid cyclers

Back 341

Most rapid cyclers are women (90%)

occurrence of 4 or more mood episodes during previous 12
months

identifying rapid cycling is important

antidepressants may accelerate rapid cycling

Individuals w rapid cycling have poorer prognosis

Front 342

Common seen of BP d/o speech

Back 342

~rapid
~loud
~pressured
~difficult to interrupt
~joking, irreverent, amusing
~word clanging in severely ill

Front 343

Common affect of BP d/o

Back 343

~labile
~irritable
~overly theatrical and dramatic

Front 344

Appearance of BD d/o pt

Back 344

~psychomotor restlessness or agitation
~frequent change of dress
~prone to light colored, often sexualized dress
~dramatic or flamboyant dress usually out of character for person when compared to nonsymptomatic periods

Front 345

Mood in manic

Back 345

euphoric
~cheerful
~high
~expansive
~irritable

Front 346

thought process in BP d/o

Back 346

~thought racing
~flight of ideas
~thoughts disorganized & incoherent in severely ill pts

Front 347

THough content in BP d/o

Back 347

~Inflated self-esteem
~indiscriminate enthusiasm
~inflated sense of abilities bordering on delusional
~increased sexual content

Front 348

BP d/o orientation

Back 348

Fully oriented

Front 349

BPd/o memor

Back 349

Impaired short term
Impaired recall

Front 350

BP d/o concentration

Back 350

HIGHLY distractible

Front 351

BP d/o judgement

Back 351

POOR

prone to imprudent behavioral choices with potential for consequencesnegative

Front 352

BP d/o insight

Back 352

pt usually does not recognize that they are ill

resists tx options

Front 353

Labs to order on BP d/o pt

Back 353

To r/o metabolic causes or unidentified conditions
~CBC
~chemistry profile
~thyroid dxn tests
~b12 level

Drug toxicity screenin

Front 354

lab abnormalities found in BP d/o

Back 354

NT levels: 5HT, DA, & GABA

Pharm provocation tests; increased cortisol secretion

polysomnographic findings sim to MDD

Front 355

If 1st onset of manic sx occurs after age 40

Back 355

most likely not BP d/o

most likely sx are caused by another medical conditions

Front 356

Many medical condition mimic manic sx

Back 356

~endocrine d/o
~Hyperthyroidism
~Intoxication of withdrawl from illicit drug use:
**amphetamines
**cocaine
**hallucinogens
**opiates

Front 357

Medications that can cause mimic of manic sx

Back 357

~captopril
~Cimetidine
~corticosteroids
~cyclosporine
~disulfiram
~Hydralazine
~Isoniazid

Front 358

Mania can be precipitated by tx used for MDD or other unipolar mood disorders

Back 358

~antidepressants
~ECT
~light therapy

Front 359

During acute manic episodes or significant depressive episodes bipolar pt may require brief hospitalization to....

Back 359

~ensure pt safety
~ensure pt compliance with tx to reach stabilization
~rapidly stabilize on medication

Front 360

Pharm mgmt of bipolar pts

Back 360

Pharmacological management should never entail the use of an antidepressant agent if a MOOD STABILIZING agent is not in place

~especially important in pt who are rapid cycling
~well known to precipitate manic polarity shift
~can worsen the kindling process

Front 361

Commonly used mood stabilizing agents

Back 361

~Lithium Carbonate
~Carbamazepine
~Valproic acid: divalproex Na
~Lamotrigene
~topiramate
~Oxcarbazepine
~Carbamazepine ER
~Levetiracetam
~Zonisamide

Front 362

Lithium Carbonate

Back 362

~gold standard for tx manic episodes
~action largely unknown
~long hx of use
~drug profile well established
~evidence exists showing some effectiveness on depressive sx as well as on manic sx
~Has many clinically sig side effects
~pts on this drug require careful monitoring
~narrow therapeutic index

Front 363

Gold standard for tx manic episodes

Back 363

Lithium carbonate

Front 364

Serum lithium level

Back 364

therapeutic effect and potential for adverse side effects monitored by serum lithium level

~drawn as trough level
~12hrs post-dose
~therapeutic serum range 0.5-1.2 mEq/L
Greater than 1.2 mEq/L increases risk for toxic side effects

Front 365

What baseline labs do you need before initiation of lithium to ensure safety and efficacy

Back 365

~thyroid panel
~serum creatinine
~blood urea nitrogen (BUN)
~urinalysis
~CBC
~EKG for pts older 50

Front 366

Rapid-cycling clients seldom respond to ....

Back 366

Lithium

Front 367

Anticonvulsant mood stabilizing agents

Back 367

~often considered 1st line agents and almost always 1st line agents for rapid cycling pts

~Action reduces kindling
~Response to tx with lithium or anticonvulsant medications 1-2 weeks

Front 368

How long does it take for a response with lithium or anticonvulsant medications

Back 368

1-2 weeks

Front 369

Endocrine side effect of lithium

Back 369

~weight gain
~impaired thyroid fxning

Front 370

Central nervous system side effect of lithium

Back 370

~fine hand tremors
~fatigue
~fasciculations
~mental cloudiness
~headaches
~course hand tremors with toxicity
~Nystagmus

Front 371

dermatological side effect of lithium

Back 371

~maculopapular rash
~pruritis
~acne

Front 372

GI side effects of lithium

Back 372

~GI upset
~diarrhea
~vomiting
~cramps
~anorexia

Front 373

Renal side effects of lithium

Back 373

~Polyuria with related polydipsia
~Diabetes insipidus
~Edema
~microscopic tubular changes

Front 374

Cardiac side effects of lithium

Back 374

~t wave inversions
~dysrhythmias

Front 375

Hematological side effects of lithium

Back 375

~leukocytoisis

Front 376

Lithium cabonate
trade name
dose
therapeutic plasma level

Back 376

Eskalith, Lithobid
1200-2400mg/d (acute)
900-1200mg/d (maintenance)

0.8-1.2mEq/L acute
0.6-1.2mEq/L maintenance

Front 377

Common side effects of lithium

Toxicity side effects of lithium

Back 377

Nausea, fine hand tremors, increased urination and thirst

Toxicity: slurred speech, confusion, severe GI effect

Front 378

Risk for what medical condition with lithium tx

Back 378

hypothyroidism

Front 379

Li and pregnancy

Back 379

avoid in pregnancy especially 1st trimester

Front 380

Carbamazepine
Trade name
Dose
Therapeutic plasma level

Back 380

Trade name: tegretol
Dose: 400-1600mg/d
Therapeutic plasma level: 6-12mcg/ml

Alternative to lithium or valproic acid

Hepatic enzyme inducer

Front 381

Tegretol
rare and common side effects

Back 381

carbamazepine
Rare: agranulocytosis

Common: nausea,
dizziness
sedation
headache
dry mouth
constipation
skin rash

Front 382

Carbamazepine and preggo?

Back 382

(Tegretol)
Avoid in pregnancy especially in the 1st trimester

Front 383

Tegretol monitor what?

Back 383

Monitor LFTs

Front 384

Alternative to lithium or valproic acid

Back 384

Carbamazepine (tegretol)

Front 385

Valproic acid
Trade:
dose:
therapeutic plasma level:

Back 385

Divalproex Sodium (other generic)
Trade: depakene, depakote
Dose: 15-40mg/kg/d
Therapeutic plasma level: 50-125mcg/ml

Avoid in pregnancy, especially 1st trimester

Depakote minimizes GI effects

More effective than lithium for rapid cycling and mixed bipolar

Load dose: 20mg/kg

Front 386

Divalproex sodium loading dose

Back 386

20mg/kg

Front 387

Common side effects for depakote

Back 387

Depakene, valproic acid, divalproex sodium

nausea
diarrhea
abdominal cramps
sedation
tremor

Front 388

Rare side effects for depakene

Back 388

Depakote, valproic acid, divalproex sodium

increased liver enzymes

Front 389

depakote minimizes ____ effects

Back 389

Depakene (depakote, valproic acid, divalproex sodium) minimizes GI effects

Front 390

Drug more effective than lithium for rapid cycling and mixed bipolar

Back 390

Valproic acid, divalproex sodium, depakene, depakote

Front 391

Avoid in preggos especially 1st trimester

Back 391

~Lithium carbonate
~carbamazepine
~valproic acid

Front 392

Lamotrigene
Trade
Dose
Therapeutic plasma level

Back 392

Lamictal
Dose: 25-600mg/d
T. plasma level: blood monitoring not necessary

Titrate dosages slowly

Front 393

Lamictal common side effects

Lamictal rare side effects

Back 393

Common:
~dizziness
~ataxia
~somnolence
~diplopia
~nausea
~headache
~hepatotoxicity

Rare:
life-threatening rashes
Leukopenia

Front 394

What to monitor for of lamotrigene?

Back 394

monitor for blood dyscrasia

steven Johnson's rash

Front 395

Helps in depressive phase of bipolar affective disorder

Back 395

Lamotrigene

evidence exists showing some effectiveness of lithium carbonate on depressive sx as well as on manic sx

Front 396

Topiramate
Trade
Dose

Back 396

Topamax
400-1200mg/d
blood monitoring not necessary

decreased efficacy of birth control agents and digoxin

decreases IQ

Front 397

Common side effects of topamax

Back 397

somnolence,
fatigue
altered cognition (reduce IQ)
paresthesia

WT loss (decreases appetitie)

Front 398

rare side effects of topiramate

Back 398

Kidney stones
glaucoma

Front 399

Monitor what for patients on topiramate

Back 399

monitor for glaucoma

monitor for kidney stones

make sure on 2 forms of birth control

Front 400

Oxcarbazepine
trade
dose

Back 400

Trileptal
300-24000mg/d
blood monitoring not necessary

May cause hyponatremia

Front 401

Oxcarbazepine common side effects

Back 401

~sedation
~dizziness
~headache
~fatigue
~GI distress
~abnormal vision
~weight gain

May decrease efficacy of birth control pills

Front 402

Rare side effects of oxcarbazepine

Back 402

(trileptal)

hyponatremia

Front 403

Monitor what for patients on trileptal?

Back 403

(Oxcarbazepine)

Monitor sodium levels (may cause hyponatremia although a rare side effect)

May decrease efficacy of birth control pills

Front 404

Carbamazepine ER
Trade
Dose

Back 404

Equetro
200-1600mg/d
Blood monitoring not necessary

No need to obtain blood levels as with tegretol

Front 405

Levetiracetam
trade
dose

Back 405

Keppra (mood stabilizer)
250-3000 mg/d

Monitor for leukopenia

Front 406

Keppra rare SE

Back 406

Levetiracetam (mood stabilizer)

Anemia

monitor for leukopenia

Front 407

Common SE for levetiracetam

Back 407

Keppra (mood stabilizer)
sedation
dizziness

Front 408

Zonisamide
trade
dose

Back 408

zonegran (mood stabilizer)
100-600mg/d

contraindicated w/sulfonamide allergy

may potentially cause wt loss

Front 409

what mood stabilizer is contraindicated with sulfonamide allergy

Back 409

Zonisamide
Zonegran (trade)

Front 410

common side effects of zonizamide

Back 410

Zonegran (mood stabilizer)

~sedation
~dizziness
~ataxia
~headache
~gi distress

May potential cause wt loss

Front 411

Rare side effects of zonegran

Back 411

~kidney stones
~elevated serum creatinine and blood urea nitrogen
~anemia
~Steven Johnson's syndrome
~agranulcytosis

CONTRAINDICATED WITH SULFONAMIDE ALLERGY

Front 412

During an acute phase of manic episode nonpharm mgmt

Back 412

monitor and help pt meed nutritional needs (finger foods)

~help pt meet sleep-rest needs
~monitor safety

Front 413

common comorbidities with bipolar

Back 413

substance abuse

hypothyroidism

Front 414

High risk activities from manic behavior

Back 414

sexual
~pt eduction for STIs
~assessment & monitoring for STIs
financial/legal
~pt access to community resources
~nutritional counseling

Front 415

Adolescent manic episodes present differently than adult episodes

Back 415

~more psychotic features
~often associated with antisocial behavior
~often associated with substance abuse
~prodromal period of sig behavioral problems
***school truancy
***failing grades

Front 416

tx duration & success rates w bipolar

Back 416

vary with individual characteristics and motivation

Front 417

relapse in bipolar

Back 417

relapse is common and frequently occurs

relapse plans need to be developed

pt should be taught sx of mania and depression and that the d/o are chronic illnesses

Front 418

Bipolar and women

Back 418

pharmacological agents for BP disorder especially Li are teratogenic

Women of child bearing years need effective contraceptive care while on BP disorder tx medication

Front 419

Routine use of lab tests to monitor for therapeutic serum levels of anticonvulsants and Lithium is needed

Back 419

routine evaluation of
~CBC
~renal fxn
~thyroid fxn for pt taking lithium long term is needed

Front 420

what standardized rating scales are needed to monitor clinical status in bipolar and why do do you use standardized rating scales

Back 420

Young mania rating scale YMRS
Mood disorder questionnaire MDQ

to establish baseline fxning and monitor disorder course over time

Front 421

CYCLOTHYMIC d/o

Back 421

chronic fluctuating mood disorder whose sx are similar to but less severe than BP d/o

Numerous periods of hypomanic and dysthymic sx

Front 422

Incidence and demographics of cyclothymic d/o

Back 422

lifetime prevalence 0.4-1%
~Insidious onset
~chronic course
~begins early in life
~15-50% of ppl w/cyclothymic d/o subsequently develop BP d/o

Front 423

Risk factors for cyclothymic d/o

Back 423

~genetic loading
~family hx
~BP d/o type I
~substance abuse

Front 424

Cyclothymic d/o

assess for the following in the hx

Back 424

~fluctuating mood episodes
~individuals can fxn well during hypomanic episodes
~may experience clinically significant distress or impaired fxn related to cyclicity
~unpredictable mood changes
~Often regarded by others as
TEMPERAMENTAL, MOODY, UNPREDICTABLE, INCONSISTENT & UNRELIABLE
~no psychotic episodes

Front 425

Psychiatric differential dx with cyclothymic d/o

Back 425

~BP d/o
~dysthymia
~substance abuse

Front 426

Pharmacological mgmt of cyclothymia

Back 426

~similar to MDD & BP d/o
~because of increased risk for development of BP d/o commonly tx with medication

Front 427

Life span considerations for cyclothymia

Back 427

~usually begins in adolescence
~onset in later life usually suggests general medical condition such as multiple sclerosis