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427 Cards in this Set
- Front
- Back
Most common of all psychiatric illnesses and can manifest initially as physical health states
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Mood disorders
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It has become increasingly common for mood disorders to be treated where & why?
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In primary care setting
because often pt 1st present to primary care because of the high degree of somatic symptomatology that accompanies mood disorders |
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Are mood disorders well tx in primary care?
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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
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How common or normal is depression?
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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 |
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Pathological levels of depression require _______ and generally will not _______without __________
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Pathological levels of depression require TREATMENT and generally will not RESOLVE without THERAPEUTIC INTERVENTION
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Depression is one of the most common human emotions
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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
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Do cultural differences affect depression?
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Yes cultural differences affect the behavioral manifestations of depression
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Depression can be a normal healthy reaction to life stressors that
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that motivates the person to deal with events and emotions
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Depression can be pathological if:
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~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 |
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The primary unipolar affective disorder
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Major depressive disorder
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MDD description
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~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 |
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MDD etiology
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~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 |
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Desynchronization of the circadian rhythms produce the sx constellation collectively called MDD is what theory of etiology?
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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 |
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Circadian rhythms control what biological processes that are frequently problems in depressed pts?
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*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 |
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What consistent abnormalities has neuroimaging demonstrated in certain structures of the brain in individuals w/ chronic and severe depression?
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~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 |
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Psychodynamic theories of depression's etiology
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*object loss theory (fairbairn, winnicott, guntrip)
*aggression-turned inward theory(freud) *Cognitive theory (beck) *learned helplessness-hopelessness theory (seligman) |
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Biological Theories of depression's etiology
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*Genetic predisposition
*endocrine dysfxn *abnormalities of NT fxn *structural brain changes *chronobiological theory |
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Structural brain changes biological theory of depression
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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 |
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Abnormalities of NT fxn biological theory of etiology of depression
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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 |
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In postmortem studies on individuals who commit suicide and in ppl w/ MDD showed
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Low 5HT levels
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Deregulation of one or more biogenic amind NTs
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(specifically DA, 5HT, NE)
Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn |
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Low levels of endogenous catecholamines in specific areas of the brain
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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 |
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Low levels of precursor tryptophan
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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 |
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Low levels of 5HT metabolite 5HTIAA
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Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn
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Receptor sensitivity for NTs set unusually hign in specific areas of the brain
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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 |
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Low density of receptor sites in specific areas of the brain
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Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn
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Hypometabolis in specific areas of the brain regulating mood, appetite and cognition
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Possible NT fxn abnormality causing depression according to the biological theory of etiology of MDD; abnormalities of NT fxn
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MDD NOT JUST DUE TO LOW LEVEL OF 1 NT
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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 |
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Dexamethasone suppression test
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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) |
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HPA controls?
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the physiological response to stress
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HPA is composed of.....?
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interconnective feedback pathwasys between the hypothalamus, pituituary gland, and the adrenal glands
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Desregulation of hypotahalamic-pituitary-adrenal axis
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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 |
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HPA cascade of rxns....
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~ 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 |
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Effects of cortisol on the brain
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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 |
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High incidence of postpartum mood disturbances suggests
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endocrine dysfxn as part of the etiologic picture of MDD
Endocrine dysfxn theory of MDD etiology |
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Neurovegetative sx commonly seen in MDD
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*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 |
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Genetic predisposition for MDD
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~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 |
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the earlier the age of onset of MDD & the more severe the sx the more likely it is that __________
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a person has a strong genetic load for depression
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The single strongest predictor of depression
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having a depressed parent
clear genetic predisposition |
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*sleep disturbances
*appetite disturbances *libido disturbances *lethargy *anhedonia |
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 |
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Object loss theory
etiology of MDD |
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 |
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Aggression-Turned-Inward Theory
etiology of MDD |
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 |
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kid experiences loss of mom
and rxn is mourning, despair, grief, separation anxiety |
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 |
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Kid experiences loss of mom
and rxn is anger |
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 |
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Learned helplessness hopelessness theory
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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 |
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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
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Learned helplessness hopelessness theory
psychodynamic theory of etiology of MDD |
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Cognitive theory
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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 |
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Theory that people with tendency to be depressed think differently than nondepressed
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Cognitive theory
thinking is more negative, believe that bad things are going to happen to them because of their own personal shortcomings and inadequacies |
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Thinking that is more negative, believe that bad things are going to happen to them because of their own personal shortcomings and inadequacies PROMOTES
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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 |
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When confronted by stressful events, these ppl tent to appraise them & the potential consequences in a negative, hopeless manner and therefore
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are more depressed than individuals with different cognitive styles
Cognitive theory as a etiology of MDD |
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How common in MDD ?
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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 |
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Most common psychiatric illness seen in primary care practices
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MDD
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Leading cause of disability in the US?
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MDD
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Per of people with MDD who ever receive tx?
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50%
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Average age of onset for MDD
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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 |
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MDD and women
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~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 |
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MDD mortality
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~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 |
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MDD disease course
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~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 |
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If left untreated an episode of sx of MDD usually lasts __________ or longer
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4 mo
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MDD tend to a _____, ______ illness
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chronic , recurrent
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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 |
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
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The # of prior episodes of MDD predict.....
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the likelihood of future episodes of MDD
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The is approx a ______% risk of a 2nd episode in a person w 1st episode of MDD
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There is approximately a 60% risk of a 2nd episode in a person w/ 1st episode
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There is approximately a _____%
risk of a 3rd episode after the 2nd episode of MDD |
There is approximately a 70% risk of a third episode after the 2nd episode of MDD
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There is approximately a ____% risk of a 4th episode after the 3rd episode of MDD
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There is approximately a 90% risk of a 4th episode after the 3rd episode of MDD
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Risk factors for MDD
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~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 |
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Prevention & screening of MDD
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~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 |
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Assessment
Initial presentation |
often manifests as vague somatic complaints
*bodily aches, pains *headaches *muscle pains *lack of energy *GI problems *Sleep disturbance (almost always present) |
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Women often report sx of MDD occurring>>>>
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in fixed pattern around several days before onset of menses
so assess menstrual hx |
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Sleep disturbance and MDD
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Almost always present
*typically problems occur w/ middle or terminal insomnia *hypersomnia can be present *Diurnal variations can be present |
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A prodromal episode of MDD commonly consists of
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a high level of subjective anxiety
mild depressive sx often develops over days to weeks before onset of a full episode |
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DSM-IV-TR diagnostic criteria for MDD
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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 |
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Melancholic feature of depression
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Sx worse in the morning
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PMDD is coded as WHAT?
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Depression NOS
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NOS diagnoses does not belong where?
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In differential diagnosis
NOS means didn't have enough time or doesn't meet criteria but important psych symptomalogy |
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Steps for differential diagnosis
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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) |
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To be considered Pathology in psych must have
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presence of specific distress or impairment
Axis II: the practitioner gets to observe inflexible and pervasive behavior cause distress (pt doesn't see it ) |
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Step one of Differential diagnosis
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Is the presenting sx real?
Some patients may elect to deceive the clinician by producing or feigning sx |
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Step 2 of Differential diagnosis
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R/O substance tiology
including drugs of abuse, medication, toxin exposure, environmental exposure |
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Step 3 of Differential diagnosis
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R/o d/o d/t gen medical condition
refer if need be |
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Step 4 of Differential diagnosis
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determine the specific primary disorder(s)
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Step 5 of differential diagnosis
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differentiate adjustment disorder from NOS
***bereavement sx w/o a loss is adjustment d/o |
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Step 6 of differential diagnosis
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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) |
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Individuals with certain other disorders (e.g. _____, ____, _____, _____) have a statistically significant increased risk for MDD.
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Individuals w/ certain other disorders (e.g. diabetes, myocardial infarction, carcinomas, stroke) have a statistically significant increased risk for MDD
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Physical exam findings in MDD
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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 |
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Lethality of intended suicide action
High: Moderate: Low: |
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 |
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Assessing for suicidal behavior
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~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 |
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Labs to run if think MDD
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~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 |
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Common abnormal lab findings in MDD
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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 |
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Before establish MDD diagnosis obtain baseline lab studies to r/o other differential dx
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!thyroid panel
CDC w. differential Electrolyte panel drug screen |
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Polysomnographic testing abnormalities of MDD include
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*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 |
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Med w/ altered mood states as side effects
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~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 |
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Endocrine d/o to consider in differential for MDD
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~hypothyroidsm
~diabetes ~hyperaldosteronism ~Cushing's/ Addison's disease |
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Infectious & inflammatory states to r/o in diff dx for MDD
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~Mononucleosis
~AIDS ~Pneumonia: Viral & bacterial ~Systemic lupus erythematosus ~Temporal arteritis ~Tuberculosis |
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Cardiac d/o to r/o in diff dx for MDD
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~myocardial infarction
~Congestive heart failure ~Hypertension |
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Neurological d/o to r/o in diff dx for MDD
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~Stroke
~Epilepsy ~Dementia ~Huntington's disease ~Sleep apnea ~Wilson's disease ~Neoplasms ~Head trauma ~Multiple sclerosis |
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Nutritional disorders to r/o in diff dx for MDD
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~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. |
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Other d/o to r/o in diff dx for MDD
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~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 |
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Psychiatric d/o to r/o in diff dx for MDD
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~Anxiety d/o
~Eating d/o ~Bipolar affective d/o ~substance dependence-related d/o |
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Reasons for brief hospitalization during acute episodes of MDD
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~to ensure pt safety
~to initiate med change ~to restabilize on med ~to monitor suicidality ~to ensure pt compliance w/ tx to reach stabilization |
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The top goal in the acute phase of MDD is
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ensuring pt safety
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Inform pt that therapeutic effect of pharm mgmt may take
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at least 4-6 wks
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Once started continue antidepressants for a minimum of
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8-12 mo
If pt has more than one prior episode of MDD consider longer term use |
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Research has found that the most effective intervention for MDD is
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combination of medication and counseling
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Not all sx of MDD will respond to pharm interventions how to measure response
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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 |
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Target sx of antidepressant tx
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~Depressed mood
~sleep-rest disturbances ~anxiety ~irritability ~impaired concentration ~impaired memory ~appetite disturbance ~agitation ~anhedonia |
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Classes of antidepressants
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~selective serotonin reuptake inhibitors
~tricyclic antidepressants ~monoamine oxidase inhibitors ~Serotonin norepinephrine reuptake inhibitors ~Norepinephrine dopamine reuptake inhibitors ~serotonin agonist and reuptake inhibitors |
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Selective Serotonin reuptake inhibitors (SSRIs)
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~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 |
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SSRI are effective in what d/o
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MDD
Panic d/o OCD Bulima GAD Social phobia PTSD Premenstrual dysphoric d/o (PMDD) |
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Most common sx w/ SSRI
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~headache
~dry mouth ~GI upset ~sexual dysfunction ~nervousness |
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Citalopram
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Brand: Celexa
Class: SSRI Dosage: tablet/ 20-60mg/d Side Effects: ~sedation ~sexual dysfunction ~agitation ~Yawning ~GI disturbances ~Wt gain |
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Escitalopram
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Trade: Lexapro
Class: SSRI Dose: Tablet 20-60 mg/d SE: ~Somnolence ~Headache ~sexual dysfunction ~GI disturbances |
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Fluvozamine
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Trade: Luvox
Class: SSRI Dose: Tablet, 100-300 mg/d SE: ~sedation ~sexual dysfunction ~agitation ~gi disturbances *****Black Box warning for liver toxicity!!!***** |
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Fluoxetine
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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*** |
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Paroxetine
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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 |
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Sertaline
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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 |
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SSRI dose for adolescents/ kids
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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 |
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SSRIs Start LOW and go SLOW especially for
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children
Elderly Patients with anxiety d/o |
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Indications for SSRI
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Depression,
OCD Panic d/o Social anxiety d/o PTSD Eating d/o Borderline personality d/o *from review course slides |
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Pharmacokinetics SSRIs
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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 |
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Serotonin syndrome
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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 |
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Common side effects of SSRI
*slides from review course |
~anziety
~agitation ~akathisia ~insomnia ~nausea ~diarrhea ~sexual dysfxn (may see motor restlessness, behavioral inhibition and disinhibition in kiddos) |
|
High fever in absence of dipherisis
|
It is 5HT syndrome
|
|
To pts with side effects when starting don't fear
|
~most SE will pass
~may need to add buprpion to tx sexual sE or switch to another agent |
|
Why should I take an SSRI for my anxiety when I take it the pill makes me MORE ANXIOUS than I was before?
|
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 |
|
Children and adolescents being tx with antidepressants
|
~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 |
|
TCAs are considered ______lind drugs for tx MDD
|
2nd line
|
|
TCA dirty side effect profile promotes poor patient compliance
SE include |
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 |
|
MANIA inducer psych meds
|
SSRIs in bipolar pts
TCAs are known to induce hypomania in certain pts |
|
Advantages of TCAs
|
~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 |
|
REMEMBER NOT TO Rx TCAs with _________. THIS CAN CAUSE A LETHAL REACTION
|
DO NOT Rx TCAs and MAOIs together can cause a lethal rxn
|
|
Disadvantages of TCAs
|
~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 |
|
Lethal dose of TCA
|
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 |
|
Pt on TCA & SSRI is this okay?
|
Yes but caution bc SSRI can possibly elevate TCA concentrations in the blood stream
MONITOR TCA LEVELS |
|
Pt on TCA and MAOI is this okay?
|
NO THIS CAN CAUSE A LEATHA RXN
DON"T KILL YOU PTS DONT rx TCA & MAOI together |
|
Child of TCA is this okay?
|
Unlike adults kiddos may NOT respond to tricyclics
|
|
Tricyclic antidepressants indications
|
~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) |
|
TCA pharmacokinetics
|
~Therapeutic effects within 3-4 wks
~improved Energy & sleep in 1-4 wks |
|
ALL ANTIDEPRESSANTS HAVE THE SAME _______ ONLY CAN WORK ON _______ & _______
|
All antidepressants have the same EFFICACY only can work on SE and TOXICITY
|
|
TCAs have a ____ theraputic index
|
low theraputic index
Lethal dose is 3x highest dose |
|
TCAs and bezos is this okay?
|
Can give but dose is much less
|
|
TCAs and EtOH is this okay?
|
Can give but does is much less
|
|
Have anticholinergic, antiadrenergic, cardiac and antihistaminergic SE
|
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 |
|
TCAs and Beta blockers is this okay?
|
NO
Cardiac side effects; changes ECG |
|
TCAs and benadryl is this okay?
|
NO
Antihistaminergic side effects already; sedation & wt gain |
|
How do you stop low dose of TCAs?
|
there can be abstinence syndrome so
Avoid abrupt withdrawal Taper |
|
What do should PMHNP monitor in a pt on TCA?
|
~Obtain baseline and yearly ECG
~monitor serum blood levels ~suicidality |
|
TCA in elderly is this okay?
|
Nope
Because of the potential for severe side effects and even death avoid rx to elderly (ortho hypotension--falls Anticholinergic--confusion) |
|
TCA in preggo lady is this okay?
|
NOPE
Because of the potential for severe side effects and even death avoid rx to Preggos |
|
Amitriptyline
|
Brand: elavil
Class: TCA Dose: Tablet/IM ~50-300mg/d **also used ***chronic pain ***insomnia ***sciatica ***fibromyalgia ***trigeminal neuralogia ***diabetic neuropathy |
|
Clomipramine
|
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 |
|
TCA used most often to tx OCD
|
Clomipramine (anafranil)
Pronounced Clum-IP-ra-mean |
|
Hard max dose of clomipramin (anafranil) is _______ because_______
|
250mg/d
due to increased seizure risk |
|
Desipramine
|
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 |
|
Most TCAs are used off label because
|
pts cannot tolerate the high doses needed for antidepressant, (so used for chronic pain, diabetic neuropathy, sleep)
|
|
Doxepin
|
Trade Sinequan
Class TCA Dose capsule, liquid ~100-3--mg/d **also used for insomnia |
|
Imipramine
|
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 |
|
Nortriptyline
|
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 |
|
Protriptyline
|
Trade Vivactil
Class TCA Dose Table ~15-60mg/d |
|
Trimipramine
|
Trade: Surmontil
Class: TCA Dose: Capsule ~100-300mg/d |
|
gun is a ____ lethality plan of suicide
|
High lethality
as is jumping from sig height & hanging |
|
Superficial wrist cutting is a _____ lethality plan of suicide
|
low lethality
as is holding breath |
|
Overdose of toxic agents is a ____ lethality plan of suicide
|
Moderated lethality
|
|
Suicide risk is especially high for individuals w/ certain sx or history: 5 things
|
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 |
|
Luvox generic name and class
|
Fluvoxamine (SSRI)
|
|
zoloft generic name, class and dose range
|
Sertaline
SSRI Tablet 50-200mg/d |
|
Anticholingic sx
|
~dry mouth
~blurred vision ~constipation ~memory problems from muscarinic receptor blockade Seen with TCAs |
|
What is the lethal rxn to watch out for with TCAs?
|
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) |
|
Elavil
|
Amitriptyline
TCA Also used for chronic pain insomnia sciatica fibromyalgia trigeminal neuralgia diabetic neuropathy |
|
Pamelor
|
Nortriptyline
TCA Capsule and Liquid 50-150mg/d Also used for enuresis & ADHD |
|
hypertensive crisis
|
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 |
|
Tyramine
|
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 |
|
MAOIs are never ____ or _____ for MDD because of dangerous food & drug interactions
|
MAOIs are never 1st line or 2nd line agents for MDD because of dangerous food and drug interactions
|
|
What do PMHNP worry about with a pt on an MAOI
|
Drug interxns
Food interxns (foods containing tyramine) resulting in hypertensive crisis Dirty side effect profile |
|
Sx of hypertensive crisis
|
~sudden, explosive-like headache, usually in occipital region
~elevated blood pressure ~facial flushing ~palpitations ~pupillary dilation ~diaphoresis ~fever |
|
Tx of Hypertensive crisis
|
~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 |
|
Pts on MAOIs must be on a ______ free diet & must avoid many meds including most over the counter ___ & ____ preparations
|
Patients on MAOIs must be on a tyramine-free diet & must avoid may medications including most over the counter cold and allergy preparations
|
|
What about MAOIs promote poor pt compliance
|
~ Dirty side effect profile & stringent dietary restrictions
|
|
Clinically sig side effects of MAOIs include:
|
~~insomnia
~hypertension crisis ~weight gain ~anticholinergic side effects ~light headedness & dizziness ~sexual dysfxn |
|
MAOIs are ____ in many co-occuring disorders
|
UNSAFE
|
|
Are MAOIs are expensive or inexpensive?
|
Inexpensive & most com in generic form
|
|
Isocarbozazid
|
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 |
|
Phenelzine
|
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 |
|
What does MAOI stand for?
Mech of Action for MAOI? |
Monoamine Oxidase Inhibitors
Elevate serotonin and norepinephrine levels primary by inhibiting MAO the enzyme that destroys neurotranmitters (in the cytosol) |
|
Tranylocypromine
|
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 |
|
Selegiline
|
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 |
|
EMSAM patch
|
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) |
|
Nardil
|
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 |
|
MAOIs & kiddos
|
not recommended for kiddos
|
|
Marplan
|
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 |
|
Parnate
|
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 |
|
MAOIs efficacy?
|
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 |
|
MAOIs pharmacokinetics
|
Antidepressant effects may take 3-6 weeks
|
|
Most frequent adverse effect of MAOIs
|
Orthostatic hypotension
Most providers worry about the possibility of Hypertensive crisis but this is RARE |
|
Most frequent adverse effectS of MAOIs
|
~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 |
|
Rare side effect of MAOIs
|
Tyramine-induced hypertensive crisis
Avoid food that are preserved, pickled or aged, caffeine, chocolate, soy |
|
Things NOT to mix with MAOIs
|
Tyramine
co-occuring med conditions childhood SSRIs TCAs atypicals decongestants Methyphenidate asthma meds |
|
Most MAOIs will eventually stop working in vast majority of people because
|
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 |
|
Many SSRI inhibit CDY2D6 metabolize why is this important?
|
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 |
|
Indications for MAOI
|
May be useful in the tx of depressed pts with marked anxiety or phobic sx.
Selegiline is also used for the tx of parkinsonism |
|
SSRI dosed for anxiety
|
Low doses at sub-theraputic level for anxiety because 5HT2 issues
Start low go slow |
|
SSRI dosed for depression
|
Normal dose for depression
Therapeutic effects may take 3-6 weeks |
|
SSRI dose for OCD
|
High doses for OCD
therapeutic effects may take 12-16 weeks for OCD |
|
Pt comes in has a sudden explosive-like headache in the occipital region
|
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 |
|
Tyramine effects
|
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 |
|
Switching from SSRI to MAOI anything important?
|
Must be off SSRI for at least 14 days.
SSRI + MAOI can possibly = death |
|
SSNRIs MOA
|
~Inhibit dual reuptake
~Action very selective on NTs ~Elevate 5HT & NE levels by inhibiting their reuptake |
|
SSNRI drugs
|
Effexor Venilafaxine
Must be at dose of 225 to be SSNRI, acts as SSRI at lower doses cymbalta Duloxatine |
|
Serotonin- 2 antagonist reuptake inhibitors drugs
|
SARIs
Nefazodone (serzone Trazodone (desyrel) Heterocyclic (between TCA & SARIs) class technically but close 1st cousin with serzone |
|
Venlafaxine
|
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 |
|
Duloxatine
|
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 |
|
Desyrel
|
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 |
|
Venlafaxine Side effects
|
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 |
|
Nefazodone
(pronounced NA-FAZE-A-DONE or NA-FAZ-A-DONE) |
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 |
|
Trazodone
|
Desyrel
SARI Tablet 200-600 (depression) 50-200mg/hs (insomnia) ~May potentially proong QTc interval ~Priapism possible |
|
Cymbalta
|
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 |
|
Cymbalta big risks
|
Elevated LFTs & HTN
Discontinuation syndrome |
|
Serzone
|
Nefazodone
SARI |
|
SARI stands for
MOA of SARI |
Serotonin-2 antagonist/ reuptake inhibitors
~Dual action ~Agonist of 5HT-2 receptors ~Action very selective on NTs ~Elevate 5HT levels by inhibiting serotonin reuptake |
|
Effexor XR
|
SNRI
XR 75-225 mg/d ~Potent inhibitor of CYP450 ~once a day dosing ~Can raise BP ~Significant discontinuation syndrome |
|
Bupropion
|
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 |
|
Antidepressants that generally will not as a class cause sexual side effects
|
Bupropion (wellbutrin, Zyban)
Mirtazapine (remeron) |
|
Dont give Bupropion to who
|
Pts with history of seizure
Bulimics |
|
Wellbutrin is good in what d/o
|
~bipolar
~ADHD ~dysthmic ~depression |
|
Mirtazapine
|
Remeron
Tablet 15-45mg/d ~Inverse relationship between dosage and sedation ~WT GAIN ~increased cholesterol |
|
Bupropion come in what formulations ?
|
Bupropion 150-450mg/d
Sustained release 150-400mg/d MAX 400 Extended release 150-450mg/d MAX 450 |
|
NDRI stands for what?
NDRI MOA? |
Norepinephrine dopamine reuptake inhibitors
Inhibit dual reuptake Action very selective on NTs Elevate dopamine & NE levels by inhibiting their reuptake |
|
Classes of antidepressants that elevate 5HT
|
~SSRI
~TCA ~MAOI ~SARI |
|
Classes of antidepressants that elevate norepinephrine
|
~TCA
~MAOI ~SSNRI ~NDRI |
|
Classes of antidepressants the elevate dopamine
|
~NDRI
|
|
Since psychotic features can be present with MDD should
|
routinely assess for the presence of psychotic sx during periods of sx exacerbation
|
|
Psychotic features in MDD
|
Are usually mood congruent
~Can be managed in short-term use of antipsychotic med ~psychosis is less common in kids before onset of puberty |
|
Electroconvulsive Therapy
|
ECT
~Grand mal seizure induced in anesthetized individual Usual course 6-12 treatments |
|
Usual # of tx in ECT
|
6-12
|
|
ECT MOA
|
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 |
|
Similar new methods to ECT
|
Transcranial magnetic stimulation
vegal nerve stimulation Phototherapy |
|
Individual therapy methods in MDD
|
CBT
Brief therapy (solution focused therapy) Group therapy Family therapy |
|
Goals of CBT in MDD
|
~Modify perceptions
~decrease negativity ~increase sense of internal control ~enhance coping skills ~modify environmental factores contribution to illness |
|
Goals of brief therapy (solution focused therapy) in MDD
|
~focus on precipitant stressor
~cope with immediate impact of MDD on personal life ~modify contributory environmental factors |
|
Goals of group therapy with MDD
|
~improve decision making
~improve socializations skills ~improve assessment of individual strengths ~gain new coping skills |
|
Goals of family therapy with MDD
|
~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 |
|
Clinical mgmt of suicidality
|
~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 |
|
Risk factors for suicide
|
~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 |
|
MDD sx in kiddos
|
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 |
|
MDD often has a strong ______________ component in kids
|
separation anxiety
|
|
These core sx are less common in kids before onset of puberty
|
~psychosis
~motor retardation ~hypersomnia ~increased appetite |
|
kids usually do not respond well to ______; however they do respond well to _______
|
do not respond to TCAs
do respond to SSRIs Monitor closely for suicidal behavior, agitation and aggression in kids taking antidepressants |
|
What to monitor for in kids taking antidepressants
|
SUICIDAL BEHAVIOR
inform parents so they can watch for this as well agitation aggression |
|
Individuals with MDD admitted to a long-term-care facility have _________spans than normal population
|
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 |
|
_____ & _____ sx of MDD in the elderly population often are confused with ________-related sx
|
COGNITION AND MEMORY sx of MDD in the elderly population often are confused with dementia-related sx (pseudodemntia)
|
|
In dementia there is usually a premorbid hx of _______ declining cognition
|
Slowly declining cognition
|
|
In MDD cognitive changes ahd a relatively ____ onset and are ____when compared to premorbid functioning
|
In MDD cognitive changes have a relatively ACUTE onset and are SIGNIFICANT when compared to premorbid functioning.
|
|
It is important to complete a functional assessment for elderly pts to....
|
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 |
|
Skill deficit:
|
inability to perform a functional skill despite the physical ability as in dementia
|
|
Performance deficit:
|
ability to perform a functional skill but lacks the motivation to do so as in depression
|
|
Reasons fro performing functional assessment
|
(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 |
|
Components of functional assessment
|
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 |
|
ADLs
|
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 |
|
IDLs
|
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 |
|
Executive functioning of the _______ assessment is
|
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. |
|
The degree of change over time and the speed of change of the functional assessment are better observed with
|
objective recording and when the assessment is measured at intervals such as q 6 mo
|
|
Follow-up care for MDD
|
~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) |
|
Teach patient about
|
~their diagnosis
~benefits/risks, potential SE of med tx ~sx of depression ~chronic nature of illness ~assess for suicide, psycotic sx, |
|
Drug combinations that may cause serotonin syndrome
|
~SSRIs & MAOIs
~Drug & herbal interactions ~SSRIs & St. John's wort (a weak MAOI) |
|
Symptoms of 5HT syndrome
|
~Fever w/o sweating
~Restlessness ~agitation ~myoclonis ~hyperreflexia ~hyperthermia ~diaphoresis ~altered sensorium ~tremor ~chills ~diarrhea & cramps ~ataxia ~headache ~insomnia |
|
Some SSRIs are known to increase _______ & contribute to __________ and others may elevate _____________tests.
|
Some ssris are known to increase BLOOD GLUCOSE and contribute to HYPERLIPIDEMIA and others may elevate LIVER FUNCTION tests
|
|
When discontinuing SSRIs
|
discontinue SSRIs slowly to prevent discontinuation syndrome
|
|
Sx of Discontinuation syndrome
|
~Flu like sx
~fatigues & lethargy ~myalgia (muscle pain) ~decreased concentration ~N/V ~impaired memory ~irritability ~anxiety ~insomnia ~crying w/out provocation ~dizziness and vertigo |
|
Risk factors for discontinuation syndrome
|
~medications with short half-life
~abrupt discontinuation ~non compliant, irregular use pattern ~high dose range ~long-term tx ~prior hx of discontinuation syndrome |
|
Discontinue TCAs slowly..
|
Pts can get cholinergic rebound syndrome
~Nausea ~GI upset ~Diaphoresis ~myalgias (sore muscles) especially of neck muscles |
|
Expected Course of MDD
|
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 |
|
Pts who have had 2 or more episodes of MDD usually require
|
lifelong medications
|
|
How long should pts take an antidepressant agent for how long after remission of sx
|
for at least 12mo after remission of sx
|
|
Evidence indicates the best tx outcomes if what tx is used?
|
medications are used in conjunction with appropriate therapy.
|
|
Pts who have ____ or more episodes of MDD require ______________
|
Pts who have 2 or more episodes of MDD usually require lifelong medications
|
|
DYSTHYMIC D/O
|
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 |
|
Vegatative sx
|
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 |
|
Etiology of dysthymic d/o
|
similar to MDD
|
|
Incidence of dysthymic d/o
|
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 |
|
individuals with dysthymia have an _______ risk of developing _____
|
Individuals with dysthymia have an INCREASED risk for developing MDD
|
|
_______% of individuals diagnosed with dysthymic d/o will have a lifetime episode of MDD
|
15-25% of individuals diagnosed with dysthymic d/o will have a lifetime episode of MDD
|
|
Early onset dysthymic d/o
|
dysthymic sx occur befoer age 21
~usually the type of dysthymic d/o with most sx ~Most at risk for onset of MDD |
|
Late onset dysthymic d/o
|
Dysthymic sx occur at or after age 21
|
|
In pts with onset of dysthymic d/o sx before age ____ there is a ____% likelihood they will have a lifetime episode of ______
|
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
|
|
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? |
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 |
|
2 types of dysthymic d/o
|
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 |
|
Risk factors for dysthymic d/o
|
~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) |
|
Prevention & screening dysthymic d/o
|
~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 |
|
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
|
Dysthymic d/o
Aggressive screening procedure required as sx often go unreported unless solicited by direct questioning |
|
Hx assessment findings for dysthymic d/o
|
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 |
|
" other" common sx in dysthymia d/o
|
~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 |
|
Less common sx in dysthymic d/o
|
vegetative sx
alteration in appetite Alteration in sleep-rest pattern (almost always present in depression) |
|
Mental status exam findings in dysthymic d/o
|
~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 |
|
Diagnostic and lab findings in dysthymic d/o
|
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 |
|
Differential dx of dysthymic d/o
|
similar to MDD but includes MDD too
|
|
Pharmacological mgmt of dysthymic d/o
|
because of increased risk for dev of MDD, dysthymia is usually tx with antidepressant medications in a manner similar to MDD
|
|
Dysthymic d/o diagnostic criteria
|
~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 |
|
Non-pharm mgmt of dysthymic disorder
|
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 |
|
CBT aim in dysthymic pts
|
~modify perceptions
~decrease negativity ~increase sense of internal control ~enhance coping skills ~modify enviro factors contributing to illness |
|
Brief therapy (solution-focused therapy) aim in dysthymic pts
|
~focus on precipitant stressor
~cope with immediate impact of MDD on personal life ~modify contributory enviro factors |
|
Group therapy aim in dysthymic pts
|
~improve decision making
~improve socialization skills ~improve assessment of individual strengths ~gain new coping skills |
|
Family therapy aim in dysthymic pts
|
~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 |
|
Dysthymic d/o is often superimposed on ____
|
MDD
|
|
Common comorbidities of dysthymic d/o
|
~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 |
|
What often brings people with dysthymic d/o in for tx?
|
Subjective worsening of sx or onset of new sx such as vegetative ones
|
|
Clinical mgmt of dysthmia can be more complex and outcomes less positive when....?
|
dysthymia precedes MDD
|
|
Dysthymia and kiddos
|
~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 |
|
period of sx required for kids/adol to be dx with dysthymic d/o
|
1 yr of depressed mood
mood usually describes as irritable rather than sad in kids but may report both sadness and irritable |
|
Bipolar d/o descrip
|
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 |
|
This disorder is a complex brain based illness with a primary characterc of disturbance in mood
mood disturbance often of both polarities |
BIpolar disorder
mood disturbance polarities depressive expansive or manic |
|
One of 3 patterns of sx present in bipolar pts
|
~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 |
|
Bipolar d/o manifests with ____, _____, ______, _________ sx
|
BIpolar d/o manifests with cognitive, affective, behavioral and somatic sx
|
|
Etiology of bipolar disorder
|
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 |
|
long-lasting epileptogenic changes induced by daily subthreshold brain stimulation
|
~*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 |
|
Abnormalities that lead to abnormal balances of intercellular and extra cellular levels of NT which then cause
|
subsequent disruption of electric signal transmission in brain regions
bipolar d/o etiology theory |
|
GABA dysregulation
|
Bipolar d/o etiology theory
|
|
voltage gated ion channel abnormalities
|
bipolar d/o etiology theory
|
|
kindling
|
bipolar d/o etiology theory
process of neuronal membrane threshold sensitivity dysfunction |
|
is bipolar d/o more or less common than MDD
|
less common
0.7 % of general population at risks affects 2.3 million american adults; 1.2% of us adult population |
|
Mean age of onset for bipolar d/o
|
early 20s
common in the adolescent yrs |
|
Risk factors for bipolar d/o
|
~genetic loading
~family hx of 1st order relative having MDD or BP d/o |
|
24% increased risk of BP d/o if relative had BPd/o type____
|
24% increased risk if relative has BP disorder type I
|
|
5% increased risk if relative has BP d/o type _____
|
5% increased risk if relative has BP d/o type II
|
|
25% increased risk of BP d/o if relative has ____
|
25% increased risk of BP d/o if relative has MDD
|
|
Prevention and screening general
|
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 |
|
Bipolar d/o does or does not have a prodromal sx period
|
Significant & protracted prodromal sx period usually noted before full onset of illness
usually mild manifestations of criteria sx before full clinical syndrome apparent |
|
The longer time period between onset of sx and dx of bipolar d/o....
|
the more difficult to interrupt cyclicity of illness
|
|
Bipolar I diagnostic criteria
|
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 |
|
dysthymia d/o cannot have what sx?
|
Psychosis
|
|
bipolar II d/o diagnostic criteria
|
~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 |
|
time period for abnormally or persistently elevated, expansive or irritable mood in bipolar d/o
|
Lasting for @ least 1 week
|
|
Mood episode has rapid development and escalation of s over a few days
|
think bipolar
|
|
mood disturbance may result in brief psychotic sx
|
Bipolar
psychotic sx also possible in MDD Never present in dysthymic d/o |
|
Manic episodes last _____ to ____
|
Manic episodes last DAYS to SEVERAL MONTHS
in 60% of bipolar pts major depressive episode immediately precedes or follows the manic episode |
|
____ episodes have a shorter duration and ending more abruptly than _______ episodes
|
MANIC episodes have a shorter duration and ending more abruptly than major depressive episodes
|
|
Persistance of suggestive sx such as _____ think Bipolar
|
~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 |
|
Hypomanic
|
~similar to mania
~briefer in duration ~episode not a s severe as mania ~does not require hospitalization ~does not cause significant functional impairment |
|
Type I bipolar
|
clinical hx characterized by occurrence of one or more manic OR MIXED episodes
|
|
Type II bipolar
|
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 |
|
Rapid cycling
|
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%) |
|
Things to consider r/t rapid cyclers
|
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 |
|
Common seen of BP d/o speech
|
~rapid
~loud ~pressured ~difficult to interrupt ~joking, irreverent, amusing ~word clanging in severely ill |
|
Common affect of BP d/o
|
~labile
~irritable ~overly theatrical and dramatic |
|
Appearance of BD d/o pt
|
~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 |
|
Mood in manic
|
euphoric
~cheerful ~high ~expansive ~irritable |
|
thought process in BP d/o
|
~thought racing
~flight of ideas ~thoughts disorganized & incoherent in severely ill pts |
|
THough content in BP d/o
|
~Inflated self-esteem
~indiscriminate enthusiasm ~inflated sense of abilities bordering on delusional ~increased sexual content |
|
BP d/o orientation
|
Fully oriented
|
|
BPd/o memor
|
Impaired short term
Impaired recall |
|
BP d/o concentration
|
HIGHLY distractible
|
|
BP d/o judgement
|
POOR
prone to imprudent behavioral choices with potential for consequencesnegative |
|
BP d/o insight
|
pt usually does not recognize that they are ill
resists tx options |
|
Labs to order on BP d/o pt
|
To r/o metabolic causes or unidentified conditions
~CBC ~chemistry profile ~thyroid dxn tests ~b12 level Drug toxicity screenin |
|
lab abnormalities found in BP d/o
|
NT levels: 5HT, DA, & GABA
Pharm provocation tests; increased cortisol secretion polysomnographic findings sim to MDD |
|
If 1st onset of manic sx occurs after age 40
|
most likely not BP d/o
most likely sx are caused by another medical conditions |
|
Many medical condition mimic manic sx
|
~endocrine d/o
~Hyperthyroidism ~Intoxication of withdrawl from illicit drug use: **amphetamines **cocaine **hallucinogens **opiates |
|
Medications that can cause mimic of manic sx
|
~captopril
~Cimetidine ~corticosteroids ~cyclosporine ~disulfiram ~Hydralazine ~Isoniazid |
|
Mania can be precipitated by tx used for MDD or other unipolar mood disorders
|
~antidepressants
~ECT ~light therapy |
|
During acute manic episodes or significant depressive episodes bipolar pt may require brief hospitalization to....
|
~ensure pt safety
~ensure pt compliance with tx to reach stabilization ~rapidly stabilize on medication |
|
Pharm mgmt of bipolar pts
|
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 |
|
Commonly used mood stabilizing agents
|
~Lithium Carbonate
~Carbamazepine ~Valproic acid: divalproex Na ~Lamotrigene ~topiramate ~Oxcarbazepine ~Carbamazepine ER ~Levetiracetam ~Zonisamide |
|
Lithium Carbonate
|
~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 |
|
Gold standard for tx manic episodes
|
Lithium carbonate
|
|
Serum lithium level
|
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 |
|
What baseline labs do you need before initiation of lithium to ensure safety and efficacy
|
~thyroid panel
~serum creatinine ~blood urea nitrogen (BUN) ~urinalysis ~CBC ~EKG for pts older 50 |
|
Rapid-cycling clients seldom respond to ....
|
Lithium
|
|
Anticonvulsant mood stabilizing agents
|
~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 |
|
How long does it take for a response with lithium or anticonvulsant medications
|
1-2 weeks
|
|
Endocrine side effect of lithium
|
~weight gain
~impaired thyroid fxning |
|
Central nervous system side effect of lithium
|
~fine hand tremors
~fatigue ~fasciculations ~mental cloudiness ~headaches ~course hand tremors with toxicity ~Nystagmus |
|
dermatological side effect of lithium
|
~maculopapular rash
~pruritis ~acne |
|
GI side effects of lithium
|
~GI upset
~diarrhea ~vomiting ~cramps ~anorexia |
|
Renal side effects of lithium
|
~Polyuria with related polydipsia
~Diabetes insipidus ~Edema ~microscopic tubular changes |
|
Cardiac side effects of lithium
|
~t wave inversions
~dysrhythmias |
|
Hematological side effects of lithium
|
~leukocytoisis
|
|
Lithium cabonate
trade name dose therapeutic plasma level |
Eskalith, Lithobid
1200-2400mg/d (acute) 900-1200mg/d (maintenance) 0.8-1.2mEq/L acute 0.6-1.2mEq/L maintenance |
|
Common side effects of lithium
Toxicity side effects of lithium |
Nausea, fine hand tremors, increased urination and thirst
Toxicity: slurred speech, confusion, severe GI effect |
|
Risk for what medical condition with lithium tx
|
hypothyroidism
|
|
Li and pregnancy
|
avoid in pregnancy especially 1st trimester
|
|
Carbamazepine
Trade name Dose Therapeutic plasma level |
Trade name: tegretol
Dose: 400-1600mg/d Therapeutic plasma level: 6-12mcg/ml Alternative to lithium or valproic acid Hepatic enzyme inducer |
|
Tegretol
rare and common side effects |
carbamazepine
Rare: agranulocytosis Common: nausea, dizziness sedation headache dry mouth constipation skin rash |
|
Carbamazepine and preggo?
|
(Tegretol)
Avoid in pregnancy especially in the 1st trimester |
|
Tegretol monitor what?
|
Monitor LFTs
|
|
Alternative to lithium or valproic acid
|
Carbamazepine (tegretol)
|
|
Valproic acid
Trade: dose: therapeutic plasma level: |
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 |
|
Divalproex sodium loading dose
|
20mg/kg
|
|
Common side effects for depakote
|
Depakene, valproic acid, divalproex sodium
nausea diarrhea abdominal cramps sedation tremor |
|
Rare side effects for depakene
|
Depakote, valproic acid, divalproex sodium
increased liver enzymes |
|
depakote minimizes ____ effects
|
Depakene (depakote, valproic acid, divalproex sodium) minimizes GI effects
|
|
Drug more effective than lithium for rapid cycling and mixed bipolar
|
Valproic acid, divalproex sodium, depakene, depakote
|
|
Avoid in preggos especially 1st trimester
|
~Lithium carbonate
~carbamazepine ~valproic acid |
|
Lamotrigene
Trade Dose Therapeutic plasma level |
Lamictal
Dose: 25-600mg/d T. plasma level: blood monitoring not necessary Titrate dosages slowly |
|
Lamictal common side effects
Lamictal rare side effects |
Common:
~dizziness ~ataxia ~somnolence ~diplopia ~nausea ~headache ~hepatotoxicity Rare: life-threatening rashes Leukopenia |
|
What to monitor for of lamotrigene?
|
monitor for blood dyscrasia
steven Johnson's rash |
|
Helps in depressive phase of bipolar affective disorder
|
Lamotrigene
evidence exists showing some effectiveness of lithium carbonate on depressive sx as well as on manic sx |
|
Topiramate
Trade Dose |
Topamax
400-1200mg/d blood monitoring not necessary decreased efficacy of birth control agents and digoxin decreases IQ |
|
Common side effects of topamax
|
somnolence,
fatigue altered cognition (reduce IQ) paresthesia WT loss (decreases appetitie) |
|
rare side effects of topiramate
|
Kidney stones
glaucoma |
|
Monitor what for patients on topiramate
|
monitor for glaucoma
monitor for kidney stones make sure on 2 forms of birth control |
|
Oxcarbazepine
trade dose |
Trileptal
300-24000mg/d blood monitoring not necessary May cause hyponatremia |
|
Oxcarbazepine common side effects
|
~sedation
~dizziness ~headache ~fatigue ~GI distress ~abnormal vision ~weight gain May decrease efficacy of birth control pills |
|
Rare side effects of oxcarbazepine
|
(trileptal)
hyponatremia |
|
Monitor what for patients on trileptal?
|
(Oxcarbazepine)
Monitor sodium levels (may cause hyponatremia although a rare side effect) May decrease efficacy of birth control pills |
|
Carbamazepine ER
Trade Dose |
Equetro
200-1600mg/d Blood monitoring not necessary No need to obtain blood levels as with tegretol |
|
Levetiracetam
trade dose |
Keppra (mood stabilizer)
250-3000 mg/d Monitor for leukopenia |
|
Keppra rare SE
|
Levetiracetam (mood stabilizer)
Anemia monitor for leukopenia |
|
Common SE for levetiracetam
|
Keppra (mood stabilizer)
sedation dizziness |
|
Zonisamide
trade dose |
zonegran (mood stabilizer)
100-600mg/d contraindicated w/sulfonamide allergy may potentially cause wt loss |
|
what mood stabilizer is contraindicated with sulfonamide allergy
|
Zonisamide
Zonegran (trade) |
|
common side effects of zonizamide
|
Zonegran (mood stabilizer)
~sedation ~dizziness ~ataxia ~headache ~gi distress May potential cause wt loss |
|
Rare side effects of zonegran
|
~kidney stones
~elevated serum creatinine and blood urea nitrogen ~anemia ~Steven Johnson's syndrome ~agranulcytosis CONTRAINDICATED WITH SULFONAMIDE ALLERGY |
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During an acute phase of manic episode nonpharm mgmt
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monitor and help pt meed nutritional needs (finger foods)
~help pt meet sleep-rest needs ~monitor safety |
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common comorbidities with bipolar
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substance abuse
hypothyroidism |
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High risk activities from manic behavior
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sexual
~pt eduction for STIs ~assessment & monitoring for STIs financial/legal ~pt access to community resources ~nutritional counseling |
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Adolescent manic episodes present differently than adult episodes
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~more psychotic features
~often associated with antisocial behavior ~often associated with substance abuse ~prodromal period of sig behavioral problems ***school truancy ***failing grades |
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tx duration & success rates w bipolar
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vary with individual characteristics and motivation
|
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relapse in bipolar
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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 |
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Bipolar and women
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pharmacological agents for BP disorder especially Li are teratogenic
Women of child bearing years need effective contraceptive care while on BP disorder tx medication |
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Routine use of lab tests to monitor for therapeutic serum levels of anticonvulsants and Lithium is needed
|
routine evaluation of
~CBC ~renal fxn ~thyroid fxn for pt taking lithium long term is needed |
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what standardized rating scales are needed to monitor clinical status in bipolar and why do do you use standardized rating scales
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Young mania rating scale YMRS
Mood disorder questionnaire MDQ to establish baseline fxning and monitor disorder course over time |
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CYCLOTHYMIC d/o
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chronic fluctuating mood disorder whose sx are similar to but less severe than BP d/o
Numerous periods of hypomanic and dysthymic sx |
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Incidence and demographics of cyclothymic d/o
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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 |
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Risk factors for cyclothymic d/o
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~genetic loading
~family hx ~BP d/o type I ~substance abuse |
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Cyclothymic d/o
assess for the following in the hx |
~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 |
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Psychiatric differential dx with cyclothymic d/o
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~BP d/o
~dysthymia ~substance abuse |
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Pharmacological mgmt of cyclothymia
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~similar to MDD & BP d/o
~because of increased risk for development of BP d/o commonly tx with medication |
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Life span considerations for cyclothymia
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~usually begins in adolescence
~onset in later life usually suggests general medical condition such as multiple sclerosis |