mood disorders depr 2013 student handout
TRANSCRIPT
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Mood Disorders:
Depressive Disorders
Maureen Eisenstein, RN, MS
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Definition page 100 ATI
Dysregulation of Mood/Affect
Disturbances in functioning:
Physical somatic symptoms, neurovegetative
Cognitive negative, pessimistic, slowed
Emotional worthlessness, hopelessness, no pleasure
Behavioral
agitation, retardation, suicide attempt
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What Depression is NOT
A passing blue mood
A sign of personal weakness
A condition that can be willed or wishedaway People with a depressive disorder cannot
merely pull themselves together and get
better Because of inaccurate beliefs/stigma many donot seek/ cont in treatment
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DSM IV T-R Diagnoses
Major Depressive Disorder, Single 296.2
Major Depressive Disorder, Recurrent296.3
Dysthymia 300.4
Depressive Disorder Not OtherwiseSpecified 311
Mood Disorder Due to General MedicalCondition 293.83
Substance-Induced Mood Disorder
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Etiology
Exact cause remains unknown
Multifactorial Neurobiologic
Psychosocial
Cognitive factors
Mood disorder As stress response to illness
As physiologic response to pathology
As physiologic response to medication
Exacerbates due to medical pathology of Rx
Medical disorder May develop in client with mood disorder
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Etiology
Neurobiologic Factors
Altered neurotransmission: 5HT, NE, MAO, DA
Depression: underactivity
Mania: overactivity Kindling: sensitivity to future stress is created: newhardwiring of brain (plasticity)
Neuroendocrine: HPA overactive w/depression, higher cortisol levels (damages healthy
tissues, see Sx) chronobiological-circadian rhythms disrupted
Genetic transmission: 3X more often 1st degreebiological relatives
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Psychosocial Factors
Psychoanalytic Theory (few support) Related to loss Mania, defense against depression
Cognitive related to negative processing of information
Life events and Stress mediated by genetic risk factors
Learned Helplessness related perceived lack of control over stressors; dependent
personality Personality
Depressive personality disorder (research diagnosis), temperament
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Epidemiology
Who Tends to be Most Depressed? CDC 2011
persons 45-64 years of age
women
blacks, Hispanics, non-Hispanic persons of otherraces or multiple races
persons with less than a high school education
those previously married
individuals unable to work or unemployed: lowersocioeconomic persons without health insurance coverage
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Epidemiology
Mood and Medical disorders 30-50% Alzheimers SA 40% comorbidity 1/3 of patients admitted to medical units
Ages 20+ Fewer than 1/3 accurately diagnosed/ treated
WHO: by 2020 2nd largest cause of theglobal health burden
Onset: 20s-30s Can begin at any age
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Depression:
DSM criteria:
Must have a total of 5 symptoms for at least 2 weeks
One of the symptoms must be depressed mood or lossof interest (is a change from previous functioning)
Emotional Symptoms Anhedonia
Depressed mood sad, empty, hopeless, numb
Irritability anxiety, anger
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Depression: Cognitive Symptoms
Diminished ability to think, concentrate, makedecisions
Self absorbed
Preoccupation with death SI
Excessive focus on worthlessness and guilt
Negative thoughts
cognitive distortions
Sometimes delusional Psychotic symptoms
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Depression: Behavioral Symptoms
Neurovegetative S&Sx (physical)
Weight Loss or gain
Change in appetite Sleep:
Insomnia or hypersomnia
Psychomotor Retardation or agitation
Fatigue Loss of energy
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Depression: Social Symptoms
Withdrawal from family and social
interactions
Work problems
Organizing, initiating, completing
Can influence work relationships
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DSM Additional Features
Episode specifiers are provided to increasediagnostic specificity: (296.2X, 296.3X)
Mild, moderate or severe, partial/full remission
Catatonia Melancholia
Psychotic symptoms
Postpartum onset-occurs w/in wks 1-4 post
Postpartum psychosis
Seasonal pattern specifiers (SAD)
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Dysthymia
Chronic, low-level depression, most days at least 2 yrs (1for C&A) and at least 2 or more following symptoms
Poor appetite or overeating
Insomnia or hypersomnia
Low energy/fatigue Low self-esteem
Negative thinking/guilt
Poor concentration/decision making
Hopelessness Irritability/anger
Anhedonia/withdrawal
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Mood Disorders Across the Life
Span/Special Populations p 265-266
ATIDEPRESSION IN CHILDREN Extraordinary pain & distress
not prepared to understand/deal with emotions and behaviors
Initiates major difficulties during development/social
learning influence rest of life span
Stress, concern for family
Presentation vary from one childhood stage to another
Sick, irritable, sadness, crying, decreased interest, poorconcentration, critical, sarcastic, poor grades, dropping out ofactivities, skip school, runaway, SA
Suicidal ideation-adols (1in 12 experience past year): 3rd leadingcause of death age 15-24 (firearm, suffocation, poisoning)
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DEPRESSION IN ELDERLY
NOT normal part of aging (5-10%
Usually present with physicalsymptoms
High co-morbidity-stroke, DM,CA, Parkinsons
Older men & barriers to care-reluctant to discuss-weak
Widely underrecognized/treated-up to 75%saw PCP w/in month
Suicide/rates-highest suiciderate WM 85+ y.o. Symptoms can result in life-
threatening situation within ashort time
Brief psychotherapy useful
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DEPRESSION IN MEN
Men are less likely to admit to depression
healthcare providers less likely to suspect it
Nearly 4X as many men suicide
Typically shows as being irritable, angry,
and discouraged
Often masked by: SA
Excessive working
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PROGNOSIS/CLINICAL COURSE
Can improve within 9 months if nocomplications
Up to 40% have symptoms after 1 year
50-85% experience a subsequent episode; Nearly 2/3 experience recurrence within ten
years
> 50% of those with dysthymia go on toMDD
Approximately 15% commit suicide
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With treatment prognosis favorable
Can be well controlled with Medications
Psychotherapy Self-help strategies
Including exercise
Need for education, lifetime monitoring,maintenance treatment
Lack of adherence, resistance of symptoms may lead to some impairments in daily functioning for
long periods of time
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Assessment
Physiologic- see lab studies to r/o organic causes Appetite
Vital signs
Hydration Sleep pattern changes
Activity level
Fatigue-energy level
Constipation
Weight loss
Sex drive
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Diagnostic Evaluation
Assessment ofMood
mood, affect, temperament, emotion,
emotional/affective reactivity, emotional
regulation, range of affect
Rating Scales: Hamilton, Becks, Zung,
Scale of 1-10
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Nursing Process: NANDAs
Imbalanced nutrition:more/less than
Disturbed sleep
patterns Activity intolerance
Sexual dysfunction
Risk for self directed
violation Hopelessness
Anxiety
Noncompliance/nonadherence
Ineffective therapeuticregimen management
Self care deficit
Social isolation
Self esteemdisturbance
Spiritual distress
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NOCs
Patient will not harm self-no gestures/plans
Approach staff if feeling suicidal
Meets basic needs
Will function at highest level of (independent)functioning possible
Make decision, state positive & helpful coping strategies
Participates in experiences/interactions that
increases socialization Speak with others, initiate conversation, go to groups
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NOCs
Participates in experiences/interactionsthat promote self esteem Self care (bathing, grooming, eating, etc.)
Decreased anxiety Identify stressors, coping strategies Demonstrates knowledge/understanding
about diagnosis, prognosis, treatment
needs, triggers Follow up with community based care
Adherent/compliant with meds and treatment
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Intervention:Avoid Pitfalls
Failing to recognize the severity of patientssymptoms depth to which depression can reach
Equating depression with own normalblues/passing moods of sadness Lack of empathy & insight
Stereotyping, rigid thinking, inexperience,
unrealistic expectations, stigma, lack ofunderstanding and empathy Interferes with developing NPR/trust, adequate
treatment
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TWO GENERAL PRINCIPLES to
Help Depressed Clients1. It is impossible to make depressed people feel better
by being cheerful Overly cheerful attitude can make them feel worse, it belittles
their feelings
Adopt more neutral emotional attitude
Maintain and communicate confidence that they will feel better-ittakes time
1. Working with depressed may lower your mood andmake you feel down; it may cause you to feel angry,
anxious while caring for them Stay in touch with your feelings, use supervision/ support frompeers
Change patient population if need be
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NICs
Prevent suicide/promote safety () ongoing risk assessment weeks 1-6 crisis plan encourage verbalizing of feelings, not ruminating calm reassuring
Promote self esteem provide distraction from self-absorption begin doing NOW, not waiting until feels better counseling: problem solving, assertiveness, etc.
Promote self care activities plan when has energy reduce choices, easier decision making simple concrete directions
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Monitor I&O, food intake and weight Assist patient in verbalizing feelings
Make observations vs asking questions, give time to respond
Instill hope clients who feel hopeless tend to be dependent
encourage client responsibility assist dont do for
Enhancing socialization brief frequent contacts, develop trust, over time socialize w/others
Help patient identify external sources of stress assist in coping in more effective manner
Teach patient and SOs about disorder & Tx Medication teaching/management
Identify the patients social support system are relationships impaired?
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TREATMENT MODALITIES:
Psychotherapeutic InterventionsCBT (cognitive behavioral therapy): Helps people learn new ways of thinking and behaving enables patients to correct false self-beliefs (cognitive
distortions) that can lead to negative moods andbehaviors
Interpersonal Therapy: Emphasis: social functioning & interpersonal
relationships; (how are relationships effected by thedisorder? Are they considered a stressor?)
Understand and work through troubled personalrelationships Psychodynamic (Freud), analysis, early loss, work through
repressed memories
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Treatments: Complementary
Therapies Family Intervention:
education
family conflicts
communication Group Intervention-(can include psychoeducation)
Benefits:
education, socialization-decrease isolation &
hopelessness need to assess readiness for: can be overwhelming
community meetings/activities, groups less
structured/imposing, better tolerated
P h h l
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Psychopharmacology-
antidepressantspage 186 ATI
SSRI/SSNRI,TCAs, MAOIs
Selecting effective drug & dosage often a difficultprocess
Lag time-initial effect 1-6 weeks
Therapeutic Improvements 3-4+ weeks
Recommend continue Rx: 3-6 months
1 year prevent relapse
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TCAs Amitriptyline (Elavil), imipramine (Tofranil), desipramine (Norpramin)
MAOIs-atypical/refractory depression Marplan, Nardil, Parnate
SSRIs
fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), citalopram(Celexa), escitalopram (Lexapro)
SSNRIs venlafaxine (Effexor), desvenlafaxine (Pristiq-active metabollite)
duloxetine (Cymbalta)
Others:
Antianxiety meds Antipsychotic meds Herbal-St. Johns Wart
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Biological Treatments for
Depression
ECT-electroconvulsant therapy
TMS-transcranial magnetic stimulation
VNS-vagus nerve stimulation Phototherapy
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ECT Page 82 ATI book
Severe/refractory depression Relieve severe symptoms e.g. psychosis (hallucinations,
delusional thinking), persons refusing to eat, unable to takeantidepressants, Suicidal
Brain defibrillator
Need informed consent Contraindicated: Recent MI, intracranial lesions/tumors,
w/increased ICP (CVA), arrhythmias, aneurysms, acute Respinfection
NPO at least 8-12H Assess vital signs, memory
Anesthesia preparation atropine like prep-decrease secretions, short acting anesthetic
(Brevital) IV
skeletal muscle relaxant-Anectine to prevent injuries during the
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Ventilate until muscle relaxant fully metabolized
Electrical current passed through brain by means of uni-or bilateral electrodes placed on the temples causes a grand mal seizure (effects often masked by muscle
relaxant) Meds affecting Sz threshhold should be d/cd prior to ECT
lasts about 30-60 seconds
Increases BP & P; HTN, dysrhytmias, cardiac conditions treated prior to ECT
small risk of death, (same as w/other procedures in whichanesthesia is used)
SE: Headache, nausea, vomiting, muscle aches jaw pain
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Post Procedure Care
Monitor VS Lateral recumbent
facilitate drainage, prevent aspiration
Reorient frequently Acetaminophen for headache Short-term memory loss
from several minutes to several hours occasionally, may last several days-quite distressing
ECT not curative encourage Tx & meds to prevent relapse
Usually up to 12 treatments, 3X/week(individualized)
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TMS
Oct. 2008, FDA approved for Tx of adult unipolardepression unresponsive to Rx
Uses magnetic fields to alter brain activity Large electromagnetic coil held against the scalp near
the forehead, (left side) electric current is switched on & off
Electric current creates a magnetic pulse that travelsthrough the skull, causing small electrical currents in thebrain Currents stimulate nerve cells in the region of the brain involved
in mood regulation and depression Seizure rare Treatment in medical facility for seizure management
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VNS
Vagus nerve: one of the primary communicationpathways from the major organs of the body to the brain
Implanted pulse generator and lead wire stimulate partsof the brain that affect mood-to decrease depression
precise mechanisms of how it works is unknown Affects blood flow to different parts of the brain
Affects neurotransmitters including Serotonin andNorepinephrine which are implicated in depression
FDA approved 2005 for long term, chronic depression (atleast 2 yrs) in conjunction with standard treatment
Utilize when Depression has not improved after @ least4 other Tx (can be antidepressants)
http://en.wikipedia.org/wiki/Serotoninhttp://en.wikipedia.org/wiki/Norepinephrinehttp://en.wikipedia.org/wiki/Norepinephrinehttp://en.wikipedia.org/wiki/Serotonin -
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VNS (cont)
Pulse approx every 5 min
Approx 30 sec duration
No seizure/memory loss Response in 3-6+ months
Highly individual
Adjunct to treatment SE: voice, SOB, cough, dif swallowing
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Phototherapy
For SAD Light therapy (phototherapy)
exposure to light that is brighter than indoor light, not as bright as directsunlight.
Outdoor light is preferred
May help reset "biological clock" (circadian rhythms) controls sleeping and waking.
Sit in front of high-intensity fluorescent lam 15/30 minutes to 1.5- 2 hours QAM
Can be used in different ways & employ different types of lightboxes, light visors, and lamps
All designed to bring in extra light to the eyes. Check to be sure a light box filters out harmful ultraviolet light.
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Other Biological Treatments:
Cranial Electrotherapy Stimulation Almost undetectable doses of electricity
Mimics bodys own natural electrical function
Microcurrents (thought to) stimulate areas of brainresponsible for neurotransmitter and hormone function
depression, anxiety, insomnia, and pain 20-60 min/day or QOD, electrodes to the area between
the mastoids and the jaw
Almost NO side effects can be used in any age group
Clinical studies have shown an increase in bothserotonin and beta endorphin
FDA approved, Class III
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Other biological treatments
MST: Magnetic Seizure therapy
Investigational brain stimulation
Uses high doses of repetitive TMS
Induces focal seizure under anesthesia for
Depression No impedance by scalp and skull
Less severe cognitive side effects vs ECT
More rapid recovery of orientation SE: H/A, scalp pain
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Other biological treatments
Deep Brain StimulationNeurosurgery-1st: frontal cortexElectrodes implanted, pacemaker sends continuous
impulses
Brodmanns 25 cingulate area of the cerebral cortex
Role with emotion and other areas involved with appetite & sleep (hypothalmus, brainstem), mood & anxiety (amygdala), memory (hippocampus) and self esteem (frontalcortex)
Metabolically over active in treatment-resistant depression (may also betreatment resistant to CBT)
Chronic deep brain stimulation in the white matter adjacent to the area is asuccessful treatment for some patients
Nucleus accumbens another possible area (reward circuit: dopamine-desire;and serotonin-satiety)
Experimental
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Goals for discharge
Verbalizes plans for future absence of suicidal thoughts or behavior
Verbalizes realistic perceptions of self and abilities
Relates realistic expectations for self and others
Sets realistic attainable goals Identifies psychosocial stressors that may have negative
influences begins to modify them
Identifies signs and symptoms of prodromal phase ofdisorder early symptoms may mark onset of the disorder
clear deterioration in function before the active phase
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Describes methods for minimizing stressors States therapeutic effects, dose, frequency,
untoward effects, and contraindications formedications
Makes and keeps follow-up appointments Expresses guilt and anger openly, directly, and
appropriately Engages family of significant others as sources
of support Structures life to include healthy activities and
diversions