Mood Disorders Depr 2013 Student Handout

7/29/2019 Mood Disorders Depr 2013 Student Handout

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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

Mood Disorders Depr 2013 Student Handout

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