Depression

all depressive disorders share symptoms of…

sadness, irritability, somatic concerns, impairment of thinking

all impact ability to function

assessment for depressive pt and key assessment findings

assessment tools/ depression screenings

suicide screenings

key assessment findings:

• depressed mood/ anhedonia

• anergia

• anxiety (70%)

• psychomotor retardation or agitation

• vegetative signs

• comorbidity: chronic pain

planning for depression pt is geared towards…

phase of depression they are in

when is the greatest risk of suicide?

when recovering from severe depression/ when depression lifts

explain the recovery model concepts:

• focus on pt strengths

• tx goals mutually developed

• based on pt’s personal needs and values

• consider pt age and stage of life

depression is the leading cause of… in the US

disability

types of depressive disorders

DMDD

dysthymic disorder

SAD

substance abuse depressive disorder

PMDD

depressive disorder associated with another medical condition

explain disruptive mood dysregulation disorder

Introduced in 2013 in response to the overwhelming number of children and adolescents misdiagnosed with bipolar disorder. This resulted in exposure to unnecessary powerful medications, and attaching a stigma of bipolar to the child for the lifetime.

 Many of these individuals went on to no longer present with the symptoms associated withbipolar disorder in adulthood.

 Most of them converted to MDD or GAD in adulthood.

 Treatment is symptom based and may include: antidepressants, ADHD meds, antipsychotics,and CBT.

( no tx for DMDD)

criteria for dysruptive mood dysregulation disorder

 Criteria for diagnosis includes: frequent and severe irritability and anger in individuals between the ages of 6 and 18.

 Onset occurs before the age of 10

 Temper tantrums and outburst occur at least 3 times per week.

 Tantrums must occur in at least 2 of the following settings: school, home, with peers.

 Prevalence rate is 2-5 percent of the overall population of 6-18 year olds.

 More common in males than females and more common in children than adolescents.

explain dysthymic disorder: (Persistent depressive disorder)

doesnt meet criteria for major depression!

 Milder form of depression; chronic condition

 depressed mood most of the day, more days than not

 duration 2 or more years

 often begins in childhood or adolescence

 More than two of the following symptoms: Appetite disturbance, Sleep disturbance, fatigue, low self-esteem, problems making decisions, feelings of hopelessness

low level depressive symptoms lasting 2 yrs in adults and 1 yr in children

usually not severe enough for hospitalization

tx similar to MDD- antidepressants and psychotherapy

 with significant distress or impairment

explain premenstrual dysphoric disorders

 Symptom cluster in last week prior to onset of a woman’s period include:

 Mood swings, irritability, depression, anxiety, feeling overwhelmed, and difficulty concentrating

 Symptoms decrease significantly or disappear with the onset of menstruation

 Symptomatic treatment. Exercise, eating habits, rest, light therapy, YAZ, SSRI’s,diuretics. BC pills to regulate hormones

explain seasonal affective disorder (SAD):

 Depressive symptoms brought on by shorter days experienced in the fall and winter months.

 Treatment for SAD may include light therapy (phototherapy), medications and psychotherapy

 The specific cause of seasonal affective disorder remains unknown. Some factors that may come into play include:

• Your biological clock (circadian rhythm). The reduced level of sunlight in fall and winter may cause winter-onset SAD. This decrease in sunlight may disrupt your body's internal clock and lead to feelings of depression.

• Serotonin levels. A drop in serotonin, a brain chemical (neurotransmitter) that affects mood, might play a role in SAD. Reduced sunlight can cause a drop in serotonin that may trigger depression.

• Melatonin levels. The change in season can disrupt the balance of the body's level of melatonin, which plays a role in sleep patterns and mood.

explain substance induced- depressive disorder

Person does not experience depressive symptoms in the absence of drug or alcohol use or withdrawal

 Symptoms appear with in 1 month of use

 When the substance is removed, depressive feelings subside

**Pt wasnt depressed until started taking med; med causes depression

explain depressive disorder associated with another medical condition:

Can be caused by kidney failure, Parkinson’s disease, Alzheimer’s disease, dm, heart failure, cancer, CHRONIC PAIN, mobility issues, etc.

 Symptoms that result from medical diagnoses or certain medications are not considered major depressive disorder 

****Major depressive disorder assessment of patient:

Five (or more) of the following in 2-week period:

 Weight loss or gain and appetite changes 5% increase or decrease in weight over 1 month

 Sleep disturbances increase or decrease

 change in level of physical activity

 Fatigue

 Worthlessness or guilt

 Loss of ability to concentrate or make decisions

 Recurrent thoughts of death or suicide

 Depressed mood

 Loss of interest or pleasure (anhedonia) loss of interest in all activities

Exceptions: grief, substance, medical

somatic complaints associated with MDD:

(very common symptom profile for older adults)

 GI complaints (constipation)

 Pain

 Irritability

 Palpitations

 Dizziness

 Appetite changes

 Lack of energy

 Change in sex drive

 Sleep disturbances 

explain epidemiology of MDD:

 Females are twice as likely as men to be affected by MDD

 Leading cause of disability in the United States

 Children and adolescents- manifests differently, may cry, refuse to go to school, withdraw, exhibit sexual behavior, display a

preoccupation with death or suicide.

 Older adults- often overlooked as a normal part of the aging process. Fatigue pain weakness, difficult to determine origin.

 Comorbidity:

Schizophrenia, substance abuse, eating disorders, borderline personality disorders, anxiety,

 Anxiety is seen in approx. 70% of cases of MDD

biological and biochemical factors influencing development of MDD

biological factors:

 Genetic predisposition

 Biochemical (Stressful life events cause changes in the central nervous system, neurotransmitters and brain)

 Alterations in hormonal regulation (cortisol, estrogen)

 Inflammatory process

 Diathesis stress model (interplay between genetic and biological predisposition toward depression and life events)

Biochemical factors:

 Serotonin (target of antidepressants)  Norepinephrine  Acetylcholine  Glutamate  GABA  Dopamine

 Treatment of anti-depressants is geared primarily toward regulating these neurotransmitters 

considerations for OAs and depression

Particularly complex

 Often missed in older adults, not sure if isolating because of pain of chronic aging/mobility issues or if depressed.

 Often mis-diagnosed- presentation often non-traditional

 Common somatic complaints

 Lowered intellectual function and a loss of interest in sex, hobbies, and activities often mis-diagnosed as brain disease (dementia) instead of depression!! 

______: outward representation of person’s internal state of being and is objective finding based on nurses assessment (poor posture, flat expression, no eye contact)

depression affect will appear exhausted

affect

thought processes associated with depression

poor judgement- lack of ability to make sound decisions

lack of focus

indecisiveness

_______: prolonged emotional state that influences person’s whole personality and functioning

pt’s subjective experience of how they feel emotionally

depressed mood and anhedonia (lack of pleasure) are the key depression symptoms

mood

feelings associated with depression

Worthlessness, guilt, helpless, despair, hopeless, pessimistic, angry, low self image. 

physical behaviors associated with depression

anergia

movements are slowed, expressions are decreased, gaze is fixed

vegetative signs of depression

 MDD is recurrent and chronic. Care must be directed toward ______________ of the condition across the lifespan. 

resolution of the acute phase and long term management

some individuals with depression are so withdrawn they are unwilling to communicate at all- _________

catatonia

is depression in person’s voluntary control

NO, but it can be managed through meds and lifestyle changes

long term management works best on psychotherapy and meds

normal greif is displayed as _____

shock and anger

_______ grief is prolonged supression of grief

abnormal

______________ grief is when society doesnt accept it; loss of loved one, abortion, loss of pet, natural disaster, school shooting)

disenfranchised grief

________ grief is guilt, anxious, irritable, tearful, empty feelings, unable to visit grave after 2 years

delayed grief

___________- when bereavement is after 12 months in adults and after 6 months in children

persistant bereavement disorder

 _________ - relates to a person’s reaction to the death of a loved one 

Bereavement

 _______ - subjective feelings after experiencing a loss

Grief

___________ - process individuals experience in different ways; anxiety, anger, pain, despair, and hope 

Mourning

old vs new tx for grief:

 OLD:

discouraged early tx for grief by not allowing it until 2 months after

 NEW:

states you can treat for depression in the 1st 2 months to help with early treatment of depression associated with grief.

behaviors associated with delayed grief reaction

 Excessive hostility and grief

 Prolonged feelings of emptiness

 Numbness

 Irritable, tearful, guilty, low self-esteem

 Use of present tense when referring to deceased

 Persistent dreams

 Retention of clothing of deceased

 Inability to visit grave site after 2 years of death

list some assessment tools and standard rating scales for those with depression and anxiety

MMSE, Becks depression index (BDI), patients health questionare 9 (PHQ9)

what are some things to consider when assessing for suicide potential

✓ Patient history of depression or family history of depression

✓ Having experienced recent negative stressors/loses

✓ Childhood experiences in a negative home environment

✓ Lack of social support system

✓ Co-morbid physical disease

✓ Co-morbid substance abuse

what to note in a behavioral assessment in regards to the patients responses

note when pts usual responses to things change there is a mood disturbance

talk to family, need reliable information on pt baseline (collateral)

ex: no longer enjoy things they used to, new isolation, decline in self care tasks

what to ask to evaluate suicide

✓ “Do you ever think about harming yourself?” ✓ “Do you have a plan for harming yourself?” ✓ “What is your plan for harming yourself?” ✓ Determine the availability of the method chosen.. ( do they have loaded gun at bedside)

**Matter of factly, dont be mistinterpretable

treatments for depression

 Electroconvulsive therapy (ECT) See Video  Transcranial magnetic stimulation  Vagus nerve stimulation  Deep brain stimulation  Light therapy  St. John’s wort  Exercise, Nutrition, Social Interaction, Adequate Sleep Hygiene  CBT, Psychotherapy  Medications 

At the cellular level, mood disorders are caused by problems with the ___________. Antidepressants aim to regulate these chemicals.

neurotransmitters

explain SSRIs

 (Citalopram, fluoxetine, sertraline, paroxetine, escitalopram) 

 First-line therapy

 Potential toxic effects

 Teach it takes 3-4 weeks for positive effects, remind to prevent poor compliance

 Safest antidepressant classification for patients with potential for overdose.

 Improvement can occur as early as one week

possible SE of SSRIs

May induce agitation, anxiety, sleep disturbance, tremor, sexual dysfunction (primarily anorgasmia), or tension

headache.

 The effect of the SSRIs on sexual performance may be the most significant undesirable outcome reported by

patients.

 Mood Blunting- common side effect where SSRIs reduce your ability to feel intense emotions, affecting

roughly 40% to 60% of patients. You may feel emotionally numb, detached, or unable to experience high joy

or deep sadness

 Autonomic reactions (e.g., dry mouth, sweating, weight change, mild nausea, and diarrhea) may also be

experienced with SSRIs.

SNRIs:

 _______________- avoid in pregnancy 

 _____________- great for somatic complaints. Can also treat chronic pain and anxiety disorder

 _______________- contraindicated in bleeding/clotting d/o and anticoagulant therapy.

 ____________- monitor patients BP for ^. Warn of discontinuation syndrome. Must take daily and taper slowly. 

Desvenlafaxine (Pristiq)

Duloxetine (Cymbalta)

Levomilnacipran (Fetzima)

Venlafaxine (Effexor)

explain MAOIs

Monoamine oxidase inhibitors (MAOIs)

 Neurotransmitter effectshinders

the monamine oxidase enzyme from breaking down the serotonin, dopamine, norepinephrine

and tyramine thus, increasing the amount available to neurotransmitter receptors. This elevates the

mood, but when eating foods high in tyramine which is already being increased by this med =

TROUBLE (Hypertensive crisis, CVA)

 Indications

unconventional depression, mood reactivity, over sleeping and over eating, panic disorders, social

phobia, GAD, OCD, PTSD, Bulimia.

 Adverse/toxic effects

Intracranial hemorrhage, coma, hypertensive crisis (Table 14.8 p. 256)

 Interactions

 Drug-(OTC, TCA’s, antihypertensives, sedatives, stimulants.) (See box 14.4 p. 255)

 Food ( Avoid high tyramine content foods and other vasopressors)chocolate, fava beans, ginseng, large amounts

of caffeine, Cheese, milk and most milk products, food with yeast, beer, wine, some fish, sausage, and red meats

prepared certain ways and fruits and vegetables under certain categories.( See Table 14.7 p. 256)

 Contraindications: liver/kidney failure, HTN, CVA, MI. severe migraines

 Pt teaching Instruct to : Always look at food labels and drug facts.

explain buproprion (wellbutrin)- NDRI

 Monitor for increased sexual desire, decreased appetite, smoking cessation and risk for

seizures in those with disorder or predisposed (head injuries etc. ) Lowers seizure threshold.

Great for those whom experience mood blunting on SSRI’s. Great for “atypical depression”

with vegatative symptoms. Tends to be “activating/stimulating”

explain mirtazipine (remeron)

May work faster than SSRIS but stimulates appetite so watch for fast weight gain, very helpful

for sleep because of sedating side effects. Usually taken at night, great for older adult

population.

explain the SARIs

Trazodone (Desyrel, Oleptro) – an antidepressant used mostly at night as a

sedative due to its sedating s/e’s. priapism

 Nefazodone (Serzone) not used much, Serzone was taken off he market, high risk for liver failure.- kills ppl

 Vilazodone (Viibryd)- take with food, s/e’s palpitations, PVC’s

 Vortioxetine (Trintellix)- memory and cognitive enhancement properties, watch for QT prolongation- good for dementia

explain TCAs

 Lethal OD, must watch for hypotension and educate to not stand up fast. Don’t put anyone suspected Suicide or SI on this. (like giving them a loaded gun) More side effects than SSRI’s

 Examples :

 Amitriptyline.

 Amoxapine.

 Desipramine (Norpramin)

 Doxepin.

 Imipramine (Tofranil)

 Nortriptyline (Pamelor)

 Protriptyline (Vivactil)

 Trimipramine (Surmontil)

explain the NMDA receptor agonist

Esketamine (Spravato)- intranasal microdosing of anesthetic ketamine (derivative of dissociative drug PCP) newly approved by FDA for treatment resistant depression. Highly regulated due to abuse potential. Frequent dosing in clinic. Must monitor for 2 hours after administration.

explain ECT

 The most effective non-pharmacological depression treatment

 Electric impulses induce mild seizures

 Psychotic illnesses = second most common indication

 ECT the primary treatment for depression in patients with:

 Severe malnutrition, exhaustion, and dehydration due to lengthy depression

 Safer than meds with certain medical conditions

 Delusional depression

 Failure of previous medication trials

 Schizophrenia with catatonia

explain transcranial magnetic stimulation (TMS)

 Noninvasive

 Uses MRI-strength magnetic pulses to stimulate focal areas of the cerebral cortex

 Presence of metal is the only contraindication

 Adverse reactions

 Headache and lightheadedness

 No neurological deficits or memory problems

 Seizures rarely

 Most are mild and include scalp tingling and discomfort at the administration site.

explain vagus nerve stimulation (VNS)

 Delivers electrical impulses directly to the patients vagus nerve. (electrodes placed and physically

wrapped around the vagus nerve)

 Originally used to treat epilepsy

 Decreases seizures and improves mood

 Electrical stimulation boosts the level of neurotransmitters

 Side effects:

 Voice alteration (nearly 60% of patients)

 Neck pain, cough, paresthesia, and dyspnea, which tend to decrease with time

**INVASIVE, surgically implanted electrodes

explain deep brain stimulation (DBS)

Surgically implanted electrodes (in the brain)

 Stimulates those regions identified as underactive in depression

 More invasive than VNS

 Electrodes placed directly into the brain

MOST INVASIVE

explain light therapy

 First-line treatment for seasonal affective disorder (SAD)

 Efficacy due to influence of light on melatonin

 Effective as medication for SAD

 Negative effects: headache and jitteriness

explain st johns wort

Flower processed into tea or tablets

 Thought to increase serotonin, norepinephrine, and dopamine in the brain

 Useful in mild to moderate depression

 Due not take with other serotonin drugs = ^ risk serotonin syndrome

explain exercise tx for depression

 Biological, social, and psychological effects

 Increases serotonin availability

 Dampens HPA axis (thought to be overly active in depression)