DEPRESSION

MODERATOR: PRESENTED BY:

DR. SUNITA SHARMA SHAILJA SHARMA
LECTURER MSc. NURSING 2nd YEAR
NINE, PGIMER, NINE, PGIMER,
CHANDIGARH CHANDIGARH
INTRODUCTION
 Depression is a widespread mental health
problem affecting many people.
 Depression is one of the leading causes of
disability across the world.
 The world health organization 2006
estimates that the depression will rank
second to heart disease by 2020 in terms
of global disability.
Incidence
 The lifetime risk of depression in male is
8-12% and in females it is 20-26%.
 Depression occurs twice in women as in
men.
 An estimate 3-4% of India’s 100 crore
population suffer from major mental
disorders and about 7-10% of the
population suffers from minor depressive
disorders (Sinha 2011).
Classification of depression (ICD10)
 F32: Depressive episode
 F32.0: Mild depressive episode
 F32.1: Moderate depressive episode
 F32.2: Severe depressive episode without
psychotic symptoms
 F32.3: Severe depressive episode with
psychotic symptoms
 F32.8: Other depressive episodes- atypical
depression
 F32.9: Depressive episode, unspecified
 F33: Recurrent depressive disorder.
Etiology
i) Biological Theories
 Neurochemical: level of serotonin and nor
epinephrine decreases, dysregulation of
acetylcholine and GABA occurs.

 Genetic theories: occur more in first degree

relatives and identical twins.

 Endocrine theories: Due to malfunction of HPA

axis it creates cortisol, thyroid and hormonal
abnormalities.
 Circadian rhythm theories: changes in
circadian rhythm which can be caused by
medications, nutritional deficiencies physical or
psychological illness, hormonal fluctuations can
lead to depression.

 Changes in the brain anatomy: Loss of

neurons in the frontal lobes, cerebellum and
basal ganglia
Medication side effects: Anxiolytics,
Antipsychotics , sedative- hypnotics, anti
hypertensives such as propranolol and
reserpine, certain acne medications such as
isotretinion. Other drugs includes:
 Antibacterial and antifungal drugs: ampicillin,
cycloserin, tetracycline and sulfonamides.
 Anti neoplstics: vincristine and zidovudine
 Analgesics and anti inflammatory drugs:
opiates, ibuprofen and phenylbutazone
 Anti ulcer: cimentadine
 Harmones: estrogen and progesteron
 Steriods: prednisone and cortisone
 Neurological disorders: Individuals who
suffered from CVA, Brain tumors particularly of
temporal lobe, Alzheimer's disease, Parkinson's
disease, Huntington’s disease, Multiple sclerosis
may experience symptoms of depression.

 Electrolyte disturbances: excessive level of

sodium bicarbonate or calcium can produce
symptoms of depression as can deficits in
magnesium and sodium.
 Nutritional deficiencies: deficiencies in vit. B1,
B6, B12, B3,Vit. C, iron, folic acid, zinc, calcium
and potassium.
ii) Psychosocial Theories
 Psychoanalytic theory: Acc. to Freud,
depression results due to loss of ‘loved
object’ and fixation in the oral sadistic phase
of development.
 Behavioural theory: depression is conditioned
by repeated losses in the past.
 Learning theory: a state of helplessness
occurs in the person who experience
repeated failures and individual abandons any
further attempts to succeed. The individual
becomes depressed because they have
learned that whatever they do is futile.
 Cognitive theory: depression occurs due to
negative cognitions related to environment,
self and future. These cognitive distortions
arises out of a defect in cognitive
development and causes the individual to feel
inadequate, worthless and rejected by others.

 Sociological theory: stressful life events e.g.

Death, marriage, financial loss can also lead to
depression.
Transactional model of
stress/adaptation
Clinical features
 Depressed mood: pervasive and persistent sadness.
 Depressed cognitions: hopelessness, helplessness,
worthlessness, unreasonable guilt and self blame.
 Suicidal thoughts because of gloomy preoccupations
 Psychomotor activity : retarded, monotonous voice. In
older patients, agitation is common with marked anxiety,
restlessness and feeling of uneasiness.
 Psychotic features: delusions specially Nilhistic delusions
, delusion of guilt, delusion of poverty and hallucinations.
Clinical features
 Somatic features ( melancholic features):
 Significant decrease in appetite or weight
 Early morning awakening, atleast 2 or more hours
before the usual time of wakening
 Diurnal variations with depression being worst in
morning
 Pervasive lack of interest and lack of reactivity to
pleasurable stimuli
 Psychomotor agitation or retardation
Clinical features
 Other features :
 Difficulties in thinking and concentration
 Subjective poor memoryOther symptoms
Common symptoms
 MenstrualApathy
or sexual disturbancesFatigue
 Vague physical
Sadness symptoms such as fatigue,
Thoughts of death aching
discomfort, constipation etc Decreased libido
Sleep disturbances

Hopelessness Dependency

Helplessness Spontaneous crying

Worthlessness Passiveness

Guilt, anger
Diagnosis
 Psychological tests: Beck depression
inventory, Hamilton rating scale to assess
the severity and prognosis.
 Dexamethasone suppression test showing
failure to suppress cortisol secretions
 Toxicology screening in case of drug
induced depression
 History collection and mental status
examination.
 Based on ICD 10 criteria.
ICD 10 DIAGNOSTIC CRITERIA
Prognosis of mood disorders
 An average manic episode lasts for 3-4
months, while a depressive episode lasts
for 4-9 months.
 Good Prognostic Factors
• Abrupt or acute onset
• Severe depression
• Typical clinical features
• Well-adjusted premorbid personality
• Good response to treatment
Prognosis of mood disorders
 Poor Prognostic Factors
• Double depression
• Co-morbid physical disease, personality
disorders or alcohol dependence
• Chronic ongoing stress
• Poor drug compliance
• Marked hypochondriacal features or
mood incongruent psychotic features
Treatment modalities

Psychopharmacology

Physical therapies

Psychosocial therapies
 PSYCHOPHARAMACOLOGY
 Antidepressants

Selective
Tricyclic Monoamine
serotonin
antidepressants oxidase inhibitors
reuptake inhibitors

Serotonin – Other
Norepinephrine Tetracyclics antidepressants
reuptake inhibitors drugs
Selective serotonin reuptake
inhibitors ( SSRIs)
 Their action is a specific to serotonin reuptake
inhibition
 Have fewer sedating, antichollinergic and
cardiovascular effects.
 Should be used cautiously along with MAOI
 Serotonin syndrome may occur with concomitant
use of SSRIs and Metaclopramide, Sibutramine,
Tramadol or 5HT receptor agonists
 E.g. Fluoxetine (20-80mg), fluvoxamine (50-300mg),
paroxetine(10-50 mg), sertaline (25-200 mg),
escitalopram (10-20 mg), citalopram (20-40mg)
Tricyclic antidepressants (TCAs)
 They work by blocking the activity of nor
epinephrine and serotonin or increasing the
sensitivity of post synaptic receptor sites.
 Contraindicated in severe impairment of
liver functions and acute myocardial
infarction
 Should not be given along with MAOIs as
can lead to hypertensive crisis
 E.g. Amitriptyline (50-300mg), clomipramine
(25-250 mg), imipramine (30-300mg),
trimipramine (50-300 mg), nortriptyline (30-
100 mg), doxepin (25-300 mg).
Monoamine oxidase inhibitors
(MAOIs)
 These drugs act on MAO (monoamine
oxidase) which is responsible for the
degradation of catecholamines after
reuptake which finally helps in increasing the
level pf NE and 5HT at receptor site.
 Has many side-effects therefore, it is used
less frequent.
 Hypertensive crisis can occur with
amphetamines, levodopa, dopamine,
epinephrine, guanethidine, reserpine or
vasoconstrictors.
Monoamine oxidase inhibitors
(MAOIs)
 Serious potentially fatal adverse reactions
occur with concurrent use of all other
antidepressants, carbomazepine,
cyclobenzaprine, buspirone,
sympthatomemtics, tryptophan,
dextromethophan, anesthetic agents.
 Hypertensive crisis may occur with ingestion
of food or other products containing high
tyramine ( aged cheese, raisins, red wine ,
smoked and processed meats, yeast etc)
Monoamine oxidase inhibitors
(MAOIs)
 E.g. Isocarboxazid (20-60mg), phenelzine
(45-90 mg), selegiline trandermal system
(6/24 hr- 12/24 hr patch)
Serotonin- Nor epinephrine
reuptake inhibitors
 Works by blocking the reuptake of
serotonin and nor epinephrine
 E.g.Venlafaxine (75-375 mg), duloxetine
(20-60 mg), desvenlafaxine (50 mg),
milnacipran (12-100 mg)
Tetracyclic antidepressants
 Prevents the reuptake of NE and 5HT.
 E.g. Amoxapine (150-300 mg), Maprotiline
(75-200 mg)
Other antidepressant drugs
 Bupropion (150-450 mg)
 Vilazodone (10-40 mg)
 Mirtazapine (15-45 mg)
 Nefazadone (300-500 mg)
 Trazodone (150-300 mg)
PHYSICAL THERAPIES

ECT

Repetitive
transcranial Light
magnetic
stimulation
therapy (used
(TMS) and for seasonal
vagus nerve depression in
stimulation winters)
(VNS)
PSYCHOSOCIAL TREATMENT
 Psychotherapy: using psychoanalytic techniques to
help the patient gain insight into the cause of
depression.
 Cognitive therapy
 Supportive psychotherapy: reassurance, ventilation,
occupational therapy, relaxation and other activity
therapies
 Group therapy
 Family therapy: to decrease intrafamilial and
interpersonal difficulties
 Behaviour therapy: social skill training, problem
solving techniques, assertive training, self control
therapy, activity scheduling and decision making
techiques.
NURSING MANAGEMENT
1. Risk for suicide
 Short-Term Goals
● Client will seek out staff when feeling urge
to harm self.
● Client will make short-term verbal (or
written) contract with nurse not to harm
self.
● Client will not harm self.
 Long-Term Goal
● Client will not harm self.
 Interventions
a. Create a safe environment for the client. Remove all
potentially harmful objects from client’s access.
b. Formulate a short-term verbal or written contract with
the client that he or she will not harm self during a
specific time period.
c. Encourage verbalizations of honest feelings. Through
exploration and discussion, help the client to identify
symbols of hope in his or her life.
d. Secure a promise from the client that he or she will seek
out a staff member or support person if thoughts of
suicide emerge.
e. Maintain close observation of client. Depending on level
of suicide precaution, provide one-to-one contact,
constant visual observation, or every-15-minute checks.
f. Teach the family members regarding the non verbal cues
which patient gives like good bye letters, saying that now
things are going to get better etc.
II. Complicated grieving
 Short-Term Goals
● Client will express anger about the loss.
● Client will verbalize behaviors associated
with normal grieving.
 Long-Term Goal
● Client will be able to recognize his or her
own position in the grief process, while
progressing at own pace toward
resolution.
 Interventions
a. Determine the stage of grief in which the client is fixed.
Identify behaviors associated with this stage.
b. Develop a trusting relationship with the client. Show
empathy, concern, and unconditional positive regard. Be
honest and keep all promises.
c. Help the client to discharge pent-up anger through
participation in large motor activities
d. Teach the normal stages of grief and behaviors associated
with each stage. Help the client to understand that feelings
such as guilt and anger toward the lost concept are
appropriate and acceptable during the grief process, and
should be expressed rather than held inside.
e. Assist the client in problem solving as he or she attempts
to determine methods for more adaptive coping with the
experienced loss. Provide positive feedback for strategies
identified and decisions made.
III. Low Self-Esteem/Self-Care Deficit
Short-Term Goals
● Client will verbalize areas he or she likes about self.
● Client will participate in ADLs with assistance from
healthcare provider.
Long-Term Goals
● By time of discharge from treatment, the client will
exhibit increased feelings of self-worth as evidenced
by verbal expression of positive aspects of self, past
accomplishments, and future prospects.
● By time of discharge from treatment, the client will
exhibit increased feelings of self-worth by setting
realistic goals and trying to reach them, thereby
demonstrating a decrease in fear of failure.
● By time of discharge from treatment, the client will
satisfactorily accomplish ADLs independently.
 Interventions
 Be accepting of the client and spend time
with him or her even though pessimism and
negativism may seem objectionable. Focus
on strengths and accomplishments and
minimize failures.
 Encourage the client to recognize areas of
change and provide assistance toward this
effort.
 Encourage the client in participation of
group activities and provide positive
reinforcement of the desired behaviour.
 Other nursing diagnosis
 Altered communication process related to depressive
cognitions, evidenced by being unable to interact with others,
withdrawn, expressing fear of failure or rejection.
 Altered sleep and rest, related to depressed mood and
depressive cognitions evidenced by difficulty in falling asleep,
early morning awakening, verbal complaints of not feeling
well-rested.
 Altered nutrition, less than body requirements related to
depressed mood, lack of appetite or lack of interest in food,
evidenced by weight loss, poor muscle tone, pale conjunctiva,
poor skin turgor.
 Self-care deficit related to depressed mood, feelings of
worthlessness, evidenced by poor personal hygiene and
grooming.