Transcript lecture 2 MDD.ppt

Mood Disorder
Major Depressive Disordered I
Jawza F. Al-Sabhan, Msc.
College of Pharmacy
Clinical Pharmacy Department
Introduction
Everyone experiences variations in mood, blues that come and go,
disappointments, the normal grief that accompanies the loss of someone
you love. But a severe or prolonged depression that interferes with the
ability to function or feel pleasure is not a mere
case of the blues. It is an illness.
Depression affects many people of all ages.
It is the 8th leading cause of death for males, and 19th leading cause of
death for females.
Epidemiology
Lifetime incidence of depression is 13-20%.
Life time incidence of depression in KSA 17%.
Life time prevalence 5-12%(US,Europe)
Most common age is late 20s.
Pathophysiology hypotheses
Biogenic amine
1. Central nervous system (CNS) deficiency in dopamine,
norepinephrine, and/or serotonin
2. Based on knowledge that antidepressants increase monoamine
neurotransmission
Permissive
An underlying deficiency of serotonin accompanied by
decreased noradrenergic transmission
Pathophysiology hypotheses
Neuroendocrine finding
1.
2.
3.
Pituitary and adrenal glands are enlarged in depressed
patients, and hypothalamic function may be abnormal.
Serotonin exerts a strong influence on HPA axis.
Approximately 45% to 60% of patients with major
depression have a neuroendocrine abnormality,
including hypersecretion of cortisol
NORADRENERGIC TRACTS
Noradrenaline, a key neurotransmitter
involved in the control of mood and
emotional behavior, is believed to inhibit
or stimulate a variety of emotional
responses such as anxiety, aggression,
stress, and sleep
SEROTONERGIC TRACTS
Serotonin is involved in the
regulation of pain, pleasure,
anxiety, panic, appetite , and sleep
behavior (the sleep-wake cycle).
Risk factors
1. Family history of depression
a. 1st degree relative of patients with depression are 1.5 to 3 times
more likely to develop depression
b. Twin studies
• Monozygotic twins have a 65% concordance rate for depression
• Dizygotic twins have a 14% concordance rate for depression
2. Female gender
3. Previous depressive episode
4. Chronic medical illness
5. Substance abuse
Diagnostic Criteria (DSM-IV)
for MDD
1.
2.
At least 5 symptoms present for 2 weeks most of day nearly every day
Represents change from previous functioning
a. Depressed mood*
b. Loss of interest or pleasure*
c. Appetite or weight change
d. Sleep disturbance
e. Psychomotor agitation/retardation
f. Fatigue/loss of energy
g. Feelings of worthlessness/guilt
h. Decreased concentration/indecisiveness
i. Recurrent thoughts of death/suicidal ideation/suicide attempt
3. Symptoms cause social or occupational impairment
4. Symptoms are not due to substance abuse or medical condition
5. Symptoms are not due to gereavement
Depression Sub-classification
A-Melancholia (endogenous)
1.
2.
3.
4.
5.
Weight loss
Early morning awakening
Extreme listlessness
Intense guilt
Inability to cheer up even for a
moment
C-Atypical depression (exogenous)
1.
2.
3.
4.
5.
Increased appetite
Weight gain
Excessive sleep
Leaden sensation in the arms
and legs
Mood reactive
B- Psychotic (or delusional)
D-Postpartum Depression
1. Mood congruent
2. Poverty, physical illness,
moral transgressions
3. Occur in 10–25%
1. Onset of depression
within 4 weeks
2. occurs in 10% to 26%
Specific features of diagnosis
1) Mild
a) Minimum requirement to make diagnosis
b) Minor functional impairment
2) Moderate
a) Greater degree of functional impairment
3) Severe
a) Marked interference with social and/or occupational
functioning
b) Suicidal ideation
Assessing Depression
Target
symptoms
Rating
scales
Laboratory
studies
Assessing
Depression
Hospitalization
Prognosis
Target symptoms
D — depressed mood
S — sleep
I — interest
G — guilt
E — energy
C — concentration
A — appetite
P — psychomotor
S — suicide
Laboratory studies
There are no diagnostic lab tests for depression, although the
following should be obtained to rule out other medical
illnesses which mimic depression
a. Complete blood count (CBC; i.e., anemia)
b. Thyroid function tests (TFTs; i.e., hypothyroidism)
c. Rapid plasma reagin (RPR; i.e., syphilis)
d. Urine drug screen (i.e., substance abuse)
Prognosis
One episode
1. 70% of patients are responsive to antidepressant therapy
• ↑ risk of recurrance by 50 %
2. Relapse
a. Following 1st episode, 50% experience another episode
Two episodes
b. Following 2nd episode70% experience another episode
• ↑3nd
riskepisode
by 70 %90% experience another episode
c. Following
Three episodes
• ↑ risk by 90 %
Hospitalization
1. Patients who lack capacity to cooperate with
treatment
2. Patients at risk for suicide or other violent
behavior
3. Patients who lack psychosocial supports
4. Patients who have other psychiatric or
general medical problems.
Rating scales
General purpose
a. Brief Psychiatric Rating Scale (BPRS), investigator-rated
b. Hopkins Symptom Checklist (SCL-90), patient-rated
Disease-specific rating scales (depression)
a. Investigator-rated
1) Hamilton Rating Scale for Depression (Ham-D, HRSD)
2) Montgomery-Asburg Depression Rating Scale (MADRS)
b. Patient-rated
1) Beck Depression Inventory (BDI)
2) Zung Self Rating Scale
Treatment Goals
Treatment
Psychotherapy
Electroconvulsive
therapy
Choices
Of
Treatment
Medication
and
psychotherapy
Medication
Choices of Treatment
Psychotherapy
a. Less severe
b. Less chronic
c. No psychotic
d. Past positive response
e. Medical contraindication to
medications
Medication
a. More severe
b. Chronic
c. Recurrent
d. Psychotic
e. Melancholic
f. Past positive response
g. Family history
h. Failure to respond to
psychotherapy
Choices of Treatment
Medication and
psychotherapy
a. More severe
b. Chronic
c. Partial response to either
therapy alone
d. Personality disorder
Electroconvulsive therapy
a. Psychotic
b. Severe or extremely severe
c. Past positive response
d. Failure of several
medications or combined
treatment trials
e. Need for rapid response
f. Medical contraindications to
medications
Antidepressant therapy
Initiation of therapy
1. Initiate therapy with divided doses to minimize
adverse drug reactions
2. Consider age of patient and adjust accordingly
3. Target dose should be achieved as quickly as
tolerated
4. Improvement in 3–4 weeks of therapy
5. Maximal response in 8 weeks of therapy
Phases of Treatment
Acute
treatment
Continuation
treatment
Maintenance
treatment
Acute treatment
1. Duration usually 6–12 weeks
2. Response (symptom remission)
a) Definition
i) Complete (> 50% reduction)
ii) Partial (> 20% but < 50%)
iii) No response (< 20%)
b) Rate of response
i) First week
• Decreased anxiety
• Improvement in sleep
• Improvement in appetite
ii) 1–3 weeks
• ↑ Activity, sex drive, self-care,
memory
• Thinking and movements normalize
• Sleeping and eating patterns
normalize
iii) 2–4 weeks
• Relief of depressed mood
• Less hopeless/helpless
• Thoughts of suicide subside
Continuation treatment
1. To prevent relapse
2. Continue antidepressant 6–9 months after 1st
episode at same dose
3. Continue with the same treatment and the
same dose in acute phase.
Maintenance treatment
1.
2.
3.
4.
1 year duration
Use full therapeutic doses
Goal is to prevent new episode (recurrence)
Potential candidates
a) Three episodes of MDD or
b) Two episodes of MDD and:
i) Family history of borderline personality disorder/recurrent MDD in 1st
degree relative
ii) Recurrence within 1 year after medicine discontinued
iii) Onset before age 20 or after age 60
iv) Severe, sudden or life threatening depression
Factors to be consider on Selection of
an antidepressant
Neurotransmitter profile family history
Side effect profile potential drug interactions
Patient age
cost
ease of administration (compliance)
Safety profile
Class
Drug
Dose
No per pack
Cost
Cost/month
TCA
Imipramine
10 mg
60 tablets
16.80 SR
100 mg
84 SR
TCA
Clopimramine
25 mg
30 Capsules
28 SR
100 mg
112 SR
SSRI
Fluvoxamine
100 mg
30 tablets
92 SR
92 SR
SSRI
Escitalopram
10 mg
28 tablets
117 SR
125 SR
SSRI
Citalopram
20 mg
28 tablets
122 SR
130 SR
SSRI
Fluoxetine
20 mg
28 tablets
122 SR
462 SR
Novel
Duloxetine
60 mg
28 Capsules
179 SR
191 SR
Dual
Mirtazapine
30 mg
30 tablets
177 SR
265.5 SR
Dual
Venlafaxine
150 mg
14 capsules
135 SR
289 SR
ANTIDEPRESSANT
MEDICATION: REVIEW
Treatment
F:\WFGSG_DEPRESSION.pdf
Psycho
therapy
Medication
Electroconvulsive
Therapy ECT
Tricyclic
Antidepressants
TCA
Monoamine Oxidase
Inhibitors MAOI
Selective serotonin
reuptake inhibitors
(SSRIs)
Dual Reuptake
Inhibitors
Drugs with Novel
Mechanism
Benzodiazepine
(Adjunctive Therapy )
ANTIDEPRESSANT MEDICATION
Antidepressants can be classified in several
ways, including by chemical structure and the
presumed mechanism of antidepressant
activity.
All antidepressants are potentially effective in the
treatment of depression, they show similar efficacy
when used in adequate dosages.
Antidepressants
1. TCA = Tricyclic Antidepressants
2. MAOI = Mono- Amines Oxides Inhibitor
3. SSRI = Selective Serotonin Reuptake
Inhibitor
4. SNRI = Serotonin Reuptake Inhibitor
ANTIDEPRESSANT MEDICATION
ANTIDEPRESSANT MEDICATION
Tricyclics “TCAs”
Amitriptyline 50 –300 mg/day
Clomipramine 50 –250 mg/day
Doxepin 25 –300 mg/day
Trimipramine 50 –300 mg/day
Imipramine 50 –300 mg/day
Desipramine 50 –300 mg/day
Nortriptyline 25 –150 mg/day
Protriptyline 10 – 60 mg/day
Tertiary amines
Secondary amines
Mechanism Of Tricyclic Antidepressants TCA
ANTIDEPRESSANT MEDICATION
Tricyclics
Block the reuptake of both norepinephrine
(NE) , serotonin (5HT), muscarinic, alpha1
adrenergic, and histaminic receptors.
The extent of these effects vary with each
agent resulting in differing side effect profiles.
TCA have effects on cardiac action potentials
typical of class IA antiarrhythmics
Possible Adverse Effects of Reuptake Blocking of
Antidepressant Drugs*
Serotonin
Reuptake
Blocking
Nausea, Diarrhea and Gastrointestinal
disturbances (including weight loss early in
treatment, weight gain late in treatment)
Nervousness, Insomnia, Fine tremors
Increase or decrease in anxiety (dose dependent)
Sexual dysfunction (including decreased libido)
Extrapyramidal adverse effects
Possible Adverse Effects of Reuptake Blocking of
Antidepressant Drugs*
Nor epinephrine
Reuptake
Blocking
Blurred vision, Dry mouth, Constipation, Urinary
retention (Act synergistically with anticholinergics)
Tremors, Increased arousal and Insomnia
Tachycardia
Raised blood pressure
Blockade of antihypertensive effects
Possible Adverse Effects of Receptor Blocking of
Antidepressant Drugs*
Blocking
Muscarinic
Receptors
Dry mouth, Constipation, Urinary retention
Sinus tachycardia
Blurred vision
Attack or exacerbation of narrow-angle glaucoma
Cognitive impairment
Memory dysfunction
Blocking
Histamine 1
Receptors
Night-time sedation
Impairment of psychomotor coordination during the
daytime, Drowsiness
Weight gain
Potentiation of central depressant drugs
Tricyclic Antidepressants
Managements of Anticholinergic side effects.
Impaired visual accommodation may be counteracted through the use of
pilocarpine eye drops.
Urinary hesitation may be treated by prescribing bethanechol, 200 mg/day
Dry mouth may be counteracted by advising the patient to use sugarless
gum or candy or by prescribing an oral rinse of 1% pilocarpine used three
or four times daily.
Constipation is best dealt with through adequate hydration and the use of
bulk laxatives.
Tricyclic Antidepressants
Sedation
TCAs also have affinity for histaminergic receptors
and produce varying degrees of sedation.
In general, tertiary amines cause greater sedation,
whereas secondary amines cause less.
Patients with major depressive disorder with
insomnia may benefit from sedation when their
medication is given as a single dose before bedtime.
Tricyclic Antidepressants
Weight gain.
TCAs have the capacity to induce weight gain possibly
through their histaminergic properties.
The degree of weight gain appears to vary by agent (e.g.,
greater weight gain with amitriptyline and less with
desipramine), be dose dependent, and be reversible with
cessation of tricyclic antidepressant therapy.
Tricyclic Antidepressants
Neurological effects.
TCAs can induce mild myoclonus, this may be a sign of
toxicity.
Amoxapine, a TCA with antipsychotic properties, can also
cause extrapyramidal side effects and tardive dyskinesia.
In overdoses, tricyclic antidepressants can precipitate seizures
especially (Maprotiline).
ANTIDEPRESSANT MEDICATION
Monoamine oxidase irreversible, non
selective inhibitors “MAO Is”
Phenelzine 15 –90 mg/day
Tranylcypromine 10 – 60 mg/day
Inhibit the enzymatic breakdown of 5HT and NE.
They are usually reserved for atypical or resistant depression
due to their toxicity profile.
ANTIDEPRESSANT MEDICATION
Reversible monoamine oxidase
inhibitors ”RIMA”
Moclobemide
This unique mechanism results in a good tolerability
profile and unlike traditional MAOIs, there is no need
to restrict dietary tyramine.
Monoamine oxidase inhibitors
Hypertensive crises.
A hypertensive crisis can occur when a patient taking an
MAOI ingests large amounts of tyramine or other pressor
amines in foods or medications.
This reaction is characterized by the acute onset of severe
headache, nausea, neck stiffness, palpitations, profuse
perspiration, and confusion, possibly leading to stroke and
death.
Monoamine oxidase inhibitors
Hypertensive crises.
Dietary restrictions include avoiding such foods as aged
cheeses or meats, fermented products, yeast extracts
The list of medications that must be avoided includes all
sympathomimetic and stimulant drugs as well as over-thecounter decongestants and cold remedies.
Monoamine Oxidase Inhibitors
Cardiovascular effects.
Orthostatic hypotension is commonly seen during MAOI
treatment.
Possible treatments for this side effect include the addition
of salt to increase intravascular volume or use of the
steroid fludrocortisone.
MAOI use can also be associated with the development of
peripheral edema, which may be helped by the use of
support stockings.
Major Depressive Disordered II
Jawza F. Al-Sabhan, Msc.
College of Pharmacy
Clinical Pharmacy Department
ANTIDEPRESSANT MEDICATION
COMPARATIVE EFFICACY
SSRIs have a flat dose-response curve. There is seldom any
advantage in dosing higher than the usually effective minimum
dose.
TCAs, and other atypical antidepressants appear to have an
ascending dose-response curve, thus higher doses are usually
associated with increased efficacy.
COMPARATIVE SAFETY
Most current literature considers the SSRIs to be better
tolerated than TCAs, especially when used at the minimally
effective dose.
One meta-analysis has disputed this, arguing that dropout
rates (~32%) are not significantly different for either group.
ANTIDEPRESSANT MEDICATION
Selective serotonin reuptake inhibitors “SSRIs”
Fluoxetine 20–40mg/day
Sertraline 50 –200 mg/day
Paroxetine 20–40 mg/day
Fluvoxamine 50 –300 mg/day
Citalopram 20 – 40 mg/day
Escitalopram 10-20 mg/day
Mechanism of SSRI
Possible Adverse Effects of Reuptake Blocking of
Antidepressant Drugs*
Serotonin
Reuptake
Blocking
Nausea, Diarrhea and Gastrointestinal
disturbances (including weight loss early in
treatment, weight gain late in treatment)
Nervousness, Insomnia, Fine tremors
Increase or decrease in anxiety (dose dependent)
Sexual dysfunction (including decreased libido)
Extrapyramidal adverse effects
ANTIDEPRESSANT MEDICATION
Selective Serotonin Reuptake Inhibitors
Block the reuptake of 5HT and increase synaptic 5HT
transmission.
They have little or no effect on other
neurotransmitters, results in fewer anticholinergic
(ACH) and sedative effects.
Selective serotonin reuptake inhibitors
Gastrointestinal.
SSRIs cause nausea, vomiting, and diarrhea to a greater extent
than tricyclic antidepressant medications.
These adverse events are generally dose dependent and tend to
dissipate over the first few weeks of treatment.
Selective serotonin reuptake inhibitors
Activation/insomnia.
In some patients, SSRIs may precipitate or exacerbate
restlessness, agitation, and sleep disturbances.
These side effects often attenuate with time.
Anxiety may be minimized by introducing the agent at a low
dose; insomnia may be effectively treated by the addition of
trazodone, up to 100 mg at bedtime.
Selective serotonin reuptake inhibitors
Sexual side effects.
loss of erectile or ejaculatory function in men and loss of
libido and anorgasmia in both sexes may be complications
SSRIs.
Lowering the dose, discontinuing the antidepressant, or
substituting another antidepressant such as bupropion
Specific pharmacologic treatments that can be added for
arousal or erectile dysfunction include sildenafil, yohimbine.
Selective serotonin reuptake inhibitors
Effects on weight.
Fluoxetine has been shown to cause an initial reduction in
weight but this tends be gained back subsequently.
The literature differs as to whether patients taking SSRIs
beyond the acute phase do or do not experience weight
gain as a medication side effect.
Selective serotonin reuptake inhibitors
Serotonin syndrome.
SSRI used associated with the rare
development of a syndrome due to
an excess of serotonergic activity.
Features of serotonin syndrome
include:
(abdominal pain, diarrhea, flushing,
sweating, hyperthermia, lethargy,
mental status changes, tremor and
myoclonus, rhabdomyolysis, renal
failure, cardiovascular shock, and
possibly death.)
it is usually associated with the
simultaneous use of multiple
serotonergic agents such as SSRIs
together with MAOIs.
When patients are being switched from
an SSRI with a short half-life to an
MAOI, a waiting period of at least 2
weeks is needed between the
discontinuation of one medication and
the initiation of the other.
When switching from fluoxetine to an
MAOI, a waiting period of at least 5
weeks is needed before the MAOI is
started.
ANTIDEPRESSANT MEDICATION
Atypical Antidepressants
Norepinephrine-serotonin modulator
Mirtazapine 15 – 45 mg/day
Serotonin-norepinephrine reuptake inhibitors
Venlafaxine 75 –375 mg/day
Dopamine-norepinephrine reuptake inhibitors
Bupropion 150 – 450 mg/day
MIRTAZAPINE
The drug mainly affects serotonin (5-HT) receptors of the 5HT2 and 5-HT-3 subtypes, possessing low affinity for 5HT1A, 5-HT1B, and 5-HT1C receptors; as a 5-HT2
antagonist.
mirtazapine has strong alpha-2 receptor blocking actions, but
unlike mianserin it has no significant effect on the synaptic
reuptake of catecholamines.
MIRTAZIPINE SIDE EFFECTS
The most common side effects from mirtazapine
include sedation, dry mouth, and weight gain.
Mirtazapine has also been shown to increase serum
cholesterol levels in some patients.
Although agranulocytosis has been observed to occur
in patients taking mirtazapine.
VENLAFAXINE
Venlafaxine is selectively inhibits neuronal
uptake of serotonin, norepinephrine.
The initial recommended dosage of regularrelease venlafaxine is 75 milligrams (mg)/day;
the dose may be titrated at 4-day intervals to a
maximum dose of 375 mg/day.
Major Side Effect: Hypertension
BUPROPION
Bupropion is a very weak inhibitor of
norepinephrine uptake and a weak inhibitor of
dopamine uptake.
Side effect including headaches, tremors,
and seizures.
Pharmacologic Effects Of Antidepressants
Reduce depression
Psychomotor activation
Antiparkinsonian effects
Sedation/drowsiness
Hypotension
Weight gain
Blurred vision
Dry mouth
Constipation
Sinus tachycardia
Urinary retention
Cognitive dysfunction
H1
block
ACh
block
DA
reuptake
inhibition
5HT2
block
Antidepressant
Alpha2
block
Alpha1
block
Anxiety
Postural hypotension
Dizziness
Reflex tachycardia
Memory dysfunction
Reduce depression
Reduce suicidal behavior
Antipsychotic effects
Hypotension
Ejaculatory dysfunction
Sedation
5HT reuptake
inhibition
NE
reuptake
inhibition
Reduce depression
Antianxiety effects
GI disturbances
Sexual dysfunction
Reduce depression
Antianxiety effects
Tremors
Tachycardia
Erectile/ejaculatory dysfunction
Algorithm for Treatment Major
Depressive Disorder.
Treatment
Psycho
therapy
Medication
TCA
MAOI
SSRIs
Dual Reuptake
Inhibitors
Drugs with
Novel
Mechanism
Benzodiazepine
(Adjunctive Therapy )
Electro-convulsive
Therapy ECT
Electroconvulsive Therapy ECT
MECHANISM OF ECT
Electroconvulsive therapy involves applying a brief
electrical pulse to the scalp while the patient is under
anesthesia. This pulse excites the brain cells causing
them to fire in unison and produces a seizure.
Cont.
Psychiatrist
ECT
Anesthesiologist
Nursing staff
Cont. ECT
Bilateral Placement
Right Unilateral Placement
Comparative Pharmacokinetics
Drug Interactions
Newer antidepressants and CYP P450 inhibitory enzymes
Drug Interactions
TCAs
a) TCA + anticoagulant → ↑ anticoagulant effect
b) Enzyme inhibitors → ↑ TCA effect
c) Enzyme inducer → ↓ TCA effect
d) TCA + centrally-acting antihypertensive → ↑ BP
e) TCA + sympathomimetic → ↑ BP plus
arrhythmias
f) TCA +MAOI → hypertensive crisis
Drug Interactions
MAOIs
a) MAOI + stimulant → hypertensive crisis
b) MAOI + antidiabetics → hypoglycemia
c) MAOI + insulin → hypoglycemia
d) MAOI + levodopa → hypertensive crisis
Drug Interactions
SSRI
a) SSRI + TCA → ↑ TCA effect
b) SSRI + carbamazepine → ↑ carbamazapene
d) SSRI + antipsychotic → ↑ antipsychotic effect
e) SSRI + warfarin → ↑ bleeding time
f) SSRI + MAOI → serotonergic syndrome
Special Populations
Pregnancy
1) Treatment
a) Mild depression—psychotherapy
b) Severe depression with decreased oral intake, suicidality,
or psychosis—pharmacotherapy or electroconvulsive
therapy (ECT)
2) Antidepressants of choice
a) Well-studied during pregnancy (tricyclic antidepressants
[TCAs], fluoxetine)
b) Short-acting (sertraline, paroxetine)
Special populations
Lactation
1) Antidepressants of choice
a) Well-studied (?)
b) Improved pharmacokinetic profiles
c) Limited metabolites
d) Greater receptor selectivity
2) Specific agents
a) Sertraline, paroxetine
b) Nortriptyline, desipramine
Special populations
Elderly
1. Treatment considerations
a) Pharmacokinetic and pharmacodynamic changes
b) Coexisting medical conditions (e.g., cardiovascular disease)
c) Anticholinergic side effects
d) Depression-related cognitive dysfunction (pseudo-dementia)
2. Agents of choice
a) Short-acting selective serotonin reuptake inhibitors (SSRIs)
b) Bupropion
Concurrent medical disorders
Asthma
a) Avoid monoamine oxidase inhibitors (MAOIs) which interfere with
sympathomimetic bronchodilators
Cardiac disease
a) Ventricular arrhythmia, subclinical sinus node dysfunction, conduction
defects
b) Avoid TCAs
c) Use bupropion, SSRIs or ECT
d) MAOIs do not affect cardiac conduction, rhythm, or contraction but
may induce orthostasis
Concurrent medical disorders
Dementia
a) Avoid TCAs or antidepressants with
anticholinergic properties
Epilepsy
a) Avoid bupropion, maprotiline, amoxapine, TCAs
Glaucoma (narrow-angle)
a) Avoid TCAs
Concurrent Medical Disorders
Hypertension
a) TCAs may antagonize the therapeutic actions of
guanethidine, clonidine, or methyldopa
c) Concurrent antihypertensive treatment, especially
with diuretics, increases likelihood that TCAs,
MAOIs, or trazodone will induce orthostasis
d) β-blockers, esp. propranolol may cause depression
Parkinson’s disease
a) Avoid amoxapine (dopamine-receptor blocker)
Patient Education
Treat the patient with the same empathy, respect, and concern that you would treat
a patient with a medical illness
Do not be afraid to discuss the symptoms of depression
Be sensitive to the patient’s fear of being stigmatized
Emphasize the common occurrence of depression as well as the many successful
treatment options
Compare depression to a common and accepted medical illness (e.g., diabetes or
hypertension)
Compare the need for medication compliance with antidepressants to the need for
compliance with other maintenance medications (e.g., insulin or antihypertensive
agents).
Thank god for his mercy,
who carry a hope for us
with every sunrise!