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DEPRESSION
Dr.Iqra Osman
CONTENTS
• INTRODUCTION
• DEFINITION
• TYPES OF DEPRESSION
• EPIDEMIOLOGY
• ETIOLOGY
• PATHOPHYSIOLOGY
• CLINICAL MANIFESTATIONS
• DIAGNOSIS
• INVESTIGATIONS
• TREATMENT
• CONCLUSION
• REFERENCES
INTRODUCTION
• Depression is a affective disorders.
• Affective disorders : mental illnesses characterized
by pathological changes in mood.
• Depression : pathologically depressed mood
DEFINITION
• DEPRESSION (By WHO) : Common mental
disorder that presents with depressed mood, loss of
interest or pleasure, feelings of guilt or low self-
worth, disturbed sleep or appetite, low energy, and
poor concentration.
TYPES OF DEPRESSION
• Major depressive disorder : recurrence of long
episodes of low moods, or one extended episode that
seems to be ‘never-ending.
- Atypical depression
- Post partum depression
- Catatonic depression
- Seasonal affective disorder
- Melancholic depression
• Manic depression (bipolar disorder)
Four ‘Episodes’of Bipolar Disorder
- depressive episode
- manic episodes
- hypomanic episode
- mixed-mood states
• Dysthymic depression
- lasts a long time but involves less
severe symptoms.
- lead a normal life, but we may not
be functioning well or feeling good
• Situational depression
• Psychotic depression
• Endogenous depression
EPIDEMIOLOGY
• Globally more than 350 million people of all ages
suffer from depression. (WHO)
• For the age group 15-44 major depression is the
leading cause of disability in the U.S.
• Women are nearly twice as likely to suffer from a
major depressive disorder than men are.
• With age the symptoms of depression become even
more severe.
• About thirty percent of people with depressive
illnesses attempt suicide.
ETIOLOGY
• Genetic cause
• Environmental factors
• Biochemical factors : Biochemical theory of
depression postulates a deficiency of
neurotransmitters in certain areas of the brain
(noradrenaline, serotonin, and dopamine).
• Dopaminergic activity : reduced in case of
depression, over activity in mania.
• Endocrine factors
- hypothyroidism, cushing’s syndrome etc
• Abuse of Drugs orAlcohol
• Hormone Level Changes
• Physical illness and side effects of medications
DRUGS
• Analgesics
• Antidepressants
• Antihypertensives
• Anticonvulsants
• Benzodiazipine withdrawal
• Antipsychotics
PHYSICAL ILLNESS
• Viral illness
• Carcinoma
• Neurological disorders
• Thyroid disease
• Multiple sclerosis
• Pernicious anaemia
• Diabetes
• Systemic lupus erythematosus
• Addison’s disease
PATHOPHYSIOLOGY
• The BiogenicAmine Hypothesis
• The Receptor Sensitivity Hypothesis
• The Serotonin-only Hypothesis
• The Permissive Hypothesis
• The Electrolyte Membrane Hypothesis
• The Neuroendocrine Hypothesis
• The BiogenicAmine Hypothesis
- caused by a deficiency of monoamines,
particularly noradrenaline and serotonin.
- cannot explain the delay in time of onset of
clinical relief of depression of up to 6-8 weeks.
• The Receptor Sensitivity Hypothesis
- depression is the result of a pathological
alteration (supersensitivity and up-regulation) in
receptor sites.
- TCAs or MAOIs causes desensitization (the
uncoupling of receptor sites) and possibly down-
regulation (a decrease in the number of receptor sites).
• The Serotonin-only Hypothesis
- emphasizes the role of serotonin in
depression and downplays noradrenaline.
- But the serotonin-only theory has shortcomings:
- it does not explain why there is a delay in
onset of clinical relief
- it does not explain the role of NA
in depression.
• The Permissive Hypothesis
- the control of emotional behavior results from a
balance between noradrenaline and serotonin.
- If serotonin and noradrenaline falls to
abnormally low levels, the patient becomes depressed.
- If the level of serotonin falls and the level of
noradrenaline becomes abnormally high, the patient
becomes manic.
• The Electrolyte Membrane Hypothesis
- hypocalcemia may be associated with mania.
- hypercalcemia is associated with depression.
• The Neuroendocrine Hypothesis
- pathological mood states are explained or
contributed to by altered endocrine function.
CLINICAL MANIFESTATIONS
• DEPRESSIONS
o Thinking is pessimistic and in some cases suicidal.
o In severe cases psychotic symptoms such as
hallucinations or delusions may be present.
o Insomnia or hypersomnia, libido, weight loss, loss of
appetite.
o Intellectual or cognitive symptoms include a
decreased ability to concentrate, slowed thinking, & a
poor memory for recent events.
DIAGNOSIS
• ICD 10 Diagnostic criteria for a depressive
episode {who}
USUAL SYMPTOMS
• Depressed mood.
• Loss of interest and enjoyment.
• Reduced energy leading to increased
fatiguability and diminished activity.
COMMONSYMPTOMS
• Reduced concentration and attention.
• Reduced self esteem and self confidence.
• Ideas of guilt and unworthiness.
• Bleak and pessimistic views of future .
• Ideas or acts of self harm or suicide.
• Disturbed sleep.
• Diminished appetite.
MILD DEPRESSIVE EPISODE
• For at least 2 weeks, at least two of the usual
symptoms of a depressive episode plus at least two
common symptoms.
MODERATE DEPRESSIVE EPISODE
• For at least 2 weeks, at least two or three of the
usual symptoms of a depressive episode plus at
least three of the common symtoms.
SEVERE DEPRESSIVE EPISODE
• For at least 2 weeks all three of the usual
symptoms of a depressive episode plus at least 4
of the common symptoms some of which should be
of severe intensity.
INVESTIGATIONS
• RATING SCALES
o Beck depression inventory
o Hamilton depression rating scale
• DEXAMETHASONE SUPPRESSION TEST
TREATMENT
ANTIDEPRESSANTS
1. MAO inhibitors:
• Irreversible: Isocarboxazid, Iproniazid, Phenelzine
and Tranylcypromine.
• Reversible: Moclobemide and Clorgyline.
2. Tricyclic antidepressants (TCAs)
• NAand 5 HT reuptake inhibitors : Imipramine,
Amitryptiline, Doxepin, Dothiepin and
Clomipramine.
• NAreuptake inhibitors : Desimipramine,
Nortryptyline,Amoxapine.
3. Selective Serotonin reuptake inhibitors:
• Fluoxetine, Fluvoxamine, Sertraline and Citalopram
4.Atypical antidepressants:
• Trazodone, Mianserin, Mirtazapine, Venlafaxine,
Duloxetine, Bupropion and Tianeptine
NON– PHARMACOLOGIC THERAPY
• LIFESTYLE CHANGES
o Stress reduction
o Social support
o Sleep
• PSYCHOTHERAPY
o Cognitive behavioral therapy
o Interpersonal therapy
o Psychodynamic therapy
• ELECTROCONVULSIVE THERAPY – ECT
o Safe & effective disorder for all subtypes of major
depressive disorder.
o ADR : Cognitive dysfunction, cardiovascular
dysfunction, prolonged apnoea etc.
CONCLUSION
• Affective disorders remain one of the most commonly
occurring mental illnesses in adults.
• It is often undiagnosed and untreated.
• Both pharmacological and nonpharmacological
interventions acts as cornerstone in the treatment of
affective disorders.
• Pharmacist plays an important role in accomplishing
these treatment goals.
THANK YOU

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Depression by Dr Iqra Osman Abdullahi.MD

  • 2. CONTENTS • INTRODUCTION • DEFINITION • TYPES OF DEPRESSION • EPIDEMIOLOGY • ETIOLOGY • PATHOPHYSIOLOGY • CLINICAL MANIFESTATIONS • DIAGNOSIS • INVESTIGATIONS • TREATMENT • CONCLUSION • REFERENCES
  • 3. INTRODUCTION • Depression is a affective disorders. • Affective disorders : mental illnesses characterized by pathological changes in mood. • Depression : pathologically depressed mood
  • 4. DEFINITION • DEPRESSION (By WHO) : Common mental disorder that presents with depressed mood, loss of interest or pleasure, feelings of guilt or low self- worth, disturbed sleep or appetite, low energy, and poor concentration.
  • 5. TYPES OF DEPRESSION • Major depressive disorder : recurrence of long episodes of low moods, or one extended episode that seems to be ‘never-ending. - Atypical depression - Post partum depression - Catatonic depression - Seasonal affective disorder - Melancholic depression
  • 6. • Manic depression (bipolar disorder) Four ‘Episodes’of Bipolar Disorder - depressive episode - manic episodes - hypomanic episode - mixed-mood states
  • 7. • Dysthymic depression - lasts a long time but involves less severe symptoms. - lead a normal life, but we may not be functioning well or feeling good • Situational depression • Psychotic depression • Endogenous depression
  • 8. EPIDEMIOLOGY • Globally more than 350 million people of all ages suffer from depression. (WHO) • For the age group 15-44 major depression is the leading cause of disability in the U.S. • Women are nearly twice as likely to suffer from a major depressive disorder than men are. • With age the symptoms of depression become even more severe. • About thirty percent of people with depressive illnesses attempt suicide.
  • 9. ETIOLOGY • Genetic cause • Environmental factors • Biochemical factors : Biochemical theory of depression postulates a deficiency of neurotransmitters in certain areas of the brain (noradrenaline, serotonin, and dopamine). • Dopaminergic activity : reduced in case of depression, over activity in mania. • Endocrine factors - hypothyroidism, cushing’s syndrome etc
  • 10. • Abuse of Drugs orAlcohol • Hormone Level Changes • Physical illness and side effects of medications DRUGS • Analgesics • Antidepressants • Antihypertensives • Anticonvulsants • Benzodiazipine withdrawal • Antipsychotics
  • 11. PHYSICAL ILLNESS • Viral illness • Carcinoma • Neurological disorders • Thyroid disease • Multiple sclerosis • Pernicious anaemia • Diabetes • Systemic lupus erythematosus • Addison’s disease
  • 12. PATHOPHYSIOLOGY • The BiogenicAmine Hypothesis • The Receptor Sensitivity Hypothesis • The Serotonin-only Hypothesis • The Permissive Hypothesis • The Electrolyte Membrane Hypothesis • The Neuroendocrine Hypothesis
  • 13. • The BiogenicAmine Hypothesis - caused by a deficiency of monoamines, particularly noradrenaline and serotonin. - cannot explain the delay in time of onset of clinical relief of depression of up to 6-8 weeks. • The Receptor Sensitivity Hypothesis - depression is the result of a pathological alteration (supersensitivity and up-regulation) in receptor sites. - TCAs or MAOIs causes desensitization (the uncoupling of receptor sites) and possibly down- regulation (a decrease in the number of receptor sites).
  • 14. • The Serotonin-only Hypothesis - emphasizes the role of serotonin in depression and downplays noradrenaline. - But the serotonin-only theory has shortcomings: - it does not explain why there is a delay in onset of clinical relief - it does not explain the role of NA in depression.
  • 15. • The Permissive Hypothesis - the control of emotional behavior results from a balance between noradrenaline and serotonin. - If serotonin and noradrenaline falls to abnormally low levels, the patient becomes depressed. - If the level of serotonin falls and the level of noradrenaline becomes abnormally high, the patient becomes manic.
  • 16. • The Electrolyte Membrane Hypothesis - hypocalcemia may be associated with mania. - hypercalcemia is associated with depression. • The Neuroendocrine Hypothesis - pathological mood states are explained or contributed to by altered endocrine function.
  • 17. CLINICAL MANIFESTATIONS • DEPRESSIONS o Thinking is pessimistic and in some cases suicidal. o In severe cases psychotic symptoms such as hallucinations or delusions may be present. o Insomnia or hypersomnia, libido, weight loss, loss of appetite. o Intellectual or cognitive symptoms include a decreased ability to concentrate, slowed thinking, & a poor memory for recent events.
  • 18.
  • 19. DIAGNOSIS • ICD 10 Diagnostic criteria for a depressive episode {who} USUAL SYMPTOMS • Depressed mood. • Loss of interest and enjoyment. • Reduced energy leading to increased fatiguability and diminished activity.
  • 20. COMMONSYMPTOMS • Reduced concentration and attention. • Reduced self esteem and self confidence. • Ideas of guilt and unworthiness. • Bleak and pessimistic views of future . • Ideas or acts of self harm or suicide. • Disturbed sleep. • Diminished appetite.
  • 21. MILD DEPRESSIVE EPISODE • For at least 2 weeks, at least two of the usual symptoms of a depressive episode plus at least two common symptoms. MODERATE DEPRESSIVE EPISODE • For at least 2 weeks, at least two or three of the usual symptoms of a depressive episode plus at least three of the common symtoms.
  • 22. SEVERE DEPRESSIVE EPISODE • For at least 2 weeks all three of the usual symptoms of a depressive episode plus at least 4 of the common symptoms some of which should be of severe intensity.
  • 23. INVESTIGATIONS • RATING SCALES o Beck depression inventory o Hamilton depression rating scale • DEXAMETHASONE SUPPRESSION TEST
  • 24. TREATMENT ANTIDEPRESSANTS 1. MAO inhibitors: • Irreversible: Isocarboxazid, Iproniazid, Phenelzine and Tranylcypromine. • Reversible: Moclobemide and Clorgyline. 2. Tricyclic antidepressants (TCAs) • NAand 5 HT reuptake inhibitors : Imipramine, Amitryptiline, Doxepin, Dothiepin and Clomipramine. • NAreuptake inhibitors : Desimipramine, Nortryptyline,Amoxapine.
  • 25. 3. Selective Serotonin reuptake inhibitors: • Fluoxetine, Fluvoxamine, Sertraline and Citalopram 4.Atypical antidepressants: • Trazodone, Mianserin, Mirtazapine, Venlafaxine, Duloxetine, Bupropion and Tianeptine
  • 26. NON– PHARMACOLOGIC THERAPY • LIFESTYLE CHANGES o Stress reduction o Social support o Sleep • PSYCHOTHERAPY o Cognitive behavioral therapy o Interpersonal therapy o Psychodynamic therapy
  • 27. • ELECTROCONVULSIVE THERAPY – ECT o Safe & effective disorder for all subtypes of major depressive disorder. o ADR : Cognitive dysfunction, cardiovascular dysfunction, prolonged apnoea etc.
  • 28. CONCLUSION • Affective disorders remain one of the most commonly occurring mental illnesses in adults. • It is often undiagnosed and untreated. • Both pharmacological and nonpharmacological interventions acts as cornerstone in the treatment of affective disorders. • Pharmacist plays an important role in accomplishing these treatment goals.