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» Home » CAD » Psychiatry » Psychiatry Disorder » Depression
Background
Depression is a mood disorder and serious mental illness characterized by persistent sadness, feelings of hopelessness, and a lack of interest or pleasure in previously enjoyable activities.
It can interfere with daily life, such as work, school, and relationships. Depression affects more than 264 million people globally and is a leading cause of disability worldwide.
Depression occurs at any age, but it mostly develops during the teenage years or early adulthood. It is common in women than men. Depression can be a recurring illness, and people who have had one episode of depression are at risk for subsequent episodes.
Epidemiology
Prevalence: According to the WHO, depression is the leading cause of disability worldwide, affecting more than 264 million people globally.
Age and Gender: Depression may affect people of any age, including children and older adults. However, the onset of depression is most common during adolescence or early adulthood. Women are more common to experience depression than men, with a female-to-male ratio of about 2:1.
Geographic Variations: The prevalence of depression varies widely across different countries and regions. According to the study from Journal of Affective Disorders, the prevalence of major depressive disorder ranged from 0.5% in China to 21% in Ukraine.
Mortality: Depression is also associated with increased mortality, particularly from suicide. According to the WHO, suicide is the second leading cause of death among people aged 15 to 29 years globally, with depression being a major risk factor.
Anatomy
Pathophysiology
Depression is a complex psychiatric disorder with multifactorial etiology and pathophysiology. Although the exact underlying mechanisms remain unclear, several factors are thought to contribute to the development of depression.
Monoamine Hypothesis
The monoamine hypothesis suggests that depression is caused by an imbalance in neurotransmitters such as serotonin, norepinephrine, and dopamine. Low levels of these neurotransmitters are associated with depressive symptoms.
The hypothesis also suggests that antidepressants work by increasing the availability of these neurotransmitters.
Neurotrophic Hypothesis
The neurotrophic hypothesis suggests that depression is caused by a decrease in neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF).
These factors are responsible for the growth, development, and maintenance of neurons in the brain. A decrease in these factors can lead to the atrophy and dysfunction of brain regions involved in mood regulation.
Inflammatory Hypothesis
The inflammatory hypothesis suggests that depression is caused by an increase in pro-inflammatory cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α).
These cytokines are produced by the immune system in response to stress and inflammation. Chronic activation of the immune system can lead to the development of depressive symptoms.
HPA Axis Dysregulation Hypothesis
The HPA axis dysregulation hypothesis suggests that depression is caused by a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis.
The HPA axis is responsible for the stress response in the body. Chronic stress can lead to the dysregulation of this system, resulting in abnormal cortisol levels and increased susceptibility to depression.
Genetic Predisposition
Multiple genes have been identified that may play a role in the development of depression, including those involved in neurotransmitter regulation, neurotrophic factor production, and immune system function.
Etiology
Depression is caused by genetic, environmental, and psychological factors. Some of the major etiological factors of depression are discussed below:
Genetics: Genetic factors are believed to be involved in the development of depression. Studies have shown that there is a higher incidence of depression in families with a history of the disorder.
Neurotransmitter imbalances: Changes in the levels of neurotransmitters such as serotonin, norepinephrine, and dopamine are associated with depression.
Environmental factors: Stressful life situations, like the death of a loved one, divorce, financial difficulties, and job loss, can trigger depression.
Medical conditions: Depression is also caused by medical conditions such as chronic pain, cancer, heart disease, and stroke.
Substance abuse: Drug and alcohol abuse can lead to the development of depression.
Medications: Certain medications such as corticosteroids, beta-blockers, and hormonal therapies can cause depression.
Hormonal imbalances: Changes in hormonal levels, such as those that occur during pregnancy, postpartum, and menopause, can also contribute to depression.
Cognitive factors: Negative thinking patterns, low self-esteem, and a pessimistic outlook on life can all contribute to the development of depression.
Genetics
Prognostic Factors
Severity of depression: Patients with severe depression may have a poorer prognosis than those with milder symptoms.
Co-occurring medical or psychiatric conditions: Patients with other medical or psychiatric conditions, such as anxiety or substance abuse, may have a worse prognosis for depression.
Age: Older patients may have a worse prognosis for depression than younger patients.
Social support: Patients with adequate social support may have a better prognosis for depression than those who are socially isolated.
Treatment response: Patients who respond well to treatment may have a better prognosis for depression than those who do not respond well.
Clinical History
CLINICAL HISTORY
A clinical history of depression typically includes an assessment of the patient’s emotional, behavioral, and physical symptoms. The patient may present with feelings of sadness, hopelessness, worthlessness, and guilt that persist for more than two weeks. They also experience loss of interest, changes in appetite and sleep patterns, fatigue, and difficulty concentrating.
The clinical history may also include a review of the patient’s suicide risk factors, including past suicide attempts, suicidal ideation, and access to lethal means. This information is critical in developing a treatment plan that addresses the patient’s specific needs and reduces their risk of self-harm.
The clinician may use standardized questionnaires or scales to assess the severity of the patient’s symptoms and monitor their progress over time. Overall, a thorough clinical history is essential in diagnosing and treating depression effectively.
Physical Examination
PHYSICAL EXAMINATION
The physical examination is usually done by perform the following:
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
DIFFERENTIAL DIAGNOSIS
Major depressive disorder: persistent feelings of sadness or emptiness, loss of interest in activities, feelings of worthlessness or guilt, fatigue, changes in sleep or appetite, and thoughts of death or suicide.
Dysthymia: a form of depression that is less severe and chronic, lasts for at least two years.
Bipolar disorder: episodes of both depression and mania, which is characterized by elevated or irritable mood, increased activity, racing thoughts, and decreased need for sleep.
Adjustment disorder: a reaction to a significant life stressor such as a divorce, job loss, or illness, which results in depressed mood.
Substance-induced mood disorder: depressive symptoms that are caused by substance use or withdrawal.
Schizophrenia: a chronic mental disorder that may present with depressive symptoms.
Personality disorders: some personality disorders such as borderline personality disorder and avoidant personality disorder may have depressive symptoms.
Medical conditions: various medical conditions such as thyroid disorders, vitamin deficiencies, and neurological disorders may present with depressive symptoms.
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Antidepressant medications: Antidepressant medications are commonly used to treat depression. These medications act by altering the levels of certain chemicals in the brain, such as serotonin and norepinephrine.
Selective serotonin reuptake inhibitors (SSRIs): Examples include sertraline (Zoloft), fluoxetine (Prozac), and citalopram (Celexa). They act by increasing the neurotransmitter serotonin levels in the brain.
Serotonin-norepinephrine reuptake inhibitors (SNRIs): Examples include venlafaxine (Effexor) and duloxetine (Cymbalta). They work by increasing the levels of both serotonin and norepinephrine in the brain.
Tricyclic antidepressants (TCAs): Examples include amitriptyline (Elavil) and nortriptyline (Pamelor). They work by blocking the reuptake of neurotransmitters like serotonin and norepinephrine.
Monoamine oxidase inhibitors (MAOIs): Examples include phenelzine (Nardil) and tranylcypromine (Parnate). They work by blocking the activity of monoamine oxidase, an enzyme that breaks down neurotransmitters like serotonin, norepinephrine, and dopamine.
Psychotherapy: Psychotherapy, or talk therapy, is another common treatment for depression. It involves talking with healthcare professionals to help identify and change negative thought patterns and behaviors that may be contributing to your depression. Cognitive-behavioral therapy (CBT) is a type of psychotherapy that has been shown to be particularly effective in treating depression.
Electroconvulsive therapy (ECT): ECT involves sending electrical impulses through the brain to induce a seizure. It is used in cases of severe depression that have not responded to other treatments. ECT is typically administered under general anesthesia.
Transcranial magnetic stimulation (TMS): TMS involves using magnetic fields to stimulate nerve cells in the brain. It is used for patients who have not responded to other treatments for depression.
Lifestyle changes: Making certain lifestyle changes can also be helpful in managing depression. These may include regular exercise, a healthy diet, getting enough sleep, and reducing stress.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
25 mg-50 mg IM or subcutaneously or 5 mg-25 mg IV administered slowly repeat the dose in 5-10 minutes as needed
20
mg
Orally
every day
and increase up to 20-50 mg/day orally
The Maximum dose for a day is 50 mg
0.5
mg
Tablet
Orally
every day
Do not exceed 3mg/day
Initial dose-10mg/day and increase the dose upward every 5-7 days then,
15-60mg/day orally every 6-8 hours
Do not exceed 60mg/day
25
mg
Capsule
Orally
every 6 -8 hours
Do not exceed 150mg/day
The medication dosage of 150-300 mg orally once a day is prescribed for depression
10 mg orally every 6-12 hours; increase the dose by 10-40
mg/kg divided every 6-12 hours by the end of the first week
Increase the dose by a maximum of 20 mg/week to 60 mg/day
After the 1st week, increase the dose from 20 mg/week to 60 mg/day
After achieving the maximum effect, decrease upto maintenance dose
Initially, 15 mg orally every 8 hours; increase the dose to 60 mg/day with patient tolerance; do not exceed more than 20-30 mg every 8 hours
Continue the treatment with 60 mg for 4 weeks in the patients who do not show clinical response
Decrease the dose after the maximum response is achieved in 2-6 weeks
Maintain it as low as 15 mg each day or every other day
Monitor the blood pressure during the same
100 mg orally every 12 hours
Increase the dose by 50-100 mg/dose
Maintenance dose- 300-600 mg orally each day
The dose is increased by 100-200 mg per day at an interval of a minimum of 1 week
Long-term patients require 52 weeks for the treatment
15 mg orally every night; increase the dose every 1-2 weeks
Do not exceed the dose of more than 45 mg orally each evening
25 mg orally every 8-12 hours
Increase the dose to 200-300 mg orally every night after 5-7 days
If the dose exceeds more than 300 mg/day, divide the dose every 12 hours
Do not exceed the dose of 400 mg each day
Inpatients may need higher doses; administer up to 600 mg/day as divided doses twice daily
Indicated for depression because of Bipolar I Disorder
Initially, 20 mg fluoxetine with 5 mg olanzapine orally every evening
Dose Adjustment
According to the tolerance and efficacy, take 20-50 mg of fluoxetine and 5-12.5 mg of olanzapine
100 - 200
mg
Orally
at bedtime or divided 2 times daily
may be increase up to 300 mg daily when severely ill
Outpatient:
75
75 orally daily; may be increase up to150 mg/day in divided doses
do not exceed 200 mg a day
Inpatient:
100-150 mg orally daily
may increase up to 200 mg daily
after 2 weeks if there is no response, increase dose up to 250-300 mg
do not exceed 300 mg daily
the Maximum dose given is 50-100 mg orally daily
25
mg
daily; titrate gradually
5 - 7
days
the dose range is 25-300 mg orally daily,
do not exceed 150 mg daily
Outpatient
Initial dose 75 mg orally daily 2 weeks; may increase to 25 mg
Maximum dose is 150 mg daily
Maintenance dose: decrease dose to 75-150 mg orally daily if symptoms achieved in control
inpatient
100-150 mg orally daily 2 weeks
Do not exceed 225 mg daily
OP:
25-50 mg orally every night at bedtime
May increase up to 25 mg for every 5-7 days; following 100-200 mg daily
And may increase 300 mg/day if required
IP:
100-300 mg orally daily
OP:
25-50 mg orally every night at bedtime
May increase up to 25 mg for every 5-7 days; following 100-200 mg daily
And may increase 300 mg/day if required
IP:
100-300 mg orally daily
ansofaxine (Pending FDA Approval)
FDA approval pending for major depressive disorder
Apply 1 patch concurrently each day
Increase the dose by 3 mg each day, every 2 weeks
Do not exceed more than 12 mg every day
No dose adjustment is required in the case of mild to moderate renal or hepatic impairment
Initial dose: Administer 300mg in two divided doses every day. May gradually increase the dose beginning a week after the therapy.
Do not exceed 600mg/day.
Dosage recommendations may vary, follow the leaflet instructions
75 to 225 mg of dosulepin in 1 to 3 divided doses (the maximum single dose is 150 mg)
Administer orally divided into four to three times daily within the range of 8-12 grams/day
Reduced dosage demonstrates efficacy when utilized alongside alternative antidepressant medications
240 to 480 mg is given orally every day
In Severe depression: a maximum dose of 720 mg is given orally every day
There is insufficient data available
Take an initial dose of 30 to 40 mg daily in divided doses or as a single dose at bedtime
Daily dose should not be more than 200 mg in divided doses
Indicated for Depression
150 mg to 300 mg orally every day
Primary Fibromyalgia Syndrome
100 mg orally three times a day for nearly one month
Indicated for Antidepressant
There is limited information available
Body surface area (BSA): 0.5 mg/kg or 16.7 mg/m2 IM or SC every 4-6 hours
<12 years: Safety and efficacy not established
>12 years: 15-20mg/day orally every day
<6 years: Safety and efficacy not established
6-12 years:1-3mg/kg/day orally divided every 6-8 hours
>12 hours:30-50mg orally every day
Age > 12 years:
25 - 50
mg
Orally
every day
increase up to 100 mg daily if required divided 2 times a day
maximum dose is 150 mg daily
1.5
mg/kg
divided every 8 hours
may increase 1mg/kg every 3-4 days
do not exceed 5 mg/kg
Adolescents:
30-40 mg orally divided 3 times a day
do not exceed 100 mg a day
Adolescents
25-50 mg orally daily in divided doses
May increase to 100 mg daily in divided doses
Children (Off-label)
On Day 1,2,3 1 mg/kg in divided doses 3 times daily
1.5 mg/kg in divided doses 3 times daily
Initial dose: 5 mg orally every day
Maintenance dose: 5-10mg every 3-7 days when necessary
Initial: 30-50mg orally every day. Do not exceed 100mg/day
10 mg orally every 6-12 hours; increase the dose by 10-40 mg/kg divided every 6-12 hours by the end of the first week
Increase the dose by a maximum of 20 mg/week to 60 mg/day
After the 1st week, increase the dose from 20 mg/week to 60 mg/day
After achieving the maximum effect, decrease upto maintenance dose
Initially, 15 mg orally every 8 hours; increase the dose to 60 mg/day with patient tolerance; do not exceed more than 20-30 mg every 8 hours
Decrease the dose after the maximum response is achieved in 2-6 weeks
Maintain it as low as 15 mg each day or every other day
Monitor the blood pressure during the same
Indicated in depression, with significant episodes without melancholia
15 mg orally every 12 hours; increase the dose by 5 mg/dose; every 1-3 weeks
Do not exceed more than 60 mg per day
Once the response gets adequate, slowly decrease the dose
7.5 mg orally every night
Increase the dose by 7.5-15 mg/day
Do not exceed the dose of more than 45 mg orally each day
Dose Consideration
In geriatric patients, clearance of mirtazapine is reduced hence, increases the plasma levels of the drug
Use the drug cautiously
25 mg orally every 8-12 hours
Increase the dose to 200-300 mg orally every night after 5-7 days
For outpatients, do not exceed the dose of 400 mg each day
For inpatients, a higher dose of 600 mg/day is required, divided twice daily
6 mg as transdermal; refer to adult dosing
Initially, 240 mg is given orally every day. Maximum dose is 480 mg/day
Future Trends
References
https://www.ncbi.nlm.nih.gov/books/NBK568733/
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» Home » CAD » Psychiatry » Psychiatry Disorder » Depression
Depression is a mood disorder and serious mental illness characterized by persistent sadness, feelings of hopelessness, and a lack of interest or pleasure in previously enjoyable activities.
It can interfere with daily life, such as work, school, and relationships. Depression affects more than 264 million people globally and is a leading cause of disability worldwide.
Depression occurs at any age, but it mostly develops during the teenage years or early adulthood. It is common in women than men. Depression can be a recurring illness, and people who have had one episode of depression are at risk for subsequent episodes.
Prevalence: According to the WHO, depression is the leading cause of disability worldwide, affecting more than 264 million people globally.
Age and Gender: Depression may affect people of any age, including children and older adults. However, the onset of depression is most common during adolescence or early adulthood. Women are more common to experience depression than men, with a female-to-male ratio of about 2:1.
Geographic Variations: The prevalence of depression varies widely across different countries and regions. According to the study from Journal of Affective Disorders, the prevalence of major depressive disorder ranged from 0.5% in China to 21% in Ukraine.
Mortality: Depression is also associated with increased mortality, particularly from suicide. According to the WHO, suicide is the second leading cause of death among people aged 15 to 29 years globally, with depression being a major risk factor.
Depression is a complex psychiatric disorder with multifactorial etiology and pathophysiology. Although the exact underlying mechanisms remain unclear, several factors are thought to contribute to the development of depression.
Monoamine Hypothesis
The monoamine hypothesis suggests that depression is caused by an imbalance in neurotransmitters such as serotonin, norepinephrine, and dopamine. Low levels of these neurotransmitters are associated with depressive symptoms.
The hypothesis also suggests that antidepressants work by increasing the availability of these neurotransmitters.
Neurotrophic Hypothesis
The neurotrophic hypothesis suggests that depression is caused by a decrease in neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF).
These factors are responsible for the growth, development, and maintenance of neurons in the brain. A decrease in these factors can lead to the atrophy and dysfunction of brain regions involved in mood regulation.
Inflammatory Hypothesis
The inflammatory hypothesis suggests that depression is caused by an increase in pro-inflammatory cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α).
These cytokines are produced by the immune system in response to stress and inflammation. Chronic activation of the immune system can lead to the development of depressive symptoms.
HPA Axis Dysregulation Hypothesis
The HPA axis dysregulation hypothesis suggests that depression is caused by a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis.
The HPA axis is responsible for the stress response in the body. Chronic stress can lead to the dysregulation of this system, resulting in abnormal cortisol levels and increased susceptibility to depression.
Genetic Predisposition
Multiple genes have been identified that may play a role in the development of depression, including those involved in neurotransmitter regulation, neurotrophic factor production, and immune system function.
Depression is caused by genetic, environmental, and psychological factors. Some of the major etiological factors of depression are discussed below:
Genetics: Genetic factors are believed to be involved in the development of depression. Studies have shown that there is a higher incidence of depression in families with a history of the disorder.
Neurotransmitter imbalances: Changes in the levels of neurotransmitters such as serotonin, norepinephrine, and dopamine are associated with depression.
Environmental factors: Stressful life situations, like the death of a loved one, divorce, financial difficulties, and job loss, can trigger depression.
Medical conditions: Depression is also caused by medical conditions such as chronic pain, cancer, heart disease, and stroke.
Substance abuse: Drug and alcohol abuse can lead to the development of depression.
Medications: Certain medications such as corticosteroids, beta-blockers, and hormonal therapies can cause depression.
Hormonal imbalances: Changes in hormonal levels, such as those that occur during pregnancy, postpartum, and menopause, can also contribute to depression.
Cognitive factors: Negative thinking patterns, low self-esteem, and a pessimistic outlook on life can all contribute to the development of depression.
Severity of depression: Patients with severe depression may have a poorer prognosis than those with milder symptoms.
Co-occurring medical or psychiatric conditions: Patients with other medical or psychiatric conditions, such as anxiety or substance abuse, may have a worse prognosis for depression.
Age: Older patients may have a worse prognosis for depression than younger patients.
Social support: Patients with adequate social support may have a better prognosis for depression than those who are socially isolated.
Treatment response: Patients who respond well to treatment may have a better prognosis for depression than those who do not respond well.
CLINICAL HISTORY
A clinical history of depression typically includes an assessment of the patient’s emotional, behavioral, and physical symptoms. The patient may present with feelings of sadness, hopelessness, worthlessness, and guilt that persist for more than two weeks. They also experience loss of interest, changes in appetite and sleep patterns, fatigue, and difficulty concentrating.
The clinical history may also include a review of the patient’s suicide risk factors, including past suicide attempts, suicidal ideation, and access to lethal means. This information is critical in developing a treatment plan that addresses the patient’s specific needs and reduces their risk of self-harm.
The clinician may use standardized questionnaires or scales to assess the severity of the patient’s symptoms and monitor their progress over time. Overall, a thorough clinical history is essential in diagnosing and treating depression effectively.
PHYSICAL EXAMINATION
The physical examination is usually done by perform the following:
DIFFERENTIAL DIAGNOSIS
Major depressive disorder: persistent feelings of sadness or emptiness, loss of interest in activities, feelings of worthlessness or guilt, fatigue, changes in sleep or appetite, and thoughts of death or suicide.
Dysthymia: a form of depression that is less severe and chronic, lasts for at least two years.
Bipolar disorder: episodes of both depression and mania, which is characterized by elevated or irritable mood, increased activity, racing thoughts, and decreased need for sleep.
Adjustment disorder: a reaction to a significant life stressor such as a divorce, job loss, or illness, which results in depressed mood.
Substance-induced mood disorder: depressive symptoms that are caused by substance use or withdrawal.
Schizophrenia: a chronic mental disorder that may present with depressive symptoms.
Personality disorders: some personality disorders such as borderline personality disorder and avoidant personality disorder may have depressive symptoms.
Medical conditions: various medical conditions such as thyroid disorders, vitamin deficiencies, and neurological disorders may present with depressive symptoms.
Antidepressant medications: Antidepressant medications are commonly used to treat depression. These medications act by altering the levels of certain chemicals in the brain, such as serotonin and norepinephrine.
Selective serotonin reuptake inhibitors (SSRIs): Examples include sertraline (Zoloft), fluoxetine (Prozac), and citalopram (Celexa). They act by increasing the neurotransmitter serotonin levels in the brain.
Serotonin-norepinephrine reuptake inhibitors (SNRIs): Examples include venlafaxine (Effexor) and duloxetine (Cymbalta). They work by increasing the levels of both serotonin and norepinephrine in the brain.
Tricyclic antidepressants (TCAs): Examples include amitriptyline (Elavil) and nortriptyline (Pamelor). They work by blocking the reuptake of neurotransmitters like serotonin and norepinephrine.
Monoamine oxidase inhibitors (MAOIs): Examples include phenelzine (Nardil) and tranylcypromine (Parnate). They work by blocking the activity of monoamine oxidase, an enzyme that breaks down neurotransmitters like serotonin, norepinephrine, and dopamine.
Psychotherapy: Psychotherapy, or talk therapy, is another common treatment for depression. It involves talking with healthcare professionals to help identify and change negative thought patterns and behaviors that may be contributing to your depression. Cognitive-behavioral therapy (CBT) is a type of psychotherapy that has been shown to be particularly effective in treating depression.
Electroconvulsive therapy (ECT): ECT involves sending electrical impulses through the brain to induce a seizure. It is used in cases of severe depression that have not responded to other treatments. ECT is typically administered under general anesthesia.
Transcranial magnetic stimulation (TMS): TMS involves using magnetic fields to stimulate nerve cells in the brain. It is used for patients who have not responded to other treatments for depression.
Lifestyle changes: Making certain lifestyle changes can also be helpful in managing depression. These may include regular exercise, a healthy diet, getting enough sleep, and reducing stress.
25 mg-50 mg IM or subcutaneously or 5 mg-25 mg IV administered slowly repeat the dose in 5-10 minutes as needed
20
mg
Orally
every day
and increase up to 20-50 mg/day orally
The Maximum dose for a day is 50 mg
0.5
mg
Tablet
Orally
every day
Do not exceed 3mg/day
Initial dose-10mg/day and increase the dose upward every 5-7 days then,
15-60mg/day orally every 6-8 hours
Do not exceed 60mg/day
25
mg
Capsule
Orally
every 6 -8 hours
Do not exceed 150mg/day
The medication dosage of 150-300 mg orally once a day is prescribed for depression
10 mg orally every 6-12 hours; increase the dose by 10-40
mg/kg divided every 6-12 hours by the end of the first week
Increase the dose by a maximum of 20 mg/week to 60 mg/day
After the 1st week, increase the dose from 20 mg/week to 60 mg/day
After achieving the maximum effect, decrease upto maintenance dose
Initially, 15 mg orally every 8 hours; increase the dose to 60 mg/day with patient tolerance; do not exceed more than 20-30 mg every 8 hours
Continue the treatment with 60 mg for 4 weeks in the patients who do not show clinical response
Decrease the dose after the maximum response is achieved in 2-6 weeks
Maintain it as low as 15 mg each day or every other day
Monitor the blood pressure during the same
100 mg orally every 12 hours
Increase the dose by 50-100 mg/dose
Maintenance dose- 300-600 mg orally each day
The dose is increased by 100-200 mg per day at an interval of a minimum of 1 week
Long-term patients require 52 weeks for the treatment
15 mg orally every night; increase the dose every 1-2 weeks
Do not exceed the dose of more than 45 mg orally each evening
25 mg orally every 8-12 hours
Increase the dose to 200-300 mg orally every night after 5-7 days
If the dose exceeds more than 300 mg/day, divide the dose every 12 hours
Do not exceed the dose of 400 mg each day
Inpatients may need higher doses; administer up to 600 mg/day as divided doses twice daily
Indicated for depression because of Bipolar I Disorder
Initially, 20 mg fluoxetine with 5 mg olanzapine orally every evening
Dose Adjustment
According to the tolerance and efficacy, take 20-50 mg of fluoxetine and 5-12.5 mg of olanzapine
100 - 200
mg
Orally
at bedtime or divided 2 times daily
may be increase up to 300 mg daily when severely ill
Outpatient:
75
75 orally daily; may be increase up to150 mg/day in divided doses
do not exceed 200 mg a day
Inpatient:
100-150 mg orally daily
may increase up to 200 mg daily
after 2 weeks if there is no response, increase dose up to 250-300 mg
do not exceed 300 mg daily
the Maximum dose given is 50-100 mg orally daily
25
mg
daily; titrate gradually
5 - 7
days
the dose range is 25-300 mg orally daily,
do not exceed 150 mg daily
Outpatient
Initial dose 75 mg orally daily 2 weeks; may increase to 25 mg
Maximum dose is 150 mg daily
Maintenance dose: decrease dose to 75-150 mg orally daily if symptoms achieved in control
inpatient
100-150 mg orally daily 2 weeks
Do not exceed 225 mg daily
OP:
25-50 mg orally every night at bedtime
May increase up to 25 mg for every 5-7 days; following 100-200 mg daily
And may increase 300 mg/day if required
IP:
100-300 mg orally daily
OP:
25-50 mg orally every night at bedtime
May increase up to 25 mg for every 5-7 days; following 100-200 mg daily
And may increase 300 mg/day if required
IP:
100-300 mg orally daily
ansofaxine (Pending FDA Approval)
FDA approval pending for major depressive disorder
Apply 1 patch concurrently each day
Increase the dose by 3 mg each day, every 2 weeks
Do not exceed more than 12 mg every day
No dose adjustment is required in the case of mild to moderate renal or hepatic impairment
Initial dose: Administer 300mg in two divided doses every day. May gradually increase the dose beginning a week after the therapy.
Do not exceed 600mg/day.
Dosage recommendations may vary, follow the leaflet instructions
75 to 225 mg of dosulepin in 1 to 3 divided doses (the maximum single dose is 150 mg)
Administer orally divided into four to three times daily within the range of 8-12 grams/day
Reduced dosage demonstrates efficacy when utilized alongside alternative antidepressant medications
240 to 480 mg is given orally every day
In Severe depression: a maximum dose of 720 mg is given orally every day
There is insufficient data available
Take an initial dose of 30 to 40 mg daily in divided doses or as a single dose at bedtime
Daily dose should not be more than 200 mg in divided doses
Indicated for Depression
150 mg to 300 mg orally every day
Primary Fibromyalgia Syndrome
100 mg orally three times a day for nearly one month
Indicated for Antidepressant
There is limited information available
Body surface area (BSA): 0.5 mg/kg or 16.7 mg/m2 IM or SC every 4-6 hours
<12 years: Safety and efficacy not established
>12 years: 15-20mg/day orally every day
<6 years: Safety and efficacy not established
6-12 years:1-3mg/kg/day orally divided every 6-8 hours
>12 hours:30-50mg orally every day
Age > 12 years:
25 - 50
mg
Orally
every day
increase up to 100 mg daily if required divided 2 times a day
maximum dose is 150 mg daily
1.5
mg/kg
divided every 8 hours
may increase 1mg/kg every 3-4 days
do not exceed 5 mg/kg
Adolescents:
30-40 mg orally divided 3 times a day
do not exceed 100 mg a day
Adolescents
25-50 mg orally daily in divided doses
May increase to 100 mg daily in divided doses
Children (Off-label)
On Day 1,2,3 1 mg/kg in divided doses 3 times daily
1.5 mg/kg in divided doses 3 times daily
Initial dose: 5 mg orally every day
Maintenance dose: 5-10mg every 3-7 days when necessary
Initial: 30-50mg orally every day. Do not exceed 100mg/day
10 mg orally every 6-12 hours; increase the dose by 10-40 mg/kg divided every 6-12 hours by the end of the first week
Increase the dose by a maximum of 20 mg/week to 60 mg/day
After the 1st week, increase the dose from 20 mg/week to 60 mg/day
After achieving the maximum effect, decrease upto maintenance dose
Initially, 15 mg orally every 8 hours; increase the dose to 60 mg/day with patient tolerance; do not exceed more than 20-30 mg every 8 hours
Decrease the dose after the maximum response is achieved in 2-6 weeks
Maintain it as low as 15 mg each day or every other day
Monitor the blood pressure during the same
Indicated in depression, with significant episodes without melancholia
15 mg orally every 12 hours; increase the dose by 5 mg/dose; every 1-3 weeks
Do not exceed more than 60 mg per day
Once the response gets adequate, slowly decrease the dose
7.5 mg orally every night
Increase the dose by 7.5-15 mg/day
Do not exceed the dose of more than 45 mg orally each day
Dose Consideration
In geriatric patients, clearance of mirtazapine is reduced hence, increases the plasma levels of the drug
Use the drug cautiously
25 mg orally every 8-12 hours
Increase the dose to 200-300 mg orally every night after 5-7 days
For outpatients, do not exceed the dose of 400 mg each day
For inpatients, a higher dose of 600 mg/day is required, divided twice daily
6 mg as transdermal; refer to adult dosing
Initially, 240 mg is given orally every day. Maximum dose is 480 mg/day
https://www.ncbi.nlm.nih.gov/books/NBK568733/
Depression is a mood disorder and serious mental illness characterized by persistent sadness, feelings of hopelessness, and a lack of interest or pleasure in previously enjoyable activities.
It can interfere with daily life, such as work, school, and relationships. Depression affects more than 264 million people globally and is a leading cause of disability worldwide.
Depression occurs at any age, but it mostly develops during the teenage years or early adulthood. It is common in women than men. Depression can be a recurring illness, and people who have had one episode of depression are at risk for subsequent episodes.
Prevalence: According to the WHO, depression is the leading cause of disability worldwide, affecting more than 264 million people globally.
Age and Gender: Depression may affect people of any age, including children and older adults. However, the onset of depression is most common during adolescence or early adulthood. Women are more common to experience depression than men, with a female-to-male ratio of about 2:1.
Geographic Variations: The prevalence of depression varies widely across different countries and regions. According to the study from Journal of Affective Disorders, the prevalence of major depressive disorder ranged from 0.5% in China to 21% in Ukraine.
Mortality: Depression is also associated with increased mortality, particularly from suicide. According to the WHO, suicide is the second leading cause of death among people aged 15 to 29 years globally, with depression being a major risk factor.
Depression is a complex psychiatric disorder with multifactorial etiology and pathophysiology. Although the exact underlying mechanisms remain unclear, several factors are thought to contribute to the development of depression.
Monoamine Hypothesis
The monoamine hypothesis suggests that depression is caused by an imbalance in neurotransmitters such as serotonin, norepinephrine, and dopamine. Low levels of these neurotransmitters are associated with depressive symptoms.
The hypothesis also suggests that antidepressants work by increasing the availability of these neurotransmitters.
Neurotrophic Hypothesis
The neurotrophic hypothesis suggests that depression is caused by a decrease in neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF).
These factors are responsible for the growth, development, and maintenance of neurons in the brain. A decrease in these factors can lead to the atrophy and dysfunction of brain regions involved in mood regulation.
Inflammatory Hypothesis
The inflammatory hypothesis suggests that depression is caused by an increase in pro-inflammatory cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α).
These cytokines are produced by the immune system in response to stress and inflammation. Chronic activation of the immune system can lead to the development of depressive symptoms.
HPA Axis Dysregulation Hypothesis
The HPA axis dysregulation hypothesis suggests that depression is caused by a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis.
The HPA axis is responsible for the stress response in the body. Chronic stress can lead to the dysregulation of this system, resulting in abnormal cortisol levels and increased susceptibility to depression.
Genetic Predisposition
Multiple genes have been identified that may play a role in the development of depression, including those involved in neurotransmitter regulation, neurotrophic factor production, and immune system function.
Depression is caused by genetic, environmental, and psychological factors. Some of the major etiological factors of depression are discussed below:
Genetics: Genetic factors are believed to be involved in the development of depression. Studies have shown that there is a higher incidence of depression in families with a history of the disorder.
Neurotransmitter imbalances: Changes in the levels of neurotransmitters such as serotonin, norepinephrine, and dopamine are associated with depression.
Environmental factors: Stressful life situations, like the death of a loved one, divorce, financial difficulties, and job loss, can trigger depression.
Medical conditions: Depression is also caused by medical conditions such as chronic pain, cancer, heart disease, and stroke.
Substance abuse: Drug and alcohol abuse can lead to the development of depression.
Medications: Certain medications such as corticosteroids, beta-blockers, and hormonal therapies can cause depression.
Hormonal imbalances: Changes in hormonal levels, such as those that occur during pregnancy, postpartum, and menopause, can also contribute to depression.
Cognitive factors: Negative thinking patterns, low self-esteem, and a pessimistic outlook on life can all contribute to the development of depression.
Severity of depression: Patients with severe depression may have a poorer prognosis than those with milder symptoms.
Co-occurring medical or psychiatric conditions: Patients with other medical or psychiatric conditions, such as anxiety or substance abuse, may have a worse prognosis for depression.
Age: Older patients may have a worse prognosis for depression than younger patients.
Social support: Patients with adequate social support may have a better prognosis for depression than those who are socially isolated.
Treatment response: Patients who respond well to treatment may have a better prognosis for depression than those who do not respond well.
CLINICAL HISTORY
A clinical history of depression typically includes an assessment of the patient’s emotional, behavioral, and physical symptoms. The patient may present with feelings of sadness, hopelessness, worthlessness, and guilt that persist for more than two weeks. They also experience loss of interest, changes in appetite and sleep patterns, fatigue, and difficulty concentrating.
The clinical history may also include a review of the patient’s suicide risk factors, including past suicide attempts, suicidal ideation, and access to lethal means. This information is critical in developing a treatment plan that addresses the patient’s specific needs and reduces their risk of self-harm.
The clinician may use standardized questionnaires or scales to assess the severity of the patient’s symptoms and monitor their progress over time. Overall, a thorough clinical history is essential in diagnosing and treating depression effectively.
PHYSICAL EXAMINATION
The physical examination is usually done by perform the following:
DIFFERENTIAL DIAGNOSIS
Major depressive disorder: persistent feelings of sadness or emptiness, loss of interest in activities, feelings of worthlessness or guilt, fatigue, changes in sleep or appetite, and thoughts of death or suicide.
Dysthymia: a form of depression that is less severe and chronic, lasts for at least two years.
Bipolar disorder: episodes of both depression and mania, which is characterized by elevated or irritable mood, increased activity, racing thoughts, and decreased need for sleep.
Adjustment disorder: a reaction to a significant life stressor such as a divorce, job loss, or illness, which results in depressed mood.
Substance-induced mood disorder: depressive symptoms that are caused by substance use or withdrawal.
Schizophrenia: a chronic mental disorder that may present with depressive symptoms.
Personality disorders: some personality disorders such as borderline personality disorder and avoidant personality disorder may have depressive symptoms.
Medical conditions: various medical conditions such as thyroid disorders, vitamin deficiencies, and neurological disorders may present with depressive symptoms.
Antidepressant medications: Antidepressant medications are commonly used to treat depression. These medications act by altering the levels of certain chemicals in the brain, such as serotonin and norepinephrine.
Selective serotonin reuptake inhibitors (SSRIs): Examples include sertraline (Zoloft), fluoxetine (Prozac), and citalopram (Celexa). They act by increasing the neurotransmitter serotonin levels in the brain.
Serotonin-norepinephrine reuptake inhibitors (SNRIs): Examples include venlafaxine (Effexor) and duloxetine (Cymbalta). They work by increasing the levels of both serotonin and norepinephrine in the brain.
Tricyclic antidepressants (TCAs): Examples include amitriptyline (Elavil) and nortriptyline (Pamelor). They work by blocking the reuptake of neurotransmitters like serotonin and norepinephrine.
Monoamine oxidase inhibitors (MAOIs): Examples include phenelzine (Nardil) and tranylcypromine (Parnate). They work by blocking the activity of monoamine oxidase, an enzyme that breaks down neurotransmitters like serotonin, norepinephrine, and dopamine.
Psychotherapy: Psychotherapy, or talk therapy, is another common treatment for depression. It involves talking with healthcare professionals to help identify and change negative thought patterns and behaviors that may be contributing to your depression. Cognitive-behavioral therapy (CBT) is a type of psychotherapy that has been shown to be particularly effective in treating depression.
Electroconvulsive therapy (ECT): ECT involves sending electrical impulses through the brain to induce a seizure. It is used in cases of severe depression that have not responded to other treatments. ECT is typically administered under general anesthesia.
Transcranial magnetic stimulation (TMS): TMS involves using magnetic fields to stimulate nerve cells in the brain. It is used for patients who have not responded to other treatments for depression.
Lifestyle changes: Making certain lifestyle changes can also be helpful in managing depression. These may include regular exercise, a healthy diet, getting enough sleep, and reducing stress.
https://www.ncbi.nlm.nih.gov/books/NBK568733/
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