What are the common symptoms of depression?

Symptoms of depression include low mood, negative thoughts, low self-esteem, guilt, low motivation, changes in appetite, and sleep disturbances.

How is bipolar disorder different from depression?

Bipolar disorder involves extreme mood swings between mania and depression, with alternating states lasting weeks or months.

Depression involves neurotransmitter imbalances like dopamine and serotonin.

Antidepressants increase neurotransmitter levels, affecting neuronal pathways and neurogenesis.

Selective serotonin reuptake inhibitors (SSRIs) are first-line therapy for depression.

Depression and bipolar disorder are distinct affective disorders focusing on mood changes rather than thought disturbances. Depression is characterized by low mood, negative thoughts, and changes in appetite and sleep, while bipolar disorder involves extreme mood swings between mania and depression, lasting weeks or months.
Treatment for depression includes medications like SSRIs and SNRIs that target neurotransmitter levels, affecting neuronal pathways and neurogenesis. SSRIs selectively inhibit serotonin reuptake, leading to fewer side effects but less effectiveness in severe depression, while SNRIs inhibit both serotonin and noradrenaline reuptake. Additionally, MAO inhibitors can be used, affecting serotonin, dopamine, and noradrenaline levels, with reversible effects being more common than irreversible ones.

What are the common symptoms of depression?
Symptoms of depression include low mood, negative thoughts, low self-esteem, guilt, low motivation, changes in appetite, and sleep disturbances.
How is bipolar disorder different from depression?
Bipolar disorder involves extreme mood swings between mania and depression, with alternating states lasting weeks or months.
What neurotransmitters are involved in depression?
Depression involves neurotransmitter imbalances like dopamine and serotonin.
How do antidepressants work in treating depression?
Antidepressants increase neurotransmitter levels, affecting neuronal pathways and neurogenesis.
What is the first-line therapy for depression?
Selective serotonin reuptake inhibitors (SSRIs) are first-line therapy for depression.

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Today's focus is on understanding and treating depression and bipolar disorder.
Both conditions fall under affective disorders, focusing on mood changes rather than thought disturbances like psychosis.
Depression is characterized by low mood, negative thoughts, low self-esteem, guilt, low motivation, and changes in appetite and sleep.
Depression is common globally, with half of those treated responding to therapy within 6-8 weeks, but it can recur in 40% of cases.
Bipolar disorder involves extreme mood swings between mania and depression, with alternating states lasting weeks or months.
Diagnosis of depression involves meeting specific criteria from the Diagnostic and Statistical Manual of Mental Disorders, with symptoms like appetite changes, sleep disturbances, and suicidal ideation.
Depression affects 1 in 7 Australians, with 1 million currently living with it, more prevalent in women but increasing in men.
During COVID-19, depression rates rose to 27%, with 14.6% reporting thoughts of self-harm.
Bipolar disorder includes manic episodes alongside depressive symptoms, with causes possibly linked to neurotransmitter imbalances like dopamine and serotonin.
Treatment for depression involves increasing neurotransmitter levels through medications targeting serotonin and noradrenaline, affecting neuronal pathways and neurogenesis.

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Serotonin can be broken down by monoamine oxidase after completing its function, similar to dopamine breakdown in Parkinson's.
Antidepressants can inhibit monoamine uptake, leading to increased neurotransmitter levels in the synapse.
Selective serotonin reuptake inhibitors (SSRIs) like fluoxetine and citalopram inhibit serotonin reuptake.
Tricyclic antidepressants are less specific and have more side effects than SSRIs.
Serotonin and noradrenaline reuptake inhibitors (SNRIs) like venlafaxine inhibit both neurotransmitter reuptake.
Noradrenaline reuptake inhibitors target only noradrenaline reuptake.
St. John's wort is a weak inhibitor of reuptake pumps and can interact with other antidepressants.
Monoamine receptor antagonists and monoamine oxidase inhibitors can also be used as antidepressants.
Tricyclic antidepressants act on noradrenaline and serotonin receptors, leading to side effects like dry mouth and constipation.
SSRIs selectively inhibit serotonin reuptake, making them first-line therapy with fewer side effects but less effective in severe depression.

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Inhibiting a pump leads to serotonin staying outside the neuron, enhancing its effects.
No impact on muscarinic receptors, reducing autonomic nervous system side effects.
Cardiac conduction remains unaffected, minimizing sedation.
Nausea affects 25% of patients, while only 10% experience diarrhea.
Weight loss is common, unlike TCAs which often cause weight gain.
Overdose is safer due to a higher therapeutic index.
Two to three weeks are needed for the medication to take effect, increasing suicidal thoughts risk.
Serotonin syndrome can occur, leading to severe sympathetic nervous system activation.
Combining medications that increase serotonin can trigger serotonin syndrome.
MAOIs inhibit neurotransmitter degradation, affecting serotonin, dopamine, and noradrenaline.

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Medication acts on both serotonin and noradrenaline, with reversible effects being more common than irreversible ones.
Reversible medication increases serotonin, noradrenaline, and a bit of dopamine, with no interaction with tyramine due to monoamine B presence.
Common side effects include nausea, dizziness, insomnia, and headaches, with minimal impact on the cardiovascular system.
Treatment for depression starts with psychotherapy for mild cases, progressing to SSRIs for moderate to severe cases, followed by SNRIs and MAO inhibitors if needed.
Bipolar depression treatment focuses on mood stabilization, with lithium being the primary choice, followed by anti-epileptics like sodium valproate or carbamazepine as second-line options.
Lithium's therapeutic effects are seen within a week to 10 days, excreted by the kidneys, and work by inhibiting IP3 formation, affecting sodium channels, and increasing GABA activation.