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Questions and Answers
What is primarily affected by tricyclic antidepressants in order to alleviate depression symptoms?
What is primarily affected by tricyclic antidepressants in order to alleviate depression symptoms?
Which neurotransmitter's uptake is the least affected by tricyclic antidepressants?
Which neurotransmitter's uptake is the least affected by tricyclic antidepressants?
What is a characteristic pharmacokinetic property of tricyclic antidepressants?
What is a characteristic pharmacokinetic property of tricyclic antidepressants?
What are the two main types of anticholinergic receptors influenced by tricyclic antidepressants?
What are the two main types of anticholinergic receptors influenced by tricyclic antidepressants?
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During which timeframe is the antidepressant action of tricyclic antidepressants typically observed?
During which timeframe is the antidepressant action of tricyclic antidepressants typically observed?
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What is the first phase of pharmacological treatment for depression referred to?
What is the first phase of pharmacological treatment for depression referred to?
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Which neurotransmitter is primarily associated with decreased levels in patients suffering from depression?
Which neurotransmitter is primarily associated with decreased levels in patients suffering from depression?
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Which treatment method is indicated for severe depression?
Which treatment method is indicated for severe depression?
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What is indicated as a characteristic of depression in the emotional symptoms category?
What is indicated as a characteristic of depression in the emotional symptoms category?
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Which of the following is identified as a common form of depression?
Which of the following is identified as a common form of depression?
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What is a common therapeutic application for imipramine?
What is a common therapeutic application for imipramine?
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Which side effect is associated with Tricyclic Antidepressants (TCAs)?
Which side effect is associated with Tricyclic Antidepressants (TCAs)?
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What is a pharmacodynamic interaction of TCAs?
What is a pharmacodynamic interaction of TCAs?
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What potential risk is associated with TCA overdose?
What potential risk is associated with TCA overdose?
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Which SSRIs are known to inhibit the reuptake of serotonin?
Which SSRIs are known to inhibit the reuptake of serotonin?
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What effect do oral contraceptives have on TCAs?
What effect do oral contraceptives have on TCAs?
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What condition is characterized by feelings of pain in a body part that has been amputated?
What condition is characterized by feelings of pain in a body part that has been amputated?
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Which of the following is NOT a common side effect of TCAs?
Which of the following is NOT a common side effect of TCAs?
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TCAs can potentiate the effects of which type of drugs, potentially leading to severe consequences?
TCAs can potentiate the effects of which type of drugs, potentially leading to severe consequences?
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What is a neurological side effect associated with TCAs?
What is a neurological side effect associated with TCAs?
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What is the primary neurotransmitter associated with decreased levels in depression, leading to the need for pharmacological treatment?
What is the primary neurotransmitter associated with decreased levels in depression, leading to the need for pharmacological treatment?
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What phase of treatment for depression typically involves monitoring and maintaining stability after achieving remission?
What phase of treatment for depression typically involves monitoring and maintaining stability after achieving remission?
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Which treatment method is commonly recommended as a first-line intervention for moderate depression?
Which treatment method is commonly recommended as a first-line intervention for moderate depression?
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Which emotional symptom is typically associated with depression?
Which emotional symptom is typically associated with depression?
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Which of the following is NOT classified as a common form of depression?
Which of the following is NOT classified as a common form of depression?
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Which of the following describes a primary mechanism of action of tricyclic antidepressants (TCAs)?
Which of the following describes a primary mechanism of action of tricyclic antidepressants (TCAs)?
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Which side effect is most closely associated with the antimuscarinic effects of TCAs?
Which side effect is most closely associated with the antimuscarinic effects of TCAs?
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What is a significant pharmacokinetic characteristic of tricyclic antidepressants?
What is a significant pharmacokinetic characteristic of tricyclic antidepressants?
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Which class of antidepressants is categorized as non-selective amine reuptake inhibitors?
Which class of antidepressants is categorized as non-selective amine reuptake inhibitors?
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During which timeframe is the antidepressant effect of TCAs typically initiated?
During which timeframe is the antidepressant effect of TCAs typically initiated?
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What condition, often treated with imipramine, involves painful sensations in a removed body part?
What condition, often treated with imipramine, involves painful sensations in a removed body part?
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Which side effect is most commonly associated with the antimuscarinic effects of TCAs?
Which side effect is most commonly associated with the antimuscarinic effects of TCAs?
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Which of the following is a therapeutic application of selective serotonin reuptake inhibitors (SSRIs)?
Which of the following is a therapeutic application of selective serotonin reuptake inhibitors (SSRIs)?
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What effect do monoamine oxidase inhibitors (MAOIs) have when taken with TCAs?
What effect do monoamine oxidase inhibitors (MAOIs) have when taken with TCAs?
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What is a primary mechanism of action of selective serotonin reuptake inhibitors (SSRIs)?
What is a primary mechanism of action of selective serotonin reuptake inhibitors (SSRIs)?
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Which of the following represents a significant risk in patients experiencing TCA overdose?
Which of the following represents a significant risk in patients experiencing TCA overdose?
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Which of the following describes the neurological side effect associated with tricyclic antidepressants?
Which of the following describes the neurological side effect associated with tricyclic antidepressants?
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What potential effect do oral contraceptives have on the pharmacokinetics of TCAs?
What potential effect do oral contraceptives have on the pharmacokinetics of TCAs?
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Which of the following best describes an adverse cardiovascular reaction to tricyclic antidepressants?
Which of the following best describes an adverse cardiovascular reaction to tricyclic antidepressants?
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What class of antidepressants can cause excessive sweating as a side effect?
What class of antidepressants can cause excessive sweating as a side effect?
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What is the primary action of tricyclic antidepressants (TCAs) in relation to neurotransmitters?
What is the primary action of tricyclic antidepressants (TCAs) in relation to neurotransmitters?
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Which of the following pharmacological actions of tricyclic antidepressants (TCAs) assists in improving sleep?
Which of the following pharmacological actions of tricyclic antidepressants (TCAs) assists in improving sleep?
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What characteristic of tricyclic antidepressants (TCAs) influences their side effect profiles?
What characteristic of tricyclic antidepressants (TCAs) influences their side effect profiles?
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Which class of antidepressants is known for being non-selective amine reuptake inhibitors?
Which class of antidepressants is known for being non-selective amine reuptake inhibitors?
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What is a key pharmacokinetic feature of tricyclic antidepressants (TCAs)?
What is a key pharmacokinetic feature of tricyclic antidepressants (TCAs)?
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What is a therapeutic application of tricyclic antidepressants beyond treating depressive syndromes?
What is a therapeutic application of tricyclic antidepressants beyond treating depressive syndromes?
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Which adverse effect is primarily associated with the antimuscarinic action of tricyclic antidepressants?
Which adverse effect is primarily associated with the antimuscarinic action of tricyclic antidepressants?
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What interaction do tricyclic antidepressants have with oral contraceptives?
What interaction do tricyclic antidepressants have with oral contraceptives?
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What is a common cardiovascular adverse reaction associated with tricyclic antidepressants?
What is a common cardiovascular adverse reaction associated with tricyclic antidepressants?
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Which of the following conditions can TCAs help alleviate pain for?
Which of the following conditions can TCAs help alleviate pain for?
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Which side effect is least likely to be associated with noradrenergic transmission?
Which side effect is least likely to be associated with noradrenergic transmission?
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What is the main therapeutic use of Atomoxetine?
What is the main therapeutic use of Atomoxetine?
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Which of the following compounds does NOT primarily act on serotonin reuptake?
Which of the following compounds does NOT primarily act on serotonin reuptake?
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What is a primary mechanism by which Agomelatine treats severe depression?
What is a primary mechanism by which Agomelatine treats severe depression?
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What potential serious complication is associated with the overdose of Duloxetine?
What potential serious complication is associated with the overdose of Duloxetine?
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What is the primary effect of Hypericum perforatum in the treatment of depression?
What is the primary effect of Hypericum perforatum in the treatment of depression?
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Which statement about Mirtazapine's mechanism of action is true?
Which statement about Mirtazapine's mechanism of action is true?
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Which treatment option is indicated for patients who have not responded to traditional antidepressant medications?
Which treatment option is indicated for patients who have not responded to traditional antidepressant medications?
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What common adverse effect may persist after electroconvulsive therapy?
What common adverse effect may persist after electroconvulsive therapy?
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Study Notes
Depression
- A mood disorder with cognitive, behavioral, and emotional alterations.
- A long-term disease.
- Can be treated and cured.
- Anyone can experience it at any time.
- Requires treatment by a medical specialist.
-
Symptoms:
- Emotional: Apathy, pessimism, sadness
- Biological: Low self-esteem, sleep disorders, loss of motivation, loss of appetite, suicidal thoughts, delayed thinking and action, loss of libido.
- Other forms: Postpartum depression, premenstrual disorder, affective emotional disorder.
Treatment of Depression
- Prevention: To avoid reaching the point of medication, mental health awareness and practice.
- Psychotherapy: For mild depression.
- Psychotherapy + Pharmacological treatment: For moderate depression.
- Hospitalization: For severe depression.
- ECT (Electroconvulsive Therapy): Used as a last resort for severe depression.
Pharmacological Treatment of Depression
- Associated with a decrease in the release of neurotransmitters in the synapse, particularly Dopamine and 5-HT.
-
Treatment phases:
- Remission phase: Takes 2-4 weeks for antidepressants to start working.
- Continuation phase: 6-12 months.
- Maintenance phase: Depends on the evolution of the disease.
Mechanism of Depression Onset
- Prodepressive pathways: Involve the hypothalamic and pituitary adrenal axis.
- Antidepressive pathways: Involve NA, 5-HT, and BNDF.
- BNDF: Brain-Derived Neurotrophic Factor.
Classification of Antidepressants
- Tricyclic antidepressants (TCA): Non-selective amine reuptake inhibitors.
- Selective serotonin reuptake inhibitors (SSRIs):
- Monoamine oxidase inhibitors (MAOI-A y B):
- Serotonin and Noradrenaline Uptake Inhibitors (SNRIs):
-
Others:
- Bupropion
- Reboxetine
- Atomoxetine
- Natural compounds (Hypericum perforatum)
Tricyclic Antidepressants (TCA)
- Examples: Imipramine, Desipramine, Amitriptyline, Nortriptyline, Clomipramine, Doxepin.
- Mechanism of action: Inhibit the reuptake of NA and Serotonin (less effect on Dopamine) in the synapse cleft, increasing their concentration.
- Anticholinergic receptors: Two types - antimuscarinic and antinicotinic.
-
Effects:
- Antidepressant: Improves sleep, appetite, psychomotor activity, mood.
- Anxiolytic and sedative:
- Analgesic: Especially in chronic pain, when pain is part of the somatization of depression.
-
Used to treat:
- Depressive syndromes.
- Anxiety syndromes (panic attacks).
- Hyperactivity syndrome, imipramine.
- Treatment of enuresis: Children > 5 years old.
- Pain: Neurogenic (phantom limb syndrome), oncological, headaches.
Selective Serotonin Reuptake Inhibitors (SSRIs)
- Examples: Fluoxetine, Paroxetine, Citalopram, Sertraline.
- Mechanism of action: Inhibit the selective reuptake of Serotonin in the synapse cleft, increasing its concentration.
Monoamine Oxidase Inhibitors (MAOI)
- Mechanism of action: Inhibit the enzyme monoamine oxidase (MAO), which breaks down neurotransmitters like serotonin, norepinephrine, and dopamine.
- Pharmacokinetics: Well absorbed orally, metabolized in the liver, short elimination half-life, multiple daily doses.
- Therapeutic effect: Takes 1-3 weeks to appear.
- Limited use: Due to toxicity and drug interactions.
- ADRs: Hypotension, tremors, excitement, insomnia, convulsions, increased appetite.
-
Drug interactions:
- Tyramine: Hypertensive crisis (Cheese effect).
- SSRIs or TCAs: Serotonin syndrome.
- Other drugs: Enhancement of depressant actions.
- Therapeutic applications: Reserve antidepressants when other treatments fail.
Serotonin and Noradrenaline Uptake Inhibitors (SNRIs)
- Examples: Venlafaxine, Desvenlafaxine, Duloxetine.
- Mechanism of action: Non-selective inhibition of 5-HT and NA uptake.
- Effects: Effective in some anxiety disorders, may be beneficial in treating perimenopausal symptoms, Duloxetine used for neuropathic pain, fibromyalgia, urinary incontinence.
- Pharmacokinetics: Orally active, venlafaxine has a slow-release formulation.
- ADRs: Headache, insomnia, sexual dysfunction, dry mouth, dizziness, sweating, decreased appetite, serotonin toxicity, convulsions, cardiac conduction abnormalities, hepatotoxicity.
Other Noradrenaline Uptake Inhibitors
- Bupropion: Inhibits noradrenaline and dopamine, not abuse potential, used to treat nicotine dependence, may cause seizures at high doses.
- Reboxetine and Atomoxetine: Highly selective for NA uptake, less efficacy in depression, Atomoxetine used in treatment of attention deficit/ hyperactivity disorder.
Natural Compounds
- Hypericum perforatum (St. John’s Wort): Main active ingredient is Hyperforin.
- Effects: Inhibition of reuptake or 5-HT, Dopamine, NA, GABA, and glutamate.
- Therapeutic applications: Antidepressant and anxiolytic effects.
Monoamine Receptor Antagonists
- Mirtazapine: Blocks alfa 2, 5-HT2C (antidepressant effects), and H1 receptors.
- Trazodone: Combines 5-HT2A and 5-HT2C receptor antagonism with 5-HT reuptake inhibition.
Melatonin Agonist
- Agomelatine: Agonist of MT1 and MT2 receptors, short biological half-life.
- Therapeutic applications: Treatment of severe depression.
- Effects: Correcting disturbances in circadian rhythms.
- Potential risks: Hepatotoxicity.
Electroconvulsive Therapy (ECT)
- Used for severe depression, unresponsive to antidepressant drugs.
- Effectiveness in severe suicidal depression.
- Side effects: Confusion and memory loss lasting for days or weeks.
- Repetitive transcranial magnetic stimulation (TMS): Another treatment option for patients unresponsive to drugs.
Depression
- A mood disorder affecting cognitive, behavioral, and emotional spheres.
- A long-term but treatable and curable disease.
- Can affect anyone at any time.
- Requires specialist treatment.
- Not a sign of weakness.
Depression Symptoms
- Emotional Symptoms: Apathy, pessimism, sadness, low self-esteem
- Biological Symptoms: Sleep disorders, loss of motivation, loss of appetite, suicidal thoughts, delayed thinking and action, loss of libido.
Other forms of Depression
- Postpartum depression
- Premenstrual disorder
- Affective emotional disorder
Treatment of Depression
- Prevention
- Psychotherapy: For mild depression
- Psychotherapy + Pharmacological Treatment: For moderate depression
- Hospitalization: For severe depression
- ECT (Electroconvulsive Therapy)
Pharmacological Treatment of Depression
- Depression is associated with decreased neurotransmitter release in the synapse, especially dopamine and 5-HT.
- Treatment phases:
- Remission Phase: Antidepressants start working after 2-4 weeks.
- Continuation Phase: 6-12 months.
- Maintenance Phase: Depends on disease evolution.
Mechanism of Depression Onset
- Prodepressive Pathways: Involve the hypothalamic and pituitary adrenal axis.
- Antidepressive Pathways: Involve NA, 5-HT, and BDNF (Brain-Derived Neurotrophic Factor).
Classification of Antidepressants
- Tricyclic Antidepressants (TCA): Non-selective amine reuptake inhibitors.
- Selective Serotonin Reuptake Inhibitors (SSRIs):
- Monoamine Oxidase Inhibitors (MAOI-A y B):
- Serotonin and Noradrenaline Uptake Inhibitors (SNRIs):
- Others:
Treatment of Depression: TCA
- Examples: Imipramine, Desipramine, Amitriptyline, Nortriptyline, Clomipramine, Doxepin.
- Mechanism of Action: Inhibit the reuptake of NA and Serotonin (less Dopamine) in the synaptic cleft, increasing their concentration.
-
Anticholinergic Receptors:
- Antimuscarinic
- Antinicotinic
-
Pharmacokinetics:
- Highly liposoluble drugs with good distribution (BBB)
- Taken orally with progressively increasing doses
- Fixed to plasma proteins
- Hepatic metabolization with active metabolites
- Long elimination half-life (10-80 hours), longer in elderly patients
-
Pharmacological Actions:
- Antidepressant effect seen after 4 weeks of treatment, improving sleep, appetite, and psychomotor activity.
- Improves depressed mood and feelings of despondency and hopelessness after the fourth week.
- Anxiolytic and sedative action.
- Analgesic action in chronic pain, especially when pain is part of depression somatization. Some TCAs are used for neuropathic pain.
Treatment of Depression: TCA Adverse Drug Reactions (ADRs)
- Cardiovascular: Orthostatic hypotension, palpitations, tachycardia.
- Antimuscarinic Effect: Dry mouth, constipation, urinary retention, nasal congestion, blurred vision.
- Neurological: Tremors in hands and head.
- Other: Weight gain, excessive sweating, photosensitivity, gastrointestinal discomfort.
- Intoxication: Overdose is common due to suicidal tendencies in some depressive patients. Symptoms include arrhythmias, convulsions, coma.
Treatment of Depression: TCA Drug Interactions
- Pharmacodynamic Interaction: Enhances the actions of catecholamines and MAOIs (Monoamine oxidase inhibitors).
-
Pharmacokinetic Interaction:
- Increases the activity of oral anticoagulants (warfarin) and increases the risk of bleeding (PP-binding).
- Oral contraceptives inhibit metabolism of TCAs (metabolism).
- TCAs potentiate the effects of alcohol and anaesthetic agents (unknown mechanism), potentially leading to death.
- Interfere with antihypertensive drugs.
Treatment of Depression: TCA Therapeutic Applications
- Depressive syndromes
- Anxiety syndromes (panic attacks)
- Hyperactivity syndrome: Imipramine
- Treatment of enuresis: Children over 5 years old (imipramine)
- Pain: Neurogenic (phantom limb syndrome), oncological, headaches.
Treatment of Depression: SSRIs
- Examples: Fluoxetine, Paroxetine, Citalopram, Sertraline.
- Mechanism of Action: Inhibition of Serotonin reuptake in the synaptic cleft, increasing its concentration.
- ADRs: Headache, insomnia, sexual dysfunction, dry mouth, dizziness, sweating, decreased appetite.
- Overdose: CNS depression, serotonin toxicity, convulsions, cardiac conduction abnormalities.
- Duloxetine: Can cause hepatotoxicity, contraindicated in patients with hepatic impairment.
Treatment of Depression: Other Noradrenaline Uptake Inhibitors
-
Bupropion:
- Inhibits noradrenaline and dopamine.
- No abuse potential.
- Used to treat nicotine dependence.
- May induce seizures at high doses.
-
Reboxetine and Atomoxetine:
- Highly selective for NA uptake, but less effective in depression than TCAs.
- Atomoxetine is used to treat attention deficit/hyperactivity disorder.
Treatment of Depression: Others: Natural Compounds
-
Hypericum perforatum (St. John's Wort):
- Herbal preparation containing hyperforin.
- Inhibits the reuptake of 5-HT, dopamine, NA, GABA, and glutamate.
- Antidepressive and anxiolytic effects.
Treatment of Depression: Monoamine Receptor Antagonists
-
Mirtazapine:
- Blocks alpha 2, 5-HT2C (antidepressant effects), and H1 receptors.
-
Trazodone:
- Combines 5-HT2A and 5-HT2C receptor antagonism with 5-HT reuptake inhibition.
Treatment of Depression: Melatonin Agonist
-
Agomelatine:
- Agonist of MT1 and MT2 receptors.
- Short biological half-life.
- Used to treat severe depression, usually taken once daily before bed.
- Works by correcting disturbances in circadian rhythms.
- May cause hepatotoxicity.
Treatment of Depression: Electroconvulsive Therapy
- ECT (Electroconvulsive Therapy) and TMS (Repetitive Transcranial Magnetic Stimulation): Used for patients who have not responded to antidepressant drugs.
- ECT: Effective for severe suicidal depression, but can cause confusion and memory loss.
- TMS: Less effective than ECT.
Treatment of Depression: Antidepressant Clinical Uses Summary
- Mild depression is often initially treated with non-drug measures.
- Antidepressant drugs are advisable for moderate to severe depression.
- The efficacy of antidepressant drugs varies between individuals.
- Different classes of antidepressants have similar efficacy but different side effects.
- Drug choice is based on individual aspects, including concomitant disease.
- SSRIs are preferred due to better tolerance and lower overdose risk.
- Antidepressant effects take several weeks to appear; decisions on changes in dose or drug should not be rushed.
- MAOI usage is restricted to specialists.
- An effective regimen should continue for at least two years.
- Specialist consideration for possible use of electroconvulsive therapy in urgent situations.
- Anxiolytics (e.g., benzodiazepines) or antipsychotic drugs are useful adjuncts for some patients.
Bipolar Disorder
- A mental health condition marked by extreme mood swings, including episodes of mania and depression.
- These phases can significantly impact behavior, energy levels, and daily functioning.
Treatment of Bipolar Disorder: Lithium Salts
-
Lithium Carbonate:
- Administered orally.
- Excreted by the kidneys.
- Narrow therapeutic margin, requiring monitoring of plasma concentration.
- Mechanism of action is unknown.
- Effective in both manic and depressive phases, considered a mood stabilizer.
- Increases release of NA and 5-HT in the brain.
- May have beneficial effects in neurodegenerative diseases like Alzheimer's disease.
Treatment of Bipolar Disorder: Lithium Salts ADRs
- Gastrointestinal: Gastric discomfort, nausea, vomiting, diarrhea, anorexia, weight gain.
- Renal: Polyuria, thirst due to inhibition of antidiuretic hormone.
- Neurological: Trembling hands.
- Chronic Administration: Thyroid disorders, kidney disorders.
Depression
- Maintenance phase of depression treatment depends on the evolution of the disease.
- Prodepressive pathways involve the hypothalamic-pituitary-adrenal axis.
- Antidepressive pathways involve NA, 5-HT, and BDNF.
- Tricyclic antidepressants (TCAs) are non-selective amine reuptake inhibitors
- Selective serotonin reuptake inhibitors (SSRIs) are a class of antidepressants that selectively inhibit the reuptake of serotonin in the synapse.
- Monoamine oxidase inhibitors (MAOIs) inhibit the enzyme monoamine oxidase, which breaks down neurotransmitters like serotonin, norepinephrine, and dopamine.
- Serotonin and Noradrenaline Uptake Inhibitors (SNRIs) are a class of antidepressants that work by inhibiting the reuptake of both serotonin and norepinephrine.
Treatment of Depression: Tricyclic Antidepressants (TCAs)
- Mechanism of action: TCAs block the uptake of amines, specifically inhibiting norepinephrine and serotonin reuptake (with less effect on dopamine reuptake).
- Pharmacokinetics: TCAs are highly liposoluble drugs, allowing for good distribution throughout the body, including the blood-brain barrier.
- Pharmacological actions: TCAs have antidepressant, anxiolytic, sedative, and analgesic actions.
- Adverse Drug Reactions (ADRs): TCAs can cause cardiovascular, antimuscarinic, neurological, and other side effects.
- Drug Interactions: TCAs can enhance the actions of catecholamines and MAOIs. They can also increase the activity of oral anticoagulants (warfarin) and potentiate the effects of alcohol and anesthetic agents.
Treatment of Depression: Selective Serotonin Reuptake Inhibitors (SSRIs)
- Mechanism of action: SSRIs selectively inhibit serotonin reuptake in the synaptic cleft.
- Adverse Drug Reactions (ADRs): SSRIs may cause headache, insomnia, sexual dysfunction, dry mouth, dizziness, sweating, and decreased appetite.
Treatment of Depression: Other Noradrenaline Uptake Inhibitors
- Bupropion: Inhibits both noradrenaline and dopamine; used to treat nicotine dependence.
- Reboxetine and Atomoxetine: Highly selective for NA uptake.
- Atomoxetine: Used in the treatment of attention deficit/hyperactivity disorder.
Treatment of Depression: Others
- Hypericum perforatum (St John’s wort): Depressive and anxiolytic effects; inhibits the reuptake of serotonin, dopamine, norepinephrine, GABA, and glutamate.
- Mirtazapine: Blocks alfa2, 5-HT2C, and H1 receptors.
- Trazodone: Combines 5-HT2A and 5-HT2C receptor antagonism with 5-HT reuptake inhibition.
- Agomelatine: Agonist of MT1 and MT2 receptors; used to treat severe depression.
- Electroconvulsive therapy (ECT): Effective treatment for severe suicidal depression.
- Repetitive transcranial magnetic stimulation (TMS): Less effective than ECT.
Clinical Uses of Antidepressants
- Mild depression: Often treated with non-drug measures.
- Moderate to severe depression: Antidepressant drugs are advisable.
- Efficacy: Varies between individuals. Antidepressants take several weeks to take effect.
- Choice of drug: Based on individual aspects including concomitant disease.
- SSRI preference: Generally better tolerated and less dangerous in overdose.
- MAOIs: Prescribed by specialists.
- Long-term use: Effective regimen should be continued for at least 2 years.
- Urgent situations: Specialist consideration should be given to possible use of electroconvulsive therapy.
- Anxiolytic (e.g.benzodiazepine) or antipsychotic drugs: Useful adjuncts in some patients.
Bipolar Disorder
- Marked by extreme mood swings, including episodes of mania and depression.
- Lithium salts: The drug of first choice in the control of manic phases and prophylaxis of bipolar disorder.
- Antiepileptic drugs: Effective in treating acute attacks of mania and long-term treatment.
- Atypical antipsychotic drugs: Effective against mania and bipolar depression; often used in combination with other medications.
Lithium Salts
- Pharmacokinetics: Orally administered; excreted by the kidney. Narrow therapeutic margin; requires monitoring of plasma concentration.
- Mechanism of action: Unknown; effective in both manic and depressive phases.
- Adverse Drug Reactions (ADRs): Gastric discomfort, nausea, vomiting, diarrhea, anorexia, weight gain, polyuria, tremor, thyroid disorders, kidney disorders, fetal malformations (during first months of pregnancy).
Antiepileptic Drugs
- Carbamazepine: Enzyme inducer.
- Valproate: Highly teratogenic (can cause spina bifida).
- Lamotrogine: Effective in preventing the recurrence of both mania and depression.
Atypical Antipsychotic Drugs
- Olanzapine, Risperidone, Quetiapine, Aripiprazole: Second generation drugs developed for schizophrenia; effective against mania and bipolar depression.
- Haloperidol: Indicated for prophylaxis of maniac-depressive disease.
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Description
This quiz explores the complexities of depression, a mood disorder characterized by cognitive, behavioral, and emotional changes. It covers symptoms, prevention strategies, and various treatment options, including psychotherapy and pharmacological treatments. Learn about the different forms of depression and the importance of medical intervention for those affected.