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Questions and Answers
What is the primary focus of the biogenic theory of depression?
What is the primary focus of the biogenic theory of depression?
Which neurotransmitters are believed to be deficient in key brain areas in individuals with depression?
Which neurotransmitters are believed to be deficient in key brain areas in individuals with depression?
What defines depression as an affective disorder?
What defines depression as an affective disorder?
Why are neurotransmitters like norepinephrine, serotonin, and dopamine crucial in preventing depression?
Why are neurotransmitters like norepinephrine, serotonin, and dopamine crucial in preventing depression?
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Which action is NOT associated with antidepressants?
Which action is NOT associated with antidepressants?
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In terms of antidepressants, what is a drug–drug interaction?
In terms of antidepressants, what is a drug–drug interaction?
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What differentiates a therapeutic indication from a contraindication in antidepressant use?
What differentiates a therapeutic indication from a contraindication in antidepressant use?
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What is the pharmacological action of tricyclic antidepressants (TCAs) in the central nervous system (CNS)?
What is the pharmacological action of tricyclic antidepressants (TCAs) in the central nervous system (CNS)?
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Which receptor blockade is associated with TCAs' effects on the central nervous system?
Which receptor blockade is associated with TCAs' effects on the central nervous system?
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What is a common cardiovascular side effect associated with tricyclic antidepressants (TCAs)?
What is a common cardiovascular side effect associated with tricyclic antidepressants (TCAs)?
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Which of the following TCAs is a secondary amine?
Which of the following TCAs is a secondary amine?
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What is the most potent anticholinergic action associated with tricyclic antidepressants (TCAs)?
What is the most potent anticholinergic action associated with tricyclic antidepressants (TCAs)?
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Which neurotransmitter system is mainly affected by tricyclic antidepressants (TCAs) in the autonomic nervous system (ANS)?
Which neurotransmitter system is mainly affected by tricyclic antidepressants (TCAs) in the autonomic nervous system (ANS)?
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Which TCA is commonly used for the treatment of depression and neuropathic pain?
Which TCA is commonly used for the treatment of depression and neuropathic pain?
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Which type of drug specifically blocks the reuptake of serotonin and increases its concentration in the synaptic cleft?
Which type of drug specifically blocks the reuptake of serotonin and increases its concentration in the synaptic cleft?
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What is the primary effect of ingesting foods high in tyramine while taking an MAOI?
What is the primary effect of ingesting foods high in tyramine while taking an MAOI?
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Which drug prevents the enzyme monoamine oxidase from breaking down norepinephrine, leading to increased NE levels in the synaptic cleft?
Which drug prevents the enzyme monoamine oxidase from breaking down norepinephrine, leading to increased NE levels in the synaptic cleft?
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What distinguishes SSRIs from TCAs in terms of adverse effects?
What distinguishes SSRIs from TCAs in terms of adverse effects?
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What is a common symptom experienced by patients who are depressed?
What is a common symptom experienced by patients who are depressed?
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Which drug blocks the reuptake of norepinephrine and serotonin, causing anticholinergic and sedative effects?
Which drug blocks the reuptake of norepinephrine and serotonin, causing anticholinergic and sedative effects?
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What can ingesting foods high in tyramine while on an MAOI lead to?
What can ingesting foods high in tyramine while on an MAOI lead to?
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How do deficiencies of neurotransmitters like NE and 5HT develop according to the text?
How do deficiencies of neurotransmitters like NE and 5HT develop according to the text?
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Which neurotransmitters are mentioned in the text as being deficient in depression?
Which neurotransmitters are mentioned in the text as being deficient in depression?
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What physical problems can untreated clinical depression lead to?
What physical problems can untreated clinical depression lead to?
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What theory of depression is discussed in the text?
What theory of depression is discussed in the text?
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Why might depression occur as mentioned in the text?
Why might depression occur as mentioned in the text?
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What functions are regulated by neurotransmitters like NE and 5HT, according to the text?
What functions are regulated by neurotransmitters like NE and 5HT, according to the text?
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How might rapid fire of neurons lead to depletion of neurotransmitters like NE and 5HT?
How might rapid fire of neurons lead to depletion of neurotransmitters like NE and 5HT?
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What is the principal mechanism of action of Tricyclic Antidepressants (TCAs)?
What is the principal mechanism of action of Tricyclic Antidepressants (TCAs)?
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What effect do Tricyclic Antidepressants (TCAs) have on dopamine system?
What effect do Tricyclic Antidepressants (TCAs) have on dopamine system?
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What was the original intended use of Tricyclic Antidepressants (TCAs) when they were first developed in 1949?
What was the original intended use of Tricyclic Antidepressants (TCAs) when they were first developed in 1949?
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How do Tricyclic Antidepressants (TCAs) lead to increased neurotransmitter levels in the synaptic cleft?
How do Tricyclic Antidepressants (TCAs) lead to increased neurotransmitter levels in the synaptic cleft?
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Which neurotransmitters are primarily affected by Tricyclic Antidepressants (TCAs)?
Which neurotransmitters are primarily affected by Tricyclic Antidepressants (TCAs)?
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What is the characteristic chemical structure of Tricyclic Antidepressants (TCAs)?
What is the characteristic chemical structure of Tricyclic Antidepressants (TCAs)?
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In comparison to cocaine, how important is the effect of Tricyclic Antidepressants (TCAs) on the dopamine system?
In comparison to cocaine, how important is the effect of Tricyclic Antidepressants (TCAs) on the dopamine system?
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Besides blocking reuptake, what other mechanism may Tricyclic Antidepressants (TCAs) use to increase neurotransmitter levels in the synaptic cleft?
Besides blocking reuptake, what other mechanism may Tricyclic Antidepressants (TCAs) use to increase neurotransmitter levels in the synaptic cleft?
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