Questions and Answers
Adolescent risk factors, such as obesity, can contribute to the development of mood disorders
False
Past history of schizophrenia is a strong predictor of developing mood disorders
False
The biological mechanism of mood disorders is primarily related to abnormalities in the neural processing of memory
False
Monoamine neurotransmitters, such as dopamine, play no role in the pathophysiology of depression
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Genetic risk is the only factor that contributes to the development of mood disorders
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The psychosocial mechanism of mood disorders focuses solely on genetic factors
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A single-factor approach is sufficient to understand and effectively treat mood disorders
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Interventions cannot be utilized to effectively reduce the likelihood of individuals developing mood disorders
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In depression, there is an increase in the proliferative responses of lymphocytes to mitogens.
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Natural killer cell activity is notably increased in individuals with depression.
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Inflammatory cytokine levels, such as IL-6 and TNFa, are decreased in depression.
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Disturbed sleep is not a characteristic feature of depression.
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The decrease in REM sleep latency is linked to a vulnerability to relapse in previously recovered depression patients.
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The medial prefrontal cortex is associated with impaired cognitive functions in patients with mood disorders.
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Resting state fMRI studies indicate that the default mode network is inactive during specific tasks in depressed patients.
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The anterior cingulate is linked to impaired attentional processes in individuals with mood disorders.
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Depressive disorders are solely caused by genetic factors according to the latest research.
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Behavioural studies suggest that emotional perception and appraisal are unaffected in mood disorder patients.
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The dexamethasone suppression test is primarily used to measure cortisol levels in healthy individuals.
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About 50% of individuals with depression exhibit normal suppression of cortisol after dexamethasone administration.
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The glucocorticoid receptor hypothesis suggests that glucocorticoid receptor dysfunction may be linked to depression.
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Corticotropin-releasing hormone (CRH) has only an endocrine role and does not affect neurotransmitter functions.
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A decrease in free triiodothyronine levels is commonly observed in individuals with depression.
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Cytokines may contribute to tryptophan depletion, increasing vulnerability to depression.
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CRH hypersecretion is not linked to any specific psychiatric disorders.
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Early adverse experiences are associated with short-term changes in HPA axis regulation.
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Individuals who were abused as children often show normal HPA axis responses to stress.
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The association between depression and immune function is established in recent studies.
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Study Notes
Immune Changes in Depression
- Lowered lymphocyte proliferation in response to mitogens indicates immune dysfunction.
- Reduced activity of natural killer cells contributes to impaired immune response.
- Increased levels of acute phase proteins suggest heightened inflammation during depressive episodes.
- Elevated inflammatory cytokines like IL-6 and TNF-alpha are linked to depression.
- Induction of indoleamine 2,3-dioxygenase affects serotonin metabolism and is associated with depression.
Sleep Changes in Depression
- Disturbed sleep patterns are a hallmark of depression.
- Polysomnographic recordings reveal distinct EEG changes in depressed individuals.
Development of Mood Disorders
- Mood disorders are influenced by biological and psychosocial factors.
- Recent life stressors significantly increase the risk of mood disorders.
- Adolescent traits, such as neuroticism, anxiety, and conduct issues, are risk factors.
- Genetic predispositions and a history of depression also elevate risk.
- Adverse childhood experiences can amplify vulnerability and reduce social support.
Biological Mechanism of Depression
- Abnormal emotional processing in the brain may lead to depressive symptoms.
- Key brain regions receive dense monoamine neuron innervation, central to emotional regulation.
- Alterations in serotonin (5-HT) and noradrenaline transmission relate to depressive symptoms and treatment responses.
Psychosocial Mechanism of Depression
- Mood disorders result from complex interactions among genetic, environmental, and interpersonal factors.
- The clinical experience of major depression underscores the multifactorial nature of its development.
HPA Axis and Depression
- The hypothalamic-pituitary-adrenal (HPA) axis is vital for stress regulation and its dysregulation may lead to depression.
- Dexamethasone suppression test results show about 50% of depressed individuals don’t exhibit normal cortisol suppression.
- Dexamethasone non-suppression is especially common in melancholic depression, but lacks diagnostic specificity.
Glucocorticoid Receptor Hypothesis
- This hypothesis posits that HPA axis dysregulation contributes to depression via glucocorticoid receptor abnormalities.
- Antidepressants may enhance glucocorticoid receptor expression, normalizing HPA axis activity.
Corticotropin-Releasing Hormone (CRH)
- CRH is a critical hormone in the HPA axis with neurotransmitter-like effects in the brain.
- Hypersecretion of CRH has been linked to depressive states; CRH receptor antagonists may have antidepressant effects.
Thyroid Function in Depression
- Thyroid abnormalities are common in depression; free triiodothyronine may be decreased despite normal free thyroxine levels.
- 25% of depressed individuals exhibit a reduced thyrotropin-stimulating hormone response to TRH.
Immune System and Depression
- Research indicates a connection between depression and immune function disturbances.
- Initial findings showed decreased immune responses; newer studies suggest immune activation with increased proinflammatory cytokines.
- This immune activation may compound HPA axis dysfunction.
Early Adverse Experiences Impact
- Childhood adversity can result in lasting HPA axis regulation changes, increasing susceptibility to mood disorders.
- Altered stress responses have been observed in adults with a history of childhood abuse.
Role of Cytokines in Depression
- Cytokines may contribute directly to depression, affecting tryptophan metabolism and enhancing vulnerability.
Conclusion on HPA Axis, Immune System, and Depression
- The interplay between dysregulated HPA axis, immune disturbances, and brain circuits is crucial for understanding and treating depression.
- Comprehensive treatment strategies should consider the multifaceted nature of these interrelationships.
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