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Depressive Disorders - Coggle Diagram
Depressive Disorders
MAJOR DEPRESSIVE
Diagnosis
i.e. major depressive episode: at least 5 symptoms nearly every day for at least 2 weeks, one must be anhedonia.
can include weight loss / gain, fatigue, decreased / increased appetite, worthlessness, guilt, inability to concentrate, recrent thoughts of death
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Theories
Beck's Depressive Cognitive Triad: negative feelings toward the self, world, and future
Reformulated Learned Helplessness Model (Seligman / Abramson) - depression = result of prior exposure to uncontrollable negative events coupled with tendency to attribute events to internal, stable, and global factors
Abramson's revision de-emphasized role of attributions and emphasized HOPELESSNESS as proximal cause
Seligman developed Positive Psychology Interventions, which seeks to address more permanent long-term stable factors through assessments of strength rather than pathology
RESEARCH
Prevalence
in the US = 7%. Age differences: A.)18-29 is 3x the prevalence for 60+. B.) Prior to puberty rates are about equal between M/F. C.) in early adolescence, F are 1.5-3x rate for M.
Associated Features
40-60% have EEG abnormalities during sleep: early morning awakening, reduced slow-wave sleep (stage 3/4), decreased REM latency (early onset), increased duration of REM sleep early in night
60% experience anxiety during lifespan. Comorbidity linked to more severe depression, poorer response to treatement, higher risk for suicide.
Course / Age
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Children: somatic complaints, irritability, social withdrawal
Preadolescents: aggressiveness and destructiveness, especially boys
Older adults: memory loss, distractability, disorientation. Makes it difficult to distinguish between "pseudodementia" and Major / Mild Neurocognitive Disorder
Culture
in some: depression manifests as somatic complaints. E.g., Latinos often complain of headaches while Asians often experience weakness, tiredness, or "imbalance"
Etiology
Concordance rates: A.) .50 for identical twins, B.) .20 for fraternal twins, C.) 1.5 to 3x more common among first degree relatives
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recent sutdies focus on the number and sensitivity of postsynaptic receptors (especially serotonin) rather than absolute levels
Linked to elevated Cortisol, causes atrophy of neurons in hippocampus
Risk:
Highest risk for suicide is shortly after treatment (psychotherapy / psychopharmacology) yield's improvement in symptoms. This is due to reduction in fatigue / vegetativeness, which allows individual energy to complete suicide.
TREATMENT
Research is inconsistent but generally confirm a combo of antidepressant and psychotherapy is better than any modality alone.
Tricyclics (TCAs) most effective for classic symptoms (vegetative bodily), worse in the morning, or acute onset with short duration
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Monoamine Oxidase Inhibitors (MAOIs) may benefit those with atypical symptoms (e.g., anxiety, hypersomnia, hyperphagia (insatiable hunger), interpersonal sensitivity
Serotonin norepinephrine reuptake inhibitors (SNRIs) increase both. Are newer. Some evidence they are comparable in effectiveness to SSRIs and TCAs but differ in side-effects (e.g., Venlafaxine, Duloxetine [Cymbalta]).
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Prementrual Dysphoric
for most cycles, at least 5 symptoms: