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9 Cards in this Set
- Front
- Back
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Describe the symptoms of depression and the evidence for a genetic contribution to depression. |
- feel sad and helpless every day for weeks at a time - have little energy, feel worthless, contemplate suicide, have trouble sleeping, cannot concentrate, find little pleasure, and can hardly even imagine being happy again - moderate degree of heritability based on twin studies and adoption studies - several genes linked but none have a large effect on its own |
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Explain the possible roles of genetics, stress, hormones, abnormalities of hemispheric dominance, and viruses in the onset or worsening of depression. |
-genetic: moderate heritability, several linked genes -stress: short form of the gene that controls the serotonin transporter may magnify stress reactions to environment, increased cortisol -viral infections: Borna disease -hormones: decreased estradiol & progesterone in women, decreased testosterone in men -abnormalities of hemispheric dominance: increased activity in right prefrontal cortex, decreased activity in left prefrontal cortex |
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Describe the short-term and long-term mechanisms of action of antidepressant drugs. |
- tricyclics (e.g., imipramine, trade name Tofranil) block the transporter proteins that reabsorb serotonin, dopamine, and norepinephrine (also block histamine receptors, acetylcholine receptors, and certain sodium channels) - selective serotonin reuptake inhibitors (SSRIs) block the reabsorption of serotonin (e.g., sertraline (Zoloft), citalopram (Celexa)) - serotonin norepinephrine reuptake inhibitors (SNRIs) block the reabsorption of serotonin and norepinephrine (e.g., duloxetine (Cymbalta) and venlafaxine (Effexor)) - monoamine oxidase inhibitors (MAOIs) (e.g., phenelzine, trade name Nardil) block the enzyme monoamine oxidase (MAO), a presynaptic terminal enzyme that metabolizes catecholamines and serotonin into inactive forms - atypical antidepressants (e.g., bupropion (Wellbutrin)) work in miscellaneous ways (e.g., buproprion inhibits reuptake of dopamine and to some extent norepinephrine) - prolonged use of antidepressant drugs generally increases BDNF production and improves learning and formation of new neurons |
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Which category of antidepressant drugs operates by preventing the presynaptic neuron from reabsorbing serotonin and catecholamines after releasing them? |
tricyclics |
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Tricyclic drugs and MAOIs both: |
effectively increase the amount of catecholamines in the synapse |
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Describe the possible mechanisms of action and the advantages and disadvantages of psychotherapy, electroconvulsive therapy, and altered sleep patterns. |
- antidepressant drugs and psychotherapy are about equally effective for treating all levels of depression, from mild to severe, with three exceptions: drugs work better for dysthymia; psychotherapy is better for patients that have a history of abuse or neglect or with multiple psychological disorders; psychotherapy is more likely to have long-term benefits - Brain scans show that antidepressants and psychotherapy increase metabolism in the same brain areas - electroconvulsive therapy (ECT) is used only with informed consent, usually for patients with severe depression who have not responded to antidepressant drugs; usually applied every other day for about 2 weeks; muscle relaxants or anesthetics used to reduce discomfort or injury; causes temporary memory loss; high risk of relapse; increases the proliferation of new neurons in the hippocampus; alters the expression of at least 120 genes in the hippocampus and frontal cortex -altered sleep is a lifelong trait of people who are pre-disposed to depression; a night of total sleep deprivation is the quickest known method of relieving depression; very short benefit as the depression returns at next regular night's sleep; increases pain sensitivity; going to bed earlier than usual relieves depression for at least a week in most patients and often longer |
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Describe the symptoms of bipolar disorder and the possible contributions of genetics. |
-alternate between depression and mania -bipolar I - full blown mania; bipolar II - milder manic phases (agitation or anxiety) - attention deficits, poor impulse control, and impairments of verbal memory - genetic predisposition (twin studies & adoption studies); two genes linked to bipolar II disorder; some of the genes that increase risk of depression also increase risk of bipolar disorder |
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Describe the mechanisms of action of drugs used to treat bipolar disorder. |
- Lithium (also valproate & carbamazepine) stabilizes mood, preventing a relapse into either mania or depression - decrease the number of AMPA type glutamate receptors in the hippocampus -Excessive glutamate activity is responsible for some aspects of mania. -block the synthesis of a brain chemical called arachidonic acid, which is produced during brain inflammation |
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Describe seasonal affective disorder and a treatment for it. |
-depression that recurs during a particular season, such as winter (more prevalent in countries with long winter nights) -phase-delayed sleep and temperature rhythms often from a mutation in one of the genes responsible for regulating the circadian rhythm -very bright lights (e.g., 2,500 lux) for an hour or more each day |
