Chapter 7 (Exam 2) Flashcards
what are the two primary emotions in mood disorders?
- DEPRESSION- a low, blue, sad emotional state in which this feeling is overwhelming
- MANIA- a state of frenzied energy (sometimes with a sense of euphoria or grandiosity); NOT the same as happiness- mania may include anger or irritability
how common is unipolar depression/major depressive disorder?
- prevalence rate: 7-8%
lifetime prevalence rate:
women: 26%, men: 12% - 20% of all adults experience unipolar depression at some time in their lives
- more than half of indiv who have a major depressive episode will experience another at some point (recurrence and relapse are concerns)
- 85% will recover but most will have another episode (half do not seek treatment and it gets better)
- rate of depression is higher in people with lower economic means
- women are twice as likely to be diagnosed with depression
- avg age of onset: 19 y/o
symptoms
unipolar depression/major depressive disorder
five main areas of functioning:
1. emotional symptoms (feeling miserable, empty, or humiliated; experiencing little pleasure)
2. motivational symptoms (lacking drive, initiative, spontaneity; 6-15% of those with severe depression commit suicide )
3. behavioral symptoms (less active/productive; socially withdrawn; staying in bed for long periods of time)
4. cognitive symptoms (negative self-views; blame themselves for unfortunate events; pessimistic; distracted/poor concentration)
5. physical symptoms (headaches, dizzy spells, GI symptoms, general pain, sleep disturbances, appetite changes, fatigue)
diagnostic criteria
depression
TWO MAJOR DIAGNOSES TO CONSIDER:
1. major depressive disorder/unipolar depression (crit 1 and 2 met)
2. persistent depressive disorder
- symptoms are mild but chronic
- depression is longer lasting but less disabling
- depressed mood plus 2+ other symptoms
- consistent symptoms for AT LEAST 2 years (one for children and adolescents)
- symptoms never disappear for more than two months
double depression
when persistent depressive disorder leads to major depressive disorder
what causes unipolar depression/major depressive disorder?
STRESS/STRESSFUL NEGATIVE EVENT may trigger depression
- people with depression experience a greater number of stressful life events during the month before onset of symptoms
- some clinicians distinguish reactive (exogenous) depression from endogenous depression
exogenous depression
outside of the person; related to stressful life events
endogenous depression
arise from internal factors, usually biological (neurochemical composition, etc.)
biological view: causes of
depression
genetic factors
- 30% of people with depressed relatives are depressed (compared with fewer than 10% of the population)
- heritability: 40%
- 2/3 of chromosomes carry genes related to depression
twin concordance rates:
- identical: 38%
- fraternal: 20%
biochemical factors: neurotransmitters
depression
neurotransmitters: SEROTONIN and NOREPINEPHRINE
- truly effective antidepressants release depression by increasing either serotonin or norepinephrine
- there are other NTs involved (e.g. glutamate)
- depression circuit
in the 1950s, medications for _______ were found to cause depression
HIGH BLOOD PRESSURE MEDS
- some lowered serotonin, others lowered norepinephrine
biochemical factors: hormones
depression
ENDOCRINE SYSTEM/HORMONE RELEASE
- people with depression have abnormally high levels of cortisol
- overly reactive HPA axis (in response to stress)
- depression circuit
depression brain circuit
- structural problems; interconnectivity (lowered connection between neurons)
- irregular activity and flow rate in various brain locations
GLUTAMATE
PREFRONTAL CORTEX (higher or lower levels of activity)
HIPPOCAMPUS (undersized, production of new neurons is low)
AMYGDALA (overactive; high blood flow)
SUBGENUAL CINGULATE (smaller than it should be yet overly active)
immune system theory
depression
people with depression have:
- LOWER levels of LYMPHOCYTES
- HIGHER levels of C-REACTIVE PROTEIN
- HIGHER levels of INFLAMMATION
do these cause depression or is depression a severe stressor that leads to immune system problems?
biological TREATMENTS
depression
ANTIDEPRESSANTS
- monoamine oxidase inhibitors (MAOs)
- tricyclics
- second generation antidepressants (SSRIs)
- ketamine-based drugs
BRAIN STIMULATION
- electroconvulsive therapy and other forms of brain stimulation
MAO inhibitors
depression treatment
- discovered in 1950s by accident
- Iproniazid helped improve depression
- works because they INHIBIT MAOs (which break down serotonin and norepinephrine)
- MUST be on a strict diet (can not eat anything with Tyramine because their blood pressure would sky rocket to dangerous levels)
tricyclics
depression treatment
- discovered by accident
- Imipramine was developed for schizophrenia
- serotonin and norepinephrine reuptake inhibitor
- unfavorable side effects
- success rate: 50-60%
second-generation antidepressants
depression treatment
SSRIs (selective serotonin reuptake inhibitors)
SNRIs (selective norepinephrine reuptake inhibitors)
SSNRIs (serotonin norepinephrine reuptake inhibitors)
- hard to overdose on these
- common side effects: weight gain and lowered sex drive
- downside: they take weeks to take effect
ketamine-based drugs
depression treatment
- increases GLUTAMATE activity (may aid in new neural pathway development); helps with neuroplasticity and can promote interconnectivity/synaptic connections
- 70% of people with treatment-resistant depression respond to ketamine
- ONLY done in a medically supervised setting
- ONLY used for treatment resistant/severe depression (pt must have tried at least 2 antidepressants before consideration
- typically given through IV
- does NOT have long lasting effects (wears off after 2 weeks; need booster sessions)
- side effects: dizziness, confusion, memory problems, high bp, dissociative symptoms, HIGH RISK OF ADDICTION
electroconvulsive therapy (ECT)
depression treatment
- targeted electrical stimulation, causes a brain seizure (pt is unconscious and given muscle relaxants)
- course of treatment: 6-12 sessions over 2-4 weeks
- ONLY used for treatment-resistant and severe depression
- effective and fast-acting
- memory loss/issues are potential side effects
- quicker response to treatment than drug or psychotherapy
- treatment may be bilateral or unilateral
- success rate: 50-80% improvement
other brain stimulation
depression treatment
- vagus nerve stimulation (VNS)- implanted pulse generator sends electrical signals to the vagus nerve, and then to the brain
- transcranial magnetic stimulation- stimulates the prefrontal cortex with electromagnetic currents daily for 4-6 weeks (as effective as ECT)
- deep brain stimulation- electrodes implanted deep within brain and low voltage is sent to Brodmann Area 25, which is theorized to be a “depression switch”; invasive procedure
theoretical explanation: cog behavioral
THEORETICAL PERSPECTIVES
depression
depression results from problematic behaviors and dysfunctional thinking
theoretical perspectives:
- behavioral dimension
- negative thinking
theoretical explanation: cog behavioral
LEWINSOHN
depression
- result of changes in rewards and punishments people receive in their lives (Lewinsohn suggests that the pos rewards in life dwindle for some, leading them to perform fewer and fewer constructive behaviors and they spiral towards depression)
research supports the relationship between the number of rewards received and the presence/absence of depression (social rewards are especially important
theoretical explanation: cog behavioral
BECK
depression
Beck theorizes four interrelated cog components combine to produce depression:
1. MALADAPTIVE ATTITUDES- developed in childhood; self-defeating: “if I fail, others will hate me”
2. COGNITIVE TRIAD- experiences and the future are interpreted negatively
3. ERRORS IN THINKING- minimizing the pos and magnifying the neg
4. NEG AUTOMATIC THOUGHTS- a constant, neg stream of thoughts involving inadequacy and hopelessness
***supported by research