Lecture 8: Depression Flashcards
at least 1 of the symtpoms of major depressive disorder (MDD)
- depressed mood
- loss of interest or pleasure
other symptoms of MDD
- weight loss or weight gain
- increase/decrease in appetite
- insomnia or hypersomnia
- psychomotor agitation or delay
- fatigue or loss of energy
- feelings of worthlessness or guilt
- reduced ability to think or concentrate
- recurring thoughts of death, suicidal thoughts, or plan/attempt
prevalence
refers to the number of people with the disorder at a given time or during a given period
- depression is more prevalent in women (diagnosed 1.7 times more often than men)
how many people have mood disorders
- UK: 4 million +
- Europe: 33 million +
recovery from MDD
- 54% of patients are likely to recover within 6 months
- 81% within 2 years
- relapse is highly likely (58% relapse within the next 10 years)
depressive symptoms
different from depressive disorder
- may be transient and occur in response to stressful life events without developing into a depressive disorder
unipolar depression
a purely depressive disorder
bipolar depression
bipolar patients have depression that alternates with periods of mania
bipolar I vs bipolar II
- bipolar I is the classic manic depression
- bipolar II is a milder variant
symptoms of a manic episode
- inflated sense of self-worth or grandeur
- decrease in need for sleep
- more talkative than usual or feels pressure to keep talking
- lost of ideas or feeling like thoughts are racing
- quickly distracted
- increased in purposeful activity or psychomotor agitation
- increased involvement in activities that are highly likely to produce pain
hypomania
a marked period of abnormally and persistently elevated, expansive, or irritable mood and increased goal-directed activity or energy
- lasting at least 4 days and present most of the day
endogenous depression
occurs for no apparent reason
- potentially caused by an underlying neurochemical imbalance as the critical neuropathology
- tends to respond well to pharmacotherapy
reactive depression
can be seen as a result of a stressful life event
- responds better to psychological interventions (e.g. cognitive-behavioral therapy)
factors which can cause depression
- family history
- abuse
- trauma and stress
- death or loss
- pessimistic personality
- major life events
- physical conditions
- social isolation
- lack of exposure to sunlight
- hormones
- other mental disorders
- drug abuse
twin studies of depression
estimate the heritability of depression in monozygotic twins at 40/50%
equifinality
the idea that multiple different causes or processes (e.g. genetic, environmental, or psychological factors) can lead to the same outcome, such as the development of depression
effect of the hypothalamic-pituitary-adrenal axis (HPA) for depression
norepinephrine, acetylcholine, serotonin, and GABA are mobilized in response to stress
- activates cortisol
stress diathesis model of depression
integrates environmental experiences (e.g. stressors), with genetic predisposition (diathesis)
stress theory of depression
emphasizes the role of a dysregulated HPA axis in depression
noradrenergic hypothesis
depression results from reduced norepinephrine (noradrenaline) activity
reserpine
a drug that depletes norepinephrine in the brain
- depletion leads to depressive symptoms that can be reversed by antidepressants
amphetamine
increases norepinephrine levels and produces a euphoric high
- increases monoamine levels
monoamine oxidase inhibitors (MAOIs)
among the first successful treatments for depression
- block the action of MAO, an enzyme that breaks down norepinephrine and other neurotransmitters
- increases availability of norepinephrine at the synapses
tricyclic antidepressants (TCAs)
work by inhibiting the reuptake of serotonin and norpinephrine into the presynaptic neuron
- increases the concentration of norepinephrine in the synapse, allowing it to exert its effects for a longer period of time
- tend to have more side effects than other types of antidepressants (dry mouth, blurred vision, constipation, and sedation)
alpha-2 autoreceptors
are on the presynaptic neurons and inhibit norepinephrine release when activated
- acted upon by drugs such as clonidine
- chronic use of antidepressants block these autoreceptors, reducing their inhibitory effect
serotonin hypothesis
proposes that low serotonin levels contribute to depression
- serotonin is critical for mood regulation
selective serotonin reuptake inhibitors (SSRIs)
work by preventing the reuptake of serotonin, thereby increasing its availability at the synapse
- e.g. fluoxetine (Prozac) and sertaline (Zoloft)
- relatively low side effects compared to TCAs
- may cause gastrointestinal disturbances or sleep issues
inflammation theory
suggests that elevated levels of pro-inflammatory cytokines are associated with depression
- inflammation in the brain can cause symptoms that resemble sickness behavior (fatigue, social withdrawal, loss of appetite)
neuroplasticity theory
links depression to reduced neuroplasticity (brain’s ability to adapts and reorganize
- in depression, levels of brain-derived neurotrophic factor (BDNF), a key protein involved in neuroplasticity, are lower
atypical antidepressants
include a variety of drugs that do not fit into other categories but are still effective in treating depression
- may target different neurotransmitter systems such as norepinephrine and dopamine (e.g. Bupropion)
selective norepinephrine reuptake inhibitors (SNRIs)
inhibit reuptake of both serotonin and norepinephrine
- used to treat depression, anxiety, and chronic pain
- e.g. venlafaxine (Effexor)
dual-action antidepressants
drugs that target both the serotonin and norepinephrine systems to increase their availability
- may include atypical antidepressants and SNRIs, targeting multiple neurotransmitter pathways to address symptoms of depression
lithium
primarily used in the treatment of bipolar disorder, particularly in management of manic episodes
- effective in reducing the frequency and severity of mania, but also used in combination with other antidepressants to treat the depressive phase
- increases serotonin and stabilizes mood through several mechanisms
electroconvulsive therapy (ECT)
a treatment for severe depression that has not responsed to other treatments
- involves inducing seizures through electrical stimulation of the brain
- can be very effective in treatment-resistant depression and severe cases
psychotherapy
cognitive behavioral therapy (CBT) and other therapeutic interventions are often used to treat depression
- helps patients identify and change negative thought patterns and behaviors that contribute to their depression
vagus nerve stimulaiton (VNS)
the stimulation of the vagus nerve with electrical impulses
- typically delivered through an implanted device
- used for treatment-resistant depression and has shown promise in reducing symptoms in some patients
light therapy
often used to treat seasonal affective disorder (SAD)
- patients are exposed to bright artificial light
- helps regulate mood by affecting the production of melatonin and serotonin
St. John’s wort (hypericum perforatum)
a herbal remedy often used as an alternative treatment for mild to moderate cases of depression
- thought to work by increasing serotonin levels
- still under debate
depression and co-occuring somatic disorders
depression is often associated with somatic illnesses (40-60% of depressed patients
- can reduce effectiveness of medical treatments
- 85% of patients with mild and 60% of patients with severe depression go unrecognized by primary care physicians (complaints are often not taken seriously leading to inadequate care)
psychosocial aspects to somatic conditions
patients deal with loss, trauma, limitations in self-care, work, and social or family life
- unpredictability of certain illnesses can increase likelihood of depression
psychobiological aspects to somatic conditions
depression can result from neurological damage, hormonal imbalances, or as a side effect of certain medications
conditions leading to increased risk of depression
conditions with eleveated cytokine levels, such as autoimmune diseases, chronic infections, obesity, diabetes mellitus, and cardiovascular disease increase the risk of depression
medications leading to increased risk of depression
medications for conditions such as hypertension, hormone treatments, and drugs such as alpha-interferon are known to contribute to the onset of depression
