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A comprehensive set of flashcards covering key terms and definitions related to unipolar and bipolar disorders.
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Major Depressive Episode
A period of 2 or more weeks marked by: Depressed mood for majority of the day; Decrease in interest or enjoyment across most activities for the majority of the day. AND 3 or 4 depression related symptoms: weight/appetite change, sleep changes, motor movement agitated or decreased, fatigue/lethargy, feelings of worthless/guilt, reduced concentration/decisiveness, repeated focus on death or suicide/suicide plan/suicide attempt; significant distress or impairment
Unipolar depression
is a mood disorder characterized by major depressive episodes without a history of manic episodes, leading to persistent feelings of sadness and loss of interest.
For unipolar depressive disorders there should be no:
history of mania or hypomania (mild mania)
Major Depressive Disorder
A severe pattern of depression that is disabling and not caused by factors such as drugs or a general medical condition.
Major Depressive Disorder Clinical Descriptors:
Seasonal, catatonic, peripartum, melancholic
Seasonal MDD
Changes with season
Catatonic MDD
if it is marked by either immobility or excessive activity
Peripartum MDD
occurs during pregnancy or within four weeks after delivery, characterized by mood disturbances.
Melancholic MDD
if the person is almost totally unaffected by pleasurable events.
Persistent Depressive Disorder
A chronic disorder where a person experiences either major depressive episodes or mild depression called “dysthymic syndrome” for at least 2 years (with depressive symptoms not absent for more than 2 months)
Disruptive mood dysregulation disorder
persistent depressive symptoms and recurrent outbursts of severe temper
Reactive (exogenous) depression
a consequence of stressful life events
Endogenous depression
internal factors that may play a role in depression’s onset
What are the four classes of drugs?
MAO inhibitors, tricyclics drugs, 2nd generation antidepressants, and ketamine based drugs
Monoamine oxidase (MAO) Inhibitors
works by slowing down the body’s production of MAO; MAO breaks down norepinephrine, serotonin, and dopamine; MAO inhibitors stop this breakdown from occurring. This leads to a reduction of depressive symptoms since the neurotransmitters (NTs) implicated in depression are more available. However, they pose a potential danger: people who take MAO inhibitors experience a dangerous rise in blood pressure if they eat foods containing tyramine (e.g., aged cheese, over ripe bananas, red wine, fermented foods)
Tricyclics
believed to reduce depression by affecting NT reuptake. To prevent a NT from remaining in the synapse too long, a pump-like mechanism recaptures it and draws it back into the presynaptic neuron. This reuptake process appears to be too efficient in some people. Tricyclics block this reuptake process, thus increasing NT (norepinephrine and serotonin) activity in the synapse. Side-effects can include dry mouth, slight blurring of vision, constipation, problems passing urine, drowsiness, dizziness, weight gain, excessive sweating...
2nd generation antidepressants
structurally different than MAO inhibitors and tricyclics. Most of these are labeled selective serotonin reuptake inhibitors—drugs that increase serotonin activity specifically. This class includes fluoxetine (Prozac), sertraline (Zoloft), and escitalopram (Lexapro). Selective norepinephrine reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors are also available. These 2nd generation antidepressants generally have fewer side effects than the MAO inhibitors and tricyclics, but depending on the drug, they also may have some undesired effects (e.g., similar adverse effects as tricyclics including constipation/diarrhea, dizziness, weight gain, somnolence=strong desire to sleep, plus possible reduction in sex drive, headaches)
Ketamine-based drugs
Latest group of drugs. Ketamine is a short-acting anesthetic that gained notoriety as a party drug, “Special K”. Researchers discovered that ketamine provides depression relief quickly (e.g., matter of hours or a day/two days) relative to the other classes of antidepressants (10 days to 2 weeks). Initial studies of intravenous administration of ketamine were quite promising. A version that administers ketamine via a nasal spray was approved by the FDA in 2019. Ketamine-based treatments are often combined with other antidepressant medications because ketamine-based drugs produce only a short-term impact on depressive symptoms, become addictive over time, are expensive, and in some individuals, produce side effects such as confusion, dizziness, memory problems, feelings of depersonalization/derealization, and increases in blood pressure. Ketamine-based treatments seem to work by increasing activity of the neurotransmitter glutamate. Some evidence also suggests that ketamine fosters growth of new neural pathways in the brain’s depression-related circuit.
Drug therapy facts
may not work for at least 30% or more of clients with depression. Usually, the solution to medication failure is to prescribe a different drug rather than recommending psychotherapy/counseling or a combination of psychotherapy with drug therapy (stronger alternative
Electroconvulsive Therapy (ECT)
targeted electrical stimulation to cause a brain seizure. Clinicians are not quite sure why it works, but it seems to result in changes across the brain and possibly stimulates NT activity. Usual course of treatment is 6-12 sessions spaced over 2-4 weeks. Procedures have been modified in recent years to reduce some of the negative effects, e.g., patients are given muscle relaxants and anesthetics before and during the procedure. Some memory loss can occur. ECT can be effective—it is most effective when there is some type of maintenance therapy, either drugs or ECT, after initial treatments
Psychodynamic theory as a treatment of Unipolar Depression
Freud and his student, Karl Abraham, focused on unconscious grief over real or imagined losses. Later, object relations theorists proposed that depression results when people’s relationships leave them feeling unsafe and insecure. Research has shown links between early or major losses and later depression—although this is not always the case among individuals with depression. Interventions can consist of free association, dream interpretation, interpretation of transference and resistance, and other insight-oriented strategies. Research into the efficacy of this type of treatment has demonstrated limited success in the treatment of unipolar depression. Short-term psychodynamic approaches have achieved better treatment outcomes than traditional longer-term approaches
Cognitive-Behavioral as treatment for unipolar depression
Behavioral dimension of this model suggest that depression results from a decrease in positive rewards and increase in punishments that people receive. Intervention strategies are designed to decrease punishments and increase rewards from the environment: Example, Lewinsohn’s intervention is most effective when several or a combination of behavioral strategies are used such as: a) identify pleasant events and reintroduce them into a weekly schedule. Can utilize behavioral activation, b) teaching of new skills to reduce punishments, c) the increase of positive reinforcement. When combined with cognitive strategies, behavioral intervention seems to reduce depressive symptoms
Beck’s theory and intervention
maladaptive attitudes lead people to the cognitive triad; repeatedly viewing themselves, their experiences, and their future in negative ways that lead to depression. This triad combined with errors in thinking produce negative automatic thoughts. Interventions: Know the multiple steps that are often used to reduce depressive symptoms a) increase activities, b) examine and invalidate automatic thoughts, c) identify patterns of distorted thinking and negative biases d) alter primary attitudes (central beliefs).
Cognitive Triad
Individuals repeatedly interpret (1) their experiences, (2) themselves, and (3) their futures in negative ways, leading to depression
Martin Seligman
Learned helplessness theory of depression; The original theory is based on Seligman’s work with laboratory dogs— dogs that had been subjected to inescapable shock were later placed in a condition where they could escape the shock, but the dogs made no attempt to escape. Seligman theorized that the dogs had learned to be helpless— that there was nothing they could do to change their situation. This theory was REFORMULATED to an attribution helplessness theory (internal, global, and stable).
Learned Helplessness
Asserts that people become depressed when they think that they no longer have control over the reinforcements (or punishments) in their lives. This leads to a helpless state
Learned Helplessness Attributions Matter
Example: “It’s all my fault” [internal]. “I ruin everything I touch” [global], “and i always will” [stable].
If people make other kinds of attributions, this reaction is less likely
Example: “She had a role in this also” [external], “the way I’ve behaved the past couple weeks blew this relationship” [specific]. “I don’t know what got into me – I don’t usually act like that” [unstable]
Sociocultural Theories of Unipolar Depression
Depression occurs in an interpersonal context and clarifying and renegotiating this context is important for reducing depression. Interpersonal problem areas include interpersonal loss, interpersonal role dispute, interpersonal role transition, and interpersonal deficits
Family-Social Perspective of Unipolar Depression
Sociocultural theory that views depressed people as having ineffective social skills and poor communication
Unavailability of social support (people in troubled relationships are 25x more likely to have depression); isolation and lack of intimacy are more likely to become depressed.
Interpersonal Psychotherapy (IPT)
A therapy that addresses four interpersonal problem areas that may be leading to psychopathology: interpersonal losses, interpersonal role disputes, interpersonal role transitions, and interpersonal deficits
Manic Episode
Lasts at least one week, where a person displays an abnormally high or irritable mood and increased activity or energy for most of every day, and at least three other symptoms of mania. Symptoms of mania include: grandiosity, decreased need for sleep, increased talkativeness, rapid thoughts or flight of ideas, distractibility, heightened goal-directed activities (such as socializing, work, or sexual activity), and engaging in risky behaviors.
Bipolar Disorders
A disorder marked by alternating or intermixed periods of mania and depression.
Bipolar I Disorder
Characterized by the occurrence of a full manic episode, possibly preceded or followed by hypomanic or major depressive episodes.
Bipolar II Disorder
Presence or history of hypomanic (mild manic) episodes and major depressive episodes.
Rapid cycling
if a person experiences four or more episodes of mood disturbances (manic, hypomanic, or major depressive episodes) within a one year period.
Cyclothymic Disorder
A person experiences numerous episodes of hypomania and mild depressive symptoms, a diagnosis of cyclothymic disorder is made. Note: mild symptoms for greater than two years, interrupted by periods of normal mood that may only last for days or a few weeks. This disorder may eventually become bipolar I or bipolar II.
Treatments for Bipolar Disorder
Mood stabilizers, antipsychotic drugs, and adjunctive psychotherapy
Mood stabilizers
such as lithium (lithium carbonate) to treat bipolar disorder
Antiseizure drugs
lamotrigine (Lamictal), carbamazepine (Tegretol), divalproex sodium (Depakote) to treat bipolar disorder
Antipsychotic drugs
medications used to manage symptoms of bipolar disorder.
What are antidepressant drugs combined with sometimes?
antibipolar drugs in order to address depressive episodes (though effectiveness may be limited).
Adjunctive Psychotherapy
the illness, family and social relationships, and learning more effective coping strategies is often used