Task 6 - Depression Flashcards

1
Q

Symptoms of Depression

A
  • anhedonia: loss of interest in everything in life
  • psychomotor retardation: many people with depression are slowed down, talk more quietly, report feelings of being chronically fatigued
  • psychomotor agitation: feeling physically agitated, not being able to sit still, moving around, or fidgeting aimlessly
  • thoughts: worthlessness, guilt, hopelessness, suicide
  • trouble concentrating and making decisions
  • delusions and hallucinations
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2
Q

DSM-5 Criteria for Major Depressive Disorder

A

A Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure
1. Depressed mood most of the day, nearly every day, as indicated by either subjective report or observation made by others
2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day
3. Significant weight loss when not dieting or weight gain, or decrease or increase in appetite nearly every day
4. Insomnia or hypersomnia nearly every day
5. Psychomotor agitation or retardation nearly every day
6. Fatigue or loss of energy nearly every day
7. Feelings of worthlessness or excessive or inappropriate guilt nearly every day
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day
9. Recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or suicide attempt or a specific plan for committing suicide

E There has never been a manic episode or a hypomanic episode

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3
Q

Complicated Grief

A
  • 10-15% of bereaved people
  • strong yearning for the deceased person and preoccupation with the loss
  • difficulty accepting the finality of the loss
  • having a sense that life is empty and meaningless
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4
Q

Persistent depressive disorder

A
  • depressive mood for most of the day; for more days than not; for at least 2 years
  • presence of 2 + of: poor appetite, insomnia/hypersomnia, low energy or fatigue, low self-esteem, poor concentration, and hopelessness
  • no symptoms period never longer than 2 months
  • major depressive disorder for 2 years = persistent depressive disorder
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5
Q

Subtypes of depression

A
  • anxious distress: prominent anxiety symptoms as well as depressive symptoms
  • mixed features: meet the criteria for major depressive disorder and have at least three symptoms of mania, but do not meet the full criteria for a manic episode
  • melancholic features: physiological features of depression are particularly prominent; inability to experience pleasure, distinct depressed mood, depression regularly worse in morning, early morning awakening, marked psychomotor retardation or agitation, significant anorexia or weight loss, excessive guilt
  • psychotic features: experience delusions and hallucinations, either mood-congruent or mood-incongruent
  • catatonic features: display catatonia, ranging from a complete lack of movement to excited agitation; not actively relating to the environment, mutism, posturing, agitation, mimicking other’s speech or movements
  • atypical features: positive mood reactions to some events, significant weight gain or increase in appetite, hypersomnia, heavy or leaden feelings in arms or legs, long-standing pattern of sensitivity to interpersonal rejection
  • seasonal pattern: history of at least 2 years in which major depressive episodes occur during one season of the year (usually winter) and then remit when the season is over –> Seasonal Affective Disorder (SAD)
  • peripartum onset: onset of major depressive episode during pregnancy or in the 4 weeks following delivery
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6
Q

premenstrual dysmorphic disorder

A
  • significant increases in distress during the premenstrual phase of the menstrual cycle
  • depression, anxiety, tension, irritability and anger, which might occur in mood swings during the week before the onset of menses, improve once menses begin, and become minimal or absent in the week post-menses
  • 2% of women
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7
Q

Comorbidity

A
  • 70%
  • substance abuse
  • anxiety disorders
  • eating disorders
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8
Q

Prevalence

A
  • 3-16%
  • most prevalent in 18-29-year-olds
  • least prevalent in people 65+
  • rise among people at 85+ –> severe, chronic, debilitating
  • children tend to show irritability instead of sadness
  • women are 2x more likely as men to experience a depressive disorder
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9
Q

Causes: Genetic

A
  • first-degree relatives of people with major depressive disorder, are 2-3 times more likely to have depression themselves
  • abnormalities in the serotonin transporter gene –> dysfunctional regulation of serotonin
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10
Q

Causes: Neurotransmitter

A
  • limbic system –> regulation of sleep, appetite, and emotional processes
  • abnormal levels of serotonin and norepinephrine –> cognitive, behavioral, and motivational deficits
  • low dopamine –> deficits in reward system
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11
Q

Causes: 5-HTT Gene

A
  • the 5-HTT gene interacts with life events to predict depression symptoms, an increase in symptoms, depression diagnoses, new-onset diagnoses, and suicidality
  • individuals with one or two copies of the short allele of the 5-HTT promoter polymorphism exhibit more depressive symptoms, diagnosable depression, and suicidality in relation to stressful life events
  • gene-environment (G x E) interaction: an individual’s response to environmental insults is moderated by his or her genetic makeup
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12
Q

Causes: Structural and Brain Abnormalities

A

reduced metabolic activity and reduction in the volume of grey matter in the PFC (left side)
- motivational deficits

altered activity in the anterior cingulate
- problems in attention, planning, coping, and anhedonia

smaller volume and lower metabolic activity in the hippocampus
- chronic arousal of the body’s stress response
- bodies overreact to stress and levels of cortisol do not return to normal as quickly
- cortisol hypersecretion predisposes to depression
- neurotoxicity in the hippocampus

enlargement and increased activity in the amygdala
- rumination over negative memories and negative aspects of the environment

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13
Q

Causes: Neuroendocrine

A

Hypothalamic-pituitary-adrenal axis (HPA axis):
- involved in the fight-or-flight response
- elevated levels of cortisol and CRH –> chronic hyperactivity in the HPA axis
- difficulty in the HPA axis’ returning to normal functioning following a stressor
- excess hormones –> inhibiting effect on receptors for monoamine neurotransmitters
–> overreaction of the HPA axis to minor stressors later in life

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14
Q

Causes: Behavioral

A
  • life stress leads to depression as it reduces the positive reinforcers in a person’s life
  • once a person begins engaging in depressive behaviors, these behaviors are reinforced by the sympathy and attention they engender in others
  • learned helplessness theory = people believe they are helpless to control important outcomes in their environment, which leads to loss of motivation and reduction of actions that might control the environment, or leaving one unable to learn how to control situations that are controllable
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15
Q

Causes: Cognitive

A
  • negative cognitive triad = depressed people have negative views of themselves, the world, and the future
  • reformulated learned helplessness theory = cognitive factors might influence whether a person becomes helpless and depressed following a negative event
  • hopelessness depression = develops when people make pessimistic attributions for the most important events in their lives, and perceive that they have no way to cope with the consequences of these events
  • ruminative response styles theory = focuses on the process of thinking more than on the content of thinking as a contributor to depression
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16
Q

Causes: Interpersonal

A
  • chronic conflict in their relationships with family, friends, and co-workers
  • personal conflict –> deficits in social and communication skills
  • rejection sensitivity: heightened need for approval and expressions of support from others, but at the same time easily perceive rejection by others
17
Q

Causes: Sociocultural

A
  • cohort effects exist when people’s differences on some psychological variable depend on the era in which they were born and lived
  • gender differences: women are 2x as likely as men to suffer from depression –> sexual abuse, less power, more interpersonal, rumination about negative feelings
  • ethnicity/race differences: African Americans have lower rates of depression; Native Americans have extremely high rates; Asian Americans have lower rates
18
Q

Treatment: Biological

A

Antidepressant drugs have slow-emerging effects on intracellular processes in the neurotransmitter system, on the action of genes that regulate neurotransmission in the limbic system, and on the stress response
–> reduce depression in 50-60% of patients

19
Q

Treatment: Selective Serotonin Reuptake Inhibitors

A

SSRIs: positive effects on a wide range of symptoms that co-occur with depression (anxiety, impulsivity, etc.)
–> first choice treatment
–> block serotonin reuptake channels
–> side effects: gastrointestinal symptoms, tremors, nervousness, insomnia, diminished sex drive

20
Q

Treatment: Selective Serotonin-Norepinephrine Reuptake Inhibitors

A

SNRIs: influence neurotransmission
–> advantage over SSRIs - affect both neurotransmitters
–> broader array of side effects

21
Q

Treatment: Bupropion

A

Bupropion: norepinephrine-dopamine reuptake inhibitor
–> successful in treating people suffering from psychomotor retardation, anhedonia, hypersomnia, cognitive slowing, inattention, and craving

22
Q

Treatment: Tricyclic Antidepressants

A

Tricyclic Antidepressants: increasing levels of serotonin and norepinephrine
–> blocks reuptake channels
–> used less frequently because of severe side effects

23
Q

Treatment: Monoamine Oxidase Inhibitors (MAOIs)

A

Monoamine Oxidase is an enzyme that causes the breakdown of the monoamine neurotransmitters in the synapse
–> drugs inhibit the actions of monoamine oxidase
–> decrease the action of MAO and thereby increase the level of serotonin and norepinephrine in the synapse
–> affects all monoamine neurotransmitters
–> side effects: inability to consume certain foods/drinks, interact with several drugs

24
Q

Treatment: Electroconvulsive Therapy (ECT)

A
  • a brain seizure is induced by passing an electrical current through the patient’s head
  • results in decreases in metabolic activity in several brain areas, including frontal cortex and anterior cingulate
  • can lead to memory loss and difficulty learning new infromation
25
Q

Treatment: Newer Methods of Brain Stimulation

A

Repetitive Transcranial Magnetic Stimulation (TMS):
- repeated, high-intensity magnetic pulses
- left prefrontal cortex is targeted
- few side effects (minor headaches)

Vagus Nerve Stimulation (VNS):
- vagus nerve is stimulated by a small electronic device
- implanted under the patient’s skin in the left chest wall
- increased activity in hypothalamus and anygdala

Deep Brain Stimulation:
- electrodes are surgically implanted in specific areas of the brain
- these are connected to a pulse generator that is placed under the skin and stimulates these brain areas

26
Q

Treatment: Light Therapy

A
  • exposing people with seasonal affective disorder to bright light for a few hours each day during the winter months
  • reduces SAD by resetting circadian rhythms
  • decreasing levels of the hormone melatonin –> increases levels of norepinephrine and serotonin
27
Q

Treatment: Behavioral

A
  • increasing positive reinforcers and decreasing aversive experiences to change the patient’s patterns of interaction with the environment and others
28
Q

Treatment: Cognitive-Behavioral Therapy (CBT)

A
  1. help clients discover the negative automatic thoughts they habitually have and understand the link between those thoughts and their depression
  2. help clients challenge their negative thoughts –> help them consider alternative ways of thinking about a situation and the pros and cons of these alternatives
  3. help clients recognize deeper, basic beliefs or assumptions they might hold that are fueling their depression –> help the patient question such beliefs and decide if they truly want to base their lives on these
29
Q

Treatment: Interpersonal Therapy (IPT)

A

1) Help clients face losses of a loved one and explore their feelings about them, and help clients invest in new relationships
2) Help client recognize the interpersonal role dispute and guide them in making choices about what concessions might be made to the other person in the relationship
3) Role transitions –> Therapists help clients develop more realistic perspectives toward roles that are lost and learn to regard new roles in a more positive manner
4) Therapist reviews client’s past relationships, especially important childhood relationships, and helps them understand these relationships and how they might be affecting their current relationships and directly teach clients social skills

30
Q

Treatment: Ketamine

A

Ketamine produces rapid, profound, and surprisingly durable antidepressant effects
- a single dose
- peaked within 24-72 h
- reduced all symptoms of depression
- ketamine increases neuroplasticity despite blocking NMDS receptors
- disinhibits glutamate release
- long-term treatment