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Psychopathology > Task 6 - Depression > Flashcards

Task 6 - Depression Flashcards

1
Q

DSM 5 - major depression

A

A) 5 or more symptoms during same 2 week period (at least one symptom is depressed mood or loss of interest/pleasure)

  • depressed mood
  • diminished interest/pleasure
  • weight loss, decreased/increased appetite
  • insomnia/hypersomnia
  • psychomotor agitation
  • fatigue/loss of energy
  • worthlessness/guilt
  • problems concentrating/thinking
  • thoughts about death/suicide

E) never been a manic or hypomanic episode

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2
Q

Prevalence depression

A
  • 16p in America
  • 3p in Japan
  • lowest in people over age 60
  • 2.5 of children
  • 8.3 of adolescents
  • 24 of youth will experience major depression before age 20
  • women: 2x more likely
  • people with major depression had spent an average of 16 weeks during previous years with symptoms
  • relapse: 75p
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3
Q

explanations why depression is lowest over age 60

A
  • less willing to report symptoms
  • often occurs in context of serious medical illness -> can interfere with diagnosis
  • more likely to have mild-severe cognitive impairment
  • depressive people are more likely to die before old age
  • more adapted coping skills -> psychological healthier
  • historical changes to vulnerability to depression
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4
Q

Genetic Factors depression

A
  • first degree relatives: 2/3 x more likely
  • depression begins early in life -> stronger genetic base
  • unclear if there are different genes in women/men responsible for depression
  • probably multiple genetic abnormalities contribute
  • example: seretonin transporter gene
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5
Q

Neurotransmitter theories depression

A
  • monoamines: norepinephrine, seretonin, dopamine
  • found in limbic system (sleep, appetite, emotional processes)
  • seretonin and norepinephrine are synthesized in neurons from tryptophan and tyrosine -> abnormalities in synthesis process
  • release process, which is regulated by seretonin transporter gene -> may be abnormal
  • receptors for seretonin and norepinephrine on post-synaptic neurons may be less sensitive
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6
Q

PFC abnormalities - depression

A
  • reduced metabolic activity
  • reduction in volume of gray matter, particularly left side
  • lower brain-wave activity left side
  • left PFC: motivation, goal orientation
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7
Q

Anterior cingulate - depression

A
  • subregion PFC
  • response to stress, emotional expression, social behavior
  • altered activity -> problems with attention and planning of response, coping
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8
Q

Hippocampus - depression

A
  • smaller volume
  • lower metabolic activity
  • many cortisol receptors
  • depressed people: high levels of cortisol -> kill/inhibit development of new neurons in Hippocampus
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9
Q

Amygdala - depression

A
  • increased activity

- direct attention to stimuli that are emotionally salient and have major significance for the individual

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10
Q

Neuroendocrine factors - depression

A
  • regulates hormones -> sleep, appetite, sexual drive, ability to experience pleasure
  • hormones also help to respond to environmental stressors
  • HPA axis -> active during stress, calms system down whens stress is over
  • > elevated levels of cortisol and coticotrophin-releasing hormone (CRH)
  • > hyperactivity of HPA axis
  • changes in ovarian hormones (estrogen, progesterone) -> affect seretonin and norepinephtine system
  • > could affect mood
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11
Q

Behavioral theories - depression

A

-life stress -> reduces positive reinforcers -> withdraw -> further reduction in reinforcers -> more withdrawal -> depression

-learned- helplessness theory:
uncontrollable negative event -> believe they are helpless to control -> lose motivation, reduce actions

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12
Q

Cognitive theories - depression , negative triad

A

-depressed people look through a negative triad: negative views about themselves, the world, the future -> ignore good events

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13
Q

cognitive theories depression - reformulated learned helplessness theory

A
  • role of causal attribution
  • > explain events by causes that are internal, stable, global, blame themselves
  • > experience long term learned helplessness deficits
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14
Q

cognitive theories- hopelessness depression

A

-making pessimistic attributions for most important events in their lives

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15
Q

cognitive theories depression - ruminative response styles theory

A
  • focus on process of thinking
  • focus intently on how they feel and identify many causes
  • > engage in rumination about their depression
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16
Q

cognitive theories depression - overgeneral memory

A
  • depressed people store memories in more general way (people are mean instead of jane was rude last friday)
  • > to cope with traumatic events
17
Q

interpersonal theory depression

A
  • interpersonal difficulties, losses -> triggering depression
  • rejection sensitivity
  • excessive reassurance seeking -> family and friends can become weary, frustrated, hostile
18
Q

sociocultural theory depression - cohort effects

A
  • historical changes put generations at higher risk
  • rapid changes in social values in 60s, disintegration of family unit
  • unrealistic high expectations for themselves
19
Q

sociocultural theory depression - gender differences

A

-men: turn to alcohol to cope, develop alcohol abuse

  • women:
  • ruminate about feelings, problems
  • more interpersonally oriented -> bad things happen to others or problems in relationships -> more depressive
  • base self-worth on health of their relationships
  • have less status and power -> more prejudice, discrimination, and violence
20
Q

sociocultural theory depression -ethnicity/ race differences

A
  • in US:
  • hispanics have higher prevalence -> might be due to higher rates of poverty, unemployment, discrimination
  • african americans: lower prevalance, but more anxiety disorders
21
Q

sociocultural theory depression - cross cultural differences

A

-lower levels in less industrialized and less modern countries

in modern countries:
-> fast-paced lifestyle, lack of stable social support and community values

-people in less modern cultures -> manifest depression through physical complaints rather than psychological symptoms

22
Q

Bipolar 1 DSM 5

A
  • necessary to meet criteria for manic episode (at least one)
  • major depressive episodes and hypomanic episodes possible but not necessary
23
Q

DSM 5 manic episode

A

A) -abnormally, persistent, elevated, expansive or irritable mood
and
-abnormally and persistent increased goal-directed activity or energy

B) during this, 3 or more are present: (4 or more if mood is only irritable)
1-inflated self-esteem/grandiosity
2-decreased need for sleep
3-more talkative, keep talking
4-flight of ideas/subjective experience that thoughts are racing
5-distractibility
6-increase in goal-directed activity or psychomotor agitation
7-excessive involvement in activities that have high potential for painful consequences

  • > must show this at least for 1 week
  • disturbance is sufficiently severe to cause marked impairment in social or occupational functioning or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features.
24
Q

Bipolar 2 - DSM 5

A

-necessary to meet criteria for current or past hypomanic episode
AND
current or past major depressive episode

-mania CANNOT be present for diagnosis

25
Q

Hypomanic - DSM 5

A

A) -abnormally and persistently elevated, expansive, or irritable mood

  • increased activity, energy
  • > 4 days

B) during this period, 3 or more (4 or more when mood is only irritable) 1-inflated self-esteem/grandiosity
2-decreased need for sleep
3-more talkative, keep talking
4-flight of ideas/subjective experience that thoughts are racing
5-distractibility
6-increase in goal-directed activity or psychomotor agitation
7-excessive involvement in activities that have high potential for painful consequences

-> same as bipolar 1

BUT: episode not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization. If there are psychotic features, the episode is, by definition, manic.

26
Q

Drug treatments for depression

A
  • drugs might have slow-emerging effects on neurotransmitter system and on action of genes that regulate neurotransmission, limbic system and stress response
  • reduce depression in 50-60p
  • better for treating severe and chronic depression
  • at least 6m after symptoms subsided, drugs should still be taken to prevent relapse
27
Q

selective seretonin reuptake inhibitors - depression and bipolar

A
  • fewer side effects
  • safer if taken in overdose
  • bipolar: may develop manic episodes
  • increase in suicidal thought and behavior (especially in children and adolescents) -> increased decision making
28
Q

selective seretonin-norepinephrine reuptake inhibitors

A
  • slight advantage over SSRIs

- > preventing relapse but more side effects

29
Q

Bupropion: norepinephrine- dopamine reuptake inhibitors

A
  • especially useful if suffering form psychomotor retardation, anhedonia, hypersomnia, cognitive slowing , inattention
  • overcomes sexual dysfunction side effects of SSRIs
30
Q

Triyclio antidepressants and monoamine oxidase inhibitors

A
  • increase levels of seretonin and norepinephrine

- but side effects too dangerous

31
Q

electroconvulsive therapy (ECT)

A
  • passing electric current of around 70- 130 volts through head of patient for around half a second
  • primarily used if severe depression and other treatment did not work well
  • effective short term effects
  • side effects: memory loss
  • normally delivered to right side of brain: less involved in learning and memory
  • relapse: 85p
32
Q

repetitive transcranial magnetic stimulation (rTMS)

A
  • exposes patient to repeated, high-intensity pulses
  • focused on particular structures
  • often left PFC
  • few side effects
  • one can stay awake
33
Q

vagues nerve stimulation

A
  • electrodes are attached to vagues nerve (ANS) that carries info to several areas of brain
  • results in increased activity in hypothalamus and amygdala
34
Q

deep brain stimulation

A
  • electrodes implanted in specific areas of brain
  • electrodes are connected to a pulse generator
  • placed under skin
  • > stimulates brain areas
35
Q

CBT - article Hundt results

A
  • depressive symptoms decreased while CBT skills use increased over time
  • increase in skill use -> predicted overall change in depression
  • > patients who used more skills -> higher decrease in depression symptoms
36
Q

premenstrual dysphoric disorder

A
  • increases stress during premenstrual phase of menstrual cycle
  • symptoms are often a mix between: depression, anxiety, tension, irritability and anger
  • mood swings
  • only 2p meet diagnostic criteria
37
Q

Article cowen - HPA axis

A
  • abnormal HPA axis -> vulnerability markers
  • > may be due to genetics and early adverse experiences
  • cortisol hypersecretion:
  • > inhibited Neurogenesis in Hippocampus
  • > hippocampal atrophy
  • > cognitive impairment
  • > declarative memory affected
  • > facilitates emotional memory
  • > recovered patients return to hyper secrete cortisol
38
Q

Article: lifestyle factors contributing to pathways associated with depression - Lopresti

A

1) Dysregulated inflammatory pathways (increased inflamation)
2) HPA disturbance (heightened cortisol secretion)
3) Increased oxidative and nitrosative damage
4) Neurotransmitter imbalances
5) Neuroprogression (neurogenesis and neural plasticity are compromised -> neuro degeneration)
6) mitochondira

39
Q

Article: lifestyle factors contributing to pathways associated with depression - Lopresti - 6 mechanisms

A

1) Dysregulated inflammatory pathways (increased inflamation)
2) HPA disturbance (heightened cortisol secretion)
3) Increased oxidative and nitrosative damage
4) Neurotransmitter imbalances
5) Neuroprogression (neurogenesis and neural plasticity are compromised -> neuro degeneration)
6) mitochondira

Psychopathology (15 decks)

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