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PsyPath > Task 6 > Flashcards

Task 6 Flashcards

1
Q

What are the two major mood disoreders?

A
  1. Bipolar disorder

2. Depressive disorders

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2
Q

What is the prevalence for mood disorders?

A

Lifetime: 5.2% - 17.1%

–> Could go up to 20% for men and 30% for woman

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3
Q

Comobidity

A

Around 60% of people with depression also experience anxiety disorder

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4
Q

DSM-5 criteria for major depressive dirorder

A
  1. Five or more f the symptoms have to be pressent during same 2-week period. At least one of the symptoms has to be depressed mood or loss of interest or pleasure
  2. Symptoms cause clinically significant distress or impairment in scoial, etc areas of functioning
  3. Not attributable to physiological effects of substances or medication
  4. Cannot be better explained by schizophrenia spectrum disorders or psychotic disorders
  5. There has never been a manic or hypomanic episode.
    - -> this one doesn’t apply if the episodes appear during effects of substance
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5
Q

What is Persistent Depressive Disorder?

A

When individual meets diagnostic criteria for major depressive disorder for 2 years
–> Diagnosis requires: poor appetite, insomnia/hypersomnia, low energy, lo self esteem, poor concentration, hopelessmess

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6
Q

DSM-­‐5 criteria determine when to diagnose major depressive episode, but depression can take many forms/subtypes.

Name them

A
  • Anxious distress
  • Mixed features –> presence of at least 3 manic/hypomanic symptoms but doesn’t meet criteria
  • Melancholic features
  • Psychotic features
  • Catatonic features
  • Atypical features
  • Seasonal pattern SAD (e.g. depressive episode during winter)
  • Peripatum onset (during pregnancy or in the 4 weeks after delivery)
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7
Q

What are the melancholic features?

A

Inabilityto experience pleasure, distinct depressedmood,depression regularlyworse in morning, early morningawakening, marked psychomotorretardation or agitation, significant anorexiaor weight loss, excessive guilt.

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8
Q

What are the psychotic features?

A

Presence of mood-congruent or mood-incongruent delucions or hallucinations

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9
Q

What are the catatonic features?

A

Behaviors: not relating to environment, mutism, posturing, agitation, mimicking another’s speech or movements (remember the Joker)

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10
Q

What is the Premenstrual dysphoric disorder?

considered a separate disorder in DSM-5

A

Increasesin distress during premenstrual phase of menstrual cycle that some womentend toexperience. Symptoms are often a mixture of depression, anxiety and tension,irritability and anger. These may occurinmood swings, the weekbefore onsetof period. Many women experience this mildly, with only2% meetingthe diagnostic criteria.

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11
Q

What do the Biological theories of depressions include?

A

Genetics, NT systems, and functional abnormalities in brain and neuroendocrine systems

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12
Q

Genetic factors

A
  • If one of your papis had MD then your are 2-3 times more likely to have it
  • MJ that appears early in life has stronger genetic base
  • Serotonin transporter gene abonormalities
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13
Q

Neurotransmitter theories (1)

A
  1. Sero, nore, and dopa are found in the limbic system, which is associated w/ regulation of sleep, appetite amd emotional processes
    • Low serotonin and norepinephrine may account for cognitive, behavioral and motivational deficits
    • Low dopamine levels may be responsible for deficits in rewards system –> makes them unmotivated
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14
Q

Neurotransmitter theories (2)

A
  1. Sero and nore are released by presypnaptic neuron and then bind to receptors on other neurons. This release process (regulated by serotonin trnasporter gene) may be abnormal in depression.
    Or receptors may be less sensitive than normal or malfunction
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15
Q

Neuroendocrine system theory

A

Lack of inhibitory control over the Hypothalamic-Pituitary-Adrenocortical (HPA) network is associated with depression since this system manages and reacts to stress and triggers secretion of cortisol in response to it.

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16
Q

What does the article from Cowel explain about HPA axis and depression?

A

It was proven that there is a established link between Cortisol hypersecretion and depression.

—> the elevated secretion of cortisol was also found in patients who recovered from depression —> this suggest that some aspects HPA axis abnormalities are more persistent and may be present before onset of illness (due to genetic factors or adverse experiences)

Also found in people not depressed so it has to do more with VULNERABILITY

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17
Q

If cortisol hypersecretion predisposes to depression, what is the mechanism?

A
  1. Neurogenesis (especially in hippocampus) is inhibited by excessive cortisol which leads to hippocampus atrophy —> cognitive impairments in declarative memory
  2. Cortisol may also facilitate emotional memory (more research needed)
20
Q

Structural and functional brain abnormalities

A

—> Decreased activation in PFC which results in failure to anticipate incentives - therefore no means to achieve goals
—> Decreased activation in ACC May reflect in deficit in ‘will to change’
—> Deficits in functioning of hippocampus may result in individual dissociating affective response rom relevant contexts (feel sadness in happy context)
—> Increased activation in amygdala may lead to interpreting threatening info negatively

21
Q

Behavioral theories to depression

A

Up to 80% of people with depression report a negative life event prior to onset of depression

  • Behavioral theories argue that it results from lack of appropriate reinforcement for positive and constructive behaviors. This leads to behavioral vacuum = person becomes inactive and withdrawn.
  • Learned helplessness theory
22
Q

Cognitive theories to depression

A
  1. Negative cognitive triad theory (Beck)
  2. Reformulated learned helplessness theory/Attribution theory
  3. Hopelessness theory
  4. Rumination theory
23
Q

Negative cognitive triad theory (Beck)

A

Negative views in self, world and future. Ignore good events and exaggerating negative ones.

24
Q

Reformulated learned helplessness theory/Attributional theory

A

They become depressed when they attribute negative life events to factors that cannot be controlled or are unlikely to change. They attribute negative events to internal, stable and global factors.

25
Q

Hopelessness theory

A

Develops when make pessimistic attributions about important events and perceive that they cannot cope with consequences.

26
Q

Rumination theory

A

Suggests that rumination (reflexion, meditation) predicts onset of depressive episodes, as well as relapses.

27
Q

Interpersonal theories for depression

A
  1. Depressed people are more likely to have chronic conflict with family, friends and colleagues
  2. Rejection sensitivity
  3. Parent-child interaction - having close relationship/ high-quality relationships can protect against maladaptive coping patterns
28
Q

What is rejection sensitivity?

A

Some depressed people have heightened need for approval and expressions of support from others, but a the same time they easily perceive rejection by other. Therefore, they always look for reassurance. This excessive reassurance seeking can lead to withdrawal of social support, leading to increased and longer depression.

29
Q

Sociocultural theories for depression

A
  1. Cohort effects: two explanations to why recent generations are at higher risk of having depression
    —> rapid changes in social values in the 60s, as well as to disintegration of family unit (more divorces?)
    —> younger generations have unrealistically high expectations for themselves (do not reach them so depression)
  2. Gender differences: women are twice as likely to get it as men - could be due to coping strategies women engage in or to gender socialization
30
Q

Biological therapies for depression

A
  1. Drug therapy
  2. Electro-compulsive therapy ECT
  3. Brain stimulation
  4. Light therapy
31
Q

Drug therapy

A
  • Tricyclic drugs (60-65% show improvement)and MAOIs (50%) increase levels of both serotonin and norepinephrine
  • SSRIs = serotonin re-uptake inhibitors —> fewer side effects but may be increase risk of suicide

RELAPSE IS COMMON AFTER DRUG TREATMENT HAS BEEN STOPPED

32
Q

ECT

A

Involves passing electric current through the head of the patient for around half a second

—> Used when other treatments don’t work
—> Provide effective short term effects but memory loss as side effect

33
Q

Brain stimulation

A
  • rTMS
  • Vagus nerve (ANS) stimulation: electrodes implanted to vagus nerve that carries info to brain areas
  • Deep brain stimulation: electrodes are implanted deep in the brain and connected to pulse generator placed under skin, which delivers stimulation to targeted brain areas
34
Q

Light therapy

A

People with SAD may have deficient retinal sensitivity to light —> exposing them to bright light for a few hours each day during winter can significantly reduce some symptoms

35
Q

Explanation of light therapy

A

It resets circadian rhythms, thereby normalizing production of hormones and NTs

36
Q

Psychological treatments to depression

A
  • Behavioral Therapy: increasing reinforces & decreasing aversive experiences in person’s life by changing their patterns of interaction with environment and other people
  • CBT —> brief and time limited 6-12 weeks
  • Interpersonal Therapy to deal with grievance or loss, role disputes, role transitions and deficits in interpersonal skills
37
Q

Is there attention and perception bias towards negative info in depressed people?

A

There is not a perception bias to negative information but once paying attention to it, it is harder for them to disengage from it

38
Q

Do depressed people display memory bias for negative information?

A

Yeh

And the negative memories are more accessible even after effective CBT

39
Q

What does cognitive control have to do with depression?

A

Depression involves difficulties in keeping irrelevant emotional info from WM and is also associated with difficulties removing previously relevant negative material from WM

40
Q

Does CBT work? (Hundt)

A

Yes, depression symptoms decrease after therapy and if skills learned were more frequently used in patient’s natural setting them it could predict the outcome of the CBT treatment

41
Q

Research on depression has confirmed that it is caused by a lot of factors. Which are these and how do they influence depression?

A

Diet, exercise and sleep.

It’s a bidirectional relationship between depression and these lifestyle factors, thereby creating a cycle of influence

42
Q

Bdnf

A

Brain derived…

PsyPath (10 decks)

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