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PSYC 300A > OCD & Mood Disorders > Flashcards

OCD & Mood Disorders Flashcards

1
Q

What are obsessions?

A

ego-dystonic and recurring thoughts, images, and impulses that can be accompanied with compulsive behaviors; necessary in OCD

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2
Q

Ego-dystonic

A

meaning intrusive, unwanted, foreign, and inconsistent with one’s values and beliefs

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3
Q

Common themes in obsessions

A

contamination, aggression, violence, religion, sexuality, order

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4
Q

What are compulsions?

A

a repetitive behavior or mental act that the person feels driven to perform to neutralize the obsessions, prevent some dreaded event or situation, and provide relief

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5
Q

How are compulsions related to obsessions?

A

functionally but not necessarily logically

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6
Q

What are the 5 associated features of compulsions?

A

mental rituals, fluctuating insight, family involvement, avoidance of objects that prompt obsessions, continuous reassurance-seeking

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7
Q

Fluctuating insight

A

recognizing that one’s behavior doesn’t make sense from time to time; doesn’t apply to kids

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8
Q

Lifetime prevalence of OCD

A

3% for everyone (no sex/ethnic differences)

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9
Q

Onset and course of OCD

A

onset is typically during early adolescence or adulthood but can be earlier; often chronic with only ~40% seeking treatment and most having multiple obsessions

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10
Q

What disorders are comorbid with OCD?

A

anxiety, mood disorders, depression (in 80% of cases)

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11
Q

Biological factors of OCD

A

moderately heritable, associated with a lack of serotonin or 5-HT, structural and functional brain abnormalities

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12
Q

How do SSRIs affect OCD?

A

they increase serotonin, which reduces the emotional force (i.e. intensity or urgency) of obsessions and decreases anxiety

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13
Q

Brain abnormalities causing OCD

A

slight structural abnormalities in the basal ganglia (responsible for motor control, learning, and reward processes); higher metabolic levels or more activity in other parts of the brain (e.g. thalamus for cleaning and checking)

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14
Q

Psychological factors of OCD

A

higher attention to disturbing material relevant to the obsessions, thought-action fusion, self-blame, attempts to suppress thoughts increase them, conditioning (behavioral theory)

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15
Q

Thought-action fusion

A

believing that the mere thought of a bad action or event will influence them happening

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16
Q

How does the behavioral theory explain OCD?

A

(1) the initial fear or obsession is classically conditioned; (2) compulsions negatively reinforce obsessions through operant conditioning; (3) the stimulus or feared object is generalized into a broader category

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17
Q

Social factors of OCD

A

social reinforcement or accomodation of obsessions (e.g. telling the person with OCD to avoid the feared object or removing it from their surroundings)

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18
Q
A
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19
Q

Orbitofrontal cortex

A

responsible for the role of emotion in reward/punishment anticipation

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20
Q

How do people with OCD experience over-importance of thoughts?

A

believing it’s possible and necessary to control their thoughts; cognitive distortions (e.g. catastrophic thinking) that are neutralized by doing compulsions; thought-action fusion

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21
Q

Biological symptoms of OCD

A

increased activity in the basal ganglia (associated with severity of OCD) and orbitofrontal cortex (OFC)

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22
Q

Psychological presentation of OCD

A

over-importance of thoughts, overestimation of threat (an inflated sense of personal responsibility), perfectionism (doing compulsions perfectly), intolerance of uncertainty

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23
Q

4 kinds of cognitive distortions

A

black and white thinking, catastrophizing, threat overestimation, mind-reading

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24
Q

Social presentation of OCD

A

the content of obsessions and whether or not OCD is deemed a problem that needs to be treated depends on one’s culture

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25
Q

Basal ganglia

A

responsible for the control of motor behavior, learning and reward

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26
Q

Biological treatment of OCD

A

antidepressants like SSRIs or cingulotomy or surgical correction for extreme cases

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27
Q

Defining feature of mood disorders

A

extremes of emotion

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28
Q

Cingulum

A

responsible for limbic system communication; emotional force is decreased when it’s removed through cingulotomy

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29
Q

Psychological treatment of OCD

A

behaviorally through exposure and response prevention or ERP (reduces compulsions); cognitively by challenging maladaptive thinking patterns

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30
Q

Social treatment of OCD

A

behavioral change in family/support system by stopping accomodation and gradual/low-intensity exposure to feared object

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31
Q

3 kinds of unipolar depressive disorders

A

major depressive disorder (MDD), chronic/persistent depressive disorder (PDD), double depression

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32
Q

Extreme emotions experienced in depression and mania

A

profound sadness and dejection in depression; intense and unfounded elation in mania

33
Q

2 types of mood disorders

A

unipolar (only depressive episodes) and bipolar (depressive and manic episodes)

34
Q

2 main features of major depressive disorder

A

sad/depressed mood (low 5-HT)and loss of interest/pleasure (low dopamine); need at least 1

35
Q

Accompanying features of MDD

A

sleep difficulties, lethargy or agitation, psychomotor retardation (low NE), appetite problems and weight fluctuations, loss of sexual desire, extreme fatigue, unfounded feelings of worthlessness and guilt (low 5-HT), difficulty concentrating, recurrent thoughts of death or suicide (low 5-HT)

36
Q

Prevalence of MDD

A

~11% lifetime prevalence and ~4.5% 1-year prevalence with a sex ratio of 2:1 (women:men)

37
Q

How many depressive episodes do people with MDD experience and for how long?

A

~80% experience more than 1 episode with an average number of 4 episodes and an average duration of 3-5 months (12% of episodes last more than 2 years)

38
Q

Kindling hypothesis

A

each episode makes you more likely to have another one

39
Q

Persistent depressive disorder (PDD)

A

chronic low-grade depression lasting for at least 2 years (average duration of 4-5 years) with intermittent normal moods

40
Q

Double depression

A

when major depressive episodes are superimposed on PDD

41
Q

Biological factors of MDD

A

~35% heritability with 3x higher risk of development when 1st degree relatives have MDD and as a reaction to high levels of stress; dysfunctional serotonin

42
Q

Heritability

A

estimate of the likelihood of a disorder happening based on genes; not causal

43
Q

How is dysfunctional serotonin associated with MDD?

A

linked to one’s temperament (neuroticism); makes a person hyperresponsive to aversive stimuli and stress, increasing vulnerability for anxiety (as a diathesis or risk factor) and depression

44
Q

Permissive theory

A

serotonin regulates other neurotransmitters (e.g. NE and DA) so when it’s dysfunctional, NE and DA become dysfunctional too

45
Q

Norepinephrine and dopamine levels during mania vs during depression

A

high NE and DA in mania; low NE and DA in depression

46
Q

Biological mystery on effect of SSRIs on MDD

A

giving someone SSRIs increases serotonin (a biological shift) and neurotransmitters eventually return to homeostasis BUT before symptoms (e.g. mood) improve

47
Q

In what cases of MDD are low metabolite or serotonin levels found?

A

more often found in those who have suicidal ideation and behavior, not in those with severe depression

48
Q

Effect of alleles of the 5-HTT (serotonin reuptake) gene on depression

A

short or “s” allele lowers 5-HT function and is more likely to lead to depression; long or “l” gene is less likely to lead to depression

49
Q

Effect of stress on the relapse of depression

A

high cortisol levels result in a high risk of relapse and eventually, after 4-5 episodes, a depressive episode occurs even without the experience of a stressful event

50
Q

Changes in brain activity during depression

A

decreased activity in left PFC and anterior cingulate cortex (ACC), increased activity in right PFC and amygdala

51
Q

Left PFC

A

responsible for approach behavior, emotion regulation, and turning off the amygdala alarm

52
Q

Right PFC

A

responsible for the avoid behavior, inhibition, and negative thinking

53
Q

Psychological factors of MDD

A

beck’s cognitive theory, negative cognitive triad, helplessness and hopelessness theory

54
Q

Beck’s cognitive theory

A

recurring cycle between negative interpretations of situations/events and feelings of depression

55
Q

Evidence of beck’s cognitive theory

A

people with depression are primed to think negatively, lack a positivity bias, and have greater accessibility of negative content

56
Q

Negative cognitive triad

A

having negative views about oneself, the world, and one’s future

57
Q

Helplessness theory

A

experiencing an uncontrollable event leads to attributions, which leads to learned helplessness, then emerging depression

58
Q

Depressive/pessimistic attributional style in learned helplessness

A

making internal (blaming oneself), stable (long-lasting effect), and global (wide-ranging effect) attributions to negative outcomes

59
Q

Hopelessness theory

A

experiencing an uncontrollable event leads to attributions or other cognitive factors, a sense of hopelessness, then emerging depression

60
Q

How does the hopelessness theory explain the comorbidity between anxiety and depression?

A

while helplessness leads to anxiety, persistent helplessness and hopelessness leads to depression

61
Q

Difference between helplessness and hopelessness theories

A

helplessness theory only has 1 diathesis (a pessimistic attributional style) but hopelessness theory has 2 diatheses (a pessimistic attributional style and a state of hopelessness)

62
Q

Psychoanalytical theory (Freud)

A

depression is anger turned inward

63
Q

Why do more women experience depression (2:1 ratio)?

A

higher cortisol levels, tendency for rumination, greater emotional importance of interpersonal relationship, exposure to traumatic events/chronic negative events (e.g. sexual harassment)

64
Q

Rumination

A

unproductive, repetitive, and passive focus on distress and its possible causes/consequences

65
Q

Social factors of depression

A

people who are depressed have a negative effect on others (e.g. become irritable) and alienate themselves from their social support network

66
Q

Evidence for interpersonal theories of depression

A

people who are depressed tend to have limited social networks and fewer positive social behaviors, initially elicit sympathy and care then hostility and rejection, be insecure in relationships

67
Q

Biological treatments for depression

A

pharmacotherapy (e.g. MAOIs, tricyclics, SSRIs, SNRIs) and light therapy

68
Q

How long does pharmacotherapy take to work?

A

3-5 weeks

69
Q

Light therapy

A

exposure to a certain amount of full spectrum light at certain times of day; typically used for seasonal depression

70
Q

Biological treatments for treatment-resistant depression

A

ECT, TMS, ketamine through IV

71
Q

Potential benefit and risk of ECT on depression

A

works quickly when it works but may cause brain fog (confusion and memory loss)

72
Q

Potential benefit and risk of TMS on depression

A

non-invasive and less intense than ECT but still relatively new in use

73
Q

Potential benefit and risk of ketamine on depression

A

works quickly (blocks NMDA receptors and reduces inflammation) but mechanisms and long-term effects are unclear

74
Q

ECT vs TMS

A

electric current induces a seizure; magnetic stimulation in parts of the brain

75
Q

Psychological treatment of depression

A

psychodynamic therapy focused on the importance of early loss and one’s attachment to their mother/parent, CBT

76
Q

Primary vs secondary control in CBT

A

taking action to change a situation if you have control over it; changing the way you perceive a situation if you have no control over it

77
Q

What is the gold standard treatment for depression?

A

behavioral treatment or behavioral activation

78
Q

Behavioral activation

A

doing activities that are worth exerting your energy in (e.g. those that give you pleasure and increase your sense of mastery)

79
Q

Social treatment for depression

A

interpersonal therapy, family and marital therapy

PSYC 300A (11 decks)

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