Psychopathology - Bipolar & Depressive Disorders Flashcards

1
Q

What are the 3 Bipolar Disorders

A

The bipolar disorders include bipolar I disorder, bipolar II disorder, and cyclothymic disorder.

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2
Q

Diagnosis of bipolar I requires:

A

The diagnosis of bipolar I disorder requires at least one manic episode that may or may not have been preceded or followed by one or more major depressive or hypomanic episodes.

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3
Q

The diagnosis of bipolar II disorder requires:

A

At least one hypomanic episode and at least one major depressive episode.

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4
Q

The diagnosis of cyclothymic disorder requires

A

Numerous periods of hypomanic symptoms that do not meet the criteria for a hypomanic episode and numerous periods of depressive symptoms that do not meet the criteria for a major depressive episode.

The minimum duration of symptoms for cyclothymic disorder is two years for adults or one year for children and adolescents.

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5
Q

Etiology of Bipolar Disorder

A

Bipolar disorder has been linked to heredity, neurotransmitter and brain abnormalities, and circadian rhythm irregularities.

In terms of heredity, twin, family, and adoption studies have confirmed that bipolar disorder has a strong genetic component. For example, twin studies report concordance rates of .67 to 1.0 for monozygotic twins and about .20 for dizygotic twins (Dubovsky, Davies, & Dubovsky, 2003).

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6
Q

Neurotransmitters linked to bipolar disorder

A

norepinephrine,
serotonin,
dopamine,
and glutamate (Ayano, 2016)

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7
Q

Structural and functional abnormalities found in the brain (bipolar)

A

The prefrontal cortex, amygdala, hippocampus, and basal ganglia (Miklowitz & Johnson, 2014).

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8
Q

Circadian rhythm irregularities linked to bipolar disorder

A

Abnormalities in the sleep-wake cycle, the secretion of hormones, appetite, and core body temperature (Nusslock & Frank, 2012).

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9
Q

Differential Diagnosis of bipolar I and ADHD, and what are the shared symptoms?

A

It can be difficult to distinguish between bipolar I disorder and ADHD because they share several symptoms, including distractibility, irritability, and accelerated speech. Geller et al. (2002) propose that consideration of mania symptoms that do not overlap with symptoms of ADHD can help avoid over- or under-diagnosing bipolar disorder in children and adolescents. Their research found that the most manic-specific symptoms for youth 7 to 16 years of age were elation, grandiosity, flight of ideas/racing thoughts, decreased need for sleep, and hypersexuality (e.g., unusual interest in or preoccupation with sex, using sexually explicit sexual language, engaging in developmentally inappropriate sexual behavior).

With regard to adults, Salvi et al.’s (2021) review of the research found that manic episodes are typically characterized by a euphoric, elevated, or irritable mood; increased self-esteem or grandiosity; distractibility caused by thought acceleration; and a decreased need for sleep, usually without physical discomfort. In contrast, ADHD in adults is characterized by a labile, dysphoric mood; reduced self-esteem; distractibility due to wandering (but not acceleration) of thoughts; and fatigue and discomfort after a loss of sleep. Studies on sexuality generally confirm that increased sexual activity is common for adults experiencing manic episodes. However, research is inconsistent with regard to ADHD: The results of some studies suggest that adult ADHD is not associated with increased sexual activity but is associated with higher rates of sexual disorders and greater involvement in risky sexual behaviors (e.g., Barkley, Murphy, & Fisher, 2008; Soldati et al., 2020).

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10
Q

Psychosocial Interventions to treat Bipolar Disorder

A

Psychoeducation

Interpersonal and Social Rhythm Therapy

Cognitive-behavior therapy

Family-focused therapy (which is based on the assumption that high expressed emotion by family members can trigger relapse in the family member with this disorder).

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11
Q

Pharmacotherapy for Bipolar

A

Lithium is usually most effective for “classic bipolar disorder” which is characterized by a low likelihood of mixed mood states and rapid cycling, long periods of recovery between episodes, and an onset between 15 and 19 years of age.

In contrast, anticonvulsant drugs (e.g., carbamazepine, valproic acid) and second generation antipsychotic drugs are most effective for “atypical bipolar disorder,” which is characterized by mixed mood states, rapid cycling, a lack of full recovery between episodes, and an onset between 10 and 15 years of age (Aiken, 2018).

Note that the distinction between classic and atypical bipolar disorder is not a DSM-5-TR categorization and that DSM-5-TR provides the specifier “with atypical features” for bipolar disorder that involves mood reactivity and at least two of the following: significant weight gain or increase in appetite, hypersomnia, leaden paralysis, interpersonal rejection sensitivity.

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12
Q

What are the 4 Depressive Disorders

A

major depressive disorder, persistent depressive disorder,
disruptive mood dysregulation disorder.

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13
Q

The diagnosis of major depressive disorder requires

A

five or more symptoms of a major depressive episode for at least two weeks with at least one symptom being depressed mood or loss of interest or pleasure in most or all activities.

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14
Q

The diagnosis of persistent depressive disorder requires

A

a depressed mood with two or more characteristic symptoms (e.g., poor appetite or overeating, insomnia or hypersomnia, feelings of hopelessness) for at least two years in adults or one year in children and adolescents.

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15
Q

Diagnosis of disruptive mood dysregulation disorder requires

A

the presence for at least 12 months of (a) severe and recurrent temper outbursts that are verbal and/or behavioral, are grossly out of proportion to the situation or provocation, and occur three or more times each week; and (b) a persistently irritable or angry mood that is observable to others most of the day and nearly every day between outbursts.

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16
Q

What are the specifiers provided in DSM-5-TR for major depressive disorder

A

with peripartum onset
and with seasonal pattern

17
Q

The specifier with peripartum onset applies when:

A

The onset of symptoms occurs during pregnancy or the four weeks after delivery.

Up to 80% of women experience “baby blues” (sadness, irritability, anxiety) after the birth of their children, while a smaller percent experience symptoms that meet the criteria for MDD.

Of those who do develop MDD, about 50% experienced the symptoms prior to delivery.

18
Q

Prevention and treatment of peripartum depression

A

Cognitive-behavioral therapy and interpersonal therapy are evidence-based psychotherapies for the prevention and treatment of peripartum depression (e.g., O’Connor et al., 2019; Sockol, Epperson, & Barber, 2011).

Antidepressants (especially sertraline) are also effective, but several factors must be considered before they are prescribed including the potential negative effects for the developing fetus and newborns who are being breast fed and the impact of untreated maternal depression on both the woman and her child.

There is evidence that exercise reduces symptoms of peripartum depression, but the studies have produced inconsistent results about the magnitude of its effects due in part to differences in methodology: For example, the type of exercise varies from study to study, and some studies evaluate its effects as an adjunctive intervention while others have evaluated it as a stand-alone treatment. However, a meta-analysis of research comparing aerobic exercise alone to aerobic exercise with co-occurring interventions found that exercise alone had a non-significant beneficial effect on depressive symptoms, while exercise with co-interventions was significantly more effective than the co-interventions alone (Pritchett, Daley, & Jolly, 2017).

19
Q

The specifier with seasonal pattern applies when…

Also known as….

Linked to lower than normal levels of…

Higher than normal levels of…..

What is SAD responsive to?

A

When there’s a temporal relationship between mood episodes and time of year, which is usually winter.

This disorder is also known as seasonal affective disorder (SAD), and its symptoms include hypersomnia, overeating, weight gain, and a craving for carbohydrates.

It’s been linked to a lower-than-normal level of serotonin and a higher-than-normal level of melatonin, which is a hormone that plays an essential role in the sleep-wake cycle.

SAD is often responsive to phototherapy which involves exposure to bright light that suppresses the production of melatonin.

20
Q

Rates of depression for boys and girls

Developmental and physiological impacts

A

During childhood, the rates of depression are similar for boys and girls.

However, the rate for females increases in early adolescence while the rate for males remains fairly stable.

Explanations for this gender difference incorporate the impact of biological and psychological factors. For example, there’s evidence that the increase of hormonal levels at puberty sensitizes females but desensitizes males to the stress of negative life events (Allen, Barrett, Sheeber, & Davis, 2006).

The higher rate for females persists into adulthood, with female adolescents and adults having a rate that is 1.5 to 3 times higher than the rate for male adolescents and adults.

21
Q

What is the rate of female adolescents and adults with MDD compared to male adolescents and adolescents?

A

The higher rate for females persists into adulthood, with female adolescents and adults having a rate that is 1.5 to 3 times higher than the rate for male adolescents and adults.

22
Q

Etiology of Major Depressive Disorder

A

Major depressive disorder has been linked to heredity; neurotransmitter, hormone, and brain abnormalities; and cognitive and behavioral factors.

23
Q

Genetic components of MDD (twin, family, and adoption studies)

A

With regard to heredity, twin, family, and adoption studies have confirmed a genetic component. For example, Strakowski and Nelson (2015) found that concordance rates for unipolar depression obtained in high-quality twin studies ranged from about .30 to .50 for monozygotic twins and .20 to .30 for dizygotic twins. They also found that gender is one factor that accounts for variability in concordance rates, with rates being higher for female twins than male twins.

24
Q

Neurotransmitters related to depression

A

low levels of serotonin, dopamine, and norepinephrine

25
Q

Depression and the HPA axis

A

Depression has also been associated with abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis, which plays an important role in the body’s reaction to stress:

Exposure to chronic stress (especially early in life) has been found to lead to persistent hyperactivity of the HPA axis and hypersecretion of cortisol, the primary stress hormone, which are associated with an increased risk for depression (Nandam et al., 2020).

26
Q

Structural and functional abnormalities in the brain associated with depression

A

In addition, neuroimaging studies have linked depression to structural and functional abnormalities in the prefrontal cortex, cingulate cortex, hippocampus, caudate nucleus, putamen, amygdala, thalamus, and several other areas of the brain (e.g., Pandya, Altinay, Malone, & Anand, 2012).

27
Q

Prefrontal cortex and depression

A

With regard to the prefrontal cortex, the studies have found that depression is associated with abnormally high levels of activity in the ventromedial prefrontal cortex (vmPFC) and abnormally low levels of activity in the dorsolateral prefrontal cortex (dlPFC) and that remission of depressive symptoms in response to psychotherapy or an antidepressant is associated with the opposite pattern – i.e., to decreased activity in the vmPFC and increased activity in the dlPFC (Koenigs & Grafman, 2009).

28
Q

3 behavioral and cognitive explanations (theories and models) for MDD

A

Lewinsohn’s social reinforcement theory

Seligman’s learned helplessness model

Beck’s cognitive theory

29
Q

How does Lewinsohn’s social reinforcement theory describe depression?

A

Lewinsohn’s (1974) social reinforcement theory describes depression as the result of a low rate of response-contingent reinforcement for social behaviors due to a lack of reinforcement in the environment and/or poor social skills. This results in social isolation, low self-esteem, pessimism, and other characteristics of depression that, in turn, further decrease the likelihood of positive reinforcement in the future.

30
Q

How does Seligman’s learned helplessness model/hopelessness theory describe depression?

A

Seligman’s (1974) original version of the learned helplessness model links depression to repeated exposure to uncontrollable negative life events that results in a sense of helplessness, and a reformulated version stresses the role of a negative cognitive style that involves attributing negative life events to stable, internal, and global factors.

The most recent revision of the model (referred to as hopelessness theory) describes a sense of hopelessness as the proximal and sufficient cause of depression which, in turn, is the result of exposure to negative events and a negative cognitive style (Abramson, Metalsky, & Alloy, 1989).

31
Q

How does Beck’s cognitive theory describe depression?

A

Beck’s (1974) cognitive theory attributes depression to a negative cognitive triad that consists of negative thoughts about oneself, the world, and the future.

32
Q

Risk factors for younger adults for depression

A

For younger adults, the risk has been linked to genetics, stressful life events, and limitations in problem-solving and other cognitive abilities.

33
Q

Risk factors for older adults for depression

A

For older adults, chronic medical illness has been consistently identified as one of the strongest risk factors, especially when the illness decreases physical functioning and contributes to social isolation (Blazer & Hybels, 2005; Caine, Lyness, & King, 1993; Lyness & Caine, 2000).

34
Q
A