Sectional 2 Exam Flashcards
Identify the symptoms of a Major Depressive Episode.
At least 5 of the following symptoms (sxs) (at least 1 of which must be ):
1. Depressed Mood
2. Anhedonia* (loss of interest or pleasure in normally enjoyed activities)
3. Significant decrease/increase in appetite or weight
4. Insomnia or hypersomnia (changes in sleep)
5. Psychomotor agitation or retardation (changes in speed of motor movements)
6. Fatigue or loss of energy
7. Feelings of worthlessness or excessive/inappropriate guilt
8. Problems concentrating, or indecisiveness
9. Recurrent thoughts of death or suicide
- Symptoms must be present together, most of the day, nearly every day, for at least 2 weeks
- Symptoms must represent a marked change
Distinguish between and explain the key features of a Major Depressive Episode, Major Depressive Disorder (MDD), and Persistent Depressive Disorder (PDD).
Major Depressive Episode:
At least 5 of the following symptoms (sxs) (at least 1 of which must be ):
1. Depressed Mood
2. Anhedonia* (loss of interest or pleasure in normally enjoyed activities)
3. Significant decrease/increase in appetite or weight
4. Insomnia or hypersomnia (changes in sleep)
5. Psychomotor agitation or retardation (changes in speed of motor movements)
6. Fatigue or loss of energy
7. Feelings of worthlessness or excessive/inappropriate guilt
8. Problems concentrating, or indecisiveness
9. Recurrent thoughts of death or suicide
- Symptoms must be present together, most of the day, nearly every day, for at least 2 weeks
- Symptoms must represent a marked change
Major Depressive Disorder:
A) Presence of a major depressive episode
B) Not better accounted for by another disorder
C) No history of a manic, mixed or hypomanic episode
D) Distress and/or impairment
Persistent Depressive Disorder:
Key difference from MDD: PDD is more chronic (longer lasting) (can be less severe than MDE’s)
At least 3 of the following (1 of which must be ) symptoms most of the day, more days than not, for at least 2 years:
1. Depressed mood
2. Decrease/increase in appetite
3. Sleep problems
4. Low Energy
5. Low self-esteem
6. Problems concentrating
7. Feelings of hopelessness
A) In addition to experiencing the symptoms (for at least 2 years) described on the previous slide…
B) Not better accounted for by another disorder
C) No history of a manic, mixed or hypomanic episode
D) Distress and/or impairment
Key feature: frequency and duration of depressed mood
MDE: almost all day, nearly every day
PDD: more than half the day, more than half of the days
Identify the prevalence of MDD and PDD and describe sex and age differences in MDD.
MDD: 1 in 6 (~16% experience MDE in lifetime)
Untreated: 4-9 months on average
25-50% single episode, 50-75% recurrent
Severity: Longer MDEs, shorter OK periods, presence of sxs between episodes
Twice as common in women as in men (see Girgus & Yang, 2015)
Much more likely in LGBTQ+ populations (see Marshal et al., 2011)
Leading cause of disease burden (e.g. loss of productivity)
PDD: 1 in 20
Untreated: 30 years on average
Depressive Disorders (Rank of how liking depending on Ethnicity, least to most likely):
White, Hispanic, Black, American Indian
Depressive Disorders (Rank of how liking depending on Age, least to most likely):
Highest in: 15-29
Lowest: 65-84
Rise in: 85+
Explain how genes and environment interact to increase risk of depression.
Family Studies
- First-degree relatives of people with MDD –> 3-4x more likely to also have depression
Twin Studies
- Higher concordance in mono than dizygotic twins
L/L = 2 long alleles
S/L = 1 short allele, 1 long allele
S/S = 2 short alleles
With the number of stressful life events and S/S alleles it increased probability of MDE significantly
Identify neurotransmitters, brain structures, and neuroendocrine factors implicated in depression.
- Serotonin
- Norepinephrine
- Dopamine
- Potential processes of neurotransmitter dysfunction:
–Production (synthesis)
–Release
–Reception
Prefrontal cortex (motivation, goal orientation): ↓ volume, ↓ activation
Anterior cingulate (attention, coping with stress): ↓ volume, ↑ activation
Amygdala (attention): ↑ volume, ↑ activation
Hippocampus (learning and memory): ↓ volume, ↓ activation
Neuroendocrine Factors:
Hypothalamic-Pituitary-Adrenal (HPA) Axis
– Involved in fight or flight responses and release of stress hormones
In depression – chronic hyperactivity (↑) of HPA axis & elevated (↑) levels of cortisol
– Possibly involved in damage to hippocampus
Explain how abnormalities in neurotransmitters, brain structure, and HPA axis functioning relate to depressive symptoms.
Abnormalities in Serotonin Transporter Gene –> not enough serotonin –> impact mood stability
Prefrontal cortex (motivation, goal orientation): ↓ volume, ↓ activation
Anterior cingulate (attention, coping with stress): ↓ volume, ↑ activation
Amygdala (attention): ↑ volume, ↑ activation
Hippocampus (learning and memory): ↓ volume, ↓ activation
(HPA Axis) In depression – chronic hyperactivity (↑) of HPA axis & elevated (↑) levels of cortisol
Name the four classes of drug treatments for MDD.
Selective serotonin reuptake inhibitors (SSRIs) – Prozac, Zoloft
Selective serotonin & norepinephrine reuptake inhibitors (SSNRIs) – Cymbalta, Effexor
Monoamine oxidase inhibitors (MAOIs) – Nardil, Emsam
Tricyclic antidepressants – Amitriptyline, Norpramine
Identify biological treatments for treatment-resistant MDD.
- For treatment-resistant depression:
Electroconvulsive therapy (ECT) (brief seizures)
– Pros: pretty good at treating very severe depression
– Cons: learning and memory difficulty; high relapse rate - Repetitive transcranial magnetic stimulation (rTMS) (noninvasive brain stimulation with electromagnet)
- Ketamine
Explain behavioral theories of depression (incl. role of stressful events, reduced reinforcers, behavioral withdrawal).
Depression arises as a reaction to stressful negative event(s), and is maintained by behaviors
- Diathesis-stress model!
- ~80% negative life event before onset of depression
- History of traumatic life events common
- Chronic life stressors
Depression involves interaction between reduced positive reinforcers & behavioral withdrawal
- Self-perpetuating cycle!
- e.g. difficulties w/romantic partner -> avoid conversations with partner -> fewer positive interactions with partner -> worsening relationship -> increased withdrawal, etc.
e.g. do poorly on exam -> stop studying -> do poorly on exam -> stop attending class -> do poorly on exam, etc.
Describe cognitive theories of depression (incl. cognitive triad, cognitive errors, causal attributions).
Inaccurate (often negative, automatic) thoughts (maladaptive attitudes)
Negative Cognitive Triad (Beck, 1967):
- The Self: “I’m ugly”
- The World: “no one loves me”
- The Future: “I’m hopeless because things will always stay this way”
Inaccurate thoughts maintained by cognitive errors:
1. Black-and-white thinking
2. Fortune-telling
3. Mind-reading
4. Discounting the positive
Causal attributions:
Didn’t get a promotion
- Internal: “It’s my fault.”
- Stable: “I’ll never be worthy of a promotion.”
- Global: “I’m not good enough at anything.”
someone perceives that a punishment or negative event is inevitable and out of their control, they learn to endure it.
Describe the cognitive-behavioral learned helplessness theory.
Depression happens when people feel unable to control/impact the events/outcomes in their lives
- Reduced actions (behavioral) to impact environment/outcomes
- Causal attributions (cognitions) for negative events: personal, stable, and global
Cognitive-Behavioral Theory
someone perceives that a punishment or negative event is inevitable and out of their control, they learn to endure it.
Apply components of cognitive and behavioral theories to examples/cases of individuals with depression.
Negative Cognitive Triad (Beck, 1967):
- The Self: “I’m ugly”
- The World: “no one loves me”
- The Future: “I’m hopeless because things will always stay this way”
Inaccurate thoughts maintained by cognitive errors:
1. Black-and-white thinking
2. Fortune-telling
3. Mind-reading
4. Discounting the positive
Causal attributions:
Didn’t get a promotion
- Internal: “It’s my fault.”
- Stable: “I’ll never be worthy of a promotion.”
- Global: “I’m not good enough at anything.”
someone perceives that a punishment or negative event is inevitable and out of their control, they learn to endure it.
Identify and describe key components of evidence-based treatments for MDD.
Cognitive-Behavioral Therapy:
brief and time-limited i.e., 6-12 weeks
1) Change negative, hopeless thinking patterns
2) Identify reinforcing ways of interacting with the environment
Cognitive-side:
1. Monitor thoughts
2. Cognitive restructuring
A. Identify thinking errors
B. Challenge thoughts
- Evidence/for and against thought
(e.g. Is there any evidence that
you are not an idiot?)
C. Generate rational responses
- e.g. Even though I did poorly on
that quiz, my overall average is
still an A- (I can do poorly on one
exam without being an idiot)
Behavioral-side:
1. Monitor behaviors (and associated thoughts)
- e.g. Louis graduated from FSU in
marketing, but hasn’t found a job
yet. He spends most of his days
watching TV and playing video
games.
2. Behavior experiments (to test assumptions)
- e.g. have Louis apply to one job a week to test his assumption that he’s not qualified enough and will never get a job
Behavioral Activation:
1) Generate list of values in multiple domains (e.g. being good friend/mom/pet owner, working hard in my studies)
2) Generate activities in line with those values (e.g. calling a friend once a week, attending my classes)
3) Track behaviors/mood to determine how client is using their time and effect of specific behaviors on mood
4) Change behaviors to incorporate more that are in line with values (continue tracking to see impact on mood)
Identify symptoms of a manic episode (be able to recognize behaviors/thoughts/feelings that someone might experience during these episodes).
Manic & Hypomanic Episodes:
1) Very elevated (or irritable) mood
2) Very high energy
(These two symptoms are required)
3) Grandiosity
- Unrealistic sense of superiority,
specialness
4) Reduced need for sleep
5) Talkativeness
6) Racing thoughts
7) Distractibility
8) Increased goal-directed activity
9) Impulsive, risky behavior
Describe similarities and key differences between manic and hypomanic episodes (including in symptoms, duration, severity, and impairment).
HYPOMANIA (hypo = less):
- 4-6 days
- Observable by others, but not much
impairment
- No hospitalization or psychosis
MANIA:
- 7+ days
- Marked impairment
- Often hospitalized
- May include psychosis
Hospitalization or psychotic symptoms = are automatically considered a manic episode
Identify diagnostic criteria of Bipolar I and Bipolar II and distinguish between the two (including differences in distress and impairment).
- Episode: a discrete period of time characterized by certain experiences
- Disorder: label applied to syndromes
- Most mood disorders require at least one or the combination of some episodes to meet criteria for diagnosis
– Exception: Persistent Depressive Disorder
Bipolar I Disorder:
Marked impairment OR Hospitalization required
+
at least 7 days (can be less if hospitalized) = manic episode
=
Bipolar I Disorder
Can have major depressive episodes, but not required.
Bipolar II Disorder:
NO marked impairment/
Hospitalization (during hypomanic episode)
+
At least 4 days = hypomanic episode
+
Major depressive episode
=
Bipolar II Disorder
Major depressive episodes required.
Distress and/or impairment…
…needed for a diagnosis of any disorder (with few exceptions)…
What does this look like with the bipolar disorders?
Bipolar I
- Mania = needs MARKED impairment
(don’t need distress, but can be
distressing)
Bipolar II
- Hypomania may not be distressing,
and by definition does NOT result in
MARKED impairment, BUT common for
depressive episodes to be distressing
and/or impairing
Describe prevalence rates, demographics, and predictors of prognosis of Bipolar I and Bipolar II.
Bipolar I: 1 in 100 (lifetime)
- Mean onset: 18
- 90% have 2+ mood episodes
- 60% of manic episodes immediately
followed by MDEs
Bipolar II: 1 in 200 (lifetime)
- Mean onset: mid-20’s
- Most start with MDD diagnosis
- 5-15% go on to Bipolar I
Note: all bipolar disorders less common than depressive disorders
- No overall gender differences (Diflorio & Jones, 2010)
- No major differences in prevalence by race/ethnicity (Breslau et al., 2006)
- Sexual orientation minorities at higher risk (Bolton & Sareen, 2011; Bostwick et al., 2010; Sandfort et al., 2001)
Best predictors of good prognosis (i.e. lower impairment and more likely to achieve remission):
- Medication adherence
- Higher socioeconomic status
Describe biological theories of Bipolar Disorders (genetic factors, neurotransmitters).
Genetic Factors:
- MZ Twins 65% likely to have Bipolar
Disorder if the other twin does
Neurotransmitters:
Dopamine
- High during mania, low during
depression
Serotonin
Discuss psychosocial theories of Bipolar Disorders (reward sensitivity, stressful events, social rhythms).
Reward Sensitivity: greater sensitivity to reward; associated with impulsive behavior
- Stressful Life Events: may be trigger for new episodes
- Social Rhythms: changes in social rhythms (regular eating, sleep, work routines) may trigger episode
Identify pharmacological and psychological treatments for Bipolar Disorders, as well as potential issues with treatment compliance.
Mood stabilizers (e.g., lithium)
– Helpful for manic & depressive sxs
Atypical antipsychotics (e.g., Seroquel)
– Helpful for manic & depressive sxs
– Especially helpful with psychotic-like sxs of mania (e.g. grandiosity)
Anticonvulsants (e.g., Depakote)
– Helpful for manic sxs
Medications are the front-line treatment for bipolar disorders
Interpersonal and Social Rhythm Therapy (type of CBT)
- Techniques to help patients maintain
regular social rhythms (routine for
sleeping, eating, and activity), increase
stability in their relationships, and
develop coping skills for stressors
Family Focused Therapy
- Goal to reduce interpersonal stress
(esp. w/in families) – trained in
communication & problem solving
skills
Identify diagnostic criteria for Anorexia Nervosa (AN), Bulimia Nervosa (BN), and Binge Eating Disorder (BED).
Anorexia Nervosa (AN)
- Restriction of energy intake leading to significantly low body weight.
How thin is too thin?
General guidelines for adults – less than 85% of weight expected based on age/height
BMI ≤ 18.5
Severity specifiers in DSM-5 based on BMI
DSM-5 lets clinician determine what is low weight for an individual
- Intense fear of gaining weight or becoming fat, or persistent behavior that interferes with weight gain.
- Disturbance in experience of body weight, undue influence on self-evaluation, or denial of the seriousness of low weight.
Subtypes:
Restricting: dieting, fasting, excessive exercise
Binge/Purge: eat a lot of food, and then purging episodes
Bulimia Nervosa (BN)
- Recurrent episodes (occurring at least 1/wk on average for 3 months) of binge eating characterized by both:
a. Eating within a 2-hour period an amount of food that is definitely larger than most people would eat in similar conditions.
b. A sense of loss of control during the episode.
- Recurrent (occurring at least 1/wk on average for 3 months) inappropriate compensatory behaviors in order to prevent weight gain.
- Undue influence of weight and shape on self-evaluation
- No low weight (e.g., not anorexia nervosa)
- Disorder often starts with (and is maintained by) ‘normative’ dieting (restrictive eating)
- Impulsivity, difficulties with emotion regulation/coping
- Binge eating episodes frequently preceded by negative emotional states/stress
- Binge episode followed by guilt/shame –> compensatory behaviors
- Cycle develops
– Dieting –> binging –> compensatory behaviors (including dieting) –> binging, and so on…
Binge Eating Disorder (BED)
- Recurrent (occurring at least 1/wk on average for 3 months) episodes of binge eating (same core features as in BN required).
- Binge episodes accompanied by ≥3 associated symptoms:
a. Eating much more rapidly than normal.
b. Eating until feeling uncomfortably full.
c. Eating large amounts of food when not feeling physically hungry.
d. Eating alone because offeeling embarrassed by how much one is eating.
e. Feeling disgusted with oneself, depressed, or very guilty afterward. - Distress regarding binge eating is present.
- Not low weight and no compensatory behaviors.
- i.e. it’s not AN or BN
Identify associated medical complications of eating disorders (EDs). ***
Anorexia Nervosa (AN)
Symptoms of starvation:
- Dry, brittle hair, skin, nails
- Fine hair grows on body (lanugo)
- Constipation
- Amenorrhea (absence of monthly menstrual periods)
- Osteoporosis & bone fractures
- Impaired immune system
- Muscle loss
- Major organ failures
- Cardiovascular complications
— E.g. arrhythmia, heart failure
Bulimia Nervosa (BN)
- Electrolyte imbalance from purging - self-induced vomiting/diuretic/laxative misuse (can lead to heart failure)
- Erosion of dental enamel
- Hypersensitive gag reflex
- Ruptured esophagus or stomach
Binge Eating Disorder (BED)
- medical complications not really associated with this eating disorder
Describe the prevalence, demographics, and course of eating disorders. ***
Anorexia Nervosa (AN)
- 1-2% lifetime prevalence (0.3% for men)
- More common in women, 90-95% of people diagnosed with AN are women
– Underdiagnosed in men
– More common in Caucasian women, in particular - Onset in adolescence (ages 15-19)
- Very chronic: 7 yrs on avg, ~50% remission rate
- Death rate is 5-10%
- 31x higher risk for suicide than general population
– Among the highest of all mental disorders
BN: Prevalence & Course:
- 1-3% lifetime prevalence
- More common in women
- Among men, more common among gay men
- More prevalent in Hispanics and
African-Americans than Asian-Americans or Caucasians - Onset in adolescence to young adulthood (ages 15-29)
- Chronic: ~50% remission rate 7.5x higher suicide rate than the general population
- Comorbidity with depression and NSSI
BED: Prevalence & Course:
- Most prevalent of EDs, overall 2-4% lifetime prevalence
- ~ 30% in weight-loss programs
- Slightly more common in women than in men (more comparable than other EDs)
- No major racial/ethnic differences
- Onset in adulthood (later than other EDs)
- Chronic: Duration 8-15 yrs on avg.
Discuss similarities and differences between AN, BN, and BED; distinguish between cases of AN, BN, and BED.
AN
BN
BED
Severely Underweight
YES
NO
NO
Binge Eating
OK
YES
YES
Compensatory Behaviors
OK
YES
NO
