Sectional 2 Exam Flashcards

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1
Q

Identify the symptoms of a Major Depressive Episode.

A

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
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2
Q

Distinguish between and explain the key features of a Major Depressive Episode, Major Depressive Disorder (MDD), and Persistent Depressive Disorder (PDD).

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

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

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3
Q

Identify the prevalence of MDD and PDD and describe sex and age differences in MDD.

A

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+

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4
Q

Explain how genes and environment interact to increase risk of depression.

A

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

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5
Q

Identify neurotransmitters, brain structures, and neuroendocrine factors implicated in depression.

A
  • 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

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6
Q

Explain how abnormalities in neurotransmitters, brain structure, and HPA axis functioning relate to depressive symptoms.

A

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

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7
Q

Name the four classes of drug treatments for MDD.

A

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

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8
Q

Identify biological treatments for treatment-resistant MDD.

A
  • 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
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9
Q

Explain behavioral theories of depression (incl. role of stressful events, reduced reinforcers, behavioral withdrawal).

A

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.

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10
Q

Describe cognitive theories of depression (incl. cognitive triad, cognitive errors, causal attributions).

A

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.

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11
Q

Describe the cognitive-behavioral learned helplessness theory.

A

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.

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12
Q

Apply components of cognitive and behavioral theories to examples/cases of individuals with depression.

A

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.

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13
Q

Identify and describe key components of evidence-based treatments for MDD.

A

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)

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14
Q

Identify symptoms of a manic episode (be able to recognize behaviors/thoughts/feelings that someone might experience during these episodes).

A

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

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15
Q

Describe similarities and key differences between manic and hypomanic episodes (including in symptoms, duration, severity, and impairment).

A

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

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16
Q

Identify diagnostic criteria of Bipolar I and Bipolar II and distinguish between the two (including differences in distress and impairment).

A
  • 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

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17
Q

Describe prevalence rates, demographics, and predictors of prognosis of Bipolar I and Bipolar II.

A

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

18
Q

Describe biological theories of Bipolar Disorders (genetic factors, neurotransmitters).

A

Genetic Factors:
- MZ Twins 65% likely to have Bipolar
Disorder if the other twin does

Neurotransmitters:
Dopamine
- High during mania, low during
depression
Serotonin

19
Q

Discuss psychosocial theories of Bipolar Disorders (reward sensitivity, stressful events, social rhythms).

A

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

20
Q

Identify pharmacological and psychological treatments for Bipolar Disorders, as well as potential issues with treatment compliance.

A

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

21
Q

Identify diagnostic criteria for Anorexia Nervosa (AN), Bulimia Nervosa (BN), and Binge Eating Disorder (BED).

A

Anorexia Nervosa (AN)

  1. 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

  1. Intense fear of gaining weight or becoming fat, or persistent behavior that interferes with weight gain.
  2. 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)

  1. 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.

  1. Recurrent (occurring at least 1/wk on average for 3 months) inappropriate compensatory behaviors in order to prevent weight gain.
  2. Undue influence of weight and shape on self-evaluation
  3. 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)

  1. Recurrent (occurring at least 1/wk on average for 3 months) episodes of binge eating (same core features as in BN required).
  2. 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.
  3. Distress regarding binge eating is present.
  4. Not low weight and no compensatory behaviors.
    - i.e. it’s not AN or BN
22
Q

Identify associated medical complications of eating disorders (EDs). ***

A

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
23
Q

Describe the prevalence, demographics, and course of eating disorders. ***

A

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.
24
Q

Discuss similarities and differences between AN, BN, and BED; distinguish between cases of AN, BN, and BED.

A

AN
BN
BED

Severely Underweight
YES
NO
NO

Binge Eating
OK
YES
YES

Compensatory Behaviors
OK
YES
NO

25
Q

Describe the key features of binge eating episodes.

A
  • Impulsivity, difficulties with emotion regulation/coping
  • Binge eating episodes frequently preceded by negative emotional states/stress
  • Binge episode followed by guilt/shame –> compensatory behaviors
26
Q

Generate examples of compensatory behaviors.

A

Purging:
- misuse of laxatives
- self-induced puking

Non-Purging:
- fasting
- excessive working out

27
Q

Discuss the biopsychosocial model of eating disorders.
a. Explain biological theories related to weight and eating disorders.
b. Describe psychological theories of eating disorders.
c. Explain sociocultural theories of eating disorders; discuss the role of media and weight stigma.

A

Biological theories

Genetic Influences

  • Family & twin studies suggest general risk for EDs (not specific risk for one type or another)
  • Heritability rates of 40-60% for AN, BN, & BED
  • Biological (hormonal) changes at puberty activate genetic risk for EDs in girls

Neurotransmitters

  • Hypothalamus plays a central role in regulating eating behaviors.
    • Signals to rest of body when to
      eat/not eat via neurotransmitters
      • Dopamine
      • Serotonin
      • Norepinephrine

^ Abnormalities associated with EDs

  • Related to the rewarding & pleasurable aspects of eating

Hormones

GLP-1 (Ghrelin) – The “Hunger Hormone”
- Short-term regulatory hormone –
triggers eating
- Abnormalities in EDs involving binge-
eating in particular

Leptin (signals to hypothalamus –> reduce appetite)
- Long-term regulatory hormone

  • Lipostatic theory: set-point for body fat
    • Loss of body fat (& leptin) -> increase
      hunger
    • Weight gain after dieting
  • Leptin resistance: high leptin in blood but not brain
    • Satiation signals not being received

Psychological Theories

Emotion regulation
Personality factors
- Perfectionism, negative affect
common among all
- Impulsivity common in BN/BED but
not AN
- Narcissism?
Cognitive models: rigid thinking
Family dynamics: enmeshed families

Sociocultural Theories

Media influences
Internalization of “thin ideal”/”appearance-ideal”/”muscular ideal”
Media exposure linked to:
- increase body dissatisfaction,
- increase investment in appearance,
- increase endorsement of ED
behaviors.
Social media may be even more detrimental when used in certain ways

Becker et al., 2002
- Evaluated the impact of the
introduction of Western television on
body image and disordered eating in
Fiji (media-naïve population)
- EDs were rare; cultural preference
for “fuller-bodied” women

Compared samples of Fijian adolescents before (1995) and after (1998) prolonged television exposure.
- Self-induced vomiting to control
weight: 0% in 1995 -> 11.3% in 1998
- Adopted the belief that reshaping
one’s body might also change one’s
life trajectory

  • Media influences
  • Internalization of “thin ideal”
  • “Fat talk” - thin friends talking about
    how fat they are, associated with
    increased body dissatisfaction
28
Q

Identify the front-line treatments for eating disorders and the core components of those treatments.

A

Biological Treatment of EDs

Inpatient or partial hospitalization
- Weight-restoration in AN
Medications
- SSRI’s effective for BN & BED
- None found effective for treatment of
AN

Treatments for Eating Disorders

Cognitive-Behavioral Therapy
- Regular eating (behavioral)
- Exposure to feared foods (behavioral)
- Challenging thoughts (cognitive
restructuring)
Family Therapy
- Most effective for adolescents with
AN

29
Q

Describe barriers to treatment-seeking for eating disorders and difficulties in treating eating disorders, particularly AN.

A
  • Social stigma; relatively more severe for ED’s than other mental health disorders in Western cultures (e.g., anxiety, depression) – why?
  • Poor understanding of EDs among general public (poor mental health literacy)
  • Individuals with EDs often fail to see the severity of their problem
    • Often difficult for clinicians as well
    • Continuum model – where is the line
      between normal/adaptive and
      abnormal/maladaptive behaviors?
  • Doctors undertrained (can encourage
    ED behaviors, unintentionally)
  • Poor detection among health professionals of EDs, esp. in minorities and men
  • Appropriate, effective treatment hard to find and expensive
    • Insurance won’t cover a lot unless
      severely underweight
    • Demands severe impairment before
      covering treatment
  • Even when men recognize they have an ED, they are less likely to seek treatment for one than women with EDs
30
Q

Recognize what is considered a substance, and the difference between illicit and non-illicit substances

A

Substance - Any natural or synthesized product that has psychoactive effects
(changes perceptions, thoughts, emotions, & behaviors)

Illicit substances = illegal to consume for recreational purposes

non-Illicit substances = not illegal to consume for recreational purposes

31
Q

Define intoxication and withdrawal

A

Intoxication - The physiological, behavioral, and psychological changes that occur as a direct result of the substance’s effects on the central nervous system

Type
- Related to length of intoxication
Amount
- Larger dose -> more bx and
psychological changes

Withdrawal: physiological, behavioral, and psychological symptoms that result when people have been using substances heavily for a long time suddenly stop or reduce their use
- Opposite of the intoxication
symptoms

32
Q

Identify the six categories of illicit drugs

A

Depressants
- Alcohol, benzodiazepines, &
barbiturates
Cannabis
- Marijuana
Stimulants
- Cocaine, amphetamines, nicotine, &
caffeine
Opioids
- Morphine, heroin, codeine, &
methadone
Hallucinogens
- LSD, psilocybin, peyote, molly
(ecstasy), PCP
Inhalants
- Solvents, medical anesthetic gases, &
nitrites

33
Q

Describe the demographics of illicit drug use, the overall prevalence of substance use, and how prevalence has changed over time.

A

Roughly ½ of the US population admits to having tried an illicit substance in their lives

Men are more likely than women to have used illicit substances (across cultures)

Regular substance use varies by age group, ethnicity, and cohort…

Substance Use Overtime:
- Peak in the 80s
- Steady decreases, overall (exception of alcohol,
ecstasy)

Demographics of Illicit Substance Use: Age
- 18 to 20 is when Illicit Substance Use peaks
- 65+ is the lowest

Demographics of Substance Use: Race/Ethnicity
- White highest for Alcohol Consumption
- Tobacco highest among Native Americans
- Illicit is highest in Native Americans, though everything doesn’t seem statistically significant

34
Q

Understand the continuum model of substance use

A

Substance use along the continuum

Abstinence/Functional <—–> Severe Substance Use Disorder/Dysfunctional

35
Q

Name and describe the key features of Substance Use Disorders (SUDs)

A

2+ of any of the following symptoms in a 12-month period:
1. Using more than planned
2. Trouble cutting down
3. Lots of time spent
4. Craving — Impaired Control
5. Not meeting responsibilities
6. Interpersonal dysfunction
7. Giving up important activities — Social Impairment
8. Physical danger
9. Continued use despite problems — Risky Use
10. Tolerance
11. Withdrawal — Pharmacological

Severity:
- Mild: 2-3 symptoms
- Moderate: 4-5 symptoms
- Severe: 6+ symptoms

36
Q

Describe the demographics of SUDs

A

SUDs In The Past Year Among Adults Aged 18 Or Older:
- No SUD in the past year: 91.6%

SUD in the past year: 8.4%
- 16.3% Alcohol Use Disorder
- 6.2% Illicit Drug Use
- 3.5% Marijuana Use Disorder

Demographics of SUDs: Race/Ethnicity
- Native Americans highest in SUDs, lowest in Asian

Demographics of SUDs: Gender & Sexual Orientation
- People who identify as gay, lesbian, or bisexual have higher rates of substance use disorders, regardless of gender.

37
Q

Describe the intoxication and withdrawal effects of specific substances

A

Alcohol

Intoxication:
Low Doses: Self-confidence, relaxation, disinhibition
High Doses: Motor problems, depressed mood, confusion, impaired sexual functioning, dizziness, loss of consciousness

Withdraw:
3 Stages:
1. 2-8 hours: hangover; tremulousness (the “shakes”),
weakness, perspiration, headache, nausea, abdominal
cramps
2. 1-3 days: convulsive seizures
3. > 3 days: delirium tremens (the DTs): hallucinations,
delusions, fever, perspiration, agitation, irregular
heartbeat
- Less than 15% of people with severe alcohol use
disorder
- Of those who experience DTs: Fatal in 10% of cases

Stimulants

Intoxication:
- Lower Doses: Alertness, energy, competence,
euphoria
- Higher Doses: Grandiosity, impulsiveness, compulsive
behavior, agitation, anxiety, panic & paranoia,
perceptual illusions, cardiac failure

Withdrawal:
- Exhaustion and depression

Opiates/Opioids: Use & Effects

Intoxication
- Low Doses: Euphoria, pervasive sense of warmth,
lethargy, drowsiness, slurred speech, vivid dreams
- Higher Doses: Unconsciousness, coma, seizures,
reduced cardiovascular function
Withdrawal
- Dysphoria, anxiety, agitation, achy feeling, vomiting,
diarrhea

Hallucinogens

Intoxication
- Perceptual changes, sense of clarity & connectedness,
euphoria
- Sometimes: anxiety, paranoia, loss of motor control
Withdrawal
- Depression, lethargy

Cannabis

Intoxication
- Low Doses: Relaxation, dizziness, grandiosity or
lethargy, short-term memory impairment, motor
impairments, dry mouth
- High Doses: Hallucinogenic effects, perceptual
distortions, depersonalization, paranoia

Withdrawal
- Anxiety, loss of appetite, hot flashes, sweating

Inhalants

Intoxication
- Behavioral changes, dizziness, euphoria, lethargy,
psychomotor retardation, tremors, muscle weakness,
blurred vision, coma
Chronic Use
- Respiratory irritations, rashes, permanent damage to
central nervous system (brain lesions), severe
dementia, hepatitis, liver and kidney disease, death

38
Q

Describe heritability estimates of SUDs

A
  • Genetic Influence
  • Explain 50% variation in risk
  • .48 (MZ), .32 (DZ)
  • Broad, not specific
  • Greater reward sensitivity
39
Q

Identify which neurotransmitters and brain areas are involved with SUDs broadly, and which neurotransmitters are involved with specific substances

A

IT ALL COMES BACK TO DOPAMINE REWARD PATHWAYS

Mesolimbic pathway: Main dopaminergic pathway in the brain

Ventral Tegmental Area -> nucleus accumbens

Drugs increase availability of dopamine along this pathway

Cravings: when dopamine levels are chronically elevated, dopamine response to other (non-drug) rewards become blunted

SUDs are thought to occur when cravings from these reward networks overpower signals from control network

Neurotransmitter Effects
Dopamine: Reward pathways are augmented by essentially all drugs of abuse
Serotonin: MDMA (ecstasy), LSD, cocaine, alcohol
Norepinephrine: Cocaine, amphetamines, MDMA
GABA: Alcohol & other depressants
Endorphins: Opioids

40
Q

Describe how sociocultural, behavioral/learning, cognitive, and personality models/theories explain the development of SUDs

A

1. Behavioral Theories
Substance abuse is modeled (i.e., social learning); learn most from those most similar

2. Cognitive Theories
Expectations about effects
Beliefs about coping with substance use

3. Personality Trait Theories
Trait disinhibition (behavioral under-control, impulsivity)
Sensation-seeking
Reward Sensitivity
- Note: these traits less common in women, which
may help explain why SUDs less common in women

Sociocultural Theories
Effects of drugs appear to be more attractive to people under chronic stress
- Poverty
- Women in abusive relationships
- Children whose parents frequently fight

Context Matters:
Robins conducted a large-scale study of 898 U.S. soldiers during the Vietnam War.
- The researchers found widespread drug use (over
90 percent) among U.S. soldiers.
- One in five soldiers returned to the United States
addicted to drugs.
- Once home, approximately 95 percent of the
soldiers addicted to drugs quit using them.

Biopsychosocial Model

Exposure is necessary
- Early age of first use
- Genetic factors mean some people get “hooked”
- Social stressors & beliefs might change likelihood of
using

41
Q

Compare and contrast the disease model and the harm reduction model of SUDs and explain how this impacts treatment

A

Disease Models:
- Assume individual cannot modify use
- Abstention a must (AA model)

Harm-Reduction Models:
- Assume individual can modify use
- Moderation, not abstinence

42
Q

Name and describe biological and psychological treatments available for SUDs

A

Biological Treatments
Antagonist drugs block or change the effects of addictive drugs by:
- Reducing reinforcement (e.g. naltrexone for
opioids; blocks effects of endorphins)
- Making it uncomfortable to consume the substance
(e.g. Antabuse for alcohol; drinking  sick, dizzy,
vomit, faint)
Antidepressants & Benzodiazepines (for alcohol) to “weather” withdrawal

Agonists = Less intense drug substitutes
- e.g., methodone; buprenorphine
- Methadone Maintenance Programs
- Methadone = synthetic, orally administered opiate
- Reduces extreme withdrawal symptoms
- Reduces intense euphoria by blocking receptors
- Goal is to taper off of 1) heroin & 2) methadone

Behavioral Treatments

Cue Exposure & Response Prevention
- Exposure to cues for substance use, prevent actual
drinking/drug use

Aversive Classical Conditioning
- Medications – e.g., taking antabuse
- Covert Sensitization Therapy- use imagery to
associate alcohol use with unpleasant images

Cognitive Treatments
1. Identify situations in which they are most likely to use substances
2. Identify & challenge core beliefs
- Substance as coping
- All-or-nothing thinking
- Coping with cravings

Other Psychotherapies

Motivational Interviewing:
- Therapist doesn’t challenge client’s substance use
- Client develops own reasons to change (or not)

Relapse prevention programs
- Alcoholics/Narcotics Anonymous (AA/NA) [disease
model, abstinence goal]
- View ‘slips’ as temporary and situationally caused

Harm Reduction Programs
- Daily records of consumption
- Learn to calculate BAL
- Risks vs. benefits of moderate use