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substance use
consumption without impairment
substance misuse
problematic, risky, or harmful use
substance use disorder
meets dsm-5 criteria
polysubstance use
use of more than one drug/ substance
tolerance
needing more of the substance to achieve the same effect
diminished effect with continued use of the same amount
withdrawal
physical and psychological symptoms when reducing/ceasing use
components of substance use disorder
craving
diminished control
withdrawal
symptoms experienced when drug is discontinued
most severe for alcohol, opinoids, and sedatives/hypnotics
evidence of physiological dependence
tolerance
nervous system becomes less sensitive to effects of substance, so increased quantities needed for same effect
mechanisms
metabolic tolerance
pharmacodynamic tolerance
behavioral conditioning
reasons for overdose risk spiking after abstinence
loss of physiological tolerance
after detox, tolerance goes down, previously “normal” dose becomes dangerous
loss of conditioned tolerance
usual environment triggers body to prepare
new setting → no compensatory response → drug hits harder
public health impact
cause of preventable death
linked to accidents
enormous economic cost
depressants
examples
alcohol, benzodiazepines (valium, xanax)
barbiturates
core effects
decrease cns activity, reduce anxiety, impair coordination
risks & consequences
accidents, aggression, liver disease
tolerance and dangerous withdrawal
cross-tolerance
prevalence of alcohol use disorder
more common in men and transgender
large sex difference in alcohol metabolism
alcohol use course
initiation often in adolescence
peaks at 18
tobacco onset rarely after 25
adolescents: heightened reward sensitivity, impulsivity
younger drinking initiation associated with higher dependence risk
problematic drinking decreases with age
periods of heavy use alternates with relative abstinence
fetal alcohol spectrum disorders
6-9 out of 1,000 live births
spectrum disorder 2-5% in US
stimulants
examples
cocaine, amphetamines (adderall, methaphetamine), nicotine, caffeine
core effects
increase cns activity, heightened alertness, euphoria, decreased appetite
risks & consequences
cardiovascular strain, sleep disruption, paranoia, high potential for dependence
tobacco
natural source of nicotine
short term effects
stimulation of norepinephrine, dopamine, and serotonin
long term consequences
3.5 million ppl die prematurely
80% lung cancer deaths
opiod
examples
natural: opium, morphine, codeine
synthetic: heroin, oxycodone, fentanyl
core effects
pain relief, euphoria, drowsiness
risks & consequences
overdose (respiratory failure)
withdrawal: flu-like symptoms
major public health crisis (opioid epidemic)
opiod epidemic
origins
prescription surge (1990s)
misleading claims of low addiction risk
escalation
prescription crackdowns → shift to heroin
fentanyl enters drug supply (2010s)
impact
80k US overdose deaths
fentanyl drives most fatalities
hits rural and marginalized communities hardset
hallucinogens
LSD
alter perceptions, trigger panic and psychosis
cannabis
THC, CBD
relaxation, increased appetite, altered time perception
heavy use → memory, motivation, and attention problems
issues
rising THC potency
edibles, vaping
debate over medical and recreational use
tranquilizers
used to decrease anxiety or agitation
sedatives
general term for drugs that calm people
examples
barbiturates
benzodiazepines
behavioral addictions
def
repetitive behavior that becomes compulsive, causes impairment/distress; compulsive behavior without substance
gambling (recognized in dsm)
classificatory debate
argued that behavioral addiction research must move beyond simply applying substance use disorder frameworks
frequency of behaviors is not an addiction
many SUD criteria (tolerance, withdrawal) may not map cleanly to behaviors
importance of considering triggers, reinforcement patterns
moral incongruence rather than impairment
DSM for substance
groups
substance use disorder
long-term problematic use (like alcohol use disorder)
substance induced disorder
symptoms caused directly by the substance (like intoxication or withdrawal).'
old DSM
line between abuse and dependence
now it is a spectrum
epidemiology of SUD
prevalence
alcohol is most commonly used and misused
10-12% meet criteria for SUD
opioid misuse has surged
polysubstance use is common
demographic
higher rates in men
faster progression to dependence (telescoping) for women'
influenced by cultural, socioeconomic, and policy factors
prevalence of drug & nicotine use disorder
SUD for any controlled substance: 9.9%
lifetime rate of nicotine dependence 24%
current rate of smoking is 11.5% which is lowest rate
biological factors for SUD
genetics and family history
family history increases risk from 2-4x
twin studies
Identical twins: high similarity
Fraternal twins: less similarity
neurobiology
dysregulation of dopamine reward pathways
Addictive drugs release dopamine in a huge surge → brain learns to seek the drug over natural rewards
Endogenous opioids, GABA, and glutamate
Opioids mimic natural opioid peptides
Alcohol affects GABA (inhibition) and glutamate (excitation)
Nicotine & stimulants increase dopamine indirectly
altered stress response (HPA axis)
sociocultural factors
people influence
selection and socialization
alcohol- parental modeling matters more
drug use- peers have greater effect
treatment for SUD
detoxification
may be medically indicated to reduce withdrawal symptoms
additional psychopharmacological methods: antabuse, revia, cambral
CBT
identify triggers
motivational interviewing
relapse prevention
12-step problems
spiritually oriented
high early drop out rates but big sobriety rates for those who stay
highly available, free
3 common evidence based treatment
CBT
motivational interviewing
medication assisted treatment
12 step programs
evidence for
support for abstinence-based recovery
evidence against
many recover without full abstinence (natural recovery)
controlled drinking can be sustainable for some AUD
alternatives offer secular and flexible options
harm reduction for SUD
goal
reduce negative consequences of use, even if use continues
core principles
pragmatic, nonjudgemental
feeding disorder
avoidant, restrictive, or irregular eating without body/shape concerns found in eating disorders
dsm includes
pica
rumination disorder
avoidant/restrictive food intake disorder
dsm criteria for anorexia nervosa
restriction of energy intake leading to significantly low body weight
intense fear of gaining weight
disturbance in the way one’s body weight is experienced
restricting or binge/purging type
dropped amenorrhea criterion
epidemiology for anorexia
common in women
lifetime prevalence is 0.5-3.7 but textbook says 0.62%
peak ages of onset 14-18 years (bimodal)
3rd leading cause of chronic illness in adolescents after asthma and obesity
crosses over to BN
health consequences of anorexia
osteopenia and osteoporosis
increased bone resorption and decreased bone formation
only partial reversal of osteoporosis
cardiac complication
frequent cause of death in anorexia patients
signs: coldness of extremities, dizziness, and palpitations
renal complications
kidney failure (Frequent cause of death), results from dehydration
cns
apathy, poor concentration
reproduction
amenorrhea, low estrogen
metabolic
cold intolerance
easy
yellow skin, brittle nails, lanugo hair, muscle weakness, and restricted facial expression
dsm criteria for bulimia nervosa
recurrent episodes of binge eating
recurrent inappropriate compensatory behaviors in order to prevent weight gain
at least once a week for 3 months
self-evaluation is unduly influenced by body shape and weight
compensatory behaviors for bulimia nervosa
most common = vomiting
among patients with type I diabetes, giving themselves less insulin than is needed “diabulimia”
physical signs of bulimia
russell’s sign
sores on hand from inducing vomiting
dental complications from vomiting
small red dots around eyes
enlarged parotid glands “chipmunk cheeks”
epidemiology for bulimia nervosa
black women have lower rates of restrictive dieting, higher rates of laxative use, and same rate of recurrent binge eating
rates higher among sexual minorities
health consequences for bulimia
electrolyte abnormalities (hypokalemia)
metabolic alkalosis
dental erosion
parotid gland enlargement
cardiac arrhythmias
dsm for binge eating
recurrent episodes of binge eating
2 hours
at least once a week for 3 months
eating more until uncomfortably full
epidemiology for binge eating
more common in female and minority groups
higher prevalence than bulimia
health consequences for binge eating
obesity
not everyone with BED is obese and not everyone who is obese has BED
GI issues
bariatric surgery complications
eating disorder mortality
anorexia has highest mortality rate of any psychiatric disorder
up to 21%
0.56% per year
eating disorder variation by culture
increasing prevalence in asia
increasing rates among black and latino americans in US
food insecurity →higher risk of bulimia or binge eating
bulimia is culture bound, anorexia is not
eating disorder in men
muscle dysmorphia
body image problems involving desire to increase muscularity
30% of teen boys trying to gain weight or bulk up
22% of young men engage in muscle enhancing behaviors
eating differently
supplements
anabolic steroids
more common in gay men
eating disorder etiology
genetic risk factor
heritability: 58-76%
anorexia > bulimia
as high as schizo or bipolar
first degree relatives have higher rates of anorexia and mood
run genetic locus shared with type I diabetes
genetic risk emerges id-adolescence
personality factors
restricting anorexia
emotional constriction, perfectionism, conscientiousness, obsessiveness, introversion, socially conforming
bulimia and binge eating anorexia
high impulsivity
sensation seeking
emotional lability
family factors for eating disorders
anorexia
lots of family enmeshment
bulimia
lots of neglect and hostility
high rates of childhood sexual disorders among bulimia
orthorexia
obsession with healthy eating leading to malnutrition
treatment for anorexia
motivational interviewing
inpatient hospitalization
necessary for those that are 20`30% below expected weight or if cardiac sx occur
little research on efficacy
goal: use behavioral principles to restore weight
family based approach (maudsley family therapy)
effective for adolescents within first 3 months
very intensive so whole family needs to be on board
20 sessions over 12 months
phase 1: weight restoration
phase 2: returning control over eating to adolescent
phase 3: establishing healthy adolescent identity
strong empirical support
treatment for bulimia and binge eating
CBT
targets weight and body concerns
considered first-line treatment
interpersonal psychotherapy
targets interpersonal problems
dialectical behavioral therapy
adopted from Linehan’s borderline personality disorder
binge/purge viewed as self-harming behavior with maladaptive emotion regulation function
schizophrenia
brain disorder involving abnormal dopamine signaling that shows a disturbance in thought shaped by psychological stressors
early conceptualizations
emil kraepelin
divided mental illness into manic depressive insanity (bipolar disporder) and dementia praecox (brain deterioration)
believed dementia praecox was due to autointoxication or a poisoning of the brain by toxins produced in the body
early biological/degenerative model of psychotic illness
eugen bleuler
coined the term schizophrenia
believed the disorder was characterized by a splitting of psychic functions rather than splitting of personality
not always degenerative
kurt schneider
first rank symptoms
dsm for schizophrenia
+ symptoms
hallucinations
delusions
disorganized speech and behavior
- symptoms
flat affect, avolition, anhedonia, alogia
greater link to functional outcomes
cognitive symptoms
global and specific deficits in cognition
social cognition deficits
two or more present during 1 month period has to be at least
delusions
hallucinations
disorganized speech
continuous signs for 6 months
primary psychotic disorders
schizoaffective disorder
threshold level criterion a psychotic symptom
presence of a major mood episode (depression or mania) for >50% duration of psychotic illness
symptoms present outside of mood episode
brief psychotic disorder
episode lasts at least 1 day but less than 1 month
schizophreniform disorder
psychotic episode lasting at least 1 month but less than 5 months
delusional disorder
2 or more delusions lasting 1 month or longer
no marked disruption to functioning
related disorders to schizophrenia
schizotypal personality disorder
pattern of acute discomfort in close relationships, cognitive or perceptual distortions, and eccentricities of behavior
schizoid personality disorder
pattern of detachment from social relationships and restricted range of emotional expressions
( _ ) with psychotic features
many dsm disorders can have specifier or qualitative descriptor
genetics for schizo
heritability
highly heritable about 70-80%
first degree relatives
-10% risk
monozygotic twins
40-50% concordance
polygenic and complex inheritance
no single schizo gene
risk is polygenic (many genes contributing toward overall symptoms) and pleiotropic (genes that contribute toward schizo also linked to other disorders)
genome wide association studies identify genes related to synpatic function, dopamine, and glutamate signaling, and immune pathways
shared genetic liability
substantial genetic overlap with bipolar disorder, major depression, and autism
helps explain blurred diagnostic boundaries and psychosis spectrum conceptualizations
biological models for schizo
dopamine hypothesis
classical model
excess dopamine activity, particularly in the mesolimbic pathway, produces positive symptoms
modified model
dopamine dysregulation- too much subcortical, too little prefrontal
evidence for
antipsychotic drug effects (D2 blockade reduces psychosis)
drugs that heighten dopamine trigger/increase psychotic symptoms (stimulants like cocaine or amphetamines
limitations
doesn’t explain negative/cognitive symptoms
dopamine changes may be downstream, not casual
neurodevelopment models
say early disruptions in brain maturation create lifelong impairment and psychotic symptoms
pregnancy complications
abnormal fetal development
maternal stress during pregnancy
birth during winter months???
altered synaptic pruning, gray matter loss, or circuit dysconnectivity emerge in adolescence
psychological models
cognitive models
abnormal salience hypothesis
benign stimuli feel personally significant
cognitive biases maintain delusional beliefs
psychological stress and trauma interact with vulnerability to shape symptom content
learning and social models
social defeat hypothesis
repeated exclusion or marginalization may sensitize dopamine systems
social deafferentation model
the social brain, when deprived of input, creates its own (hallucinations, delusions)
psychotic experiences gain meaning through reinforcement and interpretation; delusions/voices maintained by cognitive biases
integrated models for schizo
original diathesis-stress model
genetic predisposition/ vulnerability (diathesis) and environmental triggers (Stress) are both necessary but not sufficient for onset of illness
longstanding framework
strengths: flexible, predicts variability
weaknesses: broad, vague
modern conceptualizations
neurodevelopmental elements
early brain disruptions (prenatal infection, obstetric complications, adolescent synaptic pruning) create latent risk
environmental elements
interaction with later stress, substance use, or trauma triggers symptoms
neurodegenerative elements
research suggests accelerated aging across neural and biological systems
slightly faster cortical thinning, inflammation, and oxidative stress that can accumulate over time
prodromal phase for schizo
subtle early changes
social withdrawal
can last weeks to years
clinical high risk for psychosis
research/clinical designation for people showing attenuated psychotic symptoms or a steep decline in functioning
about 20-35% transition to a full psychotic disorder within two years
focus of early-intervention efforts
acute phase for schizo
emergence of threshold level characteristic psychotic symptoms
hallucinations, delusions
accompanying features
heighted emotional arousal, fear
decline in self-care
typically begins in late adolescence to early adulthood
men: often earlier onset (late teens to early 20s)
women: often later (mid to late 20s)
common precipitating events
major life stressors
cannabis use
often represents the first clear recognition of illness by family or clinicians
frequently leads to first hospitalization or crisis evaluation
duration: typically 1-6 months before partial remission
treatment response
antipsychotic medication reduces positive symptoms
supportive psychotherapy
family involvement
residual phase
reduction in acute symptoms but ongoing difficulties
negative symptoms cognitive deficits, social and occupational impairment
medication for schizophrenia
antipsychotic medications
primary mechanism: block dopamine D2 receptors in mesolimbic pathway
most effective in reducing positive symptoms
limited effects on negative and cognitive symptoms
medication classes
first generation (typical) antipsychotics
effective for psychosis but high risk of extrapyramidal symptoms and tardive dyskinesia
second generation (atypical) antipsychotics
lower risk of EPS; broader receptor activity (dopamine and serotonin)
higher risk of metabolic effects
clozapine
most effective for treatment-resistant schizophrenia but carries risk of agranulocytosis
limitations of medication treatment for schizo
partial response
30% of patients hae persistent symptoms despite treatment
side effects
metabolic syndrome, sedation, weight gain→ major contributors to poor adherence
long-acting injectables
improve adherence and reduce relapse risk
emerging targets
glutamate modulation, inflammation, and personalized medicine approaches
integrated treatment
CBT for psychosis
focuses on coping strategies and reducing distress rather than eliminating symptoms
family psychoeducation
social and functional rehabilitation
skills training
emphasizes recovery as participation in life
coordinated specialty care
early intervention model for first episode psychosis
combines psychotherapy, medication, family education, and supported education/work
shown to improve outcomes when started soon after onset
category vs continuum for schizophren
dimensional models
psychosis exists on a continuum
RDoC and HiTOP frameworks
move beyond categories to study dimensions (cognition, reward, social processing)
blurring boundaries
overlap with mood, developmental, and cognitive disorders
schizophrenia and schizoaffective debate
many patients shift between diagnoses over time; shared genetics and symptom overlap challenge categorical distinctions
somatic disorder
defining features
physical symptoms or fears about illness that cannot be explained by organic impairment
unnecessary medical treatment
excessive worry about symptoms
last more than 6 months
prevalence 5-7%
often comorbid with depression or anxiety
more than one severe somatic complaint
functional neurological symptom disorder
previously known as conversion disorder
neurological like symptoms linked with psychological roots
onset linked to stress or conflict
ex
blindness, deafness
illness anxiety disorder
formally known as hypochondriasis
preoccupation with having or acquiring a serious illness
few or no physical symptoms
health related checking or avoidance
lasts more than 6 months
1-2%, gender balanced
factitious disorder (munchausen’s syndrome)
imposed on self
intentional symptom production or falsification
motivation: assume the “sick role”
no external reward (distinguishes from malingering)
psychologically complex, often rooted in early neglect/need for nurturance
imposed on another
same criteria but on another person
malingering
intentionally faking symptoms to receive tangible benefits
not a formal diagnosis but listed as a v code (other conditions that may be a focus of clinical attention)
social shit w somatic
gender
all somatic symptom disorders are much more common in women except for illness anxiety disorder (equal)
somatic symptoms disorders more common among
lower socioeconomic status
less than a high school education
african americans
puerto rico
role of cultural norms
higher rates in latin american cultures
korean syndrome 화병
some cultures express emotional concerns physical because of limited insight or social tolerance of psychological complaints
etiological models of somatic symptom disorders
perils of diagnosis by exclusion
freud/psychodynamic
consequence of traumatic experiences overwhelming coping abilities
primary gain
symptoms protect conscious mind by expressing the psychological conflict unconsciously
secondary gain
symptoms help a patient avoid work, gain attention, etc.
cognitive behavioral
learned assumption of sick role, positive and negative reinforcement
alexithymia (deficit in ability to recognize and express emotions)
misattribution of normal somatic symptoms
dissociative disorder
dissociation
two or more distinct personality states within an individual that take control over behavior
characterized by persistent, maladaptive disruptions in the integration of memory, consciousness, identity, or perception
symptoms are involuntary, not psychotic
frequently related to trauma
dissociative amnesia (+- fugue)
dissociative amnesia
sudden inability to remember extensive and important personal information
response to trauma or extreme stress
not result of head trauma or organic cause
can be localized (specific period) or generalized (Entire life)
dissociative fugue
sudden, unplanned travel away from home
inability to recall the past, confusion about identity, or the assumption of a new identity
depersonalization/ derealization disorder
persistent detachment from
self→ feeling outside one’s body (depersonalization)
world→ surroundings feel unreal (derealization)
triggered by trauma
~2%
DID
formally multiple personality disorder
two or more distinct personality states within an individual that take control over behavior
some memory loss occurring between personalities
personalities can range from two to hundreds
considered controversial because prevalence is based on a small sample
heavy reliance on retrospective reports
memories can be selectively recalled or distorted
DID cases are from clinicians who already believe in the disorder so there is bias
etiology of dissociative disorders
trauma
clear role in dissociative amnesia & fugue
likely DID
data retrospective
iatrogenesis (sociocognitive model)
genetics
no evidence
research for both etiology and treatment is limited
personality
enduring patterns of thinking and behavior
personality disorder
An enduring pattern of inner experience and behavior that deviates markedly from cultural expectations, is rigid, leads to distress, and is stable across time.
must affect these four areas of functioning
cognition (perceiving things)
affect (range, intensity)
interpersonal functioning
impulse control
epidemiology for personality disorders
prevalence
10-14% have a PD in community samples
gender
overall equal
antisocial personality disorder has clearest gender diffs (5x more common in men)
age
not diagnosed in children
antisocial personality disorder
must show at least 3 of these behaviors occurring since 15
person must be 18 to diagnosis
must be evidence of conduct disorder before 15
behavior cannot be explained by another disorder like schizo or bipolar
dialectical behavior therapy
marsha linehan received treatment development grant to target suicidal behavior
required a diagnosis of borderline personality disorder
core: you can accept yourself and also change unhealthy behaviors
as a world view
reality is whole and interrelated
reality is complex and in polarity
change is continual and transactional
borderline personality disorder
a pervasive pattern of instability of interpersonal relationships and maked impulsivity beginning by early adulthood and present in a variety of contexts as indicated by 5+
emotion dysregulation
interpersonal dysregulation
self dysregulation
behavioral dysregulation
cognitive dysregulation
core feature
instability in emotions, self-image, and interpersonal relationships, accompanied by impulsivity and fear of abandonment
most effective treatment: DBT
biosocial theory
biological factors →emotion dysregulation←invalidating environment
biological vulnerability
emotional sensitivity
emotional intensity
slow return to baseline
invalidating environment
rejects communication of experiences
actively self-invalidate and depend on social environment cues
punishes emotional displays and intermittently reinforces emotional escalation
oscillate between emotional inhibition and extreme emotional styles
oversimplifies problem solving
form unrealistic goals
comprehensive dialectical behavioral therapy
individual therapy
weekly individual sessions
keeps patient in treatment
treatment hierarchy
life threatening behaviors
treatment interfering behaviors
quality of life interfering behaviors
group skills training
mindfulness
distress tolerance
emotion regulation
interpersonal effectiveness
24 phone coaching
aim: generalize skill usage across contexts
up to 15 mins at a time
structure
brief overview of situation
what did they try
what should they do
they do it
DBT consultation team
therapy for therapist
prevent burnout
APA code of ethics
first introduced in 1952, last amended in 2017
includes
principles
aspirational
general
nice
responsibility
integrity
justic
respect
violations not defined or enforceable
standards
enforceable
applies to a specific task
confidentiality
belongs to patient
limits
danger to self
danger to others
child abuse
victim under age 18
mandated reporters
elder abuse (not for NY)
tarasoff vs regents of the uni, of cali.
introduces duty to warn
psychologists must break confidentiality to warn potential victims when
there’s a treat to harm
there’s an identifiable victim
complications of duty to warn
sometimes no specific victim
risk is not always clear
attempts to warn public are often stonewalled by bureaucracy
what constitutes harm and victim
when victim is minor
legal perspective
clinical perspective
ethical guidelines
multiple relationships
psychologist is in a professional role with a person
has a relationship with the person
has a relationship closely associated with the person
will have a future relationship with the person
insanity defense
criminal responsibility
requires that a person
has been proven to have committed the act, and
was legally sane at the time
sane/insane
legal terms
insane: not legally responsible for actions because of mental disease
m’naughten test
whether the defendant could distinguish right from wrong at the time of the offense
ngri vs gbmi
NGRi
focuses on mental state at the time of the crime
used rarely and succeeds even more rarely
more difficulty bc of Hinckley verdict
result is treatment at hospital, not freedom
GBMI
results in criminal conviction with mental health treatment in prison
competence to stand trial
refers to defendant’s current mental state
proceedings are suspended when a defendant is judged to be incompetent
more people institutionalized for this reason than ngri/gbmi
civil commitment
what it is
legal process that allows involuntary hospitalization of a person with a mental illness when certain criteria are met
typical criteria
mental illness
danger to self, danger to others, or grave disability (unable to care for basic needs)
key points
focuses on safety, not punishment
requires legal authority
duration is short term
balances individual rights with public safety
inpatient or outpatient
patients retain rights, such as treatment in least restrictive environment and refusal of treatment
main sociocultural factors contributing to eating disorders
thing-ideal internalization
fatphobia
weight discrimination
orthorexia trends
media emphasis on appearance
difference between APA general principles and ethical standards
principles are aspirational values guiding psychologists
ethical standards are enforceable rules that can lead to sanctions for violations
core idea of Beneficence and Nonmaleficence
psychologists must strive to help others and avoid causing harm in all professional activities