Week 1 Flashcards
Chapter 9, chapter 10 (112 cards)
1
Q
What are the main features of schizophrenia?
A
Schizophrenia involves disordered thinking, faulty perception and attention, lack of emotional expression, and disturbances in behavior. Individuals may have delusions, hallucinations, social withdrawal, and struggle with daily functioning.
2
Q
How does stigma affect people with schizophrenia?
A
Schizophrenia is highly stigmatized. Studies show derogatory use of terms like #schizophrenia on social media. This stigma contributes to misinformation and social rejection, worsening the disorder’s impac
3
Q
How does schizophrenia affect a person’s daily life and health?
A
It disrupts thinking, emotion, and behavior—making it hard to maintain relationships, jobs, or independence. There are high rates of substance use and suicide; mortality rates exceed those of smokers.
4
Q
What is the lifetime prevalence of schizophrenia and who is more affected?
A
Around 1% of the population is affected. Men are slightly more likely to be diagnosed than women. Diagnosis is more frequent in Black and Latino Americans, possibly due to diagnostic bias and systemic racism.
5
Q
When does schizophrenia typically begin, and what are early signs?
A
It usually starts in late adolescence or early adulthood, earlier in men. Psychotic-like experiences in childhood may indicate higher risk, especially in Black and Latino children, often linked to discrimination
6
Q
What are the criteria for diagnosing schizophrenia?
A
At least two symptoms, with one being delusions, hallucinations, or disorganized speech. Other symptoms include disorganized/catatonic behavior and negative symptoms like lack of emotion or motivation.
7
Q
What are the three major symptom domains of schizophrenia?
A
- Positive: Delusions, hallucinations
- Negative: Avolition, alogia, anhedonia, blunted affect, asociality
- Disorganized: Disorganized speech and behavior
Cultural context should be considered when assessing symptoms.
8
Q
What are positive symptoms of schizophrenia?
A
Excesses and distortions including hallucinations and delusions, often referred to as psychotic symptoms.
9
Q
What is a delusion?
A
A belief contrary to reality that is firmly held despite disconfirming evidence.
10
Q
What is thought insertion?
A
Belief that thoughts not one’s own have been placed in the mind by an external source.
11
Q
What is thought broadcasting?
A
Belief that one’s thoughts are being broadcast so others can hear them.
12
Q
What is a delusion of reference?
A
Belief that unimportant events have personal significance.
13
Q
What is a delusion of control?
A
Belief that an external force controls one’s thoughts or behavior.
14
Q
What is a grandiose delusion?
A
Belief in one’s exaggerated importance, power, or identity.
15
Q
What is a persecutory delusion?
A
Belief that others are trying to harm, harass, or conspire against the individual.
16
Q
What are hallucinations?
A
Sensory experiences without relevant external stimuli, most often auditory in schizophrenia.
17
Q
Which brain areas show greater activity during auditory hallucinations?
A
Broca’s area and Wernicke’s area.
18
Q
What are negative symptoms of schizophrenia?
A
Deficits in motivation, pleasure, social closeness, and emotional expression.
19
Q
What is avolition?
A
Apathy or lack of motivation in routine activities.
20
Q
What is asociality?
A
Lack of interest in social relationships.
21
Q
What is anhedonia?
A
Reduced ability to experience or anticipate pleasure; particularly anticipatory pleasure.
22
Q
What is blunted affect?
A
Lack of outward emotional expression despite experiencing emotion internally.
23
Q
What is alogia?
A
Significant reduction in speech output.
24
Q
What are the two domains of negative symptoms?
A
Motivation/pleasure domain and expression domain.
25
What is disorganized speech?
Incoherent or loosely associated speech, making it hard to follow the person's thoughts.
26
What is disorganized behavior?
Unusual or purposeless behavior like agitation, odd clothing, or wandering.
27
What is catatonia?
Motor abnormality that may include repetitive gestures or immobility
28
How does schizophreniform disorder differ from schizophrenia?
Same symptoms but lasts 1–6 months, not 6+ months.
29
What is brief psychotic disorder?
Psychotic symptoms lasting 1 day to 1 month, often stress-induced.
30
What is schizoaffective disorder?
A mix of schizophrenia symptoms and a mood episode (depressive or manic).
31
What is delusional disorder?
Persistent delusions without other major symptoms of schizophrenia.
32
What contributes to the development of schizophrenia over time?
Genetic, neural, and social factors (e.g., early adversity) interact bidirectionally during development to produce symptoms of schizophrenia.
33
What is the heritability estimate of schizophrenia from behavior genetics studies?
Between 0.77 and 0.81, indicating strong genetic influence, though schizophrenia is genetically heterogeneous.
34
What do family studies reveal about schizophrenia risk?
Risk increases with genetic closeness:
General population: <1%
One parent: 7%
Both parents: 27.3%
MZ twins: 44.3%
DZ twins: 12.08%
Siblings: 7.3%
Children: 9.35%
35
What did the Danish family study (Gottesman et al., 2010) reveal about schizophrenia and bipolar disorder?
Risk is highest if both parents have schizophrenia (27.3%), and risk increases further when one parent has schizophrenia and the other has bipolar disorder (15.6%), suggesting shared genetic vulnerability.
36
What do familial high-risk studies show?
Children of parents with schizophrenia are at highest risk for schizophrenia and are nearly twice as likely to develop any severe psychological disorder compared to children of parents with no psychological disorders.
37
What do twin studies tell us about schizophrenia?
MZ twin concordance is 44.3%, DZ is 12.08%—indicating high heritability, but also some environmental influence (since MZ is <100%).
38
How do adoption studies support genetic influence?
Adopted children of mothers with schizophrenia had an 8.1% risk of schizophrenia (vs. 2.3% in controls), showing risk remains even when reared in non-schizophrenic environments.
39
What is the focus of molecular genetics in schizophrenia research?
Identifying specific genes or mutations that contribute to vulnerability—like CNVs (copy number variations) and SNPs (single nucleotide polymorphisms).
40
What are CNVs and how are they related to schizophrenia?
CNVs are rare DNA deletions or duplications. Certain CNVs (e.g., 22q11.21, 15q13.3, 1q21) are more common in schizophrenia and also seen in autism and intellectual disability, indicating non-specific genetic vulnerability.
41
What are SNPs and what do they reveal?
SNPs are single base-pair changes. GWAS show SNPs are associated with schizophrenia, bipolar disorder, ADHD, and other disorders—again indicating shared genetic vulnerability.
42
What are the main findings from the GWAS conducted by the Psychiatric Genomics Consortium (PGC)?
- 2014: Found 108 genetic loci linked to schizophrenia in >36,000 cases.
- 2022: Larger sample (76,000 cases, 240,000 controls) confirmed and added more loci.
- Supports schizophrenia being polygenic (involving many genes).
43
How significant are CNVs and SNPs in accounting for schizophrenia risk?
CNVs account for <1% of genetic variance; SNPs <25%. Many people with these mutations do not develop schizophrenia, and these mutations are not specific to it.
44
What do the findings imply about the genetic basis of schizophrenia?
Schizophrenia is genetically heterogeneous; it likely results from a combination of many rare mutations, most of which are not specific to schizophrenia and also raise risk for other disorders.
45
How did the dopamine theory of schizophrenia originate, and why is it considered insufficient on its own?
The theory originated from the observation that antipsychotic drugs reduce dopamine activity and produce Parkinson-like symptoms. These drugs block D2 dopamine receptors. However, the theory is insufficient because it mainly explains positive/disorganization symptoms, not negative symptoms like avolition or anhedonia, and schizophrenia involves multiple brain systems and neurotransmitters.
46
What is the connection between dopamine and negative symptoms of schizophrenia?
Research suggests that motivational deficits (e.g., avolition and anhedonia) are linked to dopamine dysfunction in the striatum. However, this link is weaker compared to dopamine’s role in positive symptoms. Dysfunction in anticipatory pleasure and reward processing is implicated.
47
What evidence supports a role for glutamate and NMDA receptor dysfunction in schizophrenia?
Low glutamate levels and reduced NMDA receptor activity (especially in the prefrontal cortex) are observed in people with schizophrenia. Drugs like PCP and ketamine mimic schizophrenia symptoms by blocking NMDA receptors. Cognitive and disorganization symptoms are linked to NMDA deficits, but glutamate-targeting meds show only modest efficacy.
48
What are the key structural brain abnormalities observed in schizophrenia?
Common findings include enlarged ventricles (indicating brain tissue loss), reduced cortical thickness (especially in the frontal and temporal lobes), reduced hippocampal volume, and decreased dendritic spines. These abnormalities disrupt neural connectivity and are seen early in the illness—even before treatment.
49
How does the loss of dendritic spines contribute to schizophrenia symptoms?
Dendritic spines are critical for synaptic communication. Their loss disrupts connectivity between neurons, potentially leading to disorganized thought and behavior. This is referred to as “disconnection syndrome” and may stem from genetic abnormalities such as CNVs.
50
What has functional imaging revealed about connectivity in schizophrenia?
fMRI studies show reduced connectivity within and between key networks (e.g., frontoparietal, default-mode). Lower connectivity correlates with worse cognition and negative symptoms. Connectivity deficits also appear in healthy relatives, suggesting a heritable component.
51
What are key environmental risk factors for schizophrenia, and how do they interact with brain development?
Risk factors include birth complications (hypoxia), prenatal infections (e.g., T. gondii), maternal stress, and adolescent cannabis use. These interact with genetic vulnerability and affect brain regions like the hippocampus and HPA axis, possibly triggering symptoms when the prefrontal cortex matures in adolescence.
52
Why might schizophrenia symptoms emerge during adolescence despite early brain abnormalities?
The prefrontal cortex matures in adolescence and undergoes synaptic pruning. Excessive pruning may remove critical connections, contributing to symptom onset. Increased dopamine activity and stress reactivity during adolescence may also trigger the first episode.
53
What are the primary components of schizophrenia treatment?
A combination of short-term hospitalization, antipsychotic medications, and psychosocial interventions.
54
How do first-generation antipsychotics work and what are key side effects?
They block dopamine receptors to reduce positive symptoms. Side effects include extrapyramidal symptoms (e.g., tremors, rigidity), sedation, sexual dysfunction, and tardive dyskinesia.
55
How do second-generation antipsychotics compare to first-generation ones?
They were expected to be more effective and have fewer side effects but studies (e.g., CATIE) show similar efficacy and equally unpleasant side effects (e.g., weight gain, metabolic syndrome).
56
What is tardive dyskinesia and which drugs can cause it?
A late-onset movement disorder causing involuntary facial and body movements, mostly caused by long-term use of first-generation antipsychotics.
57
What are some concerns related to antipsychotic drug prescription disparities?
Black patients are more likely to be prescribed first-generation antipsychotics, which may cause more side effects in this population, reflecting racial disparities in treatment.
58
What is the role of transcranial direct current stimulation (tDCS) in schizophrenia treatment?
tDCS can reduce auditory hallucinations and alleviate negative symptoms by stimulating the frontal/temporal cortex with weak electrical currents.
59
How does social skills training help in schizophrenia?
It teaches everyday interpersonal skills (e.g., job interviews, social interactions) and has been shown to reduce relapse and improve quality of life.
60
What are key components of effective family therapy for schizophrenia?
Education about the illness, medication info, blame reduction, communication skills, problem-solving, social support expansion, and instilling hope.
61
How common is substance use and substance use disorder in the U.S.?
In 2018, ~32 million people (age 12+) used illicit drugs in the past month; 36.4M used marijuana; 133.1M used alcohol. In 2021, 46.3M had a substance use disorder—29.5M had alcohol use disorder, 24M had drug use disorder, and 7.3M had both.
62
What are the defining symptoms of a substance use disorder (DSM-5-TR)?
Trouble meeting obligations
Use despite danger or relationship issues
Withdrawal and tolerance
Using more than intended, or failed efforts to cut back
Excessive time spent obtaining/using
Cravings
Giving up activities
Note: Tolerance = needing more for effect or reduced effect at same dose; Withdrawal = negative effects after stopping/reducing use.
63
What are the key characteristics and comorbidities of alcohol use disorder (AUD)?
AUD is the most common substance use disorder. Tolerance and withdrawal (e.g., tremors, insomnia, hallucinations—DTs) often indicate severe AUD. AUD frequently co-occurs with nicotine use due to cross-tolerance and shared brain reward pathways (dopamine).
64
How does alcohol use disorder vary by sex and ethnicity?
Men: 12.1% | Women: 9.1%
Highest rates: Native Americans (15.6%) and Multiracial (14.7%)
Lowest: Asians (6.0%)
Sex differences in alcohol problems have narrowed significantly since mid-20th century.
65
What are the short-term effects of alcohol and how is it metabolized?
Alcohol is metabolized mostly in the liver (1 oz of 100-proof/hr), with absorption slowed by food. Effects vary by body weight, fat, and liver efficiency. Alcohol affects GABA (tension reduction), dopamine/serotonin (pleasure), and inhibits glutamate (slows cognition/memory). Even legal limits (0.08 BAC) impair decision-making and motor control.
66
What are long-term effects of heavy alcohol use?
- Organ damage (esp. liver cirrhosis)
- Vitamin deficiency (B-complex) causing memory loss
- Fetal Alcohol Spectrum Disorders (FASD): Includes fetal alcohol syndrome (FAS), the most severe, with intellectual disability and physical anomalies
- Brain damage: Reduced gray matter in memory areas like the hippocampus
67
What are the risks of alcohol use during pregnancy?
Even moderate drinking can harm fetal development. FAS is the most severe form of FASD and can cause slowed growth, facial abnormalities, and intellectual disability. Estimated 1–5% of U.S. children may be affected. Total abstinence is advised during pregnancy.
68
Does moderate alcohol consumption offer health benefits?
Earlier studies suggested lower coronary risk, but recent evidence (2023 meta-analysis, 5M people) found no mortality benefit for light/moderate drinkers. Health advantages seen may reflect lifestyle factors (e.g., diet, exercise) rather than alcohol itself.
69
What role does nicotine play in tobacco addiction, and what brain area is involved?
Nicotine is the primary addictive component in tobacco. It activates neural pathways that stimulate dopamine neurons in the mesolimbic area, which contributes to the reinforcing effects of most drugs.
70
What are the health consequences of smoking and the trends in smoking prevalence?
Smoking causes emphysema, various cancers, cardiovascular diseases, complications during pregnancy, and more. Although over 20 million Americans died from smoking between 1964–2014, 45 million quit. Smoking declined more among the educated (83%) than the less educated (39%). It remains the leading preventable cause of death.
71
How do income and race affect smoking-related outcomes?
Smoking is more prevalent among lower-income individuals, exacerbating health disparities. Black smokers metabolize nicotine more slowly and often smoke menthol cigarettes, which are inhaled more deeply and increase health risks. Menthol cigarettes are targeted via marketing and are under proposed FDA regulation.
72
What are the dangers of secondhand smoke (environmental tobacco smoke)?
ETS contains higher concentrations of toxins than inhaled smoke. It causes lung damage, increased cardiovascular and cancer risk, and harms infants and children (e.g., low birth weight, infections). The Surgeon General recommends smoke-free environments, and 23 states + DC enforce strict laws.
73
What are e-cigarettes and their associated health risks and trends?
E-cigarettes deliver liquid nicotine via vapor. While less toxic than cigarettes, they still contain harmful chemicals. Vaping surged among high school students 2017–2019 but declined during COVID. Vaping is most common among adolescents and may lead to tobacco, alcohol, and marijuana use.
74
How are e-cigarettes regulated and what does research say about their health effects?
Since 2016, the FDA regulates e-cigarettes like tobacco products (age restrictions, warning labels). The National Academies report finds that e-cigarettes are:
- Less toxic than cigarettes
- Potentially helpful for adult smoking cessation
- Risky for youth (gateway effect)
- Harmful through secondhand aerosols
75
What are the usage trends and effects of cannabis and synthetic cannabis?
Marijuana is the most used drug in the U.S., especially among youth. 36.4 million reported use in the past month (2021). THC causes intoxication; CBD does not. Synthetic cannabis (e.g., Spice, K2) is banned. Potency has increased (e.g., edibles, blunts), leading to greater cognitive and psychological risks.
76
What are the cognitive and health effects of long-term cannabis use, and what are its therapeutic uses?
Chronic cannabis use is linked to cognitive deficits, IQ decline, and reduced hippocampus volume. It impairs driving and lung function, and may cause withdrawal symptoms. Therapeutically, it helps with nausea, glaucoma, pain, and muscle spasms. Legal in 22 states and medically in most others, though it remains federally illegal.
77
What are common types of opioids and examples of prescription medications?
Opioids include opium, morphine, heroin, and codeine. Prescription opioids include:
- Hydrocodone: Vicodin, Lortab, Norco
- Oxycodone: OxyContin, Percocet, Percodan
- Morphine: Avinza, MS Contin
- Fentanyl: Actiq, Fentora
- Others: Tramadol (Ultram), Oxymorphone (Opana), Hydromorphone (Dilaudid), Buprenorphine (Suboxone), Methadone
Buprenorphine and methadone are also used to treat opioid addiction
78
How common is opioid misuse and what are the recent trends?
In 2021:
- 8.7 million misused prescription pain meds
- 5.5 million met criteria for opioid use disorder
- 1.1 million used heroin
- Misuse often starts with prescription pain meds.
- White Americans misuse opioids more than other groups.
- Misuse is slightly more common in men, though women use more prescriptions.
- Rates may have plateaued or declined slightly since 2016.
79
What are the three waves of opioid overdose deaths in the U.S.?
1990s – Driven by prescription opioids (e.g., OxyContin)
~2010 – Driven by heroin
~2013–present – Driven by synthetic opioids (esp. fentanyl)
80
What are the psychological and physical effects of opioid use?
- Psychological: euphoria, rush (warm ecstasy), drowsiness, confidence, worry-free state
- Physical: drowsiness, lack of coordination, stupor after high
- Effects last 4–6 hours, followed by a severe letdown
- Mechanism: stimulate brain's opioid receptors (endorphins/enkephalins); heroin converts to morphine in brain
- Pleasure linked to dopamine and nucleus accumbens activity
81
What role did pharmaceutical companies and regulation play in the opioid crisis?
- Companies claimed addiction risk was low → encouraged overprescribing
- Lawsuits followed once addiction risks became clear
- Pills (e.g., OxyContin, Opana) originally easy to crush/snort/inject
- Reformulated as extended-release to prevent misuse
- Stricter regulation decreased prescription-related deaths, but fentanyl deaths increased dramatically since 2015
82
What are the withdrawal symptoms of opioids and how do they progress?
Withdrawal from heroin (aka "dopesick") begins ~8 hours after last use in tolerant individuals.
Early symptoms:
- Muscle pain, sneezing, sweating
- Yawning, tearfulness (flu-like)
At ~36 hours:
- Muscle twitching, cramps, chills, flushing, high BP & heart rate
- Insomnia, vomiting, diarrhea
Symptoms last ~72 hours and gradually decline over 5–10 days.
83
What are stimulants and how do amphetamines affect the body?
Stimulants (e.g., amphetamines, cocaine) increase alertness, motor activity via the sympathetic nervous system.
Amphetamines (e.g., Adderall, Dexedrine):
- Increase norepinephrine & dopamine release
- Block their reuptake
Effects: Wakefulness, energy, euphoria, confidence; appetite suppression
Side effects (high doses): Nervousness, palpitations, agitation, paranoia
Tolerance can develop in as little as 6 days.
84
What are the patterns and effects of methamphetamine use?
- Over 2.5 million used meth in 2021
- More common among men; prevalent in rural areas
- Common names: crystal meth, ice
- Taken orally, injected, or snorted
Effects: Intense high (rush), increased blood flow & body temp
Crash phase: agitation (“tweaking”)
Craving lasts years and predicts relapse
Overdose deaths quadrupled between 2015–2021
85
What are the effects of chronic meth use on the brain?
- Damages dopamine and serotonin systems
- Reduces brain volume in frontal & temporal lobes
- Shrinks hippocampus → linked to memory problems
- Affects insula, striatum, and decision-making regions
Low activation in these areas predicts relapse
Unclear if brain changes cause or result from meth use
Hard to isolate effects due to co-use of other substances
86
What characterizes dependence and withdrawal from amphetamines and meth?
- Tolerance builds quickly → higher doses needed
- Withdrawal symptoms include fatigue, depression, irritability
- Physiological dependence common in chronic users
- Cravings are intense and long-lasting
- Risk of overdose is high and often fatal
- Meth causes more severe and lasting brain damage than other stimulants
87
What are the methods, effects, and risks of cocaine use?
Comes from coca shrub; crack is a smokable rock-crystal form (named for crackling sound)
Methods: snorted, smoked, swallowed, injected; often mixed with heroin
In 2021: 4.76M used cocaine (1.7% of 12+), ~1M used crack
Men use more than women
Mechanism: Blocks dopamine reuptake → more dopamine in synapse → euphoria
Effects: Confidence, stamina, well-being
Overdose: chills, nausea, insomnia, paranoia, hallucinations (e.g., bugs under skin)
Chronic use: irritability, social issues, sleep/eating disturbances, paranoia
Tolerance may develop; withdrawal is severe
Health risks: vasoconstriction → heart attack, stroke, cognitive impairments (memory, attention)
88
What are the effects of LSD and other classic hallucinogens?
Hallucinogens: LSD, psilocybin, mescaline, Ecstasy (MDMA)
2021: 7.4M people (12+) used hallucinogens
LSD use rose in recent years; peak among teens since 2000
Acts on serotonin system, especially 5-HT2A receptor
Effects (start within 30 mins, last up to 12 hrs): hallucinations, time distortion, mood swings, expanded awareness
No withdrawal symptoms, but tolerance develops quickly
Risks: anxiety, fear of losing control (“going crazy”), flashbacks
Hallucinogen Persisting Perception Disorder = lingering flashbacks after drug use ends
Therapeutic potential: modest success in reducing anxiety in terminal illness
89
What are the effects and developments surrounding psilocybin and MDMA?
Psilocybin gaining popularity; researched for end-of-life & mental health benefits
2020: Oregon decriminalized & approved medical use; trend toward legalization
Ecstasy (MDMA) = hallucinogen + amphetamine properties
2021: 2.1% of adults (18+) used MDMA
Common among college students & 2% of high schoolers
Street form “Molly” marketed as purer MDMA (but often adulterated)
Mechanism: releases & then reuptakes serotonin
Effects: enhanced emotional insight, aesthetic awareness, euphoria, empathy
Side effects: muscle tension, eye movement, jaw clenching, chills, nausea, anxiety, confusion
Therapeutic potential: MDMA-assisted therapy more effective than placebo for PTSD (2021 study)
90
What are the effects and dangers of PCP (phencyclidine) use?
PCP (angel dust) and ketamine classified as phencyclidine use disorder in DSM-5-TR
More men use than women
Mechanism: Affects multiple brain neurotransmitters
Effects: Severe paranoia, hallucinations, potential for violence
High doses: coma and death possible
Chronic use → cognitive & neuropsychological impairments
Hard to isolate PCP’s effects due to frequent co-use with other drugs
91
What is the role of genetic and gene–environment interactions in substance use disorders?
Heritability estimates for substance use disorders: 0.40–0.60
Genetic influence is shared across substances, supported by GWAS studies
Twin studies support genetic involvement in:
Alcohol use disorder
Smoking
Heavy marijuana use
General drug use disorders
Gene–environment interactions:
Risk for alcohol use disorder higher after divorce in those with family history
Peer influence increases genetic effects (e.g., teens whose friends drink/smoke show higher heritability)
Popularity of smoking in school peers increases genetic risk for teen smoking
Genes do not act in isolation but interact with environment to influence substance use behavior
92
Which specific genes influence alcohol and nicotine use, and how might genetics be protective?
Alcohol metabolism genes:
ADH2, ADH3 → involved in alcohol dehydrogenase (alcohol breakdown)
ADLH → aldehyde dehydrogenase; GWAS link to alcohol use disorder
~75% of some Asian populations experience flushing from small alcohol doses due to enzyme deficiency, reducing alcohol use
Nicotine metabolism gene:
CYP2A6: slower metabolism → nicotine stays longer in brain
Faster metabolism → more smoking, greater addiction risk
Slower metabolism → fewer cigarettes, less nicotine dependence, lower lung cancer risk
Variants in CYP2A6 linked to lung cancer risk and smoking behavior
Marijuana use:
GWAS on 32,000+ people identified 4 genes, but none reached genome-wide significance, showing challenges in finding specific marijuana-linked genes
93
How is the dopamine system involved in substance use disorders?
Dopamine pathways, especially the mesolimbic pathway, are linked to pleasure and reward
All drugs, including alcohol, stimulate dopamine pathways (Koob & Le Moal, 2008; Volkow & Boyle, 2018)
Two models explain dopamine’s role in SUDs:
Vulnerability model: dopamine dysfunction increases risk
Toxic effect model: dysfunction is a result of drug use
Both models have support for substances like cocaine and opioids
94
How do withdrawal and stress contribute to continued substance use and relapse?
People often use drugs to relieve withdrawal symptoms, not just for pleasure
Withdrawal can be severe (e.g., alcohol, meth, heroin)
Stress after quitting increases vulnerability to relapse
Study: people with alcohol use disorder had greater stress responses after stopping use (Moberg et al., 2017)
Animal research supports that stress triggers drug-seeking behavior
95
What is the incentive-sensitization theory, and how does it explain craving?
Developed by Robinson & Berridge (1993, 2003)
Distinguishes between:
"Liking" = pleasure from drug
"Wanting" = intense craving
Dopamine system becomes supersensitive to drug cues (e.g., needles, rolling papers)
Over time, "liking" decreases, but "wanting" remains intense
Cues trigger craving and drive compulsive drug-seeking behavior
96
What is the relationship between craving, drug cues, and brain inhibition?
Drug cues (e.g., videos, objects) trigger:
Increased physiological arousal, craving, and negative emotion in users
Activation of brain reward areas in fMRI studies
Anticipating drug use (e.g., seeing a cigarette) reduces stress more than use itself (Bradford et al., 2015)
Meta-analysis: exposure to cues doubles the risk of relapse (Vafaei & Kober, 2022)
Studies using the go/no-go task show:
Brain areas (basal ganglia, inferofrontal gyrus) are involved in inhibitory control
Greater activation in these regions → better inhibition, weaker link between craving and use
Longitudinal studies confirm: more craving = more use, even after trying to quit
97
How do people with substance use disorders value short-term versus long-term rewards, and what brain regions are involved?
People with substance use disorders often prefer immediate, smaller rewards over larger, delayed ones
This tendency is called delay discounting
They discount delayed rewards more steeply, seen with opioids, nicotine, heroin, cocaine (Bickel et al., 2014)
Delay discounting predicts smoking initiation in adolescents (Audrain-McGovern et al., 2009)
Brain regions:
Immediate reward → amygdala & nucleus accumbens
Delayed reward → prefrontal cortex
These brain systems compete during decision-making (Bechara et al., 2005; 2019)
98
How does risky decision making relate to substance use disorders, and what brain regions are involved?
People with substance use disorders often make risky or impulsive decisions about substance use
Difficulty tolerating ambiguous risks (e.g., "I might get caught") is linked to higher relapse rates
Known risks (e.g., "I'll be late for work") are less predictive
Brain areas involved:
Risky decisions → orbitofrontal cortex, parietal cortex, anterior cingulate cortex (rostral)
Ambiguity tolerance → dorsolateral prefrontal cortex, parietal cortex, anterior cingulate cortex (dorsal)
99
How does emotion regulation relate to substance use?
People may use drugs/alcohol to enhance positive or diminish negative emotions
Those with substance use disorders may have impaired emotion regulation, especially involving the prefrontal cortex
Substances reduce negative emotion more when there's uncertainty, unpredictability, or distraction
Alcohol creates "alcohol myopia": focus on immediate cues, reducing negative emotions temporarily
100
When do substances reduce negative emotions most effectively?
Distraction plays a key role: alcohol/nicotine reduce negative emotion more when attention is diverted
Without distraction (e.g., drinking alone), negative emotions can intensify
Nicotine + distraction reduces anxiety more than nicotine alone
101
Why might people use alcohol in social situations?
Alcohol helps shift attention from fear of rejection to social enjoyment
Alcohol increases smiling and bonding in group settings more than placebo
These effects are stronger than just expecting alcohol
102
How do expectations influence substance use?
People may drink/use drugs due to expectations of stress relief or social enhancement
Positive expectancies predict more frequent use
Expectancies form in childhood and increase with exposure
False beliefs (e.g., alcohol increases social skill) lead to heavier use
103
What personality traits are linked to substance use disorders?
High negative emotionality (neuroticism)
Low constraint (disinhibition, risk-taking)
Also linked: low agreeableness and low conscientiousness
These traits predict alcohol, nicotine, and illicit drug use
104
What sociocultural factors influence substance use?
Influences include peers, media, cultural norms, and access
Peer groups strongly predict future substance use
Social influence model: peers affect behavior
Social selection model: people choose peers who match their habits
Both models are supported
105
How does media and advertising impact substance use?
Advertising shapes expectancies and increases use among youth
Exposure to alcohol or e-cigarette ads linked to higher initiation rates
Tobacco companies target youth, especially with menthol cigarettes
Public health ads reduce likelihood of starting smoking
106
What are effective psychological treatments for quitting smoking?
Physician advice remains common and impactful.
Quitlines & digital tools (e.g., websites, texts, social media) offer accessible support.
Pleasant smells (e.g., lemon, peppermint) can reduce cravings for up to 5 minutes.
Gradual reduction in smoking is often more effective than quitting abruptly.
Coping skills training helps identify triggers and manage cravings (relapse prevention).
Project EX: A school-based global program proven effective up to 1 year post-treatment.
Cognitive-behavioral therapy (CBT) with a focus on problem-solving shows promise
107
What are the main nicotine replacement therapies (NRT) and medications for smoking
NRT forms: gum, lozenges, sprays (fast-acting); patches (slow, steady release); e-cigarettes (under study).
Gum/lozenges: Absorbed slower than smoking; may raise BP—caution in heart patients.
Patch: Daily application; improves compliance but underused (40% adherence); effective after ~8 weeks.
Combo treatments (e.g., patch + gum/spray) are most effective.
E-cigarettes: Show promise in studies, but more trials needed to confirm efficacy.
Medications:
Bupropion (Wellbutrin): Some effectiveness.
Varenicline (Chantix): Effective alone or with NRT or behavioral therapy; works for men & women.
Bupropion + Varenicline may be more effective than varenicline alone.
NRT not a cure-all: <50% abstinent at 12-month follow-up. Best used with psychological support.
108
What psychological treatments are effective for substance use disorders?
Cognitive Behavioral Therapy (CBT): Helps avoid high-risk situations, develop coping strategies, and resist relapse.
CBT4CBT: Computer-based CBT; more effective than standard counseling and even clinician-led CBT at 6-month follow-up.
Contingency Management: Rewards abstinence (e.g., vouchers/prizes); effective for many substances (e.g., cocaine, meth, nicotine).
Motivational Interviewing: Combines CBT and patient-driven solutions; effective for alcohol and drug use disorders.
All approaches emphasize coping, relapse prevention, and behavioral reinforcement
109
What are key features and outcomes of residential and legal-based treatment programs?
Residential Programs (e.g., Phoenix House):
Remove individuals from drug-using environments.
Provide structured, drug-free support with role models.
Emphasize accountability and respect.
High dropout rates limit generalizability of success.
Drug Courts:
Offer treatment instead of prison for nonviolent drug offenses.
40% completion rate in CA; 4x cheaper than prison.
Slight increase in re-arrests post-treatment vs. before the program.
Methamphetamine Treatment Project (Matrix Model):
Longer retention and reduced use during treatment.
No long-term advantage at 6-month follow-up.
Promising but more research needed.
110
What are the two main types of medications used in medication-assisted treatment (MAT) for opioid use disorder?
1. Opioid Substitutes (Agonists):
Mimic opioids but don’t produce a high.
Examples: Methadone, Buprenorphine.
Reduce cravings and withdrawal symptoms.
2. Opioid Antagonists:
Block opioid effects; no high if opioids are used.
Examples: Naltrexone, Naloxone.
Used to prevent relapse and reverse overdoses.
111
What are the pros and cons of methadone and buprenorphine in treating opioid use?
Methadone:
Requires daily clinic visits; higher doses more effective.
Works best with counseling and social support.
Side effects and stigma may cause dropouts.
Buprenorphine:
Can be taken at home; less addictive.
Barriers still exist (e.g., rural access, racial disparities).
Suboxone (buprenorphine + naloxone) reduces abuse potential and relapse.
112
How do naltrexone and naloxone help treat opioid use disorders?
1. Naltrexone (e.g., Vivitrol):
Opioid antagonist; blocks the high.
Available as pill, implant, or injection.
Implants shown to reduce cravings and use more than pills.
2. Naloxone (e.g., Narcan):
Reverses opioid overdose.
Now sold over-the-counter as nasal spray.
Often combined with buprenorphine in Suboxone.
