Module 4/Module 5

What is a substance in the context of psychopathology?

Any natural or synthesized product with psychoactive effects that changes thoughts, perceptions, emotions, or behaviors (e.g., alcohol, nicotine, cannabis, caffeine).

What is the difference between substance use, addiction, and substance use disorder?,

Substance use = necessary but not sufficient for a disorder.

Addiction = not a diagnostic term; can mean physiological dependence or compulsive use. Substance Use Disorder = meeting at least 2 of 11 DSM-5 criteria for problematic use.

Why do alcohol consumption rates vary across cultures?

Differences in cultural acceptability, genetics (e.g., gene in people of Asian descent causing aversive reactions), availability, legality, and cost

What are substance-induced disorders?

Disorders caused by substances, including intoxication and withdrawal.

What is intoxication?

Behavioral and psychological changes directly from a substance; must cause impairment/distress; depends on dose, tolerance, chronicity, expectations, and environment

What is withdrawal?

Physical and behavioral symptoms from reducing/stopping heavy/prolonged use; must cause impairment/distress.

What are the four main categories of DSM-5 SUD criteria?

Impaired control over use, social/work impairment, risky use, tolerance or withdrawal.

What are the main substance categories?

Depressants, stimulants, opioids, hallucinogens/PCP, cannabis

What are the effects of alcohol intoxication?,

Low doses: self-confidence, relaxation, mild euphoria.

High doses: motor problems, depressed mood, confusion, impaired sexual function, dizziness.

What are the stages of alcohol withdrawal?

(1) Shakes: sweating, weakness, nausea, cramps (2–48 hrs).

(2) Convulsive seizures (1–3 days).

(3) Delirium tremens: hallucinations, delusions, fever, sweating (fatal in 10% of severe cases).

What are long-term effects of alcohol?

Hypertension, cancer risk, Wernicke’s encephalopathy, alcohol-induced dementia, Fetal Alcohol Syndrome.

What are benzodiazepines and barbiturates used for?

Prescribed as anxiolytics (anti-anxiety), anti-convulsants, and sleep aids (e.g., Xanax, Valium, Ativan).

How do benzodiazepines and barbiturates compare to alcohol?

Their intoxication and withdrawal symptoms are very similar to alcohol. Overdose can be fatal.

How does cocaine work in the brain?

Cocaine is a dopamine agonist that blocks dopamine reuptake, increasing dopamine in the synapse.

What are the effects of cocaine intoxication?

Lower dose: alertness, energy, euphoria, competence.

Higher dose: grandiosity, impulsivity, compulsive behaviors, agitation, anxiety.

What are the effects of cocaine withdrawal?

Exhaustion, depression.

What are amphetamines, and how are they used?

Manufactured stimulants (e.g., Adderall); introduced as antihistamines. Taken by injection, snorting, smoking, or orally.

How do amphetamines work in the brain?

Release dopamine and norepinephrine while blocking their reuptake → fight-or-flight response.

What are possible effects of amphetamine use?

Euphoria and energy, but also risk of psychotic disorder from inability to distinguish reality. Tolerance and dependence develop quickly.

What are amphetamine withdrawal symptoms?

Depression, memory loss, confusion, paranoia, perceptual abnormalities.

What are medical consequences of amphetamine use?

Cardiovascular problems, overdose risk, death.

What are the effects of opioid intoxication?

Low dose: euphoria, warmth, lethargy, drowsiness, slurred speech, vivid dreams.

High dose: unconsciousness, coma, seizures, reduced cardiovascular function.

What are opioid withdrawal symptoms?

Dysphoria, anxiety, agitation, achy feelings, vomiting, diarrhea.

What are the effects of hallucinogen intoxication?

Perceptual changes, sense of clarity/connectedness, euphoria; sometimes anxiety, paranoia, motor control loss.

Do hallucinogens have withdrawal symptoms?

No known withdrawal symptoms.

What are the effects of MDMA?

Stimulant effects plus hallucinogenic properties: energy, euphoria, sensory distortions.

What are MDMA withdrawal symptoms?

Fatigue, loss of appetite, depressed mood, trouble concentrating.

What are long-term risks of MDMA?

Memory/learning problems, lower intelligence, hyperthermia, cardiac issues, liver failure, anxiety, depression, paranoia, psychotic symptoms.

What is the prevalence of cannabis use?

Most widely used federally illicit drug in the U.S.; more common in men; highest in ages 18–29, lower in 45+.

What are the effects of cannabis intoxication?

Low dose: relaxation, dizziness, euphoria, impaired memory, motor issues, dry mouth. Moderate/high dose: hallucinations, perceptual distortions, depersonalization, paranoia.

What are long-term consequences of cannabis use?

Can trigger psychotic episodes in vulnerable people; impairments in attention and control.

What are cannabis withdrawal symptoms?

Anxiety, loss of appetite, night sweats, hot flashes, sweating.

What is cannabinoid hyperemesis syndrome?

A condition from chronic heavy cannabis use that causes severe nausea and vomiting.

What does the dopamine hypothesis suggest about drug use?

Drugs cause dopamine release, leading to pleasure, though the process is more complex.

What is incentive sensitization in substance use?

With repeated exposure, the “wanting” of the drug increases even if “liking” stays the same or decreases. Drug cues trigger craving.

According to the opponentprocess model, why does substance use continue over time?

Process A = pleasure from use. Process B = avoidance of withdrawal. Over time, avoiding withdrawal (Process B) becomes more important.

How does social learning theory explain substance use?

Substance abuse is modeled and learned from deviant peers, consistent with research linking peer groups to increased use.

Which personality traits increase risk for substance use?

Disinhibition and high reward sensitivity.

What does the biopsychosocial model suggest about substance use?

Exposure is necessary, but genetic, social, and psychological factors shape whether someone becomes addicted.

Disease model vs harm reduction model of treatment?

Disease model = abstinence is necessary.

How do antagonist drugs help in treatment?

They block or change effects of addictive drugs, e.g., naltrexone (opioids), Antabuse (alcohol).

What is the goal of methadone maintenance programs?

Reduce withdrawal and euphoria from heroin, eventually tapering off.

In motivational interviewing, what is the therapist’s role?

Not to challenge substance use directly, but to help the client find their own reasons to change.

A client drinks after work to “cope with stress.” Which cognitive factor contributes to this use?

Expectancies and beliefs about coping with substances.

A person relapses after one drink and says, “I’ve failed, so I may as well binge.” What effect is this?

Abstinence violation effect.

Why isn’t obesity classified as an eating disorder?

It results from a mismatch between biological homeostatic processes and the current environment, not from a disordered eating pattern.

What are the negative physical health consequences of obesity?

Increased risk of coronary heart disease, hypertension, stroke, type 2 diabetes, and higher mortality.

What are the negative mental health consequences of obesity?

Weight stigma, increased risk for eating disorders, and association with other mental health issues.

Core features of anorexia nervosa?

Very low body weight (BMI < 18.5), intense fear of weight gain, distorted body image.

Common behaviors in anorexia?

Food rituals (cutting food small), excessive exercise, perfectionism, restlessness.

Subtypes of anorexia?

Restricting type (limit intake) and binge/purge type (overeating + purging).

Key medical complications of anorexia?

Lanugo, osteoporosis, amenorrhea, cardiovascular problems, slow digestion.

What is the mortality rate of anorexia nervosa?

Around 5–8%, with ~20% of deaths due to suicide.

What defines binge eating in bulimia?

Eating a very large amount of food with loss of control.

Compensatory behaviors in bulimia?

Purging (vomiting, laxatives, diuretics) or nonpurging (excessive exercise, fasting).

Medical complications of bulimia purging?

Damage to throat, salivary glands, ruptured stomach, constipation.

Key difference between bulimia and anorexia?

Bulimia occurs at normal or above normal weight.

What is the longterm course of bulimia?

Onset in adolescence/early adulthood; chronic/intermittent; ~50% still symptomatic after 15 years.

Core features of binge eating disorder?

Large food consumption with loss of control, marked distress, and no compensatory behaviors.

Indicators of binge eating disorder?

Eating rapidly, until uncomfortably full, when not hungry, or alone; guilt/disgust afterward.

Core features of ARFID?

Low interest in food, sensory avoidance, or fear of negative consequences from eating.

Consequences of ARFID?

Weight loss/failure to gain, nutritional deficiencies, dependence on supplements/feeding, psychosocial impairment.

Purging disorder vs. bulimia?

Purging disorder = purging without binge eating.

Atypical anorexia?

Significant weight loss and fear of gaining weight, but not underweight.

Night eating syndrome?

Repeated eating after waking up or excessive eating after dinner (not explained by sleep disorders).

Gender differences in eating disorders?

More common in women (thin ideal), men pressured toward muscular ideal.

Objectification theory (male gaze)?

Suggests women internalize external appearance pressures, contributing to eating disorders.

Risk in minority groups?

Higher prevalence in sexual and gender minorities.

Sociocultural theories?

Media, peer, and family pressures increase risk.

Psychological traits linked to eating disorders?

Perfectionism, impulsivity, emotion regulation difficulties, family dynamics.

Genetic heritability of eating disorders?

40–60%.

Brain and hormone involvement in eating disorders?

Hypothalamus, dopamine/serotonin dysregulation, ovarian hormones.

What is weight suppression?

Difference between highest lifetime weight and current weight; linked to hormonal changes (e.g., reduced leptin → more hunger).

First treatment goal in anorexia?

Weight restoration.

Best treatment for adolescents with anorexia?

Family based therapy.

Medications for anorexia?

No gold standard; Olanzapine shows promise.

Best treatment for bulimia?

Cognitive behavioral therapy (CBT). SSRIs (e.g., Prozac) can help.

Best treatment for binge eating disorder?

CBT is most effective. SSRIs sometimes used, Vyvanse (stimulant) controversial