DSST Substance Abuse cheat sheet

Anabolic-androgenic steroids (AAS) are synthetic testosterone analogs; medical uses include hypogonadism and wasting conditions, but nonmedical use aims at muscle mass and performance.

AAS adverse effects: acne, gynecomastia, testicular atrophy, infertility, hypertension, dyslipidemia (LDL up, HDL down), left ventricular hypertrophy, hepatic peliosis and tumors (especially oral 17-alpha-alkylated forms), and psychiatric effects including aggression and mania.

AAS withdrawal produces depression, fatigue, decreased libido, and sometimes suicidal ideation; effects can last weeks to months and are not always captured by standard withdrawal scales.

Over-the-counter (OTC) medications with abuse potential include dextromethorphan (dissociative at supratherapeutic doses), loperamide (opioid-like at high doses, cardiotoxic), and first-generation antihistamines (anticholinergic delirium).

Pseudoephedrine and ephedrine are OTC sympathomimetics subject to retail sale limits because they are precursor chemicals for methamphetamine; high doses cause hypertension, tachycardia, and arrhythmia.

Prescription drug misuse includes taking a drug without a prescription, in a manner other than prescribed, or for the experience; common classes are opioids, benzodiazepines, and stimulants.

Alcohol is a CNS depressant acting at GABA-A and NMDA receptors; chronic heavy use causes tolerance, withdrawal seizures, and Wernicke-Korsakoff syndrome (thiamine deficiency).

Opioids (heroin, fentanyl, oxycodone) act at mu receptors; acute overdose triad is pinpoint pupils, respiratory depression, and unconsciousness, reversed by naloxone.

Stimulants (cocaine, methamphetamine) increase synaptic dopamine and norepinephrine; effects include tachycardia, hypertension, hyperthermia, and risk of myocardial infarction and stroke.

DSM-5 substance use disorder (SUD) uses 11 criteria across four groups: impaired control, social impairment, risky use, and pharmacological indicators (tolerance, withdrawal).

DSM-5 severity thresholds: mild = 2-3 criteria, moderate = 4-5, severe = 6 or more; 0-1 criteria does not meet SUD diagnosis.

Tolerance is needing more of a substance for the same effect or reduced effect with continued use; it is not required for the diagnosis and is absent in some substances (e.g., hallucinogens).

Withdrawal is a substance-specific syndrome when use stops or is reduced; it is diagnosed only when the substance is known to produce withdrawal (e.g., alcohol, opioids, benzodiazepines).

Physical dependence (tolerance/withdrawal) can occur without addiction; addiction implies compulsive use despite harm and impaired control.

Craving is a strong desire to use and is a DSM-5 criterion; it is linked to cue-induced dopamine release in the nucleus accumbens and prefrontal cortex.

The mesolimbic dopamine pathway (ventral tegmental area to nucleus accumbens) is the common reward circuit for most addictive drugs; repeated stimulation produces neuroadaptation.

Relapse risk is influenced by stress, cues, and genetic factors; heritability estimates for alcohol use disorder are roughly 50%, with both genetic and environmental contributions.

Alcohol-impaired driving is a leading cause of traffic fatalities; in the U.S., legal blood alcohol concentration (BAC) for driving is 0.08% for adults 21 and older.

Substance use is associated with increased healthcare costs, emergency department visits, and productivity loss; alcohol and tobacco together account for a large share of preventable mortality.

Prenatal alcohol exposure can cause fetal alcohol spectrum disorders (FASD), including facial dysmorphology, growth restriction, and cognitive deficits; no safe amount is established.

Injection drug use is a major route for HIV and hepatitis C transmission; syringe services programs reduce transmission without increasing drug use.

Stigma reduces treatment seeking; language matters, and person-first terms (e.g., "person with a substance use disorder") are preferred over pejorative labels.

The opioid epidemic has been driven by prescription opioids, then heroin, and increasingly illicitly manufactured fentanyl; overdose deaths often involve multiple substances.

Tobacco use remains the leading preventable cause of death; secondhand smoke exposure harms children and nonsmoking adults.

Workplace and legal consequences include impaired performance, absenteeism, and criminal justice involvement; diversion programs and treatment courts aim to reduce incarceration.

The CAGE questionnaire is a 4-item screen for alcohol problems: Cut down, Annoyed by criticism, Guilty, Eye-opener; 2 or more positive answers suggest further evaluation.

The AUDIT (Alcohol Use Disorders Identification Test) is a 10-item screen developed by WHO; scores of 8 or more indicate hazardous or harmful drinking.

The DAST-10 is a 10-item screen for drug use in the past 12 months; a score of 3 or more suggests moderate problems and further assessment.

SBIRT (Screening, Brief Intervention, and Referral to Treatment) is a public health model; brief intervention is typically 5-15 minutes of motivational feedback.

DSM-5 diagnosis requires a pattern of use causing clinically significant impairment or distress, with at least 2 criteria within a 12-month period.

Urine drug testing has detection windows that vary by substance: opioids 1-3 days, cocaine 2-4 days, benzodiazepines up to weeks for chronic use, and cannabis weeks in chronic users.

False positives occur (e.g., poppy seeds for opioids, some cold medicines for amphetamines); confirmation is by gas chromatography-mass spectrometry (GC-MS).

Screening tools are not diagnostic; a positive screen requires a comprehensive assessment including history, collateral information, and physical exam.

The brain reward circuit centers on dopamine neurons from the ventral tegmental area projecting to the nucleus accumbens; most addictive drugs increase dopamine there.

Chronic drug use downregulates dopamine D2 receptors and blunts natural reward responses, contributing to anhedonia and craving during abstinence.

Prefrontal cortex dysfunction impairs inhibitory control and decision-making; this is linked to continued use despite negative consequences.

The amygdala and extended amygdala mediate stress and negative emotional states during withdrawal, driving negative reinforcement (use to relieve distress).

Alcohol enhances GABA-A receptor activity and inhibits NMDA receptors; withdrawal involves rebound glutamate activity, which can cause seizures and delirium tremens.

Benzodiazepines bind at the GABA-A receptor benzodiazepine site and increase chloride channel opening; withdrawal can cause seizures and is potentially fatal.

Opioids inhibit the locus coeruleus, reducing norepinephrine release; withdrawal causes rebound noradrenergic activity with agitation, sweating, and diarrhea.

Chronic alcohol use causes thiamine (vitamin B1) deficiency, leading to Wernicke encephalopathy (confusion, ataxia, ophthalmoplegia) and Korsakoff syndrome (amnesia, confabulation).

Stimulant use can cause cerebrovascular events (stroke, hemorrhage) and seizures; hyperthermia and rhabdomyolysis are additional neurological emergencies.