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substance use disorder

Psychiatry (Substance-Related and Addictive Disorders)Nervous SystemPsychiatric/BehavioralCardiovascularGastrointestinal/HepaticRespiratory

Summary

Substance use disorder (SUD) is a DSM-5 diagnosis defined by a problematic pattern of use of a substance (alcohol, opioids, stimulants, cannabis, sedatives, tobacco, etc.) causing clinically significant impairment or distress, with ≥2 of 11 criteria within 12 months. Severity: mild (2-3 criteria), moderate (4-5), severe (≥6). It replaced the DSM-IV categories of "abuse" and "dependence."

Detail

DEFINITION / DSM-5 CRITERIA (≥2 in 12 months; 11 total, grouped into 4 domains): - Impaired control: (1) using larger amounts/longer than intended; (2) persistent desire or unsuccessful efforts to cut down; (3) great deal of time spent obtaining/using/recovering; (4) craving (added in DSM-5). - Social impairment: (5) failure to fulfill major role obligations; (6) continued use despite social/interpersonal problems; (7) important activities given up or reduced. - Risky use: (8) recurrent use in physically hazardous situations; (9) continued use despite knowledge of physical/psychological problems caused or worsened by it. - Pharmacologic criteria: (10) tolerance; (11) withdrawal. (Not counted if the substance is taken under appropriate medical supervision, e.g., prescribed opioids.) Note: recurrent legal problems was REMOVED from DSM-5 and craving was ADDED. Severity: mild 2-3, moderate 4-5, severe ≥6. Specifiers: "in early remission" (≥3 months but <12 months without criteria, except craving), "in sustained remission" (≥12 months), "in a controlled environment," and "on maintenance therapy" (e.g., methadone, buprenorphine).

PATHOPHYSIOLOGY: - Mesolimbic dopamine "reward" pathway: ventral tegmental area (VTA) → nucleus accumbens (plus prefrontal cortex, amygdala). Drugs increase dopamine in the nucleus accumbens. - Chronic use causes neuroadaptation: tolerance, withdrawal, and sensitization; reduced prefrontal (executive control) function; and amygdala/stress-system activation (negative reinforcement) driving relapse. - Cycle: binge/intoxication → withdrawal/negative affect → preoccupation/craving. - Risk factors: family history (heritability ~40-60%), early age of first use, comorbid psychiatric disorders (ADHD, conduct/antisocial personality, depression, PTSD, bipolar), trauma, peer use, availability.

KEY SUBSTANCE-SPECIFIC HIGH-YIELD POINTS: - Alcohol: Intoxication → disinhibition, slurred speech, ataxia. Withdrawal: tremor (6-24 h), seizures (12-48 h), alcoholic hallucinosis (12-48 h), delirium tremens (48-96 h; autonomic instability, confusion, hallucinations; mortality if untreated). Treat with benzodiazepines (lorazepam/oxazepam if liver disease); give thiamine BEFORE glucose (prevent Wernicke encephalopathy). Maintenance: naltrexone, acamprosate, disulfiram. Labs: ↑ GGT, AST:ALT >2:1, ↑ MCV. - Opioids: Intoxication → miosis, respiratory depression, CNS depression; treat with naloxone. Withdrawal: mydriasis, rhinorrhea, lacrimation, yawning, piloerection, diarrhea, myalgias (flu-like, uncomfortable but rarely life-threatening). Treat with methadone (full agonist), buprenorphine (partial agonist), naltrexone (antagonist), clonidine for autonomic symptoms. - Stimulants (cocaine, amphetamines): Intoxication → mydriasis, tachycardia, HTN, euphoria, paranoia, arrhythmia, MI, chest pain; cocaine blocks reuptake of NE/DA/5-HT. Withdrawal → "crash" (dysphoria, hypersomnia, increased appetite). Avoid pure β-blockers in acute cocaine toxicity (unopposed α stimulation); use benzodiazepines first-line. - Benzodiazepines/barbiturates: Withdrawal can cause seizures and is potentially fatal. Overdose treated with flumazenil (benzos; caution as it may precipitate seizures). - Cannabis: conjunctival injection, increased appetite, dry mouth, impaired time perception; withdrawal is mild (irritability, insomnia). - Nicotine: Withdrawal → irritability, increased appetite, insomnia. Treat with nicotine replacement, bupropion, varenicline (partial α4β2 nicotinic agonist). - PCP: Violence, nystagmus (vertical or horizontal), hypertension, analgesia; LSD: visual hallucinations, pupillary dilation, "flashbacks" (hallucinogen persisting perception disorder).

MANAGEMENT PRINCIPLES: - Screen: CAGE (Cut down, Annoyed, Guilty, Eye-opener; ≥2 positive suggests alcohol use disorder), AUDIT, CRAFFT (adolescents), single-question screening. - Motivational interviewing and the stages of change model (precontemplation → contemplation → preparation → action → maintenance → relapse). - Treatment: pharmacotherapy (see above), CBT, contingency management, 12-step programs (AA/NA), residential/outpatient programs. Treat comorbid psychiatric disorders (dual diagnosis). - Harm reduction: naloxone distribution, needle exchange, supervised use. - Medical complications depend on substance and route (e.g., IV use → HIV, hepatitis B/C, endocarditis (tricuspid valve, S. aureus), abscesses).

DEFENSE MECHANISMS/ASSOCIATIONS: Denial is the classic defense mechanism in patients with SUD. Physical dependence (tolerance/withdrawal) is NOT equivalent to addiction; patients on appropriately prescribed opioids may be physically dependent without SUD.

DSM-IV → DSM-5: "Abuse" and "dependence" were merged into a single disorder with a severity continuum.

Sources

  • DSM-5-TR (American Psychiatric Association, 2022): Substance-Related and Addictive Disorders
  • First Aid for the USMLE Step 1: Psychiatry – Substance Use Disorder
  • Kaplan & Sadock's Synopsis of Psychiatry
  • UWorld Step 1/Step 2 CK: Psychiatry – Substance Use
  • Pathoma/Sketchy Medical: Psychiatry – Substance Abuse
  • NIDA (National Institute on Drug Abuse) – Drugs, Brains, and Behavior: The Science of Addiction

Reviewed by Medusa editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.