CH-11-Substance-Related, Addictive & Impulse-Control Disorders – Detailed Study Notes

Overview and Historical Context

• Substance-Related, Addictive & Impulse-Control Disorders cost U.S. society \approx\$600\text{ billion+/year} and claim (\approx 500,000) lives annually.
• DSM-5 category now covers
  • Psychoactive‐substance problems (6 chemical classes)
  • Newly recognised behavioural addiction: Gambling Disorder
  • Impulse-control disorders (IED, Kleptomania, Pyromania)
• Etiology once framed as moral weakness; modern view = complex biopsychosocial interaction.

Levels of Involvement & Core Terms

• Substance use → ingestion in moderate amounts w/o major interference (e.g., morning coffee).
• Substance intoxication → acute physiological/psychological reaction (impaired judgement, mood changes).
• Substance use disorder (SUD) (DSM-5)
  • \ge 2 of 11 symptoms within 12\text{ mo}; severity: mild (2–3), moderate (4–5), severe (\ge 6).
  • Symptoms span "impaired control, social impairment, risky use, pharmacological criteria" (tolerance & withdrawal).
• Tolerance: need for increased dose or diminished effect with same dose.
• Withdrawal: negative physical/psychological response when substance discontinued.
• Physiological vs psychological dependence: drug-seeking behaviours (craving, relapse) can exist without physical WD.

Diagnostic Issues & Comorbidity

• DSM-III (1980) first separated SUDs; DSM-5 merges “abuse” & “dependence”.
• Legal-problem criterion removed; craving added.
• (~75\%) of patients in addiction Tx have another psychiatric Dx ((>40\%) mood; (>25\%) anxiety/PTSD).
• Intoxication/withdrawal symptoms can mimic/deepen other disorders; DSM-5 requires symptom persistence >6\text{ wks} post-WD to assign independent Dx.

Depressants

Mechanism & Shared Features

• ↓ CNS activity; promote relaxation & sleep; high risk of physical dependence.
• Potentiate \gamma-aminobutyric acid (GABA) → neuronal inhibition.

Alcohol (EtOH)

• Path: mouth → esophagus → stomach (minor absorption) → small intestine → blood → organs → liver metabolism (ADH).
• Biphasic: initial apparent stimulation (inhibitory centres depressed) → overall CNS depressant.
• Effects: ↓ motor coordination, reaction time; vision/hearing impairment.
• Metabolism: (~1) drink/hr; impairment >50\,\text{mg\%}; legal intoxication 100\,\text{mg\%}.
• Withdrawal: tremor → nausea → anxiety → hallucinations → Delirium Tremens (DTs).
• Long-term: liver cirrhosis, pancreatitis, cardiomyopathy, brain damage.
  • Wernicke-Korsakoff Syndrome (thiamine deficiency): confusion, ataxia, aphasia.
  • Alcohol-related dementia; moderate wine may be neuroprotective.
• Fetal Alcohol Syndrome (FAS): facial anomalies, growth retardation, cognitive deficits; risk moderated by beta-3 ADH genotype & ethnicity (↑ African-American).
• Epidemiology (US):
  • \approx56.8\% Caucasians current drinkers vs 40.0\% Asians.
  • 24.6\% binge ((\ge5) drinks men/(\ge4) women in 2\text{ h}) monthly.
  • Lifetime AUD prevalence 29\%.
• Course: Jellinek’s 4-stage model questioned; progression not inevitable; early LOR (low level of response) predicts later AUD.

Sedative-, Hypnotic-, Anxiolytic-Related Disorders

• Barbiturates (e.g., Seconal): historical sleep aids; low dose = relaxation; high dose = coma, death via diaphragm suppression.
• Benzodiazepines (e.g., Valium, Xanax, Rohypnol): safer but abuse potential; WD similar to EtOH.
• DSM criteria parallel alcohol; GABA-A receptor involvement; synergistic fatality with EtOH.

Stimulants

• Most widely consumed class; ↑ alertness, mood; act via dopamine/norepinephrine.

Amphetamines

• Medical: ADHD (Ritalin, Adderall), narcolepsy, appetite suppression.
• Illicit: MDMA/Ecstasy/Molly, Methamphetamine (Ice).
• Intox: euphoria, lack of sleep, paranoia; OD → hallucinations, cardiovascular collapse.
• Mechanism: ↑ release & block reuptake of DA/NE.

Cocaine

• Blocks DA reuptake in pleasure pathway; short high (<1 hr) → crash (apathy, boredom).
• Cocaine-induced paranoia in \approx66\%.
• Fetal exposure: ↓ birth weight, possible cognitive issues confounded by polysubstance & environment.
• Usage: 1.5\text{ M} U.S. users/year; men 2× women; crack users younger, urban.

Tobacco/Nicotine

• Nicotinic-acetylcholine receptor agonist; reaches brain in 7–19\text{ s}.
• Dosing pattern maintains plasma \approx35\,\text{ng/ml}.
• WD: depressed mood, insomnia, ↑ appetite; relapse rates ≈ alcohol/heroin.
• Genetic & environmental interplay (maternal smoking → later SUD via environment > biology).

Caffeine

• Most common psychoactive; 85\% adults daily; small dose ↑ mood, ↓ fatigue; high dose → anxiety, insomnia.
• Blocks adenosine reuptake; tolerance & WD (headache, irritability).

Opioids

• Natural (opium, morphine, codeine) & synthetic (heroin, oxycodone, methadone); mimic endorphins.
• Effects: analgesia, euphoria, drowsiness, slowed breathing; high dose fatal.
• WD (6–12 h post): yawning, nausea, aches, lasts 1–3 d.
• US epidemic: 1.9\text{ M} prescription‐opioid disorders (2013); deaths ↑ 360\% since 1999.
• Risk: HIV/Hep-C via IV use.

Cannabis

• THC acts on brain endocannabinoid system (anandamide, 2-AG).
• Acute: mood swings, heightened sensory; chronic heavy use → memory, motivation issues.
• Tolerance mixed (reverse tolerance reported); WD: irritability, sleep disturbance.
• Medical: dronabinol, Sativex for chemo nausea, MS pain; smoke may equal tobacco carcinogens.
• Synthetic variants (Spice/K2) produce severe psychosis.

Hallucinogens

• LSD (ergot derivative), Psilocybin, Mescaline (peyote), PCP, Ketamine.
• Effects: perceptual distortions, depersonalisation, mystical experiences.
• Tolerance rapid; negligible WD; risk "bad trips"; possible flashbacks.
• Psilocybin activates 5\text{HT}_{2A/C}; fMRI shows default & attention network alteration.

Other Drugs of Abuse

• Inhalants: solvents, glue; peak age 13–14; intox like EtOH; sudden sniffing death.
• Anabolic-androgenic steroids: performance, body image; mood disturbances.
• Dissociative anesthetics / Designer drugs: GHB, Rohypnol, MDMA, ketamine; tolerance, neurotoxicity.
• Synthetic cathinones (bath salts, MDPV): stimulant + psychosis.

Causes – An Integrative Model

Biological

• Heritability across substances; genes modulate sensitivity (ALDH2 flushing), metabolism, & treatment response (OPRM1 & naltrexone).
• Reward pathway: Ventral tegmental area → nucleus accumbens (DA); GABA inhibition lifted by opioids; serotonin, glutamate involvement.
• Opponent-process theory: positive → negative after-effects; use shifts to negative-reinforcement cycle.

Psychological/Cognitive

• Positive & negative reinforcement (tension reduction, self-medication).
• Expectancy effect: beliefs formed via media/peers predict initiation & escalation.
• Cravings triggered by cues; neuroplasticity strengthens conditioned responses.

Social & Cultural

• Exposure via family, peers, media; parental supervision protective.
• Cultural norms influence prevalence & expression (Korean heavy-occasion drinking vs ALDH2 gene).
• Disease vs moral-weakness models shape policy & treatment-seeking.

Treatment Modalities

Biological

• Agonist substitution: methadone, buprenorphine for opioids; nicotine gum/patch; aims at harm reduction.
• Antagonist: naltrexone (opioids, alcohol); acamprosate for EtOH cravings.
• Aversive: disulfiram (\text{Antabuse}) for EtOH; silver nitrate gum for smoking.
• Meds for withdrawal: clonidine (opioid), benzos (EtOH).

Psychosocial

• Inpatient detox (costly) vs outpatient equally effective.
• Twelve-Step (AA, NA): disease model, spirituality, social support; best for highly motivated, severe cases.
• Controlled drinking (UK): moderate use training; controversial.
• Aversion therapy & covert sensitisation: pair drug with nausea/shock or imagery.
• Contingency management: vouchers/money for clean urines.
• Community Reinforcement Approach: spouse counselling, skills, vocational, recreational alternatives.
• Motivational Enhancement Therapy (MET): elicit intrinsic change talk.
• Cognitive-Behavioural Therapy & Relapse Prevention: ID triggers, challenge expectancies, coping skills.

Prevention

• Education alone (DARE) ineffective; comprehensive community interventions (responsible serving, law enforcement) show ↓ binge & injuries.
• Sociocultural shift (anti-smoking norms) powerful; proposal for vaccines targeting drug molecules.

Gambling Disorder (Addictive Disorder)

• Lifetime prevalence \approx1.9\%; criteria parallel SUD (tolerance, chasing losses, WD-like restlessness).
• Biological parallels: DA ventromedial PFC hypo-function, impulsivity genes.
• Tx: CBT, motivational & relapse prevention; Gambler’s Anonymous (high dropout); opioid antagonists reduce urge.

Impulse-Control Disorders

Intermittent Explosive Disorder (IED)

• Recurrent outbursts (assault/property); lifetime 7.3\%.
• Etiology: OFC–amygdala circuitry, serotonin deficits; CBT & meds (SSRIs, mood stabilisers).

Kleptomania

• Irresistible stealing, tension → relief; more females; comorbid mood/SUD; opioidergic involvement; Tx: behavioural, SSRIs, naltrexone.

Pyromania

• Deliberate fire-setting for gratification; (<4\%) of arsonists; Tx parallels IED with CBT focus.

Concept Integration

• SUDs & impulse disorders share craving, poor inhibitory control, reward pathway dysregulation.
• Multimodal treatment (biological + psychosocial + community) yields best outcomes; prevention via cultural change crucial.