123. Substance Use Disorders Flashcards
DSM5 Criteria for Substance Use Disorders
- Maladaptive use = impairment
- Two or more of the following in same 12 mo period
1. Risky, harmful use (recurrent)
2. Impaired contol (craving, unsuccessful efforts to stop, more time spent using/obtaining/recovering)
3. Social impairment (decrease in other activities, social problems)
4. Physical dependence - tolerance, withdrawal
Etiology of Alcohol Use Disorder
- Genetics 50% risk (less alcohol breakdown, low sensitivity to alcohol, depression, personality - negative emotionality (high N, low A/E) and more impulsvity (low C))
- Effects of Family, Social/Cultural, Peers, Adverse Effects (abuse, emotional neglect)
- Environment (stressors, lack of rewards, access)
What are the 4 types of motivations for alcohol use - and their risks for alcohol use disorder
- Social (increase positive mood, external drive) - low risk
- Conformity (decrease negative mood, external drive) - low-risk
- Enhancement (increase positive mood, internal drive) - at risk
- Coping (decrease negative mood, internal drive) - HIGHEST risk
How do personality traits (Big 5) map onto enhancement and coping motives?
Enhancement: less C, more sensation seeking, more impulsive
Coping: more N, less E/A, more impulsivity
What is the neurobiology for alcohol use disorders
- Abuse in increasing DA (chronic use = decrease D2 receptors = reversible if stop)
- Multiple NTs involved in regulating DA (5HT, Glu, GABA, endorphins, NE) and multiple systems (inhibitory control, motivation/drive, memory/learning, reward/salience)
Treatment principles for substance use disorders
Match Tx to Severity (dimensional scale)
Motivational tx, 12-step facilitation, CBT, couples/family therapy
Decrease drug reward/salience, decrease impulsivity/learned responses
Increase alternative rewards/salience, increase awareness
What are the mechanisms of action of alcohol? What are alcohol’s adverse effects?
Mech: Direct - increase GABA, decrease NMDA, decrease adenosine
Indirect: increase DA (KEY) increase endorphins
SE: Depression, Cognitive deficits, Wernicke’s encephalopathy (opthalmoplegia, ataxia, confusion), Wernicke-Korsakoff Syndrome (memory deficits - confabulation)
What is the pharm tx of alcohol use disorder?
- Naltrexone: Mu opioid antagonist (decrease reward, improve remission)
- Acamprosate: inhibits Glu receptors (decrease craving, improve remission)
- Disulfiram: blocks acetaldehyde breakdown (worsens flushing, nausea, vomiting), most studies are negative
- Benzodiazepines/ZaZolEz - GABA modulators: cause motor (falls, car accidents)/cognitive (memory, sedation) impairment
What are the adverse effects of marijuana use?
Cannabis use disorder Motor Vehicle Accidents Sx of Chronic Bronchitis Diminished Lifetime Achievement Schizophrenia
Difference between naturally occuring and synthetic cannabinoids
Synthetic: higher potency than THC, full agonists at CB1 receptor (not partial, no CB2 activity), higher risks of anxiety, confusion, psychosis, no dose control, no CBD (CB antagonist)
What are the types and mechanisms of stimulants?
What are adverse effects of stimulants?
Cocaine: blocks DA reuptake (brief effect)
Amphetamine: blocks DA reuptake, increases DA release (longer effect)
Direct: blocks 5HT and NE transporters two
indirect: increases Glu/endorphin release
SE: MI, stroke, Persistent Psychosis, Disinhibition, Poor Decisions (Altered risk-reward)
(Molly, Bath Salts are derivatives of amphetamines)
Opioids
- which are detected on drug screen?
- adverse effects?
- tx?
Naturals detected on screen (morphine, codeine, heroin) Semi-synthetic erratic detection (hydrocodone, oxycodone, oxymorphone) Synthetics undetected (methadone, fentanyl, buprenorphine)
SE: N/V, constipation, itching, cognitive slowing, fatigue, drowsiness, OD
tx: Methadone (mu agonist - safer opioid - decreases deaths, heroin use, increases employment)
Buprenorphine (mu partial agonist, outbinds heroin, decreases OD/heroin use)
Naltrexone (mu antagonist, CI in hepatitis, liver failure, need for opioids)