Substance use disorder Flashcards
DSM V substance use disorder
larger amounts/longer time than intended
attempts to cut down/control
time is spent obtaining, using, or recovering
craving/urge
failure to fulfill major role or obligations
use despite social/interpersonal problems
activities given up due to using/recovering
use under hazardous conditions
use despite knowledge of med/psych problem
tolerance
withdrawal
substance use disorder severity
MIld: 2-3 symptoms
moderate: 4-5
severe: >=6
Substance use disorder remission
early: 3-12 mo; only criteria left may be craving
Sustained: 12 mo or longer - craving may remain
in a controlled environment
Agent- risk factors for addiction
availability, cost , rapidity to reach brain, efficacy as a tranquilizer (to relieve withdrawal)
Host risk factors fo addiction
genetic predisposition, multi-problem family, co-morbid psych disorders
Environmental risk factors for addiction
occupation, peer group, culture, instability
sanctioned use, prohibition, restrictions
Agent risk factors for psychosis
amoutn of dopamine stimulation +/ - serotonin stimulation produced
damage to neurons
certain withdrawal states
Host risk factors for psychosis
genetic predispositions to addiction/mood/psychotic disorders
previous head injury
Environmental risk factors for psychosis
social stressors
nutrition
access to treatment
Agent risk factors for movement disorders
Exposure to substances that affect brain dopamine levels and/or damage dopamine neurons in the CNS
Host risk factors for movement disorders
genetic predisposition
family history
previous head injury
Environmental risk factors for movement disorders
occupational exposure (solvents, heavy metals)
social stressors
access to treatment
Dopamine and addiction
hallmark of an addicting substance = increased dopamine in nucleus accumbens
Dopamine/serotonin excess when using stimulants/hallucinogens/alcohol can cause psychosis
Dopamine depletion through lowered set point/damaged neurons can produce movement disorders, and low mood
D2 receptors lower in addiction
Alcohol effects
sedative-hypnotic
GABAa/glycine agonist, NMDAr antagonist
Use: increased opiate, dopamine, serotonin, GABA
- decrease in glutamate (from NMDA blockage)
Withdrawal: decrease in inhibitory NTs
increase in excitatory NTs
insomnia, irritation, tremor, risk of seizure
Genetics of alcohol
some concordance rates for alcoholism in twin studies
If biological parent was alcoholic, then sons more likely to become alcoholics
Family history positive males tend to report less intoxication from alcohol
Early lack of intoxication in males = 60% risk of later alcohol abuse/dependence, even if afmily history negative
Polymorphism at D4 receptor has been associated with novelty seeking
Genetically high risk individuals: bigger beta-endorphin rise with drinking –> more dopamine
Acetaldehyde dehydrogenase in alcohol addiction
Slow ADH and fast ALDH –> little acetaldehyde build up –> high risk for alcoholism
Fast ADH and slow ALDH –> 0% alcoholism
Wernicke-Korsicoff’s syndrome
alcohol blocks NMDA, in withdrawal glutamate slams away at NMDA receptor
oculogyric criss, ataxia, tremor
Long term use of alcohol
cerebellar cell destructions - ataxia, tremor
peripheral neuropathy - stocking-glove anesthesia/burning, can affect gait
Cannabis
endogenous cannabinoid system - infant bonding, regulates dopamine, sleep
CB1 receptors: central; CB2: peripheral
classed as hallucinogens
THC
THC
binds to CB1 and CB2
increases DA (dysregulation), stimulant/depressant
often desired - increased appetite, reduced nausea/pain
THC vs CBD
Cannabidiol (CBD) natural plant product - protective against psychosis
as marijuana THC content goes up, CBD goes down
NB inhaled cannabis not recommended for medicinal purposes, buccal spray (THC + CBD) 3-4th line for neuropathic pain
Psychosis risk with cannabis
heavy users (50+ times) by age 18 were 6x more likely to be admitted to hospital and diagnosed with schizophrenia than non-users Cannabis use associated with 2x risk of developing future psychotic states/schizophrenia
Cannabis, genetics and psychosis
COMT gene:
Alleles MM no increased risk
MV double risk
VV 10x psychosis when using cannabis
Cocaine/other stimulants
increase DA, serotonin, noradrenaline
include ritalin and other medications for ADHD
cocaine - reuptake inhibitor of all 3
methamphetamines - increase release of all 3, reverses the transporter
Potential adverse effects of stimulant use
alert, powerful, insomnia, anorexia
increased HR/BP, arrhythmias, stroke, fetal loss
anxiety, paranoia, delusions, psychosis, violence
tremor, hyperreflexia,seizure, akathisia, choreiform movements
Genetics of cocaine dependence
Genetics/exposure to drug = primary risk factors to develop cocaine dependence
making more endogenous opioids - may be protective against cocaine dependence
if slow to break down dopamine after cocaine use, can become paranoid
Stimulate induced movement disorders
Acute use:
- abnormal picking
- tremor
- myoclonic jerking
- akathisia
- choreiform
- seizures
If choreiform movements persist, then dopaminergic pathways may be damaged
Stimulant-induced abnormal gait
Dopamine overstimulation: choreiform gait
Dopamine hypofunction: Parkinsonian gait
Acutely dropping dopamine: can produce akathisia, restless legs
Serotonin syndrome
stimulant-induced rigidity myoclonic jerking hyperreflexia vasomotor instability confusion disorientation
Drug induced psychosis
largely caused by DA dysregulation if symptoms persist for weeks-mo, then an underlying psychotic disorder likely Hazard ratios: - meth: 9 - cannabis: 0 - alcohol, opioids and cocaine: 1.5-2.8
