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Flashcards in Substance use disorder Deck (30):
1

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

2

substance use disorder severity

MIld: 2-3 symptoms
moderate: 4-5
severe: >=6

3

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

4

Agent- risk factors for addiction

availability, cost , rapidity to reach brain, efficacy as a tranquilizer (to relieve withdrawal)

5

Host risk factors fo addiction

genetic predisposition, multi-problem family, co-morbid psych disorders

6

Environmental risk factors for addiction

occupation, peer group, culture, instability
sanctioned use, prohibition, restrictions

7

Agent risk factors for psychosis

amoutn of dopamine stimulation +/ - serotonin stimulation produced
damage to neurons
certain withdrawal states

8

Host risk factors for psychosis

genetic predispositions to addiction/mood/psychotic disorders
previous head injury

9

Environmental risk factors for psychosis

social stressors
nutrition
access to treatment

10

Agent risk factors for movement disorders

Exposure to substances that affect brain dopamine levels and/or damage dopamine neurons in the CNS

11

Host risk factors for movement disorders

genetic predisposition
family history
previous head injury

12

Environmental risk factors for movement disorders

occupational exposure (solvents, heavy metals)
social stressors
access to treatment

13

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

14

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

15

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

16

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

17

Wernicke-Korsicoff's syndrome

alcohol blocks NMDA, in withdrawal glutamate slams away at NMDA receptor
oculogyric criss, ataxia, tremor

18

Long term use of alcohol

cerebellar cell destructions - ataxia, tremor
peripheral neuropathy - stocking-glove anesthesia/burning, can affect gait

19

Cannabis

endogenous cannabinoid system - infant bonding, regulates dopamine, sleep
CB1 receptors: central; CB2: peripheral
classed as hallucinogens
THC

20

THC

binds to CB1 and CB2
increases DA (dysregulation), stimulant/depressant
often desired - increased appetite, reduced nausea/pain

21

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

22

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

23

Cannabis, genetics and psychosis

COMT gene:
Alleles MM no increased risk
MV double risk
VV 10x psychosis when using cannabis

24

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

25

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

26

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

27

Stimulate induced movement disorders

Acute use:
- abnormal picking
- tremor
- myoclonic jerking
- akathisia
- choreiform
- seizures

If choreiform movements persist, then dopaminergic pathways may be damaged

28

Stimulant-induced abnormal gait

Dopamine overstimulation: choreiform gait
Dopamine hypofunction: Parkinsonian gait
Acutely dropping dopamine: can produce akathisia, restless legs

29

Serotonin syndrome

stimulant-induced
rigidity
myoclonic jerking
hyperreflexia
vasomotor instability
confusion
disorientation

30

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