Substance Use Disorders Flashcards
Acute Intoxication
Transient condition following administration of alcohol and other psychoactive substance, resulting in decrease in LOC, cognition, perception, affect or
behaviour, or other psychophysiological functions and responses
Addiction
Repeated use of psychoactive substance to the extent the user is periodically or
chronically intoxicated, shows a compulsion to take preferred substance, has great difficulty
ceasing, and exhibits determination to obtain by any means
Tolerance
Physical adaptation to consumption, leading to a need for increasing
dose to achieve the same effect; Often precedes Physical Dependence
Dependence
Need for repeated administration to feel good, or avoid feeling bad
▪ Psychological – Refers to experience of impaired control (craving,
compulsions); Physical – Refers to Tolerance and Withdrawal symptoms
Dependence Syndrome
Cluster of Behavioural, Cognitive and Physiological phenomena which might develop after repeated use
o Strong desire to take the drug, Impaired control over use, Persistent use despite
awareness of harmful consequences, Higher priority given to drug than other activities, Increased Tolerance, and a Withdrawal associated when use is
discontinued; >3/6 of criteria = ICD-10 def of Dependence Syndrome
Withdrawal
Cluster of symptoms which occur on cessation/reduction of use of psychoactive
substance which was previously taken repeatedly, typically for prolonged time/high doses
o Typically, features are opposite to Acute Intoxication
o E.g. ETOH Withdrawal – Tremor, Sweating, Anxiety, Agitation, Depression, Nausea
and Malaise; Can be complicated and progress to Delirium Tremens
Harmful Use
Pattern of Psychoactive substance use that causes damage to health
o Physical or Mental; Commonly but not invariably has harmful social consequences
o Replaces non-dependent use in the ICD-10
Alcohol Metabolism
Ethanol is oxidised to Acetaldehyde by Alcohol
Dehydrogenase primarily; Acetaldehyde is highly
unstable and forms free radicals which are
highly damaged and need to be quenched by
antioxidants (E.g. Ascorbic Acid, Thiamine)
o Acetaldehyde is then converted to Acetate by Aldehyde Dehydrogenase 2 (ALDH2),
which is then subsequently converted to Acetyl CoA which can be metabolised to
produce ATP, or other biomolecules
How does alcohol affect CNS
Ethanol affects brain function by interacting with multiple neurotransmitter systems; In the
short term, believed to increase inhibitory neurotransmission (GABAA) resulting in sedation
and reduced anxiety
Alcohol Limits
Current alcohol advice (2016) states that safe levels are 14 units per week regardless of sex
o If drinking as much as 14 units, spread evenly over three days or more
o Heavy drinking sessions increase risk of death from long-term illness and accidents
o In Pregnancy – No safe level known, hence best to remain abstinent
Presentation of Acute Alcohol Intoxication
Slurred speech, Impaired Coordination and Judgment, Labile Affect; Hypoglycaemia, Stupor and Coma
Presentation of Acute Withdrawal
Malaise, Nausea, Autonomic Hyperactivity, Tremor, Labile Mood, Insomnia and Transient Hallucinations (Typically visual)
Alcohol Dependence Syndrome
Compulsion, Awareness but Persistence, Neglect,
Tolerance, Withdrawal, Stereotyped Pattern, Time Pre-occupied, Out-of-control use, Persistent wish to cut down (albeit futile)
Alcoholic Psychotic Disorders
ETOH Hallucinosis (Threatening, Second-person auditory hallucinations) or Jealousy (Paranoid delusions about Infidelity)
Alcohol Amnesic Syndrome
Korsakoff’s Psychosis, Wernicke’s
Encephalopathy
ETOH Induced Hypoglycaemia
ETOH metabolism requires
NAD, hence reducing the NAD/NADH ratio;
Gluconeogenesis is reduced as it is dependent on this ratio; Ketosis occurs due to Hypoglycaemia,
Managing Alcohol Withdrawal
Can be quantified using
CIWA-Ar (N+V, Tremor, Paroxysmal Sweats, Tactile
Disturbance, Auditory and Visual Disturbances)
o Offer Pharmacotherapy – Benzodiazepine (E.g. Chlordiazepoxide) or Carbamazepine
for prevention of DT in Acute ETOH Withdrawal
Delirium Tremens
Rapid onset Confusion typically due to acute withdrawal about 3 days
after; Exaggerated symptoms of Acute Withdrawal plus Seizures and Fever
Management of Delirium Tremens
o Oral Lorazepam first line; If persistent or oral declined, Parenteral Lorazepam or
Haloperidol alternatively; Phenytoin not used to treat withdrawal seizure
o Rehydration, Correction or Electrolyte Disturbances, Oral or Parenteral Thiamine e.g.
Pabrinex; Especially if Malnourished, Decompensated Liver Disease
Consequences of Alcohol Excess
ETOHXS leads to inadequate Nutritional Intake, Decreased Thiamine absorption in GI tract, and Impaired Thiamine Utilisation
Wernicke’s Encephalopathy
Exhaustion of B-Vitamins esp Thiamine; Many will have partial triad of ophthalmoplegia, Ataxia and Confusion
o Body has 2 – 3 weeks of Thiamine reserves which is easily exhausted if no intake, or
rapid depletion e.g. Chronic inflammatory states
o Thiamine is a co-factor in the Kreb cycle and
PPP; Necessary for Glucose metabolism,
Neurotransmitter production (E.g. Glutamic
acid, GABA), Myelin production etc
o Thiamine Deficiency – Oxidative Damage,
Mitochondrial Injury and Pro-Apoptotic
stimulation leads to neurological injury
Promoting Alcohol Abstinence
Motivational Interviewing, Psychological Therapies, Self-Help (E.g. Alcoholics Anonymous; Reduce pro-drinking activities, improves social ties with abstinent groups)
Promoting Alcohol Abstinence: Pharmacotherapy
Pharmacotherapy for after successful withdrawal from Moderate-Severe ETOH dependence
o Baseline U/Es, LFTs with GGTs,
SSRIs, GHB or Benzodiazepines should not be used to maintain abstinence
Promoting Alcohol Abstinence: Pharmacotherapy-Acamprosate TDS
Acts on NMDA and GABAA to reduce Cravings, and risk of Relapse; Up to
6/12 initially; Stopped if drinking persists 4 – 6/52 after starting
