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MANAGEMENT OF DRUG ADDICTION / SUBSTANCE ABUSE

Dr Jacinta OShea Research Registrar ERHA

DRUG ADDICTION
Chronic relapsing disorder Compulsive drug seeking & drug taking behaviour, despite serious negative consequences ICD 10 Criteria Induce pleasant states (positive reinforcer) or relieve distress (negative reinforcer) Continued use induces adaptive changes in the CNS, leading to the development of tolerance, dependence, sensitization, craving & relapse

Substances of abuse
Opiods; Heroin Alcohol Benzodiazepines & Barbiturates Stimulants: Cocaine & Amphetamines Cannabinoids Hallucinogens; LSD, Mescaline Solvents Nicotine

Patterns of Drug Use


Experimental Recreational Habitual Dependant Other: - Polysubstance use - Dual diagnosis use

Clinical situations
Harmful use Dependence syndrome Withdrawal state +/- delirium; DTs Drug induced Psychosis Cognitive impairment syndromes Acute intoxification Residual disorders

ICD-10 Criteria
A strong desire/compulsion to take the substance Difficulties in controlling substance-taking A physiological withdrawal state Evidence of tolerance Progressive neglect of alternative pleasures Persisting with substance use despite clear evidence of OVERTLY harmful consequences

Epidemiology
British Psychiatric Morbidity study 1993/2000
neurosis- 160/1000 Probable psychosis 5/1000 Personality disorder- 44/1000 Alcohol dependant- 70/1000 Drug dependant- 40/1000

UK Community surveys
3o% have tried illegal drugs; 10% in last year. <25y.o 50% lifetime; 33% in last year. At all ages, males have higher rates of drug use than females; M:F 3-4:1 Use of illegal drugs commoner in: - young adults especially males, - Lower socioeconomic groups - Those with psychiatric illness - Urban areas

Drug use prevalence Ireland 2002/03

Factors influencing drug abuse and dependence


Pharmacological & physiochemical properties of drugs Personality & Psychiatric disorder - increased risk associated with schizophrenia, BPAD, depression, ADHD. Genetic factors (that influence metabolism and the effects of drugs)

Pharmacologic and physiochemical properties


Liposolubility increases the passage through the blood-brain barrier Water solubility facilitates injection Volatility favours inhalation in vapour form e.g aerosols / solvents Heat resistance favours smoking e.g. cannabis Rapid onset and intensity of effect increase the potential for abuse A short half-life produces abrupt & intense syndromes of withdrawal

OPIATES
Strong narcotic analgesics Derived from the ripe seed capsule of the poppy Crude opium contains morphine, codeine, other alkaloids Diamorphine (heroin) made by acetylation Eaten, sniffed, smoked, injected

OPIATES
Short term effects Euphoria, analgesia, sedation & a feeling of tranquillity
Long term effects / Repeated use Rapid tolerance & physical dependence Over dose Lethal respiratory depression

Opiate Receptors
3 Major opiate receptors - , , and
3 Endogenous opiate peptides Encephalins, beta-endorphin, dynoorphin Agonist action at and receptors causes tolerance and dependence Opiates activate these receptors which then couple G proteins

Opiates &The dopamine pathway


Natural rewards and addictive drugs stimulate the release of dopamine from neurones of the presynaptic ventral tegmental area into the nucleus accumbens, causing euphoria & reinforcement of the behaviour Habituation ( rapid adaptive changes ) occur with natural rewards but not with addictive drugs & each dose stimulates the release of dopamine Dopamine binds to a G-protein coupled receptor with two subtypes, D1 like, and D2 like.

Opiates Cont
Most drugs that produce elevations in mood or euphoria, release dopamine in either the nucleus accumbens or the prefrontal cortex Opiods release dopamine mainly by an indirect mechanism that decreases the activity of GABAinhibitory neurones in the ventral tegmental area Stimulation of receptors decreases dopamine levels in the nucleus accumbens and produces aversive responses Reward & physical dependence are mediated by the activation of receptors

Opiate tolerance
Tolerance leads to increasing doses, or reduction between intervals, or both Short term administration of opiates activates the -opiod Gi/o- coupled receptor, this leads to a decrease in the number of opiod receptors and to the development of tolerance

Opiate withdrawal
Withdrawal causes reinstatement of drug use to prevent or decrease physical symptoms and dysphoria

Inhibition of neurones in the locus ceruleus by opiate is a key mechanism in withdrawal


When opiate levels fall the unopposed neurones lead to adrenergic over activity Activation of receptors in the ventral tegmental area decreases dopamine in the nucleus acumbens, leading to dysphoria and anhedonia

Opiate withdrawal
Grade 0 drug craving, anxiety, drug seeking Grade 1 yawning, sweating, runny nose, restless sleep Grade 2 dilated pupils, hot and cold flushes, goose flesh (cold turkey), aches and pains Grade 3 insomnia, restlessness and agitation, abdominal cramps, N+V, diarrhoea, increased pulse , BP and RR

Hazards
Sterility abscesses, septicaemia endocarditis Adulterants gangrene DVT and pulmonary emboli Sharing blood borne diseases HIV, Hepatitis B and C

Blood borne diseases HIV


Currently IVDUs account for 37% (1048)
Though the numbers of IVDUs with HIV increased between 1998-2001, it was followed by a reduction of almost 50% during 2001-2002. This may reflect service expansion or the delay between infection and diagnosis EMCDDA(2002) record a prevalence rate of 3.3-8.7% of HIV infection among IVDUs between 1996-2001

Hepatitis C
HCV prevalence is very high in all countries and settings in Europe, with infection rates of between 40-90% among different IDU subgroups Prevalence rates 72-73% 1996-2001 (EMCDDA) No routine data collection in Ireland 1st study 1995 HCV prevalence 84% <2 years injecting 70% +ve >2 years injecting 95% +ve

Methadone
Synthetic opiate Administered orally Half-life 24-36 hrs (10-90) ; once daily dosage Steady state 4-5 days Dosage 30-60mg Harm reduction approach Maintenance / Detoxification

Methadone Maintenance
Used in the USA since 1960s Stabilises lifestyle Harm reduction benefits 75-90% of patients Reduces HIV, Hepatitis Reduces crime Aim for a dose of 60mg and over

Harm reduction
As opposed to Abstinence / curing WHO defines Harm reduction as a concept to prevent or reduce negative health consequences associated with certain behaviours Concerns about transmission of HIV; epidemics in >110 countries; relapsing nature of Addiction Focuses on minimising health, personal and social harms associated with drug use - the spread of blood-borne diseases, overdoses etc Ongoing interventions, not short term, as a way to improve health of drug users, their families and society Marginalised groups

Interventions include
Information, education, communication Education about STDs +safer sex, family planning ; injection techniques Health care in relation to infectious diseases; screening, immunisation Substitution with oral drugs Needle exchange programmes Linking with other services e.g. medical, psychiatric, obstetric, dental ; social and forensic other

Benefits of methadone
safe substitution drug Effective in engaging and retaining people in treatment Reduces risk, reduced levels of injection A factor in improving physical/Mental health and quality of life of patients and their families Reduces criminal activity and demands on the criminal justice system

Lofexidine
Alpha-2 adrenergic agonist inhibiting noradrenaline release
Useful in short term users Detoxify over 2-3 weeks using up to 2mg daily Daily BP monitoring is essential Mainly used in in-patient units

Naltrexone
Narcotic antagonist Half-life 96 hours Dose 50mg daily Used after detoxification Best when supervised by family

Breaks the cycle of craving

Alcohol
1 unit = 10ml / 8g absolute alcohol ( pint lager, glass wine, 25ml spirits)
Hydrophilic, with rapid absorption through the gut Peak plasma levels reached 30-60 mins post ingestion Metabolized by hepatic oxidation (ADH)

Neurobiology of alcohol
Stimulant at low doses, sedative at higher concentrations Anxiolytic effects mediated by potentiation of inhibitory effects GABA at GABA-A receptors Disturbs glutamate transmission by inhibiting NMDA receptors,- related to withdrawal seizures, DTs etc Unopposed action of GABA and NMDA, increasing neuronal excitability

Alcohol related physical problems


GIT oesophagitis, gastritis, reflux, m-w tears, varices, pancreatitis, portal HT, cas Liver hepatitis, fatty liver, cirrhosis, haemochr, hepatic Ca, hepatic encephalopathy Cardiovascular arrythmias, cardiomyopathy, coronary/cerebrovascular disease, hypertension Metabolic Endocrine e.g. pseudocushings, hypogonadism, infertility, low libido/impotence Musculoskeletal e.g. gout, fractures, osteoporosis Haematological e.g. anaemia, thrombocytopaenia Respiratory Dermatological e.g. spider naevi, palmar erythema, eczema, worsening psoriasis

Alcohol Neurological problems


Acute intoxication Mania a potu pathological drunkenness with minute amounts of alcohol (not in ICD-10) Methanol poisoning Amnesic (Korsakoffs) syndrome & Wernickes encephalopathy Cerebellar degeneration Ambylyopia- retrobulbar neuritis; may be associated with peripheral neuropathy Central pontine myelinosis Dementia, amnesia/blackouts etc Fetal alcohol syndrome

Psychological related disorders


Alcoholic Hallucinosis- 10-20% > 6/12 -5-20%...schizoph Psychiatric comorbidity ECA study -psychiatric dx x3 risk of lifetime alc disor - 13% alcoholics 2nd mood disorder - 22% mood disorder also alcohol disorder Suicide approx 25% attempt; male, divorced, personality disorder, older, unemployed, medical issues, hx of DSH Pathological jealousy- Othello syndrome Anxiety states- panic, OCD, phobias PTSD - alcohol dampens hyperarousal Eating disorders bulemia Other drug use

Alcohol withdrawal
Important to recognise 25% of male medical patients are problem drinkers
Occurs from 6-24 hours after cessation, peaking at day 2-3, highest risk in first 24-48hrs Range of features sweating, tremor, nausea, anorexia, vomiting, anxiety, insomnia, restlessness, hallucinations, seizures, nightmare, confusion, hallucinosis

Delirium tremens
Toxic confusional state with somatic disturbance, occurring in < 5% Mortality rate of approx 10%( -20%) Symptoms peak at 3-4 days of withdrawal Triad of clouding of consciousness, sensory distortion and tremor Agitation, fear and insomnia, worse at night

Features of DTs
Confusion and disorientation. Clouding of consciousness. Delusions and hallucinations. Psychomotor agitation and automatic dysfx. Perceptual disturbance and fear. Insomnia and truncal ataxia. Electrolyte disturbance and dehydration . Leukocytosis and disordered LFTs. EEG shows an increase in fast activity.

Treatment
Acute withdrawal Short acting benzodiazepines; chlordiazepoxide, diazepam minimise the risk of seizures 40mg clordiazepoxide, 6hourly, (Max 300mg in 24hrs) Reducing doses over 5-10 days Consider anticonvulsants (carbamezepine) Multivitamin preparations- Thiamine / B vitamin - Wernicke-Korsakoff psychosis Treat infection, dehydration, suicidal ideation etc

In Patient Treatment
Past History of seizures or epilepsy Comorbid severe mental illness Intercurrent acute illness Previous failed OPD attempts Elderly patients

Post-detoxification
Disulfuram (Antabuse) Inhibitor of aldehyde dehydrogenase. Blocks ethanol metabolism at the acetaldehyde level. Flushing reaction Loading dose 600-800mg per day for 3-4 days Maintenance 200mg daily Hypotension and MI with heavy alcohol consumption, potentially fatal Useful in highly motivated groups and where assisted by family or friends

Post Detoxification
Naltrexone- Opiate receptor antagonist, thought to negate the euphoria associated with alcohol DOSE Acamprosate (Calcium bisacetyl homotaurine)- Synthetic GABA analogue DOSE SSRIs

Post Detoxification
Psychological interventions; Relapse prevention, MET, cue exposure with response prevention, social skills, relaxation techniques, CBT, Family therapy etc Alcoholics anonymous 12 step programme Residential rehabilitation programmesminnisota model- social skills, relaxation, structured relapse prevention

Cognitive & behavioural strategies


By identifying triggers for relapse neg/pos mood states - poor coping skills - social isolation - craving - family issues And developing global self management strategies in areas of cognitive restructuring, skills training, lifestyle changes

Brief intervention
Assessmint of intake Information on harmful drinking, advice
Decrease by 50%, as effective as more expensive specialist tx.

Motivational interviewing
Addressing ambivalence, moving through a cycle of change 5 tenets - express empathy -help see discrepancies -avoid argument - roll with resistance - support sense of self efficacy

Prognosis
Poor alcoholic brain damage, comorbidity, divorced, criminal record, low IQ, poor support and motivation Valient 2003 60 yr follow up -25% dependant -Death rate x 2-3, rare after 70; predictors of positive outcome the most and least severe alcoholics appeared to enjoy the best longterm chance of remission

Cocaine
Substantial increases in drug treatment population Increasingly reported as 2nd problem drug 50%IV ( < benzodiazepines ) Anecdotal reports- across general population No substitute drug available Some combined pharmacotherapy's; counselling, CBT, Motivational interviewing 3% general population report lifetime use; increasing

Effects and risks of cocaine


Perceived as safe Increased energy, alertness, talkative, sex drive Combined with alcohol more toxic than either alone Severe psychological dependence, cravings Tolerance develops unpleasant side effects dry mouth, sweating, palpitations, anorexia, headaches, abd pain, irritability, paranoia, hallucinations, MI Fatigue and depression; crash; mental problems; nasal / breathing problems Increased sexual risk behaviour; association with prostitution

Benzodiazepines