Substance Misuse Disorder Flashcards

1
Q

Spectrum of substance misuse

A
  • Recreational use > acute intoxication > harmful use > dependence syndrome
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2
Q

Acute intoxication

A
  • Transient condition following use of alcohol or drugs, closely related to dose and following which recovery is usually complete
  • Stimulation, excitement or impaired judgement
  • Disinhibition
  • Reduced (or heightened) conciousness
  • Euphoria/Dysphoria
  • Impaired motor co-ordination
  • Sensory disturbances ( esp Psychadellics)
  • Hyperthermia
  • Respiratory Depression
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3
Q

Harmful substance use

A
  • A pattern of substance use that causes damage to physical health, mental health or social circumstances.
  • Diagnosis requires damage to the physical or mental health of the user.
  • Social disapproval or adverse social consequences do NOT qualify for diagnosis. (misuse rather than harmful use) Such as:
    • Ingestion of excessive amounts
    • “Idiosyncratic” Reactions e.g. Diazepam
    • Method of Administration e.g. IV use
    • Chronic Use e.g.. smoking, alcohol, drugs
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4
Q

Dependence syndrome

A
  • A strong desire or sense of compulsion to take the substance
  • Difficulties in controlling substance-taking behaviour in terms of its onset, termination, or levels of use
  • A physiological withdrawal state when substance use has ceased or been reduced
  • Evidence of tolerance, such that increased doses of the psychoactive substances are required in order to achieve effects originally produced by lower doses
  • Progressive neglect of alternative pleasures or interests because of psychoactive substance use
  • Persisting with substance use despite clear evidence of overtly harmful consequences
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5
Q

Withdrawal state

A
  • A group of symptoms of variable clustering, severity & duration depending on substance
  • Occur on withdrawal or reduction of use
  • Occur after repeated use of a substance
  • Indicates dependence

NB - Can be complicated by an acute confusional state

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6
Q

Symptoms of withdrawal state

A
  • Benzodiazepines
    • Anxiety
    • Agitation
    • Irritability
    • Diaphoresis
    • Confusion
    • Nausea
    • Palpitations
    • Insomnia
    • Seizures
    • Hallucinations
    • Psychosis
  • Opioids
  • Rhinitis
  • Lacrimation
  • Yawning
  • Dilated pupils
  • Diaphoresis
  • Insomnia
  • Diarrhoea
  • Nausea & vomiting
  • Piloerection
  • Abdominal cramps
  • Dysphoria
  • Tachycardia
  • Hypertension
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7
Q

Delirium tremens

A
  • Mortality is 5-10%
  • Characterised by:
    • Hx of Alcohol
    • Confusion-Nocturnal worsening
    • Hallucinations- Lilliputian.
    • Illusions- Insects
    • Anxiety/Fear
    • Tremulousness
    • Hypertension
    • Tachycardia
    • Tachypnoea
    • Seizures
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8
Q

Psychotic disorder

A
  • Psychotic symptoms occur during or after recent (48hrs) psychoactive substance use
  • Vivid hallucinations, misidentifications, paranoid delusions, ideas of reference
  • Psychomotor disturbances
  • Abnormal affect
  • Usually improves within 1 month & resolves within 6 months
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9
Q

Amnesic syndrome

A
  • Memory impairment (recent memory)
  • Absence or defect in immediate recall, of impairment of consciousness and of generalized cognitive impairment
  • History or objective evidence of chronic use of alcohol or drugs
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10
Q

Residual and late onset psychotic disorder

A
  • Onset of the disorder should be directly related to the use of alcohol or psychoactive substances
  • Persists beyond any period of time in which direct effect of the substance
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11
Q

Mesolimbic dopamine reward pathway

A
  • Starts in the Ventral Tegmental Area (VTA) which is site of dopaminergic neurons
  • Mesolimbic domapine pathway connects it with the Nucleus Accumbens (NAc)
  • The NAc has Dopamine sensitive cells & mediates the rewarding effects
  • Dopamine is released when an addictive drug is used
  • Amygdala & Hippocampus play role in memory & whether experience is desirable
  • Prefrontal cortex co-ordinates the information & determines behaviour
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12
Q

Reward pathway activation

A
  • Natural rewards
    • Food
    • Sex
    • Nurturing
    • Exercise
  • Chemical rewards
    • Drugs
    • Alcohol
    • Coffee
    • Nicotine
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13
Q

Aetiology of addiction

A
  • Social learning model
    • Observation of others engaging in addictive behaviour/maladaptive coping leads to copying behaviour
  • Disease model
    • Addiction is a disease with biological, neurological, genetic and environmental sources of origin
    • Altered brain structure and functioning + neuroadaptation
  • Genetic vulnerability
    • Children of alcoholics 4x as likely to be alcoholics
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14
Q

Cycle of change

A
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15
Q

Psycholosocial interventions in addictions

A
  • Motivational enhancement interviewing
  • Brief interventions
  • Relapse prevention
  • Anxiety management and coping skills (CBT)
  • 12 step programmes (AA, NA, CA)
  • Peer support (addactions, St Mungo foundation, recovery cafe’s)
  • Contingency management
  • Therapeutic community/residential rehabilitation
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16
Q

Motivational interviewing

A
  • Works on facilitating & engaging intrinsic motivation to change
  • Collaborative
  • Goal-orientated
  • Client- centred
  • Guides patient to examine & resolve ambivalence
17
Q

Brief interventions

A
  • F- Feedback of risks
  • R- Responsibility Highlighted
  • A - Advice to abstain or cut down
  • M- Menu of alternative options and activities offered
  • E- Empathic Interviewing
  • S- Self efficacy enhanced
18
Q

Misuse of drugs act (1971)

A
  • Covers possession & supply of controlled drugs
  • Class A: includes heroin, cocaine, MDMA, LSD
  • ClassB: cannabis, amphetamines, ketamine, codeine
  • Class C: diazepam, GHB, tranquilisers, anabolic steroids
19
Q

Psychoactive substances act (2016)

A
  • Offence to produce, supply or offer to supply any psychoactive substance if substance likely to be used for its psychoactive effects & regardless of its potential for harm
  • Intended to act against shops and websites supplying NPS
20
Q

Substance use mortality

A
  • Mortality in drug addicts is 7x higher than the general population
  • Injecting drug users mortality is 12-22x> drug using peers
  • Alcohol is strongest single predictor of suicide
  • Most common cause of drug-related death is opoids followed by benzos
  • Generally poly-drug use
21
Q

Opoids

A
  • Analgesic, Euphoric & Anxiolytic effects
  • μ(Mu), κ (Kappa) & δ (Delta) receptors
  • Most abused substances are μ receptor agonists
  • μ receptors mediate analgesia, respiratory depression, euphoria (in some), drowsiness & constipation
  • Mediate dopamine release in VTA
  • Seek help from services in 20s
  • Detox Vs maintenance prescription
  • Lofexidine ( α2 adrenergic agonist) or Buprenorphine for detox- high relapse rates
  • Methadone & Buprenorphine for substitute prescriptions (effective for reducing heroine use)
  • Rapid loss of tolerance
  • High risk of OD if missed doses and re-instated at usual dose
  • Need for re-titration after 3 days
  • Management of overdose:
    • Symptoms – respiratory depression, pinpoint pupils, ↓ levels consciousness
    • Treatment – Naloxone – competitive opioid anatgonist, reverses depression of CNS & respiratory system caused by opioids; can be given nasally, IM, IV
    • Naloxone’s rapid blockade of opioid receptors often produces fast onset of withdrawal symptom
22
Q

Benzodiazepines

A
  • Enhance GABA at the GABAA receptors
  • Ligand gated ion channel
  • When activated. Selectively conduct Cl ions, causing hyperpolarisation which reduces likelihood of action potential
  • Sedative, hypnotic, anxiolytic & muscle relaxant effects
  • Licit- Prescribed. Normal dose but unable to stop
  • Illicit- often excessive doses (eg 20x 10mgs daily)
  • Rate of dependence increases with duration of use
  • Use for 4 weeks or less rarely leads to significant withdrawals or dependence
  • Management of overdose:
    • Sedation, drowsiness, ataxia, slurred speech, coma, respiratory depression
    • Higher risk if combined with alcohol or other CNS depressants
    • Supportive treatment
    • Flumazenil IV
23
Q

Amphetamines

A
  • CNS stimulants
  • Enhance release of Dopamine, Norepeniphrine & Serotonin from pre- synaptic neurons
  • Block catecholamine reuptake
  • Norepheneprine >sympathomimetic
  • Dopamine > Central stimulant/reward
  • Serotonin > Mood
  • Rapid onset of effects
  • Therapeutic use in ADHD
  • Withdrawal can develop rapidly with methamphetamine
24
Q

MDMA (Ecstasy)

A
  • A substituted amphetamine
  • Serotonergic
  • Partially stimulant & partially hallucinogenic
  • Harm reduction advice regarding maintaining hydration & avoiding overheating.
25
Q

Cocaine

A
  • CNS stimulant & local anaesthetic
  • Short acting
  • Direct action on Dopamine neurons blocking reuptake
  • Also blocks reuptake of Serotonin & Norepinephrine
  • Causes increased energy, increased confidence, euphoria & diminished need for sleep
  • Can precipitate psychosis
  • Associated with sudden cardiac death
  • Crack cocaine- more potent
  • Strong complusion to take & psychological dependence
  • Dysphoric “Come down”
26
Q

Cannabis

A
  • Herbal cannabis contains >400 compounds > 60 are cannabinoids
  • 9Tetrahydrocannabinol (THC) most potent psychoactive
  • Cannabis receptors are inhibitory G protein linked
  • CB1 receptors (CNS & PNS)
  • CB2 receptors (immune)
  • THC increases release of DA from the Nucleus accumbens & prefrontal cortex
  • Impaired cognitive & psychomotor performance
  • Euphoria, heightened perceptual sensitivity, depersonalisation & derealisation
  • Vasodialtion, suffused sclerae, postural hypotension, syncope
  • Tolerance
  • Psychological dependence
  • Withdrawals: restlessness, insomnia, anxiety, aggression, anorexia, muscle tremor & autonomic effects
  • Link with onset of Schizophrenia
  • Long term use may lead to subtle forms of cognitive impairment affecting memory, concentration & the integration of complex information or to an amotivational syndrome
27
Q

Volatile gases

A
  • 1 death/week in UK
    • Sudden cardiac death
    • Asphyxiation
    • Accidents when intoxicated
  • Rapid intoxication- euphoria, nystagmus, hallucinations, psychomotor retardation, blurred vision, poor co-ordination
  • Rashes around nose & mouth
  • Occular or oropharangeal irritation
  • Chronic users may develop diffuse cerebral, cerebellar and brainstem atrophy with white matter changes & leukoencephalopathy
  • Hearing loss, cerebellar signs, peripheral neuropathy, lethargy, memory less etc
  • Harm reduction advice
    • Not to take when alone
    • Reduce risk of asphyxiation
28
Q

Ketamine

A
  • NMDA antagonist but also has effects at Dopamine & Opioid receptors
  • Anaesthetic- used in Paediatrics & field medicine
  • Treatment of neuopathic pain
  • Acute experience is dose dependent
  • Short t1/2
  • ?may be beneficial in treatment resistent depression
  • Tolerance develops rapidly
  • Intense cravings related to pain & cramps
  • 1/3 experience anxiety, sweats & shakes in withdrawal
  • Acute risks include:
    • Cardiac
    • Accidental Death
    • Unprotected Sex
  • Chronic use associated with cognitive deficits
  • Can lead to ketamine bladder
    • 30% of regular Ketamine users
    • Errosion of urothelium
    • Inflammation leads to revascularisation
    • Urge incontinence
    • Decreased bladder compliance
    • Decreased bladder volume
    • Detrusor overactivity
    • Painful haematuria
    • Bilateral hydronephrosis and
    • Renal papillary necrosis
    • On stopping use
      • 1/3 recover
      • 1/3 no change
      • 1/3 deteriorate
29
Q

G Drugs GBL and GHB

A
  • Gamma Butyrolactone (GBL)
  • Pro-drug for Gamma hydroxybutyric acid (GHB)
  • Recreational use
  • Effects similar to alcohol
  • Recreational Use in MSM
  • Heavy use/dependence assoc with severe withdrawals