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Substance use disorders Flashcards

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1
Q

Terminology: intoxication, harmful use, dependency, withdrawal

A

Intoxication: transient state of emotional and behavioural change following drug use. Dose-dependent and time limited

Harmful use: pattern of use likely to cause physical or psychological damage

Dependency: a cluster of physiological, behavioural and cognitive symptoms in which the use of a substance takes on a much higher priority than other behaviours that once had greater value

Withdrawal: transient state occurring whilst readjusting to lower levels of the drug in the body

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2
Q

Theories of dependence

A

Learning theories

  • Classical conditioning: cravings become cues which trigger drug-seeking behaviour
  • Operant conditioning: behaviours repeated if they relieve unpleasant experiences (negative reinforcement); drug providing pleasure will be used again (positive reinforcement)

Neurobiological

  • All drugs of abuse affect the DOPAMINERGIC MESOLIMBIC reward pathway
  • Pathway beings in the ventral tegmental area and projects to the prefrontal cortex and limbic system; prefrontal cortex - role in motivation and plannaing; dopamine release in the nucleus accumbens causes a sensation of pleasure
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3
Q

Features of depedence

A

Tolerance: larger doses required to gain the same effect as previously

Compulsion: strong desire to use the substance; craving

Withdrawal: physioloigical withdrawal state when the substance is stopped/decreased, demonstrated by characteristic withdrawal S and substance use to prevent or relieve withdrawal Sx.

Problems controlling use: difficulties controlling starting, stopping or amounts used

Continued use despite harm: despite clear problems caused by the substance, the person can’t stop using

Salience (primary): obtaining and using the substance becomes so important that other interests are neglected

Reinstatement after abstinence: tendency to return to the previous pattern and level of use after a period of abstinence

Narrowing of the repertoire: loss of variation in use of the substance.

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4
Q

Differentials for substance misuse

A

Organic: consider physical causes for certain symptoms (e.g. ataxia, confusion); beware risk of head injury and subdural haematoma from falls

Psychiatric illness: may be primary or comorbid problem

  • Depression/mania
  • Functional psychosis
  • Anxiety disorder
  • Personality disorder
  • Which is primary prob- psych Sx fit with Sx of substance?; psych Sx while abstinent?; FHx psych illness?
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5
Q

Alcohol - harmful substance use - classification

A

Pattern of alcohol use that had caused damage to a person’s physical or mental health or has resulted in behaviour leading to harm to health of others

Pattern of alcohol use is evident over a period of at least 12 months if substance use is episodic or at least 1 month if use is continuous

Harm to health of the individual occurs to one or more of the following: behaviour related to intoxication; direct/secondary toxic effects on body organs/systems; a harmful route of administration

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6
Q

Alcohol- dependence syndrome - classification

A

Disorder of regulation of alcohol use arising from repeated or continuous use of alcohol.

Characteristic feature: strong internal drive to use alcohol which manifested by impaired ability to control use increasing priority given to use over other activities and persistence of use despite harm tor negative consequences

2 of the following:

  • Impaired control over substance use - in terms of onset, level, circumstance of termination of use, often accompanies by a subjective sensation of urge/craving
  • Substance use becomes an increasing priority in life - takes precedence over other interests, responsibilities, health, personal care
  • Physiological features - (indicative of neuroadaptation to the substance as manifested by: tolerance; withdrawal Sx following in cessation or reduction in use; repeated use to prevent or alleviate withdrawal Sx
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7
Q

Aetiology of alcohol abuse

A

Genetic factors - populations with less effective enzymes - lower dependence
Occupation
Social background
Psychiatric illness

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8
Q

Mechanism of alcohol in brain

A

Primary target: GABA-A receptor/glutamate receptor

GABA-A receptor

  • Acutely: alcohol boosts function -> anxiolysis, sedative
  • Chronically: alcohol reduces function as you develop tolerance - countered by alcohol boosting function

Glutamate-NMDA receptor

  • Acutely: reduces function
  • Chronically: boosts function - associated with impaired memory

Withdrawal leads to:

  • Increased glutamate-NMDA activity
  • Decreased GABA activity
  • Can lead to cell death and seizures
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9
Q

Clinical features of alcohol intoxication

A

Relaxation and euphoria
At higher level may make people irritable, aggressive, weepy, morose and disinhibited
Impulsivity and poor judgement can make people take risks and behave irresponsibly

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10
Q

Clinical features of alcohol withdrawal

A

Sx start at 6-12 hrs: tremor, sweating, tachycardia, anxiety, headache, nausea, retching, vomiting, insomnia

Peak incidence of seizures at 36 hrs

Delirium Tremens (med emergency): peak incidence at 48-72 hours

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11
Q

Onset, duration, Sx of Delirium Tremens

A

Peak incidence at 48-72 hrs post alcohol withdrawal
Duration: 3-4 days
Confusion
Hallucinations (especially visual e.g. formication)
Affective changes (extreme fear and hilarity may alternate)
Gross tremor (especially hands)
Autonomic disturbance (sweating, tachycarida, HTN, fever)
Delusions
5% mortality

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12
Q

Complications of alcohol misuse - general

A

Physical
Psychological
Wernicke-Korsakoff Syndrome
Social - unemployment, poor attendance/performance at work, domestic violence, separation and divorce; always ask about drink driving

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13
Q

Physical complications of alcohol miuse

A

Liver: alcoholic hepatitis, cirrhosis
GI: pancreatitis, oesophageal varices, peptic ulcer disease
Neuro: peripheral neuropathy, seizures, dementia
Cancers: bowel, breast, oesophageal and liver
CVS” HTNM cardiomyopathy
Head injuries/accidents
Foetal alcohol syndrome

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14
Q

Psychological complications of alcohol misuse

A

Depression, anxiety, self harm, suicide
Amnesia
Cognitive impairment (alcoholic dementia, Korsakoff syndrome)
Alcoholic hallucinosis (experience of auditory hallucinations in clear consciousness while drinking - often persecutory/derogatory)
Morbid jealously (overvalued idea or delusion that partner is unfaithful

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15
Q

Wernicke-Korsakoff Syndrome

A

Wernicke’s Encephalopathy

  • Caused by acute thiamine deficiency via chronic alcohol consumption: inadequate nutritional intake, decreased absorption, impaired use by cells
  • Thiamine deficiency results in abnormal cellular function in the cerebral cortex, hypothalamus and cerebellum
  • TRIAD: confusion + ataxia (wide based gait) + ophthalmoplegia (nystagmus, lateral rectus or conjugate gaze palsies
  • MEDICAL EMERGENCY

Korsakoff Psychosis

  • When Wernicke’s encephalopathy deteriorates further
  • Confusion + anterograde/retrograde amnesia + confabulation
  • Irreversible anterograde amnesia - pt register new events, but cannot recall them within a few minutes; confabulate to fill gaps in their memory
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16
Q

Screening tools for potential alcohol misuse

A

CAGE questionnaire - ever felt need to cut down drinking? people annoyed you by criticising your drinking? ever felt guilty about drinking? need to drink first thing in the morning? score 2/+ suggests excessive drinking

AUDIT - more comprehensive to identify misuse - >15 requires comprehensive assessment

SADQ or LDQ for severity of dependece

CIWA-Ar for severity of withdrawal

APQ for nature and extent of problems arising from alcohol misuse

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17
Q

Investigations for alcohol misuse

A

Hx/screening tools

FBC - macrocytosis anaemia due to B12 deficiency in alcoholism

LFTs - GGT rises with heavy alcohol use; raised ALT + AST suggests hepatocellular damage

B12/folate

U&Es

Clotting screen

Glucose

Other tests based on presentation

  • ECG
  • Urine drug screen (amphetamines, heroin, cocaine, methadone, cannabis)
  • Hepatitis if IVDU
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18
Q

Management of alcohol dependence

A

Assessment and preparation: motivation to change; identify type of support needed (reduce consumption/detox/college)

Detoxification

  • Allows metabolism and excretion of the substance whilst minimising discomfort
  • May be planned or unplanned
  • Long acting benzos (e.g. chlordiazepoxide) - replace alcohol and prevent withdrawal Sx; gradually withdrawn and stopped
  • Thiamine (vit B1) - prophylaxis against Wernicke’s encephalopathy; best given IV or IM
  • Community/home detox for uncomplicated dependency using a fixed-dosage reducing regime of benzos over 5-7 days
  • Inpatient detox if Hx of withdrawal fits, comorbid medical or psych illness or if pt lacks support at home
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19
Q

Relapse prevention

A

Psychological

  • CBT
  • Problem-solving therapies
  • Group therapy (AA)

Medical

  • Acamprosate (anti-craving drug)
  • Disulfiram (antabuse) - mimics flush reaction to alcohol thereby making alcohol consumption unpleasant
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20
Q

NICE guidelines - Interventions for harmful drinkers and mild alcohol dependence

A
  • Offer psych intervention (CBT, behavioural therapy, social network and environment-based) focussed on alcohol related cognitions
  • Offer behavioural couples therapy focussed on EtOH problems if indicated
  • Can offer alongside pscyh tx: Acamprosate, Naltrexone
21
Q

NICE guidelines - assisted alcohol withdrawal

A

Assisted alcohol withdrawal

  • Give pabrinex if at risk of Wernicke’s encephalopathy
  • Expectations: Sx worst within 1st 48 hrs; takes 3-7days to disappear completely
  • If >15 units/day/>20 on AUDIT, consider offering community bases assisted withdrawal, management in specialist alcohol service if safety concern
  • Consider in-pt if any: 30+ units/day; 30+ on SADQ; Hx epilepsy, delirium tremens or withdrawal-related seizures; also withdrawing from benzos; significant psych co-morbidity or LD; vulnerable groups; children 10-17
22
Q

NICE guidelines - drug regiments in alcohol detox

A

Fixed-dose or Sx-triggered regimen

  • Fixed dose: involves starting Tx with a standard dose , not defined by the levels of alcohol withdrawal, and reducing to zero over 7-10 days according to standard protocol
  • May be longer if concurrent benzo withdrawal Tx required

Preferred medication: clordiazepoxide or diazepam
- If liver impairment: consider lorazepam (limited hepatic metabolism)

Give not more than 2 days medication at a time

23
Q

NICE guidelines - post withdrawal

A

Consider acamprosate or naltrexone with individualised psych intervention
Consider disulfiram if above options are unsuccessful/unacceptable

24
Q

NICE guidelines - Wernicke’s Encephalopathy

A

Start high risk/suspected Wernicke’s on thiamine (Pabrinex) (oral or parenteral)

  • Malnourished or at risk of malnourishment
  • Decompensated liver disease
  • Acute withdrawal
  • Before and during a planned medically assisted alcohol withdrawal
  • Attend A&E
  • Admitted to hospital with an acute illness or injury

Offer parenteral thiamine followed by oral to suspected Wernicke’s for 5 days, unless Wernicke’s excluded

For those with Wernicke-Korsakoff syndrome offer: supported independent living for those with mild cognitive impairment; supported 24 hr care for those with moderate-severe cognitive impairment

25
Q

NICE guidlines - acute alcohol withdrawal

A

Offer admission for med-assisted withdrawal

Offer pharmacotherapy for withdrawal Sx: consider adding benzo (lorazepam) or carbamazepine; alternative: clomethiazole

Offer advice on local support (AA, etc)

Delirium tremens - 1st line: oral lorazepam, if Sx persist parenteral lorazepam or haloperidol; alternative chlordiazepoxide + IV thiamine + manage dehydration and electrolyte abnormalities

Alcohol withdrawal seizures - consider fast-acting benzos e.g. lorazepam to reduce likelihood of future seizures

26
Q

Opiates - examples, receptors, route of admin, complications of IV drug use

A

Examples: heroin, morphine, pethidine, codeine, dihydrocodeine

Bind to opioid receptors

Heroin route of admin: initially smoked, then IV; may inject SC or IM, when venous access is difficult

Complications of IVDU: local - abscess, cellulitis, DVT, emboli; systemic - septicaemia, infective endocarditis, blood-borne infections, increased risk of overdose

27
Q

Clinical features of opioid misuse

A 
Rhinorrhoea
Needle track marks
Pinpoint pupils
Drowsiness
Watering eyes
Yawning
28
Q

Clinical features of opioid intoxication

A

IV heroin - intense rush or buzz
Euphoria, warmth and wellbeing
Sedation and analgesia
Vomiting and dizziness
Bradycardia and respiratory depression (can die from aspiration)
Pinpoint pupils
non IV users may experience milder effects (e.g. constipation, anorexia, decreased libido)

29
Q

Clinical features of opioid overdose

A

Miosis
Respiratory depression
Altered mental status

ANTIDOTE: naloxone (opioid antagonist)
- pts may be plunged into withdrawal

30
Q

Clinical features of opioid withdrawal

A 
Starts 6 hrs after injection
Peaks 36-48 hrs
Should improve by 1 week
Dysphoria
Nausea
Insomnia
Agitation
The runs - diarrhoea, vomiting, lacrimation, rhinorrhoea
Feverish
Abdo cramps
Aching joints and muscles
Yawning irresistibly
Dilated pupils
31
Q

Investigations in opioid overdose/misuse

A

Phys exam (establish baselines)
Urine drug screen
U&E (malnutrition)
FBC - anaemia due to malnutrition, signs of infection
LFTs
Blood bourne infection: syphilis (RPR), hepatitis serology, HIV test

32
Q

Alcohol dependence pharmacology

A

Alcohol withdrawal regime

  • Benzos: reduce signs and Sx of withdrawal; increase frequency of Cl channels opening hence increasing effect of GABA
  • Carbamazepine: glutamatergic anticonvulsant

Abstinence follow detox

  • Acomprosate: reduces glutamate function
  • Naltrexone: opiate antagonist; leads to reduced dopaminergic activity and decreased pleasurable effects of alohol
  • Disulfiram: inhibits aldehyde dehydrogenase to cause undesirable Sx after alcohol consumption
33
Q

Management of opioid misuse

A

Harm reduction

  • Assess and minimise risk rather than insist on abstinence
  • Info on improving safety of drug use
  • Needle exchange, vaccination and testing for blood-borne viruses

Substitute prescribing

  • Deliberate prescribing in a controlled manner
  • Methadone (liquid) and buprenorphine (subligual tablet): oral to replace injectable opiates
  • Taken in supervised environment, dose titrated down
  • Detox helped with managing of Sx (anti-diarrhoeals, anti-emetics, pain killers)
  • Naltrexone (opiate antagonist) may be given after detox to prevent relapse, as it blocks the euphoric effects of opiates
34
Q

NICE: when not to routinely offer opioid withdrawal Tx

A

Concurrent med problem requiring urgent Tx
In police custody
Presenting in acute or emergency setting
Be careful with pregnant women

35
Q

NICE - meds for opioid detox

A

1st line: methadone (liquid) or buprenorphine (sublingual)

If above not acceptable, mild dependence or keen to detox over short period: consider lofexidine (alpha-2 agonist)

Duration: in-pt - upto 4 weeks (pts with sig. comorbid phy/mental problems/req. concurrent detox of another substance); community - upto 12 weeks

Withdrawal Sx: clonidine and lofexidine can help the Sx; anti-diarrhoeal, anti-emetic, pain killers

36
Q

NICE - ultra-rapid, rapid and accelerated detox

A

Withdrawal actively precipitated by using high doses of opioid antagonists e.g. naltrexone or naloxone

Ultra-rapid: 24 hrs under GA or heavy sedation - should not be offered

Rapid: 1-5 days with moderate sedation - can be considered

Accelerated: no sedation

37
Q

NICE - opioids - post detox stabilisation/maintenance and follow up

A

Promote abstinence, prevent relapse, reduce HIV and hep C risk, reduce mortality and decrease criminality

Can use opioid agonists (methadone, buprenorphine) and opioid antagonists (injectable extended release naltrexone)

Refer to drugs and alcohol service
F/U at least 6 months
Offer CBT to prevent relapse
Urine screening; incentives for neg tests; reduce freq of tests over time

38
Q

Opioid dependence pharmacology

A

Full agonist

  • Morphine and methadone
  • High efficacy, producing a full response while occupying a relatively low proportion of receptors
  • Can easily cross potentially lethal dose

Partial agonist

  • Buprenorphone
  • Produces sub-maximal response even when occupying all receptors (cannot produce maximal response)
  • Will cause withdrawal Sx if given with heroine; antagonises the effects

Antagonist

  • Naltrexone
  • Helps prevent relapse as user will not get any effect from heroin if antagonist is present
39
Q

Cannabis: psychoactive compound, where it acts

A

Delta-9 tetrahydrocannabinol (THC)

Acts on cannabinoid receptors in the brain

40
Q

Cannabis effects

A

Perceptual distortion, the munchies, nausea and vomiting
Early heavy use may precipitate psychosis
Lethargy and poor motivation are features of chronic heavy use

41
Q

Stimulants: mechanisms, effects and side effects

A

Potentiate the effects of NTs, increasing energy, alertness and euphoria; decreases need for sleep
Increase confidence and impulsivity
Side effects: arrhythmia, HTN, stroke, anxiety, panic and drug-induced psychosis
Crash after substance wears off

42
Q

Examples of stimulants

A

Cocaine - may cause formication (feeling of insects); powerful vasodilator
Crack cocaine - concentrated smokable cocaine; immediate and extremely intense high; lasts 5-10 mins
Amphetamine (speed) - dissolved or injected
Khat - mild stimulant; chewable leaves; can cause florid(acute) psychosis
Ecstacy - causes serotonin reuptake inhibition and release; usually tablet; users become chatty, dance relentlessly and show bruxism (tooth grinding); side effects - N&V; death associated with hyperthermia and dehydration

43
Q

Stimulant management

A

Harm reduction

Short term benzos may be offered to help withdrawal anxiety

44
Q

Hallucinogens - effects

A

Cause visual illusions and hallucinations
Synaesthesia may occur (experience of sensation in another modality)
Some people become acutely anxious
Behavioural toxicity - accidental harm when ppl act on drug-induced beliefs (e.g. can fly)

45
Q

Examples of hallucinogens

A

LSD - affects dopamine and serotonin transmitter systems; trips could last 12 hrs; bad risks; risks also incl anxiety, depression, psychosis
Phenylcyclidine - snorted or added to joint; associated with violent outbursts and ongoing psychosis
Ketamine - aesthetic; effects can lead to self-harm
Magic mushroom - eaten or drunk; risk of poison
Sedatives - Benzos have sedative effect; enhance GABA transmission; similar FX to EtOH; slurred speech, ataxia, stupor at higher doses; withdrawal similar to alcohol; overdose treated with flumenazil

46
Q

Benzodiazepine mechanism, uses and risks

A

Enhance effect of inhibitory GABA by increasing frequency of chloride channels

Uses: sedation, hypnotic, anxiolytic, anticonvulsant, muscle relaxant

Risks: tolerance and dependence; short term - drowsiness, reduced concentration; long term - cognitive impairment, worsening anxiety and depression, sleep disruption

47
Q

Clinical features of benzodiazepine withdrawal

A

Can occur up to 3 weeks after stopping a long acting drug

Insomnia
Irritability
Anxiety
Tremor
Loos of appetite
Tinnitus
Excessive sweating
Seizures
Perception disturbance
48
Q

Management of benzodiazepine misuse

A

Address underlying issues - anxiety, sleep, depression

Withdraw - dose reduced gradually according to severity of withdrawal Sx
Suggested protocol - switch pt to equiv dose diazepam; reduce every 2-3 weeks by 2/2.5mg; time needed for withdrawal can var 4 weeks to year+; consider oxazepam if liver failure

Psych therapy - offer CBT (address underlying MH, advice on sleep hygiene etc)

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