Substance Misuse Disorders Flashcards

1
Q

Definition of dependance

A
  • Needing to use a substance to feel or function normally, after a period of regular use. Recognised by 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 a greater value. Dependence can be both physical and psychological
    • Features of dependence include: Tolerance, compulsion, withdrawal (physiological state), loss of control, Continued use despite harm, salience (obtaining the substance becomes more impotant than other social priorities) reinstatement after abstinence and narrowing of repertoire.
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2
Q

Definition of withdrawal

A

Transient state which occurs whilst the body readjusts to lower levels of the substance

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3
Q

Lifetime prevalence of alcohol dependence, drug dependence, any use disorder

A

Alcohol dependence (5.4%), Drug dependence (3.0%), Any substance use disorder (14.6%)

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4
Q

Male to female ratios for alcohol dependence and substance use disorders

A

2:1 for alcohol use disorders, 4:1 for substance use disorders in general

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5
Q

Definition of binge drinking

A
  • (>8 units for men or >6 units for women) > constitutes 27% of UK alcohol consumption
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6
Q

Main aetiological factor in substance use disorders

A
  1. Genetics: Family, twin and adoption studies suggest that the heritability of substance use disorders is around 40-60%. This may be accounted for by personality traits in part i.e impulsivity, anxiousness/ avoidance. May also involve having low DR2 levels, making patients seek external pleasures to compensate for low endogenous dopamine stimulation
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7
Q

Other factors (aside from genetics) which predispose to substance use disorders

A
  1. Childhood and life experiences: RFs include low parental socioeconomic status, ineffective parenting, family breakdown and abuse. More commonly have conduct disorders as children
  2. Occupation: stress and sanctioned drinking increases the risk of alcohol dependency
  3. Psychiatric illness: Associated with PD, depression, BPAD, ADHD, psychosis and anxiety disorders
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8
Q

What ‘theories of dependence’ exist which explain substance use disorders

A
  • Learning Theories:
    • Classic (Pavlovian) Conditioning- Cravings become conditioned to cues and the cue itself can trigger craving, causing drug-seeking behaviour (e.g seeing a needle)
    • Operant (Skinnerian) Conditioning- depends on repetitive behaviours having predictable outcomesà Behaviours which are rewarded are repeated (positive reinforcement), and also behaviours which relieve unpleasant experiences (negative reinforcement)
  • Motivational Theory: ‘stages of change model’
  • Neurobiological Models: Most addictive drugs strongly increase synaptic dopamine levels in the reward pathway. The brain then adjusts by reducing natural dopamine production; addiction may then develop as the patient becomes dependant on this external dopamine ‘rush’
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9
Q

Clinical presentation of alcohol use

A

Clinical presentation of intoxication includes slurred speech, ataxia, increasing sedation and confusion. Withdrawal symptoms present as blood alcohol levels fall: headache, nausea, vomiting, tremor and sweating, insomnia, anxiety, agitation and tachycardia.

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10
Q

How to calculate units of alcohol and Uk guidance on consumption

A
  • 1 unit of alcohol is 8g of pure alcohol. Units= volume (litres) x alcohol by volume (ABV, %)
  • 1 unit is equivalent to: ½ a pint, 1 small glass of wine, 1 standard measure of spirits

UK low-risk drinking guidelines are the same for men as for women: maximum 14 units a week spread over 3 days in that week

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11
Q

Physical complications of alcohol misusue

A
  • Liver: alcoholic hepatitis (malaise, hepatomegaly and ascites)
  • GI: pancreatitis, oesophageal varisces, gastritis and peptic ulceration
  • Neurological: peripheral neuropathy, seizures and dementia
  • Cancer: bowel, breast, liver, oesophageal
  • CV: HTN and cardiomyopathy
  • Head injuries and accidents when intoxicated- increased risk of subdural haematoma
  • Fetal alcohol syndrome
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12
Q

Psychological complications of alcohol misuse

A
  • Depression, anxiety, self-harm and suicide
  • Amnesia
  • Cognitive impairment- either alcoholic dementia or Korsakoff’s syndrome
  • Alcoholic hallucinosis
  • Morbid jelousy
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13
Q

Social complications of alcohol misuse

A

Social issues including unemployment, absenteeism, domestic violence, sexual exploitation and divorce may follow alcoholism and perpetuate it.

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14
Q

Wernicke’s encephalopathy causes and presentation. What is the main complication

A

Wernicke’s Encephalopathy: A medical emergence caused by acute thiamine (vitamin b1) deficiency. Presents with a classic TRIAD of 1. Confusion 2. Ataxia 3. Ophthalmoplegia. If left untreated this will progress to Korsakoff’s syndrome- irreversible anterograde amnesia, whereby patients can register new events but cannot recall them after a few minutes. Patients may confabulate.

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15
Q

Delirium tremens cause and presentation

A

Delirium Tremens: A medical emergency which occurs around 48 hours after abstincence from alcohol and which may last 3-8 days. Presents with confusion, hallucinations (especially visual), affective changes (extreme fear or hilarity), gross tremor, autonomic disturbances such as sweating or tachycardia. Has a 5% mortality rate and up to 30% if untreated or complicated

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16
Q

Management of delirium tremens

A

A reducing regimen of benzodiazepines alongside parenteral thiamine (pabrinex). Need to correct dehydration and electrolyte disturbances (can use a longer-acting benzo such as diazepam or chlordiazepoxide)

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17
Q

General investigations for alcohol dependance

A
  • Physical health screen: patients with alcohol dependency can neglect themselves so need to examine fully and broadly (guided by Hx e.g ECG, BG etc)
  • FBC: may develop macrocytic anaemia due to B12 deficiency
  • LFTs: raised transaminases suggests hepatocellular damage, raised GGT suggest recent heavy alcohol use.
  • UDS
18
Q

Questionnaires used for alcohol dependance

A

AUDIT, CIWA-Ar (grades withdrawal symptoms to inform treatment), APQ (assesses the severity and extent of problems arising from the alcohol use), Severity of Alcohol Dependence Questionnaire (SADQ)

19
Q

CAGE questions

A
  • Have you ever felt you need to CUT DOWN on your drinking?
  • Do you every feel ANNOYED if people criticise your drinking?
  • Have you ever felt GUILTY about your drinking?
  • Do you ever need an EYE OPENER to steady yourself in the morning?
20
Q

Process of assisted withdrawal (uncomplicated)

A
  • Give Pabrinex if they are at risk of Wernicke’s encephalopathy
  • Council patient on expectations: withdrawal symptoms are worst within the first 48 hours, take about 3- 7 days after the last drink to completely resolve
  • Gradually reduce alcohol consumption
  • If >15 units/day or >20 on AUDIT, consider offering Community-based assisted withdrawal (best option)
    • This can be done through organisations like CGL (Change, Grow, Live)
    • Usually 2-4 meetings in the first week
    • If complex, may need up to 4-7 days per week over a 3-week period
21
Q

What is the purpose of ‘detox’

A

‘Detox’ reduces the discomfort and risk during alcohol withdrawal- it may be planned or unplanned. The severity of withdrawal symptoms should be determined using CIWA-Ar

22
Q

When can detoxification be done in the community and when should a patient be referred for inpatient detoxification

A

Community detoxification can be offered for uncomplicated alcohol dependence, using a fixed dose regimen of benzos over 5-7 days. Inpatient detoxification is required if there is a history of:

  • 30+ units/day
  • 30+ on SADQ
  • History of epilepsy, delirium tremens or withdrawal-related seizures
  • Need concurrent withdrawal of alcohol and benzodiazepines
  • Significant psychiatric comorbidity or significant learning disability
  • Lower threshold for inpatient treatment in vulnerable groups (e.g. homeless, older people)
  • Children (10-17)
  • nobody at home to support the process.
23
Q

First steps in alcohol withdrawal management

A

There is a need to establish goals: Abstinence is the best treatment goal, however, some patients may need more moderate goals. If comorbid mental health illnesses do not improve within 3-4 weeks of abstinence, must consider referring for specific treatment. > Motivational interviewing

24
Q

Acute alcohol withdrawal management

A
25
Q

How is relapse prevention achieved

A
  • Consider acamprosate (anticraving) or naltrexone with individualised psychological intervention
  • Consider disulfiram (inhibits acetaldehyde dehydrogenase making symptoms of withdrawal worse) if above options are unsuccessful/unacceptable, usually prescribed for up to 6 months
  • Carry out thorough medical assessment to establish baseline before starting medication (including U&Es and LFTs)
  • Provide information about Alcoholics Anonymous, SMART Recovery and Change, Grow, Live (CGL)
  • Provide social interventions e.g homes can be provided for up to 3 months for homeless. Consider family meetings
26
Q

Psychological interventions for alcohol misuse

A
  • Brief interventions: can help people reduce their alcohol use to safer levels. Examples include keeping an alcohol diary, choosing lower ABV drinks, eating before drinking.
  • Motivational interviewing: Aims to empower people to be able to change. Incorporates stages of change. Create goals and helps people engage with detoxification. Involves; building rapport, developing discrepancy (showing where they are and where they want to be), avoiding disagreement, encouraging change talk, supporting self efficacy
  • CBT- helps people create alternative coping strategies to alcohol use.
27
Q

Examples of opioids, clinical presentation and complications

A
  • Heroin (diamorphine) is the most notorious: A µ-opioid agonist which stimulates endogenous endorphin receptors. Initially is smoked, then used IV as tolerance builds.
  • Others include morphine, pethidine, codeine and hydrocodeine
  • Clinical presentation:
    • Intoxication: intense rush or bush, with feelings of euphoria, warmth and well-being
    • Sedation, bradycardia and respiratory depression follow, alongside pinpoint pupils and analgesia
    • Withdrawal: begins around 6 hours after injection, peaking at 36-48 hours. Extremely unpleasant but not life threatening. People feel dysphoric, sick and restless. Generally have dilated pupils, diarrhoea, vomiting, sweating, lacrimation, aching muscles, joints.
  • Overdose can kill through respiratory failure or aspiration of vomit whilst sedated.
  • Other complications include: Infection (cellulitis, absecces), DVT (most common after repeated femoral vein injection), Emboli, Infective endocarditis, sepsis, BBVs (blood borne viruses including hep B, HIV)
28
Q

Cannabinoids symptoms and complications

A
  • The main psychoactive components, delta-9-tetrahydrocannabidiol (THC) and cannabidiol (CBD), act on cannabinoid receptors in the brain to trigger dopamine release
  • Effects depend greatly on expectation and original mood state, which tends to be enhanced by the drug
  • Higher CBD levels generally cause relaxation, contentment and talkativeness whilst higher THC levels cause anxiety, panic and paranoia
  • Perceptual distortion can occur: time slows down, hunger pangs and N&V occurs
  • Other signs include bloodshot eyes, tachycardia, dry mouth
  • It was thought that cannabis didn’t cause physiological dependency, however, chronic use can cause anxiety, restlessness, irritability, nausea, headaches and poor sleep, appetite and concentration (upon withdrawal)
  • Early use in vulnerable people can trigger psychosis. The risk is increased after use of high potency cannabinoids such as skunk
  • Regular use of high THC cannabis is associated with depression, anxiety, ADHD and PTSD
29
Q

Stimulants mechanism of action, examples and presentation

A
  • Potentiate the effects of the monoamine neurotransmitters dopamine, noradrenaline and sometimes serotonin.
  • Cocaine can be snorted or dissolved and injected.
  • Crack cocaine is a concentrated and smokable form of cocaine which causes an immediate and intense high which lasts for 5-10 minutes and is highly addictive
  • Amphetamine (‘speed’) is dissolved and injected, swallowed or snorted. Dexamphetamine can be used as a replacement for IV amphetamine dependence. Methamphetamine is similar but smokeableà causes tooth decay and loss
  • Ecstasy (3,4-Methylenedioxymethamphetamine) causes serotonin release and reuptake inhibition, which makes it a cross between a stimulant and a hallucinogen. Causes a sense of empathy and closeness to others. Makes people chatty, restless and causes bruxism (tooth grinding). Death is associated with hyperthermia and dehydration.
  • All stimulants speed up the body and mind, making users energetic, alert, excited and euphoric. Stimulants also supress appetite and sleep and cause tachycardia and HTN. Associated with impulsivity. Most start working within a few minutes and last up to 3 hours.
30
Q

Complications of stimulant use

A
  • Cocaine can cause patients to experience formication (insects crawling on or below the skin.) Also a powerful vasoconstrictor- damages the nasal mucosa and can lead to necrosis and septal perforation.
  • Withdrawal: An unpleasant ‘comedown’ within 24 hours of use- depression, irritability, lethargy and cravings.
  • In overdose stimulants cause multi organ failure and in particular kidney failure due to rhabdomyolysis
31
Q

Hallucinogens mechanism of action and complications

A
  • Affect glutamate, dopamine and serotonin neurotransmission to cause visual illusions and hallucinations
  • May cause synaesthesia (experiencing a sensation in another modality) as well as depersonalisation and derealization. Ketamine and PCP also cause anaesthesia
  • Behavioural toxicity is the accidental harm that occurs when people act on drug-induced beliefs e.g. that they can fly. PCP can cause dangerous hyperthermia and ketamine causes bladder ulceration and frank haematuria
  • Can develop anxiety and depression from ‘bad trips’
32
Q

Sedatives examples, presentation and complications

A
  • Benzodiazepines are depressant drugs with enhance the inhibitory effect of GABA transmission (barbiturates are rarely seen now)
  • Swallowed or dissolved and injected IV
  • Effects are similar to alcohol – calm and mind euphoria
  • Cause slurred speech, ataxia and stupor at high doses. Withdrawal symptoms include nausea, vomiting, headaches, anxiety, depression and confusion or seizures in severe cases.
  • Overdose can kill through respiratory arrest
33
Q

Solvents presentation and complications

A
  • Generally people sniff solvents from cloth, however gases can be directly squirted into back of throat, which may cause swelling and asphyxiation
  • Intoxication is similar to alcohol, causing euphoria and disinhibition. Some people report hallucinations.
  • These cause phsycological rather than physiological dependence.
  • Some people may experience hangovers after use with severe headaches, fatigue and depression, muddled thinking and hallucinations. Tell-tale signs include blistering and redness around mouth and nose.
  • Coma and death can occur if vomit is aspirated
34
Q

Investigations for drug dependance

A

Investigations are similar as for alcohol dependence, though emphasis should be put on a UDS. Additionally, BBV screening is important for IV drug users. U&Es should be recorded since many drugs can affect kidney and bladder function (cocaine, E, ketamine)

35
Q

General management of opiate withdrawal

A

Opioid withdrawal is unpleasant but- unlike alcohol withdrawal- cant kill. Patients should be counselled on aspects of a healthy lifestyle (sleep hygiene, diet) and provided information about self-help groups (12-step groups) additional support should then be offered to family and carers. For detoxification we generally use substitute prescribing

36
Q

When should a patient be referred for inpatient opiate detoxification, what is the duration of inpatient and community detox

A
  • Duration
    • Inpatient: up to 4 weeks- Residential detoxification tends to be limited to patients with significant comorbid physical and mental health problems or require concurrent detox of other substances
    • Community: up to 12 weeks
  • For faster detox: Withdrawal is actively precipitated by using high doses of opioid antagonists (e.g. naltrexone or naloxone)
    • Ultra-Rapid: 24 hours under general anaesthesia or heavy sedation This should not be offered
    • Rapid Detoxification: 1-5 days with moderate sedation Can be considered if patient specifically requests it
    • Accelerated Detoxification: no sedation
37
Q

Process of opiate detoxification

A
  • Appoint a key worker (supports the patient as they go through detoxification)
  • 1st line: methadone (liquid- opioid agonist with a longer half-life than heroin) or buprenorphine (sublingual- partial agonist of µ receptor- blocks euphoric effects of heroin but stops withdrawal symptoms) - decision is largely based on patient preference
  • Consider lofexidine (alpha-2 agonist) if above options are unacceptable, mild dependence or keen to detoxify over a short period of time
  • Decisions about the dosing regimen should be based on severity of dependence, stability of the patient and the setting of detoxification
38
Q

Steps following opiate withdrawal/detoxification

A

Should work towards stabilisation and maintenance: should promote abstinence from illicit drugs, prevent relapse, reduce HIV and Hep risk and decrease criminality. This can be accomplished without the use of opioid agonists, but substantial evidence indicates that medication-assisted treatment is essential for a majority of patients with opioid use disorder

MUST refer to drugs and alcohol service who will follow up for at least 6 months. Psychological therapy is largely the same as for alcohol dependence. Should offer incentives for negative drug tests, test frequently at first then less frequently.

39
Q

Treatment for opiate overdose

A

Naloxone

40
Q

Management of benzodiazepine misuse

A

Abrupt withdrawal from benzodiazepine dependence carries a high risk of seizures. This can be avoided by switching to an equivalent dose of a benzodiazepine with a longer half life

  • Withdraw in steps of about 1/8 or 10% of the daily dose every fortnight (but in reality, the dose is reduced according to the severity of the withdrawal symptoms)
  • Consider switching patients to equivalent dose of diazepam (longer half-life)
  • Oxazepam may be considered instead in patients with liver failure
  • Duration: may take 3 months to a year or more
  • Warning: do not drive if feeling drowsy

OVERDOSE > Flumazenil (benzodiazepine antagonist)

41
Q

For how long will cannabis be detectable in a UDS. How long for other drugs

A

Cannabis will be detectable for 2-14 days if used casually and up to 30 days after chronic use. Most other substances can be identified in a UDS between 2-6 days after use