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Psychiatry > Substance Misuse > Flashcards

Substance Misuse Flashcards

1
Q

Define intoxication.

A

a dose dependent, transient state following drug use

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2
Q

Define harmful use.

A

a pattern of use likely to cause physical or psychological damage

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3
Q

Define dependence.

A

needing to use a substance to feel or function normally, after a period of regular use

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4
Q

What are the features of dependence?

A
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5
Q

Describe the epidemiology of substance misuse.

A
  • Alcohol use disorder
    • Male to female ratio is 2:1
  • Substance us disorder
    • Male to female ratio is 4:1
  • Using multiple substances (which may include alcohol) is not uncommon
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6
Q

Define binge drinking.

A

>8 units for men or >6 units for women in one session - constitutes 27% of UK alcohol consumption.

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7
Q

What is the aetiology behind substance use disorders?

A
  • Genetics
  • Childhood and life experiences
  • Occupation
  • Psychiatric illness
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8
Q

Describe the genetic aspect behind behind substance use disorders.

A
  • Heritability of 40-60%
  • May be mediated by personality traits e.g. impulsivity, anxiousness/avoidance, reward-seeking
  • Multiple genes implicated
    • Dopamine ‘reward’ pathways - low dopamine-2 receptor levels → compensation for low stimulation - by external pleasures
    • Ethanol → acetaldehyde → acetaldehyde dehydrogenase. Some East Asian Populations have less effective enzymes causing acetaldehyde accumulation → flush reaction → avoidance of alcohol
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9
Q

Describe the childhood and life experiences behind substance use disorders.

A

RFs:

  • lower parental socioeconomic group and educational achievement
  • parental substance dependence
  • ineffective parenting
  • family breakdown
  • childhood abuse
  • Affected adults may have had conduct disorder as child, experienced bullying and involved in antisocial peer group
  • Adolescence (vulnerability, stress, risk-taking behaviour, brain sensitive to modification of dopamine reward pathways)
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10
Q

Describe the role of occupation in substance use disorders.

A
  • Stress and socially sanctioned drinking increase the risk of alcohol use disorders in certain occupations, e.g. publicans, journalists, doctors, military personnel, people in the entertainment industry.
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11
Q

Describe the role of psychiatric illness in substance use disorders.

A

Substance use disorders are associated with:

  • personality disorders
  • depression
  • BPAD
  • ADHD
  • psychosis
  • anxiety disorders (particularly social anxiety disorder)
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12
Q

What are the 2 broad theories of dependence?

A
  • Learning theories
  • Neurobiological theories
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13
Q

Describe the learning theories of dependence.

A

Classic (Pavlovian) Conditioning

  • Cravings become conditioned to cues (e.g. needles for heroin users)
  • Cue itself can trigger craving, causing drug-seeking behaviour

Operant (Skinnerian) Conditioning

•Behaviours which are rewarded are repeated (positive reinforcement), and also behaviours which relieve unpleasant experiences (negative reinforcement)

Vicarious Learning

• Substance dependence can develop following observation of behavioural rewards in others as well as direct experience

Motivational Theory

  • Precontemplation - cant see a problem
  • Contemplation - recognises problem but doesn’t want to change (open to discussion)
  • Preparation - wants to change and plans
  • Action - cuts down or stops
  • Maintenance - remains abstinent
  • Relapse - starts using again

Relapse isn’t ‘failure’, but a learning opportunity: under-standing the triggers for relapse helps the next attempt at abstinence

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14
Q

Describe the neurobiological models of dependence.

A
  • All drugs of abuse affect the dopaminergic reward pathway
  • Starts in ventral tegmental area and protects onto the prefrontal cortex and limbic system (emotional brain)
  • Prefrontal cortex has a role in motivation and planning
  • Dopamine release in the nucleus accumbens is central to the sensation of pleasure, which is important in reward

Most addictive drugs strongly increase synaptic dopamine levels in the reward pathway.

  • The brain adjusts by reducing natural dopamine production in response to drug use and become dependent on the drug for dopamine rush.
  • Cocaine and amphetamine block dopamine reuptake → increased synaptic dopamine → pleasurable sensation
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15
Q

Describe the clinical presentation of alcohol use.

A

•Intoxication

o Slurred speech, poor coordination, exaggerated emotions, ataxia, increasing sedation and confusion

Severe intoxication (‘alcohol poisoning’) can cause vomiting, ataxia, respiratory depression, confusion, coma, and death.

•Withdrawal

o Headache, nausea, retching and vomiting, tremor and sweating

o Insomnia

o Anxiety, agitation, tachycardia and hypotension

Severe withdrawal causes delirium tremens or death

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16
Q

How can we divide the complications of alcohol use disorder?

A
  • Physical
  • Psychiatric
  • Social
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17
Q

What are the physical complications of harmful alcohol use?

A

Liver: alcoholic hepatitis (malaise, hepatomegaly and ascites)

GI: pancreatitis, oesophageal varices, gastritis and peptic ulceration

Neurological: peripheral neuropathy, seizures and dementia

Cancer: bowel, breast, liver, oesophageal

CV: htn and cardiomyopathy

Head injuries and accidents while intoxicated – increased risk subdural haematoma

Fetal alcohol syndrome

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18
Q

What are the physical complications of harmful alcohol use?

A
  • Liver: alcoholic hepatitis (malaise, hepatomegaly and ascites) → end stage liver disease (cirrhosis)
  • GI: pancreatitis, oesophageal varices, gastritis and peptic ulceration
  • Neurological: peripheral neuropathy, myopathy, Wernicke-Korsakoff syndrome, seizures and dementia
  • Cancer: bowel, breast, liver, oesophageal, mouth, pharynx, larynx, pancreas
  • CV: IHD, HTN and cardiomyopathy
  • Head injuries and accidents while intoxicated – increased risk subdural haematoma
  • Fetal alcohol syndrome
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19
Q

What is Wernicke-Korsakoff syndrome?

A

Wernicke encephalopathy

  • Medical emergency
  • Caused by acute thiamine (vitamin b1) deficiency (inadequate intake, absorption, cellular utilisation)
  • Triad: confusion, ataxia and opthalmoplegia
  • If untreated, leads to Korsakoff’s Syndrome

o Irreversible anterograde amnesia (and some retrograde)
o Patient can register new events, but cannot recall them within a few minutes o Patients may confabulate to fill gaps in memory

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20
Q

What is delirium tremens? What are the symptoms, mortality and management?

A

Medical emergency

Onset: ~48h into abstinence

Part of severe alcohol withdrawal

Onset around 48 hrs into abstinence; Duration: 3-8 days

Symptoms

o Confusion
o Hallucinations, especially visual (animals and people) and tactile (itch, burn, crawling up skin)
o Affective changes – extreme fear and hilarity may alternate
o Gross tremor (hands)
o Autonomic disturbance: sweating, tachycardia, htn, dilated pupils, fever o Delusions

5% mortality rate (30% if complications occur)

Urgent medical treatment involves a reducing benzodiazepine regime and parenteral thiamine

o Mx dehydration and electrolyte imbalance

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21
Q

What are the psychiatric complications of harmful alcohol use?

A
  • Depression, anxety, self-harm and suicide
  • Cognitive impairment – either alcoholic dementia or Korsakoff’s syndrome
  • Alcoholic hallucinosis - auditory hallucinations in clear consciousness during or after heavy drinking (often persecutory or derogatory)
  • Morbid jealousy - overvalued idea/delusion of a partner’s infidelity
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22
Q

What are the social complications of harmful alcohol use?

A
  • Social problems → alcoholism → further problems (vicious cycle)
  • Problems include unemployment, poor work attendance and performance, domestic violence, separation and divorce
  • Law-breaking may occur
  • Children at increased risk of neglect, abuse and conduct disorder
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23
Q

What is the progression of alcohol withdrawal?

A

Alcohol withdrawal

  • symptoms: 6-12 hours
  • seizures: 36 hours
  • delirium tremens: 72 hours
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24
Q

What is the differential diagnosis of alcohol use disorder?

A

Organic: head injury and subdural haematoma

Psychiatric illness

o Often a dual diagnosis

o Depression/mania
o Functional psychosis

o Anxiety disorder

o Personality disorder

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25
Q

What are the investigations for alcohol use disorder?

A

Physical health screening - people may neglect themselves

FBC: macrocytic anaemia due to B12 deficiency

LFTs: yGT increase with recent heavy alcohol use, raised transaminases suggest hepatocellular damage

ECG, urine drug screen, hepatitis screening if IVDU

MedEd

o Bloods: FBC, LFT, B12, folate, U&E, clotting screen, glucose

  • *o Blood alcohol level or breathalyser**
  • *o Urine drug screen**
  • *o Rating scale (e.g.AUDIT, CIWA-Ar, APQ)**
  • *o Severity of Alcohol Dependence Questionnaire (SADQ)**

Assessment
o Use formal assessment tool to assess severity and nature of misuse:

  • *AUDIT** – alcohol use disorders identification test (>15 requires comprehensive assessment)
  • *SADQ** – severity of dependence
  • *CIWA-Ar** – clinical institute withdrawal assessment of alcohol scale (for severity of withdrawal)

APQ – alcohol problems questionnaire (assess the nature and extent of the problems arising from alcohol misuse)

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26
Q

What are the 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?

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27
Q

How do we think about the management of patients with alcohol use disorder?

A
  1. Assess - use formal assessment tool to assess severity and nature of misuse
  2. Carry out Motivational Interview
  3. Establish Goals - Abstinence is the best treatment goal (but some may want a more moderate goal)
    o If comorbid mental health issues don’t improve within 3-4 weeks of abstinence, consider referring for specific treatment
  4. Offer interventions to promote abstinence as part of intensive structured community- based intervention for people with moderate to severe alcohol dependence who have limited social support, complex physical/psychiatric comorbidities or who have not responded to initial community-based interventions
  5. Offer a Carer’s Assessment if necessary

o Consider offering guided self-help for families and provide resources about support groups
o Consider offering family meetings, usually at least 5 weekly meetings

  1. Provide info about Alcoholics Anonymous, SMART Recovery and Change, Grow, Live (CGL)
  2. If homeless, offer residential rehabilitation services for maximum of 3 months
  3. Routinely monitor outcomes
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28
Q

What are the interventions for harmful drinkers and Mild Alcohol Dependence?

A

o Offer psychological intervention (e.g.CBT, behavioural therapy, social network and environment-based, MI) focused on alcohol-related cognitions Weekly 1 hour sessions for 12 weeks

o Offer behavioural couples therapy(if a regular partner is present)
o If no response to above or if pharmacological treatment requested, offer the following alongside psychological therapy:

Acamprosate (anti-craving)

Naltrexone

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29
Q

What should be done in assisted withdrawal?

A

o Give Pabrinex if they are at risk of Wernicke’s encephalopathy
o Expectations: withdrawal symptoms are worst within the first 48 hours, take about 3-7 days after the last drink to completely resolve

o 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 Management in specialist alcohol services if there are safety concerns

o Consider inpatient assisted withdrawal if one or more of the following: 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)

  • Hospital staff grade withdrawal symptoms using objective scales e.g. the Clinical Institute Withdrawal Assessment for Alcohol (CIWA) scale

• Should also receive family therapy for about 3 months

o Drug Regimens

Fixed-dose or symptom-triggered regimen
Preferred medication: (long-acting benzodiazepines) chlordiazepoxide or diazepam

• If liver impairment, consider lorazepam (limited hepatic metabolism)

Titrate initial dose based on severity of alcohol dependence/daily alcohol consumption
Gradually reduce the dose over 7-10 days

• This will be longer if concurrent benzodiazepine withdrawal treatment required (up to 3 weeks)

Give no more than 2 days medication at a time (installment dispensing)

o After Successful Withdrawal

Consider acamprosate (anticraving drug) or naltrexone with individualised psychological intervention

Consider disulfiram (Discourages drinking by inhibiting acetaldehyde dehydrogenase → acetaldehyde accumulation → unpleasant SEs in response to drinking) 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)

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30
Q

What should you say to patients who have alcohol use disorders?

A
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31
Q

What is Motivational Interviewing?

A

MI is a therapeutic approach which aims to empower people to change a behaviour.

Key concepts include:

  • Empathy: build rapport and identify someone’s own goals and reasons for change.
  • Developing discrepancy: help somebody recognize the gap between where they are now and where they want to be.
  • Rolling with resistance: avoid disagreement and conflict, as these undermine the relationship and distract from the goal (change).
  • Encouraging change talk: explore ambivalence and help people talk themselves into change.
  • Supporting self-efficacy: build someone’s belief in their ability to change and empower them to take small steps to change
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32
Q

What is the prognosis for patients with alcohol use disorder?

A

Alcohol disorders tend to follow a relapsingremitting course; people may relapse several times before eventually becoming abstinent. After a period of alcohol dependence, complete abstinence is often necessary, as ‘controlled drinking’ (trying to drink within healthy limits) often leads to relapse.

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33
Q

How do you manage an acute alcohol withdrawal?

A

Offer pharmacotherapy to treat the symptoms of withdrawal as follows:
o Consider offering a benzodiazepine (e.g.lorazepam) or carbamazepine

o Alternative: clomethiazole

Offer advice on local support services (alcoholics anonymous, SMART recovery)

Delirium Tremens

o 1st line: oral lorazepam
If symptoms persist: offer IV lorazepam or haloperidol

Alternative: chlordiazepoxide

o IV thiamine

Alcohol Withdrawal Seizures

o Consider fast-acting benzodiazepine (e.g.lorazepam) to reduce the likelihood of future seizures

34
Q

How were the illicit drugs traditionally grouped? What are NPS’?

A
  1. Opioids
  2. Cannabinoids
  3. Stimulants
  4. Hallucinogens
  5. Sedatives
  6. Solvents

More recently: novel psychoactive substances (NPS) have been developed in laboratories worldwide - can’t be classified or fully understood

35
Q

What are the opioids? How is it administered?

A

Heroin (diamorphine)

μ-opioid agonist

Stimulates endogenous endorphin receptors

Initially smoked, then move on to IV injection as tolerance builds

Antecubital fossa = first site use

Once venous access difficult, people inject SC or IM

  • Others include morphine, pethidine, codeine, and dihydrocodeine.
36
Q

What is the presentation of a patient with opioid use disorder?

A

Intoxication: intense rush or buzz, feeling or euphoria, warmth and well-being.

Other effects: Sedation and analgesia follow - some people vomit or feel dizzy.

Non-IV use causes milder effects.

Bradycardia and respiratory depression can cause death

Pinpoint pupils = classic sign

Naloxone = antidote

Withdrawal begins 6 hours post-injection and peaks at around 36-48 hours - extremely unpleasant but not life-threatening → Dysphoria (miserable), dilated pupils, nausea, vomiting and agitation occur.

They yawn irresistibly but can’t sleep.

As the effect on opioid receptors reverse everything ‘runs’: diarrhoea, vomiting, sweating, lacrimation, and rhinorrhea.

People will feel feverish with aching joints/muscles, abdominal cramps and Piloerection → goose flesh (hence why its called Cold Turkey).

37
Q

How does withdrawal in neonates present?

A
38
Q

What are the complications of opioid use disorder?

A
  • Overdose → death from respiratory failure or aspiration of vomit while sedated
  • Constipation, anorexia and low libido are SEs
  • Complications of IV drug use
39
Q

What are the investigations of opioid use disorder?

A

o Physical examination (establish baseline physical state)

o Urine drugs screen
o U&Es (features of malnutrition)
o FBC (anaemia due to malnutrition or signs of infection)
o LFTs(may impact medication dosing)
o Blood borne infections (RPR, hepatitis serology, HIV test)

40
Q

How should we think of managing opiate misuse?

A
  • Harm Reduction
  • General recommendations
    • Counsel on aspects of a healthy lifestyle (e.g.sleep hygiene, diet)
    • Provide information about self-help groups (e.g. 12-step groups)
    • Offer assessment for family members and carers
  • Consider withdrawal tx
  • Medication for detoxification
  • Ultra-rapid, Rapid and Accelerated Detoxification
  • Stage 2: Stabilisation and Maintenance
  • Follow-up
41
Q

What is harm reduction in opiate misuse?

A

o Pragmatic approach involving assessing and minimising risk rather than insisting on abstinence
o Information should be provided on improving safety of drug use

Provide Naloxone to heroin users and their family, friends, hostel staff (etc.) in case of overdose.

o Examples:

Needle exchanges for IV drug users

Vaccination and testing for blood-borne viruses for sex-workers and IVDU

Teaching BLS

42
Q

When should you not routinely offer opioid withdrawal treatment?

A

o Concurrent medical problem requiring urgent treatment

o In police custody

o Presenting in acute or emergency settings

o Be careful with pregnant women

43
Q

What medications do we use for detoxification in opiate misuse?

A

• Medication for Detoxification

o Appoint a key worker (supports the patient as they go through detoxification)
o 1st line: methadone (liquid) or buprenorphine (sublingual)-decision is largely based on patient preference - doses slowly titred until person experiences no withdrawal symptoms. - complete abstinence may not be realistic

  • Benefits of substitute prescribing: breaking links with dealers, cutting injection risks, offering stability to enable employment.
  • Methadone is a full agonist at opioid receptors with a longer half-life than heroin.
  • Buprenorphine is a partial agonist at the mu receptor, blocking the euphoric effects of heroin while preventing withdrawal symptoms.

o Consider lofexidine (alpha-2 agonist) if above options are unacceptable, mild dependence or keen to detoxify over a short period of time
o Decisions about the dosing regimen should be based on severity of dependence, stability of the patient and the setting of detoxification

o 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
o Withdrawal Symptoms: clonidine and lofexidine can help the symptoms
o Detox can be helped with medications to help manage symptoms (e.g.anti-diarrhoeals,anti-emetics, pain killers)

44
Q

How can be accomplish stabilisation and maintenance in opioid misuse?

A

Promotes abstinence from illicit drugs, prevent relapse, reduce HIV and hepatitis C risk, reduce mortality, and decrease criminality.

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

Long-acting opioid agonists (i.e., methadone, buprenorphine) and opioid antagonists (i.e., injectable extended-release naltrexone)

45
Q

What is the follow-up for opioid misuse?

A

o Refer to Drugs and Alcohol Service
o For at least 6 months
o Offer talking therapy (CBT) to prevent relapse and address underlying mental health issues
o Appoint a key worker
o Consider contingency management after completed detoxification

Offer incentives for every drug-negative test
Screening could be frequent at first (3/week) and then reduced Urinalysis is the preferred method of screening

46
Q

How should patients with opioid misuse be counselled?

A
47
Q

What are cannabinoids and how do they work?

A

Come from the Cannabis sativa plant

  • Weed - from leaves and flowers
  • Hash - from resin
  • skunk - newer, stronger strain of cannabis

Psychoactive component - Delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) → acts on cannabinoid receptors in the brain

Usually smoked through spliffs or bong

Can also be inhaled through an e-cigarette or vaporiser, or eaten or drunk as tea.

48
Q

What is the presentation of cannabis use?

A

Effects depend greatly on expectation and original mood state, which tends to be enhanced by the drug.

Higher CBD levels → relaxation, contentment, giggling and talkativeness

High THC levels → anxiety, panic and paranoia

Perceptual distortion can occur: time slows down, hunger pangs and N&V occurs.

Bloodshot eyes, tachycardia and dry mouth occur.

Withdrawal: identified in those with heavy and prolonged use - anxiety, irritability, restlessness, nausea, headache, poor sleep, appetite and concentration.

49
Q

What are the complications of cannabis use?

A
  • Physical - Aggravates asthma and risks lung disease and cancer
  • Psychiatric - Trigger psychosis, especially in vulnerable people using it heavily from a young age, particularly high potency (e.g. skunk)
    • Lethargy and poor motivation (with heavy chronic use)
    • Regular use associated with depression, anxiety, ADHD and PTSD.
50
Q

What are stimulants?

A

Potentiate effects of neurotransmitters (dopamine, noradrenaline and and sometimes serotonin)

They include: cocaine, crack cocaine, amphetamine-type stimulants (e.g. amphetamine, methaphetamine, ecstasy, methylphenidate) and khat.

Increase energy, alertness and euphoria

Side effects include cardiac arrhythmia, htn and stroke

Unpleasant crash after substance wears off

51
Q

What is cocaine?

A

Stimulant

White powder

Can be snorted or dissolved and injected

Can experience formication (insects crawling on or below skin)

Powerful vasoconstrictor → damages nasal mucosa and leads to necrosis and septal perforation

52
Q

What is crack cocaine?

A

Concentrated by heating cocaine in a baking soda solution until the water evaporates, leaving rocks which are heated and smoked.

Concentrated smokeable form of cocaine (makes a cracking sound)

Immediate and extremely intense high

High lasts 5-10 minutes → highly addictive

53
Q

What are amphetamines?

A

Pinkish-White powder or paste

Dissolved in drinks, dissolved and injected, swallowed or snorted, put on gums

Dexamphetime can be used as a replacement for IV amphetamine dependence

Methamphetamine also available as highly addictive, smokeable, glassy rocks known as crystal meth.

54
Q

What is ecstasy?

A

3,4-Methylenedioxymethamphetamine (E, MDMA)

Usually tablet but can be purer, crystalline powder

Serotonin release and reuptake inhibition– cross between stimulant and hallucinogen

Causes sense of empathy and closeness to others

Chatty, dance relentless and bruxism (tooth grinding)

Death associated with hyperthermia and dehydration

55
Q

What is Khat?

A

Mild stimulant, popular in East Africa

Chewable leaves → mild stimulant effects

56
Q

What is the presentation of stimulant use?

A
  • Intoxication
    • Make people energetic, alert, excited and euphoric (high)
    • May be chatty and show frenzied or prolonged activity (dancing all night)
    • Suppress appetite and sleep → High HR and BP
    • Confidence, impulsivity, poor judgement, risky behaviour
    • Work within a few minutes - last up to 3 hrs
  • Withdrawal
    • Unpleasant comedown (crash) within 24 hrs followed by several weeks of withdrawal
    • Symptoms: depression, irritability, lethargy and cravings
    • Ecstasy and khat don’t cause withdrawal → can cause psychological dependence
57
Q

What are the complications of stimulant use?

A
  • Physical: insomnia, WL, arrhythmias and hypertension
    • Overdose: multiorgan failure, seizures, strokes, coma, and death
    • Mixing stimulants with alcohol increases risk of fatal cardiac events and IV use can cause complications
  • Psychiatric: anxiety, panic, aggression and psychosis.
58
Q

What are the complications of stimulant use?

A
  • Physical: insomnia, WL, arrhythmias and hypertension
    • Overdose: multiorgan failure, seizures, strokes, coma, and death
    • Mixing stimulants with alcohol increases risk of fatal cardiac events and IV use can cause complications
  • Psychiatric: anxiety, panic, aggression and psychosis.
59
Q

What are the complications of stimulant use?

A
  • Physical: insomnia, WL, arrhythmias and hypertension
    • Overdose: multiorgan failure, seizures, strokes, coma, and death
    • Mixing stimulants with alcohol increases risk of fatal cardiac events and IV use can cause complications
  • Psychiatric: anxiety, panic, aggression and psychosis.
60
Q

How can we manage stimulant withdrawal if needed?

A

Benzodiazepines in stimulant withdrawal

61
Q

What are hallucinogens?

A
  • Drugs in this group affect dopamine, serotonin and glutamate neurotransmitters.
  • Visual illusions and hallucinations
  • Synaesthesia may occur
  • Depersonalisation and derealistion and fairly common – can become acutely anxious
  • Behavioural toxicity is the accidental harm that occurs when people act on drug- induced beliefs e.g. that they can fly
62
Q

What is LSD?

A

Lysergic acid diethylamide

Affects dopamine and serotonin transmitter system

63
Q

What is psilocybin?

A

Eaten or drunk and has similar effects to LSD but milder.

  • Magic mushrooms
64
Q

What is PCP and ketamine?

A

Both are anaesthetics - cause hallucinators and dissociative symptoms

Phenylcyclidine (PCP)

  • Snorted or smoked
  • Associated with violent outbursts and psychosis

Ketamine

  • Veterinary anaesthetic
  • Prevents brain’s awareness of pain
  • Severe harm during hallucinations due to analgesic affect
65
Q

Describe the presentation of hallucinogen use.

A

Intoxication

  • Lasts a few hours
  • Altered mood and sensory experiences
  • Synaesthesia (experiencing a sensation in another modality e.g. hearing a smell)
  • Depersonalization and derealisation
66
Q

What are the complications of hallucinogen use?

A

Physical

  • Accidents
  • May not realise they are causing damage
  • PCP → hyperthermia
  • Prolonged use of ketamine → bladder ulceration and frank haematuria
  • Magic mushrooms - main risk is eating poisonous species

Psychiatric

  • Bad trips - frightening and unpleasant → anxiety and depression
  • LSD → disturbing flashbacks to trips even yrs later
  • PCP → associated with violent outbursts
67
Q

What are sedatives?

A

Enhance inhibitory effect of GABA

68
Q

What are the types of sedatives?

A
  • Benzodiazepines
  • Alcohol and barbiturates
  • GHB
  • GBL
  • 1,4-BD
69
Q

What are benzodiazepines?

A
  • Prescribed for insomnia and anxiety usually
  • • Swallowed or dissolved and injected IV
  • • Effects are similar to alcohol – calm and mind euphoria
    • Slurred speech, ataxia and stupor at high doses
70
Q

What is GHB?

A
  • Gamma hydroxubutyrate
  • Strongly sedative anaesthetic - used in club scene
  • White powder or colourless, oily liquid and usually sipped or mixed with soft drinks
71
Q

What are GBL and 1,4-BD?

A
  • GBL(gamma butyrolactone) and 1,4- BD (1,4- butanediol) are chemicals which convert to GHB after ingestion
  • Originally legal alternatives to GHB, they’ve now also been outlawed.
  • GHB and GBL have been used to facilitate sexual assaults (‘date rape’): their salty taste can be hidden in soft drinks, and make the victim disinhibited or unconscious, often with amnesia for the assault
72
Q

What would the clinical presentation of sedative use be?

A
  • intoxication
    • calm, mild euphoria, loss of inhibition and sedation
    • GHB - mild stimulant at low doses
  • Withdrawal
    • Nausea, vomiting, headaches, anxiety, depression and uncomfortable body sensations
    • severe cases: confusion and seizures
  • Abrupt discontinuation of dependent use is discouraged without medical supervision.
  • GHB dependence can develop after a relatively short period of use and can be life- threatening
73
Q

What are the complications of sedative use?

A

At higher doses - slurred speech, ataxia, vomiting, coma and respiratory collapse

Overdose → kill through respiratory arrest (particularly in combination with alcohol or opioids)

74
Q

What are the short and long term risks of using benzodiazepines?

A

o Short-Term:drowsiness, reduced concentration

o Long-Term:cognitive impairment, worsening anxiety and depression, sleep disruption

75
Q

What are the clinical features of a benzodiazepine withdrawal?

A

o Insomnia
o Irritability
o Anxiety
o Tremor
o Loss of appetite

o Tinnitus

o Excessive sweating
o Seizures
o Perception disturbance

76
Q

How do you manage benzodiazepine misuse?

A

Overdose: flumazenil (benzodiazepine antagonist)

Address underlying issues that need benzodiazepines

o Anxiety

o Sleep

o Depression

How to Withdraw

o Withdraw in steps of about 1/8 of the daily dose every fortnight(but in reality, the dose is reduced according to the severity of the withdrawal symptoms)

o Consider switching patients to equivalent dose of diazepam
Oxazepam may be considered instead in patients with liver failure

o Duration:may take 3 months to a year or more

o Warning:do not drive If feeling drowsy

• Psychological Therapy

o Offer CBT (help address underlying mental health issues and provide advice about sleep hygiene etc.)

77
Q

How should you counsel a patient about benzodiazepines misuse?

A
78
Q

What are inhalants? How does it present?

A
  • Volatile solvents (glue gas)
    • Sniff solvents from cloth
    • Gases can be directly squirted into back of throat
    • Intoxication is similar to alcohol, causing euphoria and disinhibition
    • Some report hallucinations
  • Volatile anaesthetics
    • Commonest nitrous oxide
    • Usually inhaled from a balloon from a canister
    • Passed around in groups
    • Intoxications causes euphoria and uncontrollable fits of laughter
  • Nitrites (poppers, TNT, rush)
    • inhaled from bottles
    • Intoxication → euphoric ‘rush’ and enhancement of sexual experience (associated with male gay club scene)
  • Withdrawal: inhalants → psychological rather than physical dependence
79
Q

What are the complications of inhalant use?

A
  • Hangovers, with severe headaches, fatigue, and depression.
  • At higher doses, inhalants → ataxia, vomiting, dizziness, muddled thinking, and sometimes hallucinations.
  • Heart failure, coma, and death (from vomit aspiration) can all occur.
  • Squirting solvents into the throat can cause swelling and asphyxiation.
  • Inhalation from bags risks suffocation: tell tale signs are blistering and redness around the mouth and nose.
  • Heavy nitrous oxide use is linked to vitamin B12 deficiency and anaemia
80
Q

What are novel psychoactive substances?

A
  • NPS are chemicals synthesized to mimic standard recreational drugs
  • Though hard to categorize, they can be roughly placed in the same overall groups as established drugs, giving similar effects and risking similar complications
  • The most common NPS are cannabinoids and stimulants.
81
Q

What is the prognosis of substance misuse?

A

Tend to follow relapsing and remitting course

IVDU, chaotic use and polydrug use = poor prognosis

Psychiatry (13 decks)

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