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Psychiatry > Drug Abuse > Flashcards

Drug Abuse Flashcards

1
Q

What are the main effects (uses) of cocaine?

A
  • Anti-dysarrhythmic
  • Local anaesthetic
  • Sympathomimetic
    Symptoms: Feel on top of the world, confident, wide awake, short acting, ↓ hunger
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2
Q

Who is most likely to take cocaine?

A

Youths
Socially marginalised groups
Opiate dependent patients

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3
Q

How does physiological tolerance to cocaine occur?

A

Brain notices dopamine flood so down regulates dopamine receptors so no longer active and post-synaptic neurone not stimulated, therefore more cocaine is needed for an effect

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4
Q

How does dependence to cocaine occur?

A

Cocaine causes HR, BP & wakefulness increase so body pre-emptively decreases these reactions for next time cocaine is used to make things ‘normal’. If cocaine use is stopped the body feels abnormal as these factors are lower than normal. If meds needed to make the person feel normal

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5
Q

What are the signs of mild & severe cocaine withdrawal?

A

MILD: Depression & anxiety, fatigue, reduced conc, cravings, tiredness, inc appetite, excessive vivid dreaming (inc REM)
SEVERE: Cocaine Crash, Suicidal ideation, N&V, sensation of insects on the skin Usually leads to relapse & negative reinforcement

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6
Q

What are the complications of cocaine abuse?

A 
Excited delirium
Overdose
Crack keratitis
Mood disorders (anxiety, paranoia, panic, depression)
Renal failure
Psychosis (Magnun syndrome)
IV blood borne viruses
MI, Heart failure
Seizure
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7
Q

What is the management in cocaine abuse?

A

ACUTE: Anxiolytic & treatment of urgent complications (Lorazepam)
Drug counselling/mental health referral
ONGOING: Drug counselling/ mental health referral

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8
Q

Define amphetamine abuse

A

Involves the recreational use of a class of non-catecholamine sympathomimetic amines.

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9
Q

What are the demographics for amphetamine abuse?

A

18-25

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10
Q

What does tachyphylaxis mean?

A

User requires a higher dose to get the same effect due to down-regulation of the postsynaptic receptors & depletion of presynaptic stores of neurotransmitters

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11
Q

How do amphetamines work?

A

Monoamine agonist/antagonist
Stimulate the release of norepinephrine from central adrenergic receptors.
Higher doses: Release dopamine from mesocorticolimbic system and nigrostriatal dopamine systems.
Acts as a direct agonist on 5-HT receptors & inhibits monoamine oxidase.
Periphery: Release norA by acting on the adrenergic nerve terminals and alpha & beta receptors.

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12
Q

What are the signs of amphetamine use?

A 
Hallucinations & Paranoia
HypoN
Reduced hunger/appetite
Trismus, Bruxism
Hyper-vigilance/ wide awake
Talkative & Hyper-arousal
Increased energy
Reduced need for sleep
Comedown: Lethargy, anergia, anxiety, irritable, restless, Unable to sleep, exhaustion
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13
Q

How is amphetamine abuse investigated?

A 
Urine toxicology testing
Gas chromatography/ mass spectrometry of urine/blood
ECG: ST changes, SVT/arrhythmia
Serum sodium: <130mmol/L
Serum creatine phosphokinase: Elevated
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14
Q

How is amphetamine abuse managed?

A

ACUTE:
Activated charcoal 1g/kg <1hour
Sedative/antipsychotic (Olanzapine/Lorazepam)
ONGOING:
Psychosocial &behavioural treatment (Matrix Model, CBT)
Pharmacotherapy (Modafinil/Risperidone/Naltrexone)
Depression: Antidepressant (20-60mg/daily Fluoxetine)

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15
Q

How does cannabis work?

A

Bind to cannabinoid receptors found in NS & immune cells
Type 1: CNS- cerebellum, hypothalamus,SC, hippocampus, cerebral cortex binding slows activity in these areas & releases dopamine ADDICITIVE PATHWAY
Type 2: Immune system &peripheral nerve terminals, analgesic & anti-inflammatory effects

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16
Q

What are the long-term effects of cannabis use?

A

Airway & lung damage (hyperinflated lungs, chronic bronchitis)

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17
Q

What are withdrawal symptoms of cannabis?

A 
Not lethal as few receptors in the brainstem
Loss of appetite
Mood changes
Irritability
Anxiety
Difficulty sleeping
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18
Q

What are signs of cannabis misuse?

A

Acute chest pain in a young person
Acute psychosis +/- precipitate schizophrenia
Mood/sleep disorders (anxiety & paranoia)
Poor concentration & memory

19
Q

How is cannabis abuse managed?

A

Anti-anxiety: Buspirone
Psychotherapy: CBT, Self-help, Motivational counselling
Brief interventions
Contingency management

20
Q

What receptors do the following drugs act on:

  • LSD
  • Mephedrone
  • Mushrooms
  • Ketamine
  • Benzos
  • GBL
  • Heroin
  • Amphetamines
  • Alcohol
A
  • LSD: Dopamine & 5HT agonist
  • Mephedrone: Monoamine (ant)agonist
  • Mushrooms: 5HT partial agonist
  • Ketamine: NMDA antagonist
  • Benzos: Gaba agonist
  • GBL: GABA agonist
  • Heroin: Opioid agonist
  • Amphetamines: Monoamine (ant)agonist
  • Alcohol: GABA agonist & depressant
21
Q

How can amphetamines be taken?

A

Sniff
Smoke
Swallow
Inject (Class A)

22
Q

What are the negative risks associated with amphetamines?

A

Panic attacks, depression, aggressiveness, paranoia, hallucinations, psychosis, dependency, chronic sleep deprivation, weight loss, tremors, seizures, immune system suppression, poor concentration, cardiac problems
Severe: Skin picking, excoriations, skin lesions
Dental decay, gum disease

23
Q

What is the stronger form of amphetamine known as? What are its affect?

A

Methamphetamine (Crystal meth)
Reaches brain more easily; effects longer
Addictive, ↑MI risk, damages cognition

24
Q

What is the toxidrome for sympathomimetics?

A 
E.g: Cocaine, Epinephrine, Amphetamine
↑ HR &amp; BP &amp; RR &amp; Temp
Dilated pupils
↑ Bowel sounds
↑ Diaphoresis
25
Q

What is the toxidrome for sedatives/hypnotics?

A 
E.g: Benzos, barbituates, antihistamines
↓ HR &amp; BP &amp; RR &amp; Temp
Normal pupils
↓ Bowel sounds
↓Diaphoresis
26
Q

What is the toxidrome for opioids?

A 
E.g: Morphine, Heroin
↓ HR &amp; BP &amp; RR &amp; Temp
Constricted pupils
↓ Bowel sounds
↓ Diaphoresis
27
Q

What are the class A drugs?

A 
Heroin
Ecstasy
PCP
LSD
MDMA
Cocaine (incl. crack)
Methamphetamine
Psilocybin mushrooms
Any class B drug made for injection
28
Q

What are the class B drugs?

A 
Cannabis
Synthetic cannabinoids
Ketamine
Mephedrone
Amphetamine
Codeine
Methoxetamine
Methylphenidate
29
Q

What are class C drugs?

A 
Khat
GHB/GBL
Benzodiazepines
Tramadol
Anabolic steroids
30
Q

What are the criminal convictions for possession & supply of illegal drugs?

A 
Possession-
A: 7yrs/ unlimited fine
B: 5yrs/ unlimited fine
C: 2yrs/ unlimited fine
Psychoactive Substances: NOT an offence

Supply-
A: Life/ unlimited fine
B & C: 14yrs/ unlimited fine

31
Q

What are the exemptions of the Psychoactive Substances Act 2016?

A

Nicotine
Alcohol
Caffeine

32
Q

What are the symptoms of opioid withdrawal?

A 
Tremors
Anxiety &amp; irritability
Yawning
Sweating &amp; runny nose &amp; watery eyes
Sleep disturbance, insomnia, restlessness
nausea &amp; diarrhoea
Goose-bumps
Abdominal cramps and muscle spasms
Tachycardia, hypertension.
Dilated pupils.

Tx: Loperamide (diarrhoea), Metoclopramide, NSAIDs, Diazepam (insomnia)
Feeling hot and cold.
Increased bowel sounds.
Coughing

33
Q

What is the criteria for dependence?

A

> 3 in last 12months:

  • Tolerance
  • Withdrawal
  • Using more/ for longer than intended
  • Unsuccessful attempt to reduce
  • Large amount of time spent seeking, using and recovering from use
  • Drug use taking priority over social, work and recreational activities
  • Persistent use despite harm
34
Q

How is a patient managed who wants to come off opioids?

A

28days as in-patient, 12weeks in community
Maintenance: Heroin substitute at stable dose (Methadone, Buprenorphine)
Detox: Switch to heroin substitute and gradually taper down over time
ALL: CBT, stopping OH, support groups, incentives
Naltrexone:
• Long acting opiate antagonist
• Oral, depot, implant
• Blocks euphoric effects, little effect on cravings
• Also used in Alcohol dependency (better evidence base)

35
Q

How is opioid dependency diagnosed?

A

A strong desire or sense of compulsion to take the substance.
Difficulty in controlling use.
A physiological withdrawal state.
Tolerance.
Neglect of alternative pleasures and interests.
Persistence of use despite harm to oneself and others.

36
Q

How is cocaine detox managed?

A

Psychotherapy: CBT, motivational interviewing
Beta blockers: Symptoms of withdrawal
Benzos: <2weeks, ‘come down’ & insomnia
Disulfiram (secondary care only)

37
Q

What is the mechanism of action of cocaine?

A

Cocaine binds to dopamine, serotonin, and norepinephrine transport proteins
Directly prevents the re-uptake into pre-synaptic neurons. Dopamine effect is most responsible for the addiction

38
Q

What is the mechanism of action of opioids?

A

Mu-opioid agonist

39
Q

How do benzodiazepines work?

A

GABA agonists

40
Q

What are the signs of benzo withdrawal?

A

Mild: Decreased concentration, Tremors, N&V, Headache, Mood changes: Anxiety, panic attacks, depression, nightmares, insomnia, sweating, tachy, mild HTN
Serious symptoms: seizures, delirium, confusion. Usually due to abrupt withdrawal.
Other: anorexia, nausea, tinnitus, photo/phonosensitivity, depersonalisation & derealisation.

41
Q

What are the negative consequences of benzos?

A 
Respiratory depression
Falls
Hangover
Memory loss
Sedation
Death with injection
42
Q

How is a benzo detox managed?

A

Gradual dose reduction- withdrawal 3m-1yr
?Switch to longer acting benzo (Diazepam)
Psychotherapies: CBT, relaxation techniques
Anxiety: Propanolol
Severe: Short-term flumazenil infusions, ?Carbamezepine

43
Q

How is a benzo overdose treated?

A

Supportive

Flumazenil

Psychiatry (19 decks)

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