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Substance misuse Flashcards

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1
Q

list the 4 categories of substance misuse?

A

Intoxication - emotional and behavioural change after drug use.

  • Harmful use - use causing damage.
  • Dependency
  • Withdrawal
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2
Q

define dependency according to ICD-10?

A

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 - (ICD-10)

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3
Q

what is the ratio of substance and alcohol misuse in men vs women?

A

M:F

2:1 for alcohol disorders
• 4:1 for substances

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4
Q

what are the Main theories of dependence?

A

A. Learning theories

  • Classical (Pavlovian) conditioning
  • Operant conditioning
  • Social learning theory (vicarious learning)
    • learn from others/peer pressure

B. Neurobiological models
- drugs of reward affect reward pathway - dopaminergic
reward pathway
- pleasurable sensation from block of DA degradation

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5
Q

what is Classical (Pavlovian) conditioning?

A

cravings become conditioned to ‘cues’ (e.g. needles for heroin users), so

the cue itself can trigger cravings

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6
Q

what is operant conditioning?

A

Behaviours that are rewarded are repeated (positive

reinforcement

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7
Q

what is the effect of cocaine and amphetamines on the dopaminergic reward pathway?

A

block dopamine reuptake,

increasing synaptic dopamine levels, and causing a pleasurable sensation.

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8
Q

what is the effect of alcohol and opiates on the dopaminergic reward pathway?

A

increase dopamine

and affect other neurotransmitters.

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9
Q

outline the mechanism AND presentation of the ‘flush reaction’ ?

which ethnicity most affected?

A

Ethanol is metabolized to acetaldehyde,

which is then broken down by aldehyde dehydrogenase.

In East Asian populations,

a less effective variant enzyme occurs.

Acetaldehyde accumulates, causing flushing, palpitations, and nausea

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10
Q

list risk factors of alcohol misuse?

A

occupation

social background - difficult childhood

psychiatric illness - anxiety, depression etc

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11
Q

How can alcohol misuse present?

A
  1. Intoxication
  2. Withdrawal

intoxication;
irritable, aggressive, weepy,
morose, and disinhibited.
Impulsivity and poor judgement
Speech becomes slurred, the gait ataxic, and there may
be increasing sedation, confusion, and even coma.

withdrawal:
Headache, nausea, retching and vomiting, tremor, and
sweating are all typical. Insomnia.
anxiety, agitation, tachycardia, and hypotension

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12
Q

outline the mechanism of alcohol induced seizures?

A

Alcohol is a CNS depressant,

stimulates the GABA inhibitory system to reduce brain excitability.

When dependent drinkers suddenly stop drinking,

neural pathways
become hyper-excitable and seizures can occur.

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13
Q

what is the consequence in very severe cases of alcohol withdrawal?

A

Very

severe cases risk delirium tremens

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14
Q

a publican met an evangelist and has decided to take a new leash on life and quit 2 days ago. He is brought in with;

confusion
– hallucinations, especially visual, e.g. animals and people
– affective changes; extreme fear and hilarity may alternate
– gross tremor, especially of hands
– autonomic disturbance: sweating, tachycardia, hypertension,
dilated pupils, fever
– delusions.

diagnosis?

A

delirium tremens

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15
Q

how to manage a delirium tremens patient?

A

reducing benzodiazepine regime

and parenteral thiamine (so iv/im/sc NOT po)

rehydrate and fix electrolyte imbalance if any

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16
Q

what is the aetiology of Wernicke’s encephalopathy?

A

Caused by acute thiamine (vitamin B1) deficiency.

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17
Q

classic presentation of Wernicke’s encephalopathy?

what is the treatment?

A

triad of confusion, ataxia,
and ophthalmoplegia.

rx;
treat with parenteral thiamine:
IV thiamine given slowly (prevent anaphylaxis) +
IM thiamine for next 5 days
PO thiamine 6-12 after resolution of acute episode

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18
Q

classic presentation of Korsakoff’s syndrome ?

A

irreversible anterograde amnesia (and
some retrograde amnesia)

patient can register new events, but cannot recall
them within a few minutes.

Patients may confabulate to fill the gaps in their memory.

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19
Q

when does one get Korsakoff’s syndrome?

A

if wernickes is not treated with parenteral thiamine

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20
Q

what equates to a unit of alcohol for the following;

beer
wine
spirits
sherry

A
  • half a pint of ordinary strength beer (3.5–4%)
    • a small glass of wine (125mL)
    • a standard measure of spirits (25mL)
    • a standard measure of sherry/port (50mL)
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21
Q

what units are considered as binge drinking for

women/ men ?

A

women - more than 6 per day (35 a week)

men - more than 8 per day

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22
Q

list features of dependency?

A

Tolerance

Compulsion

Withdrawal

Problems controlling use

Continued use despite harm

Salience - other needs become neglected

Relapse/Reinstatement after abstinence

Narrowing of the repertoire - only use same type of substance, and style

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23
Q

outline the key areas of the dopaminergic ‘reward’
pathway in the brain?

where is DA released?

A

pathway starts in the ventral tegmental area (VTA)

and projects onto the prefrontal cortex

and limbic system (the ‘emotional’ brain).

Dopamine release in the nucleus accumbens -> sensation of pleasure -> reward.

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24
Q

which part of the brain has a role in motivation and

planning?

A

The prefrontal cortex

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25
Q

list some GI complications of excess alcohol consumption?

A

pancreatitis, oesophageal varices,

gastritis, and peptic ulceration.

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26
Q

list some CVS complications of excess alcohol consumption?

A

HTN

Cardiomyopathy

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27
Q

list some psychological complications of excess alcohol consumption?

A

Depression, anxiety, self-harm, and suicide are
increased.

• Amnesia (blackouts)

Cognitive impairment - occur, as either alcoholic
dementia or Korsakoff ’s syndrome

  • Alcoholic hallucinosis - auditory hallucinations in clear consciousness while drinking alcohol, or after periods of heavy alcohol use.
  • Morbid jealousy - delusion that a partner is unfaithful.
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28
Q

ivx for alcohol dependency?

results would show?

A
  1. FBC
    – Alcohol causes a macrocytic anaemia (raised MCV)
    due to B12 deficiency.
  2. LFTs
    – γGT rises with recent heavy alcohol use.
    – Raised transaminases suggest hepatocellular damage.
  3. Additional investigations e.g. an ECG for chest pain, a urine drug screen (UDS) if you suspect drug misuse, hepatitis screening if intravenous (IV) drug use.
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29
Q

what are the steps involved in alcohol dependency management?

A
  1. Assessment and preparation
    - Assess motivation to change:
    - > stages of change model
    - motivational interviewing
  2. Detoxification
  3. Relapse prevention
    • psychological and medical means
  4. Rehabilitation
    - finding work, restructuring of life etc
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30
Q

what are the steps of the stages of change model?

A

pre-contemplation

contemplation

preparation
- set SMART goals

action

maintenance

relapse - part of the learning experience

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31
Q

what is motivational interviewing?

A 
Motivational interviewing (MI) is a form of counselling
which aims to empower the person to change
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32
Q

how is alcohol detox conducted?

and where

iv/im/po?

A

Community
Admission - if risks of seizures or mental illness etc

Long-acting benzodiazepines (e.g. chlordiazepoxide)
replace alcohol and prevent withdrawal symptoms,
including seizures and delirium tremens. They are
gradually withdrawn and stopped.

• Thiamine (vitamin B1) is prescribed as prophylaxis
against Wernicke’s encephalopathy. It is best given
parenterally (IM or IV) since it is poorly absorbed in
the gut.

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33
Q

What strategies are used in relapse prevention?

A

Psych; CBT + group therapies

Meds;

1st line - Acamprosate is an anti-craving drug. if relpase into drinking, doesn’t work.

+ Disulfiram (Antabuse) mimics the ‘flush reaction’ to alcohol, making drinking highly unpleasant! causes severe reaction if they drink again.

Naltrexone

Used from 6months - 1 year
Check LFTs before use

34
Q

what is the MOA of Cannabis?

A

thc-9-tetrahydrocannabinol acts on cannabiinoid receptors ini brain?

35
Q

effects of taking cannabis?

A

enhances original mood state;

relaxation, euphoria
paranoia, anxiety

36
Q

chronic heavy use of cannabis causes?

A

lethargy, poor motivation

37
Q

describe hashish?

A

squidgy brwon/black lump - from resin and flowers

38
Q

strongest cannabis form?

A

skunk

39
Q

sidie effects of stimulant drugs?

A

cardiac arrhythmias

HTN

Stroke

Anxiety, Panic, Psychosis

40
Q

a patient has presented having taken cannabis - a stimulant. how to treat?

A

harm reduction

short term Benzo
- helps with withdrawal anxiety

41
Q

MOA of stimulants?

A

potentiate the effects of neurotransmitters

dopamine, noradrenaline, sometimes serotonin

42
Q

what sensations are associated with cocaine use?

A

euphoria - its a stimulant

formification - insects crawling on or below skin

43
Q

cocaine damages nasal mucosa because?

A

powerful vasoconstrictor

44
Q

why is crack so addictive?

A

intense high lasts only 5/10 mins

45
Q

what drug to give as replacement for iv amphetamine dependency?

A

dexamphetamine

for stabilisation and detox

46
Q

which drug causes florid psychosis?

A

Khat

47
Q

MOA of MDMA?

A

serotonin release and reuptake inhibition

its a cross between a stimulant and a hallucinogen (although hallucinations are rare).

48
Q

define synaesthesia?

A

experiencing a sensation in another modality like hearing a smell

49
Q

synaesthesia is common with the use of which drug type?

A

Hallucinogens

50
Q

what does LSD stand for?

A

lysergic acid diethylamide

51
Q

what are the effects of taking LSD?

side effects?

A

ingestion causes trips of up to 12 hours’ duration, with

perceptual changes and euphoria.

Bad trips - experiences become frightening and unpleasant.

side effects:
sudden flashbacks can occur, even years later.
anxiety, depression, and psychosis.

52
Q

which drug comes as a liquid or powder that can be snorted or added
to a joint and smoked, and is associated with violent
outbursts and ongoing psychosis.

A

Phenylcyclidine (PCP, angel dust)

53
Q

which drug causes anaesthesia ->

people have severely harmed themselves while hallucinating, e.g. pulling out their own teeth.

A

Ketamine

54
Q

which drug group has sx at high doses similar to alcohol;

causing a feeling of calm and mild
euphoria, with slurred speech, ataxia, and stupor (or
even coma) at higher doses. Withdrawal effects are similar to alcohol, e.g. seizures ?

A

Benzos

55
Q

rx for Benzo overdose?

A

flumazenil

which is a benzodiazepine antagonist.

56
Q

list some risks associated with solvent use?

A

Spraying:

  • Throat swelling
  • Asphyxiation

Bag:
-Suffocation

Coma can occur and result in death if vomit
is aspirated.

57
Q

how to spot someone on solvents?

A

Telltale signs are blistering and redness around the mouth and nose

hangover can occur afterwards with severe
headaches and fatigue

58
Q

list some poor prognostic factors for abstinence from drug use?

A

Intravenous drug use,
chaotic use,
polydrug use

59
Q

How would you assess alcohol dependency in a patient?

A
  1. AUDIT questionnaire

if result suggests depence then do the

  1. SADQ - seveerity of alcohol dependence OR
  2. LDQ - leeds dependence questionnaire
60
Q

how do you initially screen if the patient requires an in depth alcohol screen?

A

CAGE questionnaire

C Have you ever felt that you should cut down on your
drinking?
A Have people annoyed you by criticizing your drinking?
G Have you ever felt guilty about your drinking?
E Have you ever had a drink first thing in the morning, to
get rid of a hangover? eye-opener

61
Q

list mild, moderate and severe alcohol withdrawal sx?

A

mild - emotional sx, fine tremor, insomnia

moderate - mild sx more prominent, coarse tremor, agitation

severe - tonic clonic seizures, delirium/confusion, hallucinations, hyPERtheremia

62
Q

list withdrawal sx from stimulants i.e cocaine, amphetamine?

A

CRASH -> depression, lethargy

63
Q

what do withdrawals from benzo’s look like?

A

similar to alcohol including seizures

64
Q

list withdrawal sx from opiates?

A

everything runs!
- diarrhoea, vomiting, lacrimation, rhinorrhea

Yawning
dysphoria
aches, cramps, sweating
dilated pupils
insomnia

etc

65
Q

colloquial names for heroin?

A

(diamorphine, brown, smack, horse, gear, H)

66
Q

what is the MOA of heroin?

A

Heroin is a μ (mu) opiate agonist,

stimulating brain and spinal
cord receptors that are normally acted upon by endogenous
endorphins (the body’s natural painkillers).

67
Q

list local and systemic complications of ivdu?

A 
local;
abscess
cellulitis
DVT
Emboli
systemic;
septicaemia
infective endocarditis
blood-borne infections - hep b,c,hiv (hep c most common)
overdose
68
Q

how does heroin kill?

A

bradycardia and respiratory depression ->

aspiration of vomit in OD

69
Q

Managment of opiate dependency?

A
  1. Harm reduction
    - needle exchange, blood virus screening
  2. Substitute prescribing
    - methadone - liquid
    - buprenorphine - sublingual tablet
    (this is used for current addicts to get them off heroin, given until no longer experiencing withdrawal, wean off over weeks/months)

2b. Adjuncts (used to aid detox)
- Loperamide (4 diarrhoea)
- anti-emetics (metoclopramide)
- non-opiate pain killers

  1. Naltrexone
    - Blocking drug
    - Given post detox to prevent relapse
70
Q

MOA of methadone?

why is it used for decency?

A

full agonist at opiate mu receptors

longer half lofe than heroin = withdrawal longer and milder

71
Q

MOA of buprenorphine?

when is it preferred?

A

partial agonist at opiate mu receptors

blocks heroin euphoric effects, prevents withdrawal

preferred in:

  • users with bad expereicnce iwth methadone
  • want clear head
  • on cyp450 inducers; anticonvulsants etc
  • want to quit heeroin completely
72
Q

when does Withdrawal following IV heroin use typically begin?

A

around 6 hours after injection; peaking at 36–48 hours

73
Q

a patient is prescribed methadone, detoxification is then commenced. patient detriorates on detox. what is the best course of action?

A

Keep patient on a maintenance regime of Methadone so that they at least have stability;

can get and maintain a job etc etc

74
Q

what is the MOA of naltrexone?

A

Naltrexone is an opiate antagonist that blocks opiate

receptors and thus the euphoric effects of opiates.

75
Q

what is the COAT rack of wernicke-korsakoffs syndrome?

A

C - confusion
O - opthalmoplegia
A - ataxia
T - thiamine deficiency

R - retrograde amnesia
A - anterograde amnesia
C - confabulation
K - korsakoff psychosis

76
Q

in the treatment of wernicke’s what is one alternative to thiamine that could be preferable? why?

A

Pabrinex

contains nicotinamide, riboflavine, pyridoxine and ascorbic acid along with thiamine, is
often preferable to thiamine alone as this will cover the possibility of other vitamin deficiencies.

77
Q

what is charles bonnet syndrome?

A

visual hallucinations secondary to visual impairment

78
Q

if a patient undeergoing detox self discharges, what advice to give them?

A

cant give them chlordiazepoxide - only used in hospitals

tell them they must continue drinking, cant stop completely due to risk of seizures

tell them to seek further help when they feel ready - gp

refer to alcohol liason nurse/services -> can be followed up in the community

79
Q

if a patient undeergoing detox self discharges, what advice to give them?

A

cant give them chlordiazepoxide - only used in hospitals

tell them they must continue drinking, cant stop completely due to risk of seizures

tell them to seek further help when they feel ready - gp

refer to alcohol liason nurse/services -> can be followed up in the community

80
Q

treatment of opiod overdose?

A

IM naloxone

A- Psych (24 decks)

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