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CASC > Addiction > Flashcards

Addiction Flashcards

1
Q

Class A drugs

A

Ecstasy, LSD, heroin, cocaine, crack, magic mushrooms
(whether prepared or fresh), methylamphetamine (crystal meth),
other amphetamines if prepared for injection

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2
Q

Class B drugs

A

Amphetamines, Methylphenidate (Ritalin), Pholcodine.

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3
Q

Class C drugs

A

Cannabis, tranquilisers, some painkillers, GHB (Gamma-

hydroxybutyrate), ketamine

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4
Q

ICD-10 criteria for alcohol dependence

A

requires at least 3 out of following list satisfied in last 12 months:

  1. Intense desire to drink alcohol
  2. Difficulty in controlling the onset, termination and the level of drinking
  3. Experiencing withdrawal symptoms if alcohol is not taken
  4. Use of alcohol to relieve from withdrawal symptoms
  5. Tolerance as evidenced by the need to escalate dose over time tom achieves same effect
  6. Salience – neglecting alternate forms of leisure or pleasure in life
  7. The narrowing personal repertoire of alcohol use.
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5
Q

Criteria for alcohol dependence (Edward and Gross criteria)

A
  1. Narrowed repertoire
  2. Salience of alcohol-seeking behaviour
  3. Increased tolerance
  4. Repeated withdrawals
  5. Drinking to prevent or relieve withdrawals.
  6. Subjective awareness of compulsion
  7. Reinstatement after abstinence
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6
Q

What is salience?

A

refers to the neglect of all leisure and alternate forms of pleasure apart from
alcohol. One’s life revolves around getting alcohol, storing it, saving money to buy it,
making opportunities to drink, etc.

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7
Q

Time course of alcohol withdrawal

A
  • Onset of shakes (4-12 hours)
  • Onset of perceptual disturbances (8-12 hours)
  • Seizure onset (12-24 hours); peaks at 48 hours
  • Delirium onset (72 hours)
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8
Q

Peak of alcohol withdrawal sx

A

48 hours

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9
Q

When do alcohol withdrawal sx start

A

Within 12 hours of last sx

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10
Q

Initial sx of alcohol withdrawal sx

A 
Tremor
Sweating
Insomnia
GI distress
Anxiety
Craving
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11
Q

Risk factors for alcohol withdrawal seizures

A

Previous seizures
HI
Electrolyte imbalance - low sodium or K+

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12
Q

How many patients with alcohol withdrawal develop DT?

A

5%

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13
Q

Sx of DT

A

Disturbed autonomic functions (pulse, temperature and blood pressure changes in either
direction), clouded consciousness with hallucinations (often Lilliputian) and agitation can
occur.

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14
Q

Incidence of seizures in untreated alcohol dependent patients

A

8%

3% if treated

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15
Q

What causes seizures in alcohol dependent patients

A

Kindly process; episodic alcohol withdrawal sensitises brain leading to increased likelihood of seizure with each future episode

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16
Q

How many patients with withdrawal seizures develop DTs

A

30%

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17
Q

Risk factors for DT

A

Severe dependence
History of DTs
Older patient
Acute physical illness

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18
Q

How many patients with DT will die if untreated

A

10%

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19
Q

Withdrawal sx of heroin

A 
o Dysphoric mood
o Nausea or vomiting
o Muscle aches
o Lacrimation or rhinorrhea
o Pupillary dilation, piloerection (gooseflesh), or sweating
o Diarrhea
o Yawning
o Fever
o Insomnia
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20
Q

Time frame of withdrawal sx of heroin

A

Begin 6-8 hours after last dose
Peaks in 2 days
Reduces in a week

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21
Q

Withdrawal sx of cannabis

A

Irritability
Insomnia
Anorexia
Nausea

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22
Q

Withdrawal sx of benzos

A

prominent anxiety and autonomic hyperactivity,
increased tremor, insomnia, nausea or vomiting, transient visual, tactile, or auditory
hallucinations or illusions, psychomotor agitation, in some cases - grand mal seizures.
Kinaesthetic hallucinations are also reported in some individuals. Note that withdrawal
delirium can be fatal.

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23
Q

Management of benzo dependence in non-abusing patients mild dependence

A

Advisory letters

Shourt courses of relaxation

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24
Q

Management of benzo dependence moderate/severe

A

Graded discontinuation of prescribed benzos with aim of cessation

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25
Q

GHB withdrawal sx

A

In mild cases, it is limited to insomnia, tremors and anxiety.
But may extend to paranoia, hallucinations, psychotic behaviour and extreme agitation in
some.

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26
Q

Time duration of GHB withdrawal effect

A

Start in 12 hours

Last up to 12 days

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27
Q

Intoxication effects of amphetamines

A

tachycardia or bradycardia (sometimes these arrythmias can be
fatal), pupillary dilation, elevated or lowered blood pressure, perspiration or chills , nausea or
vomiting , evidence of weight loss, psychomotor agitation or retardation, muscular weakness,
respiratory depression, chest pain, or cardiac arrhythmias, confusion, seizures, dyskinesias,
dystonias, or coma, psychological effects such as euphoria, changes in sociability, anxiety,
tension, stereotyped behaviours and impaired judgment.

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28
Q

Withdrawal effects of amphetamine

A

dysphoric mood (crash) sometimes with suicidal ideation. fatigue,
vivid, unpleasant dreams, hypersomnia, increased appetite, psychomotor retardation and
small pupils.

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29
Q

MDMA withdrawal sx

A

fatigue, loss of appetite,
depression, anxiety, and trouble concentrating.
the most common mental or mood complaints are difficulty concentrating,
depression, anxiety and fatigue.

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30
Q

Harm reduction advice on MDMA

A

maintaining hydration and avoiding overheating during

use

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31
Q

Withdrawal sx of cocaine

A

Effects of cocaine are short-lived - rapid cessation occurs due to rapid
metabolism resulting in withdrawal effects that can lead to repeated use. A characteristic
feature is intense cravings for cocaine with a striking lack of much physical withdrawal
symptoms. Dysphoria (crash), anhedonia, anxiety, irritability hypersomnolence, and
sometimes agitation are seen upon withdrawal.

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32
Q

Time duration of withdrawal effects of cocaine

A

These effects usually end within 18 hours

though in heavy, dependent users this can last up to a week, peaking in 3 days.

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33
Q

Physical adverse effects of cocaine

A 
 Nasal perforation on snorting.
 Nonhemorrhagic cerebral infarctions.
 Subarachnoid, intraparenchymal, and intraventricular hemorrhages.
 TIAs
 Seizures (3 to 8% of A&E visits)
 Myocardial infarctions and arrhythmias
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34
Q

Sx of hallucinogenic intoxication

A

marked anxiety or depression, ideas of
reference, fear of losing one’s mind, paranoid ideation, perceptual changes e.g., subjective
intensification of perceptions, depersonalization, derealization, illusions, hallucinations,
synesthesias in a state of full alertness, pupillary dilation, tachycardia, sweating, palpitations,
blurring of vision, tremors, and incoordination. The usual sequence of changes follows a
pattern of somatic symptoms appearing first, then mood and perceptual changes, and, finally,
psychological changes.

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35
Q

Additional features of PCP intoxication

A

vertical or horizontal
nystagmus, numbness or diminished
responsiveness to pain, ataxia and dysarthria
with muscle rigidity.

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36
Q

Pharmacology of inhalants

A

CNS depressants

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37
Q

Pharmacology of GHB

A

a GABA-like action; also inhibits dopamine release at a low dose
but boosts dopamine availability on chronic use. GHB can also induce the release of
noradrenaline in the hypothalamus. It causes respiratory depression and coma, especially
if mixed with alcohol. But the person may remain combative despite respiratory
depression. Can produce bradycardia in 1/3rd of users.

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38
Q

Sx of alcohol hallucinosis

A

The most common hallucinations are unstructured sounds or voices that may be
characteristically malign and threatening.

The hallucinations usually last less than a week,
when patients believe in the hallucinations though afterwards they may realise the untrue
nature. These usually appear in persons abusing alcohol for a long time.
Delusions - secondary to hallucinations
Clear sensorium unlike DT

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39
Q

Difference between alcoholic hallucinosis and SCZ

A

o Atypical or late age of onset of psychotic symptoms
o Onset of alcohol drinking clearly preceding the onset
o Remission of psychotic episodes during abstinence.
o Lack of thought disorder and affect incongruence.

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40
Q

Triad of Wernickes

A

ophthalmoplegia, ataxia global confusional state.

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41
Q

Most valuable diagnostic tool for Wernickes

A

MRI

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42
Q

How many people with Wernickes develop Korsakoff if untreated

A

84%

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43
Q

Mortality rate of untreated Wernickes

A

20%

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44
Q

Why give thiamine before IV glucose in Wernickes?

A

Glucose infusion exacerbates thiamine deficiency

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45
Q

Which sx of Wernickes resolves quickest with treatment?

A

Ophthalmoplegia - within hours

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46
Q

How many patients with Wernickes develop Korsakoffs

A

80%

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47
Q

What characterises Korsakoffs

A

marked deficits in anterograde and to some extent retrograde episodic
memory, apathy, an intact sensorium, and relative preservation of other intellectual abilities
such as attention, procedural memory and working memory.

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48
Q

What memory functions are intact in Korsakoffs

A

digit span test scores and other

measures of working memory

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49
Q

Sx of hepatic encephalopathy

A

by altered sensorium, frontal

release signs, ‘metabolic’ flapping tremor, hyperreflexia, and extensor plantar responses.

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50
Q

Hallmark of amphetamine-induced psychosis?

A

Paranoia

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51
Q

Sx of amphetamine-induced psychosis different to SCZ

A

 The absence of prominent negative symptoms.
 The predominance of visual hallucinations.
 Generally appropriate affect.
 Associated with hyperactivity.
 Disinhibited sexual behaviour.
 Confusion and incoherence.
 Almost no formal thought disturbance.

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52
Q

Treatment of amphetamine-induced psychosis

A

Haloperidol short-term

Resolves after several days

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53
Q

What is flashback phenomenon?

A

Long after ingesting a hallucinogen, a person can experience a flashback of hallucinogenic
symptoms.

54
Q

Sx of flashback phenomenon

A

by seeing geometric hallucinations, false perceptions of movement in
the peripheral visual fields, flashes or intensified colours, trails of images of moving
objects, positive afterimages, halos around objects, macropsia, and micropsia.

55
Q

Triggers of flashback phenomenon

A

Emotional stress, sensory deprivation or the use of another

psychoactive substance, such as alcohol or marijuana can trigger a flashback.

56
Q

Increase in risk of alcoholism in those with first degree relatives with the disease?

A

2x increase

57
Q

Risk factors for illicit substance use

A 
•Peer drug use
•Single parenting
•Homelessness
•Poor educational
attainment
•Neighborhood
disadvantage
•Unemployment
58
Q

Risk factors for alcohol use

A 
•Disruption of family
structure
•Social networks that use
alcohol
•Recent immigration
•Small-area deprivation
59
Q

How long is alcohol present in urine

A

12 hours

60
Q

How long is ampethamine present in urine

A

48 hours

61
Q

How long is benzo present in urine

A

Up to 3 days

62
Q

How long is cannabis present in urine

A

3 days or 4 weeks if daily, chronic use

63
Q

How long is cocaine present in urine

A

6-8 hours; metabolites up to 2-4 days

64
Q

How long is codeine present in urine

A

48 hours

65
Q

How long is heroin present in urine

A

1-3 days

66
Q

How long is methadone present in urine

A

3 days or more

67
Q

How long is morphine present in urine

A

2-3 days

68
Q

How long is PCP present in urine

A

3-8 days

69
Q

How long is LSD present in urine

A

<24 hours

70
Q

What can cause false positive test for PCP?

A

Dextromethorphan

71
Q

What can cause false positive test for marijuana metabolites?

A

Ibuprogen

72
Q

What can cause false positive test for opiates?

A

Tonic water

73
Q

What can cause false positive test for amphetamines?

A

Phenylephrine decongestants

74
Q

When is longer dose tapering for benzos in alcohol withdrawal indicated?

A

Current or previous DTs

75
Q

What is front loading technique of alcohol withdrawal treatment?

A

a loading dose of diazepam is given followed by and further
doses every 90 min until light sedation is achieved. No further medication is given, and the
long half life of diazepam covers the withdrawal.

76
Q

What is symptom-triggered regime in alcohol withdrawal?

A

uses chlordiazepoxide whenever a clinical withdrawal rating
scale such as (CIWA– Clinical Institute Withdrawal Assessment Scale; 10 items score 10-20
moderate, >20 –severe, or SAWS – short alcohol withdrawal scale – self-completed; >12 needs
treatment) shows significant symptom scores.

77
Q

Advantages of symptom-triggered regime

A

Faster control and fewer benzodiazepine doses needed in total.
Waiting for withdrawal symptoms to be manifest is safer with regard to avoiding
over-sedation and increased confusion in intoxicated users seeking detoxification.

78
Q

Problems of symptom-triggered regime

A

As prevention of withdrawal symptoms is the goal this approach may be
meaningless in various settings. The distress caused to the patient may reduce his
motivation to be abstinent.

79
Q

First line alternative to benzos in alcohol withdrawal

A

Carbamazepine - not CI in liver failure

80
Q

How many people with alcohol use have spontaneous abstinence?

A

1 in 10

81
Q

When is total abstinence from alcohol advised?

A 
Age >40
Long standing alcohol problems
Mod-severe dependence
Medical/psych complications
Impulsive personality
Poor social support
Ambivalent or chooses abstinence
Monitoring not possible
82
Q

How does Acamprosate work?

A

It inhibits glutamatergic NMDA receptor function
and balances GABA-glutamate imbalance seen in alcohol dependence. It is hypothesized
to suppress the ‘urge to drink’ in response to learned cues

83
Q

Common SEs of Acamprosate

A

GI - nausea, diarrhoea

84
Q

When is Acamprosate advised to start

A

As soon after detox as possible

85
Q

How does Naltrexone help in alcohol use?

A

Naltrexone may reduce the pleasurable effects of
alcohol by blocking the effects of opioids released by alcohol; this results in reduced
stimulation of mesolimbic dopamine reward system.

86
Q

What can Naltrexone help with in alcohol use?

A

Naltrexone has been shown to be superior to placebo in maintaining abstinence, relapse
rates, time to first drink, and reduction in number of drinking days, reduction in craving
and improvement in GGT

87
Q

What does Disulfram do?

A

Disulfiram blocks aldehyde dehydrogenase, resulting in the accumulation of acetaldehyde
leading to signs and symptoms such as flushing, nausea, vomiting, headache, tachycardia
and palpitations if alcohol is consumed.
Dose-dependent reaction

88
Q

What is important for Disulfram efficacy

A

Witnessing or supervising compliance

89
Q

What can Disulfram help with

A

Disulfiram reduces the number of drinking days and reduces the quantity of alcohol
consumed, but not increase abstinence. There

90
Q

How long to continue Disulfram for?

A

3-6 months

91
Q

CI to Disulfram

A

Impulsivity, psychosis, suicidality, severe hepatic dysfunction, peripheral neuropathies,
cardiac diseases are

92
Q

Psychosocial interventions for alcohol use

A 
Motivational enhancement therapy
Coping skills training
Behavioural self-control training
Family/marital therapy
Intensive case management
93
Q

Describe Behavioural self-control training

A

The major components include placing limits on
number of drinks, self-monitoring using a drink diary, using non-alcoholic spacers, using
food to fill before / after drink, altering rate of drinking, developing assertiveness to refuse
offer of drink and to reward oneself for reaching goals. The user is encouraged to develop
awareness of antecedents and to learn alternate coping skills.

94
Q

Describe FRAME approach

A

o Feedback of risks
o Responsibility highlighted
o Advised to abstain or cut down
o Menu of alternative options and activities offered
o Empathic interviewing
o Self-efficacy is enhanced regularly throughout the intervention.

95
Q

Aim of CBT approach to alcohol relapse prevention

A

o The main aim is to enhance capacity to maintain abstinence.
o This can reduce relapse and if relapse occurs the intensity of relapse may be less
severe.
o Note that overinvestment of absolute abstinence itself contributes to the catastrophic
nature of relapses – this is called abstinence violation effect.

96
Q

Matrix model of alcohol treatment

A

The matrix model uses a combination of CBT, family education, social support,
individual counselling, regular testing of alcohol and optional 12 step program.

97
Q

Describe some residential rehab models for alcohol use

A

Minnesota rehab

Phoenix house

98
Q

Describe Minnesota rehab model

A

uses detoxification,
psychoeducation and AA attendance with 4 weeks stay in the ward. This is followed by after care
at rehabilitation residences.

99
Q

Describe phoenix house model

A

house is an example of concept houses. It works on a therapeutic community model. A
slightly confrontational style is adapted, firm feedback is given, and responsibility is emphasized.
Residents have a major role in running the house; they get an increase in privileges and
responsibilities depending on their progress.

100
Q

Harm reduction advice for opioid use

A

Not to use opiates while alone; Not to use in combination with other
drugs; Avoid IV route; Always inject in the direction of blood flow (in veins, this is towards
heart); Rotate injection sites; Avoid going for neck, groin etc.; Ensure complete dissolution
before injection – else emboli can occur; Use new sterile needles and syringes on each
occasion; Use sterile water – avoid lemon juice, which can cause Candida endophthalmitis;
Never share needles or equipment with others

101
Q

Types of pharmacotherapy for opioid withdrawal

A

Methadone
Buprenorphine
alpha2 adrenergic agonists - clonidine, lofexidine

102
Q

Best pharmacotherapy for opioid withdrawal if short duration of treatment is desirable

A

Alpha 2 adrenergic agonist

Buprenorphine (partial agonist) - abrupt discontinuation does not produce as many withdrawal sx

103
Q

How long does Methadone suppress withdrawal for

A

24-36 hours

104
Q

Options for relapse prevention with maintenance treatment for opioid use

A

Methadone
Buprenorphine
Levo-alpha-acetylmethadol
Suboxone

105
Q

Which patients with opioid use are Methadone and Buprenoprhine appropriate for?

A

Those unwilling to undergo withdrawal or have had repeated unsuccesful attempts

106
Q

What is Methadone effective in?

A

Reducing heroin use
Reducing injecting
Reducing sharing of injecting equipment

107
Q

What does Suboxone contain?

A

Buprenorphine + naloxone to deter abuse of tablets by IV injection - will produce unpleasant withdrawal if taken IV

108
Q

When is Naltrexone used

A

To nullify effects of heroin if relapse occurs - long-acting (72 hours)

109
Q

When is Naltrexone used for opioid use

A

Adjuvant in therapy
For highly motivated patients
For those who fear consequences if they do not stop opioid use

110
Q

NICE guidelines for opioid detox to those who are opioid dependent and have chosen to become dependent

A

offer detox in community with methadone and buprenorphine as first-line

111
Q

When to consider lofexidine in opioid dependence

A

Consider lofexidine for those with mild or uncertain dependence but warn patients that this necessitates use of adjunct meds for nausea/vomiting

112
Q

Psychosocial interventions for opioid dependence

A

o Offer opportunistic brief interventions focused on motivation to people in limited
contact with services
o Routinely provide information about self-help groups, often based on 12-step
principles (for example, Narcotics Anonymous and Cocaine Anonymous).
o Drug misuse services
o Contingency management with incentives such as vouchers or privileges, contingent
on each presentation of a drug-negative test result (for example, free from cocaine or
non-prescribed opioids);
o Urine tests: (three tests a week for the first three weeks, two tests a week for the next
three weeks and once weekly thereafter until stability is achieved).

113
Q

Treatment for amphetamine dependence

A

Most users do not become dependent, but in some,
dependence and craving on withdrawal can be very rapid. The evidence supporting
pharmacological treatment is weak for stimulant use. Psychosocial treatments such as
cognitive behaviour therapy and contingency management are recommended as the main
treatment approaches albeit with poor quality evidence.
Harm-reduction; do not share needles

114
Q

Treatment for cocaine withdrawal

A

No pharmacological agents can reduce the intensity of
cocaine withdrawal or craving reliably
Contingency management; positive reinforcement

115
Q

NICE guidelines recommend contingency management for what?

A

Treatment of primary stimulant misuse and for illicit drug use in methadone
maintenance treatment.

116
Q

Who is Bupropion CI for NRT?

A

Hx of seizures or eating disorders

117
Q

Meds for gambling

A

Naltrexone
SSRIs - Fluvoxamine, citalopram, sertraline
CBT

118
Q

Types of steroid use

A

patterns: ‘cycling’ (using for 4-12 weeks in a cyclical
fashion), ‘stacking’ (regular use of multiple preparations) and ‘pyramiding’(gradually
building the dose to a peak and then tapering).

119
Q

Risks with anabolic steroid misuse

A

increased risk of aggression, violence, psychosis, mania,
depression and endocrine abnormalities resulting in acne (~50%), testicular atrophy and/or
gynaecomastia (1/3rd of users)

120
Q

Most common non-genetic cause of LD

A

Fetal alcohol syndrome

121
Q

Features of fetal alcohol syndrome

A

Intellectual impairment, dysmorphic facial features and disruptive behaviour are noted.

122
Q

Alcohol in pregnancy

A

Do not drink or at max one drink a day

123
Q

Major risks in opioid use in pregnancy

A 
Major risk is the harm caused to
the baby by injections, e.g.,
infection and the effects of drug-
induced stillbirth, premature
birth, antenatal complications
(OR for antepartum hemorrhage
is 2.33 in opiate using mothers),
low birth weight (mean reduction
of ~500g in heroin/methadone users), microcephaly and neonatal withdrawal.
124
Q

Aim of treatment in pregnant opioid user

A

Stabilisation on oral substitute drug

125
Q

What to do if women on high dose methadone becomes pregnant

A

Slowly reduce dosage
Fetal monitoring
Methadone is more likely than heroin to induce withdrawal syndrome (60-80%)

126
Q

When to consider detox in pregnant opioid users

A

Middle trimester - risk of abortion in first and premature birth in third

127
Q

Principles of managing opioid users in pregnancy

A
  1. Therapeutic alliance
  2. Aim to reduce risk-taking behaviours (sharing needles, prostitution).
  3. Stabilize on non-injectable alternatives such as methadone.
  4. If considering detoxification, this should be done in the middle trimester –
    avoid first trimester for the fear of abortion and last trimester for the fear
    of premature birth.
  5. Close liaison with obstetric, midwifery, and paediatric teams, and with
    social services where appropriate.
  6. HIV and hepatitis screening (vaccination where appropriate).
128
Q

Impact of cocaine use in pregnancy on child

A

Small for gestational age

Microcephaly

129
Q

Impact of cannabis use in pregnancy in child

A

Affects neurodevelopment

2-fold risk of low brith weight

130
Q

Alcohol withdrawal sx in neonates

A

Seen within 3-12 hours after delivery. Hyperactivity, crying, irritability, poor
sucking, tremors, seizures, poor sleeping patterns, hyperphagia, and diaphoresis.
Signs usually appear at birth and features of Foetal Alcohol Syndrome may be
apparent later on further development.

131
Q

Marijuana withdrawal sx in neonates

A

A mild opiate-like withdrawal syndrome with fine tremors, hyperacusis, and a
prominent Moro reflex; mild and very rarely require treatment.

132
Q

Opiate withdrawal sx in neonates

A

Usually begins 24-48 hours after birth, depending on the time of last dose.
However, signs may not appear in the infant until 3-4 days after birth.
Hyperirritability, gastrointestinal dysfunction, respiratory distress, and vague
autonomic symptoms (e.g., yawning, sneezing, mottling, fever). Tremors and
jittery movements, high-pitched cries, increased muscle tone, and irritability are
common. Normal reflexes may be exaggerated. Loose stools are common, leading
to possible electrolyte imbalances and diaper dermatitis. Methadone withdrawal
symptoms typically appear within 48-72 hours but may not start until the infant is
aged 3 weeks. Milder with buprenorphine withdrawal.

CASC (16 decks)

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