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
2
Q
Class B drugs
A
Amphetamines, Methylphenidate (Ritalin), Pholcodine.
3
Q
Class C drugs
A
Cannabis, tranquilisers, some painkillers, GHB (Gamma-
hydroxybutyrate), ketamine
4
Q
ICD-10 criteria for alcohol dependence
A
requires at least 3 out of following list satisfied in last 12 months:
- Intense desire to drink alcohol
- Difficulty in controlling the onset, termination and the level of drinking
- Experiencing withdrawal symptoms if alcohol is not taken
- Use of alcohol to relieve from withdrawal symptoms
- Tolerance as evidenced by the need to escalate dose over time tom achieves same effect
- Salience – neglecting alternate forms of leisure or pleasure in life
- The narrowing personal repertoire of alcohol use.
5
Q
Criteria for alcohol dependence (Edward and Gross criteria)
A
- Narrowed repertoire
- Salience of alcohol-seeking behaviour
- Increased tolerance
- Repeated withdrawals
- Drinking to prevent or relieve withdrawals.
- Subjective awareness of compulsion
- Reinstatement after abstinence
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.
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)
8
Q
Peak of alcohol withdrawal sx
A
48 hours
9
Q
When do alcohol withdrawal sx start
A
Within 12 hours of last sx
10
Q
Initial sx of alcohol withdrawal sx
A
Tremor Sweating Insomnia GI distress Anxiety Craving
11
Q
Risk factors for alcohol withdrawal seizures
A
Previous seizures
HI
Electrolyte imbalance - low sodium or K+
12
Q
How many patients with alcohol withdrawal develop DT?
A
5%
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.
14
Q
Incidence of seizures in untreated alcohol dependent patients
A
8%
3% if treated
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
16
Q
How many patients with withdrawal seizures develop DTs
A
30%
17
Q
Risk factors for DT
A
Severe dependence
History of DTs
Older patient
Acute physical illness
18
Q
How many patients with DT will die if untreated
A
10%
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
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
21
Q
Withdrawal sx of cannabis
A
Irritability
Insomnia
Anorexia
Nausea
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.
23
Q
Management of benzo dependence in non-abusing patients mild dependence
A
Advisory letters
Shourt courses of relaxation
24
Q
Management of benzo dependence moderate/severe
A
Graded discontinuation of prescribed benzos with aim of cessation
25
GHB withdrawal sx
In mild cases, it is limited to insomnia, tremors and anxiety.
But may extend to paranoia, hallucinations, psychotic behaviour and extreme agitation in
some.
26
Time duration of GHB withdrawal effect
Start in 12 hours
| Last up to 12 days
27
Intoxication effects of amphetamines
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.
28
Withdrawal effects of amphetamine
dysphoric mood (crash) sometimes with suicidal ideation. fatigue,
vivid, unpleasant dreams, hypersomnia, increased appetite, psychomotor retardation and
small pupils.
29
MDMA withdrawal sx
fatigue, loss of appetite,
depression, anxiety, and trouble concentrating.
the most common mental or mood complaints are difficulty concentrating,
depression, anxiety and fatigue.
30
Harm reduction advice on MDMA
maintaining hydration and avoiding overheating during
| use
31
Withdrawal sx of cocaine
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.
32
Time duration of withdrawal effects of cocaine
These effects usually end within 18 hours
| though in heavy, dependent users this can last up to a week, peaking in 3 days.
33
Physical adverse effects of cocaine
```
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
```
34
Sx of hallucinogenic intoxication
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.
35
Additional features of PCP intoxication
vertical or horizontal
nystagmus, numbness or diminished
responsiveness to pain, ataxia and dysarthria
with muscle rigidity.
36
Pharmacology of inhalants
CNS depressants
37
Pharmacology of GHB
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.
38
Sx of alcohol hallucinosis
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
39
Difference between alcoholic hallucinosis and SCZ
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.
40
Triad of Wernickes
ophthalmoplegia, ataxia global confusional state.
41
Most valuable diagnostic tool for Wernickes
MRI
42
How many people with Wernickes develop Korsakoff if untreated
84%
43
Mortality rate of untreated Wernickes
20%
44
Why give thiamine before IV glucose in Wernickes?
Glucose infusion exacerbates thiamine deficiency
45
Which sx of Wernickes resolves quickest with treatment?
Ophthalmoplegia - within hours
46
How many patients with Wernickes develop Korsakoffs
80%
47
What characterises Korsakoffs
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.
48
What memory functions are intact in Korsakoffs
digit span test scores and other
| measures of working memory
49
Sx of hepatic encephalopathy
by altered sensorium, frontal
| release signs, ‘metabolic' flapping tremor, hyperreflexia, and extensor plantar responses.
50
Hallmark of amphetamine-induced psychosis?
Paranoia
51
Sx of amphetamine-induced psychosis different to SCZ
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.
52
Treatment of amphetamine-induced psychosis
Haloperidol short-term
| Resolves after several days
53
What is flashback phenomenon?
Long after ingesting a hallucinogen, a person can experience a flashback of hallucinogenic
symptoms.
54
Sx of flashback phenomenon
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
Triggers of flashback phenomenon
Emotional stress, sensory deprivation or the use of another
| psychoactive substance, such as alcohol or marijuana can trigger a flashback.
56
Increase in risk of alcoholism in those with first degree relatives with the disease?
2x increase
57
Risk factors for illicit substance use
```
•Peer drug use
•Single parenting
•Homelessness
•Poor educational
attainment
•Neighborhood
disadvantage
•Unemployment
```
58
Risk factors for alcohol use
```
•Disruption of family
structure
•Social networks that use
alcohol
•Recent immigration
•Small-area deprivation
```
59
How long is alcohol present in urine
12 hours
60
How long is ampethamine present in urine
48 hours
61
How long is benzo present in urine
Up to 3 days
62
How long is cannabis present in urine
3 days or 4 weeks if daily, chronic use
63
How long is cocaine present in urine
6-8 hours; metabolites up to 2-4 days
64
How long is codeine present in urine
48 hours
65
How long is heroin present in urine
1-3 days
66
How long is methadone present in urine
3 days or more
67
How long is morphine present in urine
2-3 days
68
How long is PCP present in urine
3-8 days
69
How long is LSD present in urine
<24 hours
70
What can cause false positive test for PCP?
Dextromethorphan
71
What can cause false positive test for marijuana metabolites?
Ibuprogen
72
What can cause false positive test for opiates?
Tonic water
73
What can cause false positive test for amphetamines?
Phenylephrine decongestants
74
When is longer dose tapering for benzos in alcohol withdrawal indicated?
Current or previous DTs
75
What is front loading technique of alcohol withdrawal treatment?
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
What is symptom-triggered regime in alcohol withdrawal?
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
Advantages of symptom-triggered regime
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
Problems of symptom-triggered regime
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
First line alternative to benzos in alcohol withdrawal
Carbamazepine - not CI in liver failure
80
How many people with alcohol use have spontaneous abstinence?
1 in 10
81
When is total abstinence from alcohol advised?
```
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
How does Acamprosate work?
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
Common SEs of Acamprosate
GI - nausea, diarrhoea
84
When is Acamprosate advised to start
As soon after detox as possible
85
How does Naltrexone help in alcohol use?
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
What can Naltrexone help with in alcohol use?
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
What does Disulfram do?
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
What is important for Disulfram efficacy
Witnessing or supervising compliance
89
What can Disulfram help with
Disulfiram reduces the number of drinking days and reduces the quantity of alcohol
consumed, but not increase abstinence. There
90
How long to continue Disulfram for?
3-6 months
91
CI to Disulfram
Impulsivity, psychosis, suicidality, severe hepatic dysfunction, peripheral neuropathies,
cardiac diseases are
92
Psychosocial interventions for alcohol use
```
Motivational enhancement therapy
Coping skills training
Behavioural self-control training
Family/marital therapy
Intensive case management
```
93
Describe Behavioural self-control training
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
Describe FRAME approach
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
Aim of CBT approach to alcohol relapse prevention
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
Matrix model of alcohol treatment
The matrix model uses a combination of CBT, family education, social support,
individual counselling, regular testing of alcohol and optional 12 step program.
97
Describe some residential rehab models for alcohol use
Minnesota rehab
| Phoenix house
98
Describe Minnesota rehab model
uses detoxification,
psychoeducation and AA attendance with 4 weeks stay in the ward. This is followed by after care
at rehabilitation residences.
99
Describe phoenix house model
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
Harm reduction advice for opioid use
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
Types of pharmacotherapy for opioid withdrawal
Methadone
Buprenorphine
alpha2 adrenergic agonists - clonidine, lofexidine
102
Best pharmacotherapy for opioid withdrawal if short duration of treatment is desirable
Alpha 2 adrenergic agonist
| Buprenorphine (partial agonist) - abrupt discontinuation does not produce as many withdrawal sx
103
How long does Methadone suppress withdrawal for
24-36 hours
104
Options for relapse prevention with maintenance treatment for opioid use
Methadone
Buprenorphine
Levo-alpha-acetylmethadol
Suboxone
105
Which patients with opioid use are Methadone and Buprenoprhine appropriate for?
Those unwilling to undergo withdrawal or have had repeated unsuccesful attempts
106
What is Methadone effective in?
Reducing heroin use
Reducing injecting
Reducing sharing of injecting equipment
107
What does Suboxone contain?
Buprenorphine + naloxone to deter abuse of tablets by IV injection - will produce unpleasant withdrawal if taken IV
108
When is Naltrexone used
To nullify effects of heroin if relapse occurs - long-acting (72 hours)
109
When is Naltrexone used for opioid use
Adjuvant in therapy
For highly motivated patients
For those who fear consequences if they do not stop opioid use
110
NICE guidelines for opioid detox to those who are opioid dependent and have chosen to become dependent
offer detox in community with methadone and buprenorphine as first-line
111
When to consider lofexidine in opioid dependence
Consider lofexidine for those with mild or uncertain dependence but warn patients that this necessitates use of adjunct meds for nausea/vomiting
112
Psychosocial interventions for opioid dependence
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
Treatment for amphetamine dependence
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
Treatment for cocaine withdrawal
No pharmacological agents can reduce the intensity of
cocaine withdrawal or craving reliably
Contingency management; positive reinforcement
115
NICE guidelines recommend contingency management for what?
Treatment of primary stimulant misuse and for illicit drug use in methadone
maintenance treatment.
116
Who is Bupropion CI for NRT?
Hx of seizures or eating disorders
117
Meds for gambling
Naltrexone
SSRIs - Fluvoxamine, citalopram, sertraline
CBT
118
Types of steroid use
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
Risks with anabolic steroid misuse
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
Most common non-genetic cause of LD
Fetal alcohol syndrome
121
Features of fetal alcohol syndrome
Intellectual impairment, dysmorphic facial features and disruptive behaviour are noted.
122
Alcohol in pregnancy
Do not drink or at max one drink a day
123
Major risks in opioid use in pregnancy
```
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
Aim of treatment in pregnant opioid user
Stabilisation on oral substitute drug
125
What to do if women on high dose methadone becomes pregnant
Slowly reduce dosage
Fetal monitoring
Methadone is more likely than heroin to induce withdrawal syndrome (60-80%)
126
When to consider detox in pregnant opioid users
Middle trimester - risk of abortion in first and premature birth in third
127
Principles of managing opioid users in pregnancy
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
Impact of cocaine use in pregnancy on child
Small for gestational age
| Microcephaly
129
Impact of cannabis use in pregnancy in child
Affects neurodevelopment
| 2-fold risk of low brith weight
130
Alcohol withdrawal sx in neonates
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
Marijuana withdrawal sx in neonates
A mild opiate-like withdrawal syndrome with fine tremors, hyperacusis, and a
prominent Moro reflex; mild and very rarely require treatment.
132
Opiate withdrawal sx in neonates
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.
