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MRCPsych Part B > Addiction Psychiatry 1.2 > Flashcards

Addiction Psychiatry 1.2 Flashcards

1
Q

What models explain the relationship between substance misuse and other psychiatric disorders?

A

Common factor model
Secondary use model
Supersensitivity model
Secondary illness model

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2
Q

What is the common factor model?

A

Proposes a common factor such as genetic vulnerability which predisposes to both illnesses.

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3
Q

Evidence for common factor model

A

Patients with a dual diagnosis often have more relatives with a substance use disorder.

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4
Q

What is the secondary use model?

A

Patients use substances to self-medicate and reduce social isolation.

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5
Q

What is the supersensitivity model?

A

Mentally ill patients are unusually sensitive to negative social and health consequences os substance exposure leading to diagnosis of substance misuse.

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6
Q

What is the secondary illness model?

A

Substance misuse leads to mental illness by a mechanism similar to kindling or behavioural sensitisation.

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7
Q

Which model of substance misuse and psychiatric disorders is popular with the lay public?

A

Secondary illness model

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8
Q

What is another name for pathological intoxication?

A

Idiosyncratic alcohol intoxication

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9
Q

What is pathological intoxication?

A

Severe behavioural reaction developing rapidly after consumption of small amount of alcohol.

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10
Q

Sx of pathological intoxication?

A

Confusion
Hallucinations
Psychomotor agitation
Impulsive/aggressive behaviour with risk to self or others

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11
Q

How long do sx of pathological intoxication last?

A

Few hours

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12
Q

How do sx of pathological intoxication terminate?

A

In a prolonged sleep

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13
Q

What factors have been proposed to be linked to pathological intoxication?

A

High levels of anxiety
Brain damage
Age
Sedative-hypnotic drugs
Feeling fatigued

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14
Q

What treatment may need to be considered for pathological intoxication?

A

Physical restraint
IM Haloperidol

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15
Q

Which classification has a diagnostic criterion for alcohol-induced psychotic disorders?

A

DSM

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16
Q

Most common hallucinations in alcoholic hallucinosis

A

Unstructured sounds or voices that may be threatenng

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17
Q

How long do hallucinations last in alcoholic hallucinosis

A

Less than a week

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18
Q

When do hallucinations in alcoholic hallucinosis tend to occur?

A

In patients with a chronic hx of alcohol abuse

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19
Q

Difference between alcoholic hallucinosis and delirium tremens?

A

In alcoholic hallucinosis there is clear sensorium.

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20
Q

At what point should hallucinations in alcoholic hallucinosis lead to suspicion of an underlying psychosis?

A

> 6 months

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21
Q

Differentiating factors of alcoholic hallucinosis compared to schizophrenia

A

Atypical or late age of onset of psychotic sx
Onset of alcohol drinking preceding onset
Remission of psychotic episodes during abstinence
Lack of thought disorder and affect incongruence

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22
Q

What are alcoholic blackouts?

A

Discrete episodes of anterograde amnesia that occur in association with alcohol intoxication

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23
Q

How does alcohol affect memory?

A

Blocks consolidation of new memories into old memories at the hippocampus

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24
Q

What happens to memory during alcoholic blackout?

A

Remote memory is intact but patients experience specific short-term episodic memory deficit

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25
Q

How long does memory gap tend to last in alcoholic blackouts?

A

Hours

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26
Q

What types of alcoholic dementia are there?

A

Primary alcoholic dementia
Wernickes/Korsakoffs
Marchiafava-Bignami
Hepato-cerebral degeneration
Vitamin deficiency

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27
Q

What is primary alcoholic dementia?

A

Direct toxic effects of alcohol on the brain

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28
Q

What brain findings can be reversed on abstinence of alcohol?

A

Atrophy
Other alcohol-related brain changes

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29
Q

What are the sx of Wernickes?

A

Ohthalmoplegia
Ataxia
Global confusion

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30
Q

How many patients with Wernickes present with the triad of sx?

A

10%

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31
Q

What causes Wernickes?

A

Thiamine deficiency

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32
Q

What leads to thiamine deficiency?

A

Inadequate dietary intake
Reduced GI absorption
Decreased hepatic storage
Impaired utilization

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33
Q

What factor increases risk of Wernickes?

A

Anormal thiamine-dependent transketolase

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34
Q

Brain findings in Wernickes

A

Gliosis and small haemorrhages in periventricular and periaqueductal structures - especially in mammillary bodies, hypothalamus, mediodorsal thalamic nucleus, colliculi and midbrain tegmentum

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35
Q

How many chronic alcoholics exhibit signs of Wernickes?

A

12.%

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36
Q

What is the most valuable diagnostic tool for Wernickes?

A

MRI

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37
Q

MRI sensitivity for Wernickes

A

53%

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38
Q

MRI specificity for Wernickes

A

93%

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39
Q

How many untreated patients with Wernickes go on to develop Korsakoffs?

A

84%

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40
Q

Mortality rate of untreated Wernickes?

A

20%

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41
Q

Why should Thiamine be given before glucose?

A

Glucose infusion exacerbates thiamine deficiency

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42
Q

How much PO thiamine should be given in low risk drinkers

A

300mg/day

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43
Q

How much thiamine should be given in high risk drinkers

A

250mg IM/IV OD for 3-5 days.

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44
Q

What does Pabrinex contain?

A

Thiamine
Nicotinamide
Vitamin B2 and B6
Vitamin C

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45
Q

How much thiamine should be given if Wernickes is suspected?

A

IM/IV of >500mg for 3-5 days

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46
Q

Which sx of Wernickes resolves with hours?

A

Ophthalmoplegia

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47
Q

Whatt characterises Korsakoffs?

A

Marked deficits in anterograde and retrograde episodic memory
Apathy
Intact sensorium
Preservation of other intellectual abilities: attention, procedural memory, working memory

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48
Q

Physiological process of Korsakoffs

A

Storage of information in more permanent form (consolidation by transfer of information from primary to secondary memory) are affected

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49
Q

What does diagnosis of Korsakoffs correlate with?

A

Presence of lesions in dorsomedial thalamus

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50
Q

What correlates with memory dysfunction in Korsakoffs?

A

Lesions in mammillary bodies, mammilothalamic tract and anterior thalamus

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51
Q

What leads to confabulation in Korsakoffs?

A

Double lesion - frontal and diencephalic deficits

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52
Q

What leads to cerebellar degeneration in alcohol use?

A

Degeneration of Purkinje cells in cerebellar cortex due to alcohol-induced damage

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53
Q

How many chronic alcoholics have cerebellar degeneration?

A

40%

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54
Q

What characterises hepatic encephalopathy?

A

Altered sensorium
Frontal release signs
Metabolic flapping tremor
Hyperreflexia
Extensor plantar responses

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55
Q

What sx are noted in those who make a partial recovery from hepatic encephalopathy?

A

Tremor
Choreoathetosis
Dysarthria
Gait ataxia
Dementia

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56
Q

What is the name of the sx that occur in patients who make partial recovery from hepatic encephalopathy?

A

Hepatocerebral degenaration

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57
Q

Brain changes in hepatic encephalopathy?

A

Enlargement and proliferation of protoplasmic astrocytes in basal ganglia, thalamus, red nucleus, pons and cerebellum

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58
Q

Who first described Marchiafava-Bignami syndrome?

A

Carducci in 1898 in Italian red wine drinkers

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59
Q

Who expanded the description of Marchiafava-Bignami syndrome?

A

Marchiafava and Bignami in 1903

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60
Q

Who does Marchiafava-Bignami syndrome commonly occur in?

A

Malnourished alcoholics

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61
Q

M:F ratio of Marchiafava-Bignami syndrome

A

More in males

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62
Q

Pathology of Marchiafava-Bignami syndrome?

A

Demyelination of corpus callosum and adjacent subcortical white matter - extra-pontine myelinolysis

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63
Q

Sx of Marchiafava-Bignami syndrome

A

Dementia
Spasticity
Dysarthria
Gait changes

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64
Q

Who described 2 clinical types of Marchiafava-Bignami syndrome

A

Heinrich, 2004

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65
Q

What is Type A of Marchiafava-Bignami syndrome

A

Predominant features of coma and stupor

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66
Q

What is Type A Marchiafava-Bignami syndrome associated with?

A

High prevalence of pyramidal rtact sx

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67
Q

Radiologic features of Type A Marchiafava-Bignami syndrome

A

Involvement of entire corpus callosum

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68
Q

What characterises Type B Marchiafava-Bignami syndrome?

A

Normal or mildly impaired mental status

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69
Q

Radiologic features of Type B Marchiafava-Bignami syndrome?

A

Partial or focal callosal lesions

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70
Q

Who first described central pontine myelinolysis?

A

Adams et al in 1959

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71
Q

What happens in central pontine myelinolysis?

A

Demyelination of central portion of base of pons

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72
Q

Sx of central pontine myelinolysis?

A

Pain sensation in limbs
Bulbar palsy
Quadriplegia
Disordered eye movements
VOmiting
Confusion
COma/locked-in syndrome

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73
Q

Which non-alcoholic diseases can result in central pontine myelinolysis?

A

Wilsons
Malnutrition
Anorexia
Burns
Cancer
Addisons
Severe hyponatraemia

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74
Q

What is alcoholic pancreatitis associated with?

A

Hypocalcaemia

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75
Q

Physiology underlying alcoholic pancreatitis?

A

Damaged pancreas leads to free fatty acids generated by pancreatic lipase.
Free fatty acids chelate the insoluble calcium salts resulting in calcium deposition in retroperitoneum leading to back pain.

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76
Q

How can low Mg result in alcoholic pancreatitis?

A

Low albumin leads to reduced total serum calcium
If there is emesis or poor nutritional status, low Magnesium can make things worse

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77
Q

PTH levels in pancreatitis-induced hypocalcaemia?

A

Normal
Elevated if severe hypocalcaemia

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78
Q

Treatment of alcoholic pancreatitis?

A

Parenteral ca and Mg replacement
Vitamin D levels checked

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79
Q

What type of pancreatitis is associated with depression?

A

Chronic

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80
Q

Hallmark of amphetamine-induced psychosis?

A

Paranoia

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81
Q

What is the biological mechanism behind stimulant-induced psychosis?

A

Sensitisation

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82
Q

Features of stimulant-induced psychosis compared to schizophrenia?

A

Absence of negative sx
Visual hallucinatinos
Appropriate affect
Hyperactivity
Disinhibited sexual behaviour
Confusion/incoherence
No formal thought disorder

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83
Q

How can one diagnose stimulant-induced psychosis?

A

Positive finding in urine drug screen
Rapid resolution of sx in a few days

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84
Q

Treatment of stimulant-induced psychosis

A

Short-term use of antipsychotic such as Haloperidol

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85
Q

What is hemp insanity?

A

Florid psychosis after high doses of high potency cannabis use

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86
Q

Impact of cannabis on cognition

A

Long term use can cause impairment in memory, attention and integration of complex information

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87
Q

What is amotivational syndrome?

A

Lack of motivation in a task that requires prolonged attention or effort in those with long term heavy cannabis use

88
Q

Findings in children born to mothers consuming cannabis during pregnancy

A

Mild attentional problems and impulsivity

89
Q

What is a ‘bad trip’ in LSD use?

A

Acute panic reaction
Can produce psychotic sx

90
Q

What is hallucinogen persisting perception disorder?

A

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

91
Q

Which classification has the disorder of hallucinogen persisting perception disorder?

A

DSM V

92
Q

What characterises hallucinogen persisting perception disorder?

A

Geometric hallucinations
False perceptions of movement in peripheral visual fields
Flashes/intensified colours
Trails of images of moving objects
Halos around objects

93
Q

What can trigger hallucinogen persisting perception disorder?

A

Stress
Sensory deprivation
use of another psychoactive substance such as alcohol or cannabis

94
Q

What can chronic inhalant use lead to?

A

Diffuse cerebral, cerebellar and brainstem atrophy with white matter disease

95
Q

What is seen in CT and MRI of chronic inhalant users?

A

Leukoencephalopathy

96
Q

Clinical effects of chronic inhalant use

A

Hearing loss
Peripheral neuropathy
Cerebellar signs
Motor impairment
Parkinsonism
Memory loss
Visuo-spatial dysfunction
Impaired processing of linguistic material

97
Q

What is the social learning model?

A

Views alcoholism as a maladaptive behaviour

98
Q

What is the disease model?

A

Views issues as irreversible but reduces self-blame.
Loss of control is the primary concept

99
Q

What sociocultural factors are linked with alcohol misuse?

A

Domestic Violence

100
Q

How does family systems model consider the behaviour of family members in the impact of alcohol misuse behaviours?

A

Behaviour of dysfunctional family members around drinking over time stabilizes the family system, forcing families to organise their structure and function around alcohol to preserve a degree of homeostasis

101
Q

What percentage of the general population has a FHx of alcoholism?

A

40%

102
Q

How much of the population have multiple family members affected by alcoholism?

A

7-9%

103
Q

How to calculate alcohol units based on ABV

A

Multiply ABV in % for a drink by the litres consumed.

104
Q

How many units of alcohol in men is hazardous

A

21-49 in a week

105
Q

How many units of alcohol in men is harmful

A

> 49 in a week

106
Q

How many units of alcohol in women is hazardous

A

14-35 in a week

107
Q

How many units of alcohol in women is harmful?

A

> 35 in a week

108
Q

Which study estimated heritability of alcohol disorders?

A

Virginia Adult twin study of psychiatric and substance use disorders

109
Q

Heritability of alcohol use disorders

A

0.51-0.66

110
Q

Who calculated odds of alcohol dependence in families

A

Dawson et al 1992

111
Q

Risk of alcohol dependence in individuals with both first and 2nd degree relative

A

4x increase

112
Q

Risk of alcohol dependence in those with affected first degree relative

A

2x increase

113
Q

Biomarkers found in impulsive problem drinkers

A

Low 5HT, 5HIAA and MAO

114
Q

What biomarker is reduced in alcoholics?

A

P300 amplitude
Also reduced in their children

115
Q

Physiological findings in men with FHx of alcoholism

A

Less physiological response (cortisol) when alcohol is ingested

116
Q

Genetic loci linked to alcohol misuse

A

Chromosomes 4p13-12 (GABRB1)
Chromosome 5q33-34
Chromosome 11q23.1
Chromosome 12q24.2
Chromosome 4q22 cluster

117
Q

Role of GABRB1

A

GABA receptor subunits

118
Q

Findings of GABRB1 and alcohol use

A

Linkage regions in association studies

119
Q

Role of chromosome 11q23.1

A

Dopamine D2 receptor gene (DRD2)

120
Q

What polymorphism occurs in the DRD2 gene?

A

Taq1

121
Q

Role of chromosome 12q24.2

A

Aldehyde dehydrogenase variants

122
Q

Findings of chromosome 12q24.2

A

Single base pair change in exon 12 of ALDH2 gene produces antabuse like reaction due to reduced ALDH activity.

123
Q

Ethnic significance of chromosome 12q24.2

A

Homozygous in 12% of people of South East Asia/Chinese origin, conferring protection

124
Q

Role of chromosome 4q22

A

Alcohol dehydrogenase polymorphism

125
Q

Findings of chromosome 4q22

A

High-activity variants ADH21 and ADH31 significantly decreased in people with alcohol dependence in oriental population.
They produce less acetaldehyde at slower pace.

126
Q

Risk factors for smoking

A

Low school achievement
Young among peer cohort
Poor relationship with family
Low household income

127
Q

Risk factors for alcohol use

A

Disruption of family structure
Social networks that use alcohol
Recent immigration
Small area deprivation

128
Q

Risk factors for illicit substances

A

Peer drug use
Single parenting
Homelessness
Poor educational attainment
Neighbourhood disadvantage
Unemployment

129
Q

What domains of risk factors do public health bodies focus on?

A

Individual
Family
Peer group
School
Wider society

130
Q

Risk factors for the individual in public health

A

Aggressive behaviour

131
Q

Risk factors for the family in public health

A

Poor parenting
Dysfunctional attitudes towards substances

132
Q

Risk factors in schools according to public health

A

Drug availability

133
Q

Risk factors in wider society for public health

A

Poverty
Social deprivation

134
Q

Preventive measures for the individual

A

Early identification
Targeted psychological intervention

135
Q

Preventive measures for the family

A

Parental training
Family education

136
Q

Preventive measures for peer groups

A

Academic competence
Legal policies

137
Q

Preventive measures for schools

A

Legal policies
School-based educational interventions

138
Q

Preventive measures for wider society

A

Promoting neighbourhood cohesion

139
Q

Screening tools used for alcohol disorders

A

AUDIT
CAGE
MAST

140
Q

What setting is AUDIT made for?

A

GP

141
Q

Sensitivity of AUDIT

A

83% males
65% females

142
Q

How can AUDIT be carried out?

A

Brief structured interview or
self-report questionnaire

143
Q

What subtype of AUDIT can be used in ED?

A

FAST - fast alcohol screening test

144
Q

What is the most widely used alcohol screening tool?

A

CAGE

145
Q

Disadvantages of CAGE

A

Does not include frequency of alcohol use, levels of consumption or episodes of heavy drinking - all of which identify patients in early stages of alcohol misuse.

146
Q

Who conducted a study into use of CAGE in GP?

A

Aertgeerts et al. 2001

147
Q

Sensitivity of CAGE in primary care

A

62% males
54% females

148
Q

What does MAST stand for

A

Michigan Alcohol Screening test?

149
Q

Who was MAST developed for?

A

Detecting dependent drinkers

150
Q

Structure of MAST

A

25 questions related to respondents self-appraisal of problems associated with excessive drinking

151
Q

Sensitivity of MAST

A

86-98%

152
Q

Specificity of MAST

A

81-95%

153
Q

Drawbacks of MAST

A

Focus is on lifetime rather than current occurrence of alcohol problems.
Can therefore miss early stages of alcohol misuse

154
Q

How long is alcohol present in urine?

A

Up to 12 hours

155
Q

How long is amphetamine present in urine?

A

Up to 48 hours

156
Q

How long are benzos present in urine?

A

Up to 3 days

157
Q

How long is cannabis present in urine if occasional use?

A

Up to 3 days

158
Q

How long is cannabis present in urine if heavy use?

A

Up to 4 weeks

159
Q

How long is cocaine present in urine?

A

6-8 hours

160
Q

How long is cocaine metabolite present in urine?

A

2-4 days

161
Q

How long is codeine present in urine?

A

48 hours

162
Q

How long is methadone present in urine?

A

3 days or more

163
Q

How long is heroin present in urine?

A

1-3 days

164
Q

How long is morphine present in urine?

A

2-3 days

165
Q

How long is PCP present in urine?

A

3-8 days

166
Q

How long is LSD present in urine?

A

<24 hours

167
Q

False positive test producer of PCP

A

Dextromethorphan

168
Q

False positive test producer of marijuana metabolites

A

Ibuprofen

169
Q

False positive test producer of opiates?

A

Tonic water

170
Q

False positive test producer of amphetamines

A

Phenylephrine decongestants

171
Q

What are successive episodes of alcohol withdrawal associated with?

A

Increasing severity and complications

172
Q

Goals of alcohol detox programmes

A

Symptom suppression
Avoiding complications
Completion of regime with subsequent abstinence

173
Q

What does community-based detox involve?

A

Daily contact with a nurse to assess withdrawal and monitor for complication

174
Q

Indications for inpatient alcohol detox

A

Past hx or current sx of DT/seizure
Psychiatric morbidity with risk of suicide or debilitating physical health
WE/Korsakoffs
Homelessness or social difficulties where detox may not be completed successfully

175
Q

What can benzos help with in alcohol detox?

A

Reduce severity of withdrawal
Reduce incidence of delirium and seizures
Completion of regime and subsequent rehab

176
Q

Which benzos are best in alcohol detox?

A

Those with longer half life are more effective in reducing incidence of delirium
Longer dose tapering required in those with hx of DT or having DT at present

177
Q

Which substances are suitable for patients in alcohol detox who have liver failure?

A

Substances which are eliminated without phase 1 metabolism e.g. lorazepam, oxazepam

178
Q

Typical fixed regim for uncomplicated alcohol detox

A

20mg QDS CPZ, reduced over 7 days
PRN in first 2 days for titration

179
Q

What is the front loading technique for alcohol detox?

A

Loading dose of Diazepam followed by further doses every 90 minutes until light sedation achieved.
No further medication given as long half life of diazepam covers withdrawal

180
Q

What is the symptom triggered regime for alcohol detox?

A

CPZ used when clinical withdrawal rating scale such as CIWA shows significant sx scores

181
Q

Advantages of symptom triggered regime for alcohol detox?

A

Faster control
Fewer benzo doses needed
Safer as avoid over-sedation and increased confusion

182
Q

Problems with symptom triggered regime for alcohol detox?

A

Distress caused to patient may reduce their motivation to be abstinent

183
Q

What drugs other than benzos can be used in alcohol detox?

A

Chlormethiazole
Carbamazepine
Anticonvulsants
Haloperidol

184
Q

Why should Chlormethiazole be avoided?

A

Risk of respiratory depression, especially when alcohol is consumed during detox

185
Q

First-line alternative to benzos in alcohol detox?

A

Carbamazepine

186
Q

Problems with Carbamazepine use in alcohol detox?

A

Limited evidence with respect to preventing DTs

187
Q

Problem of using haloperidol for alcohol detox

A

Do not reduce risk of seizures or delirium

188
Q

How many patients may have spontaneous abstinence of alcohol due to social changes

A

1 in 10

189
Q

Goals of relapse prevention for alcohol

A

Controlled drinking or abstinence

190
Q

Factors that favour aim of controlled drinking in rehab

A

Age <40
Early detection of alcohol problem
Minimal dependence
Mo medical/psychiatric complications
No impulsivity
Stable social support
Clear preference for controlled drinking
Partner/family who can monitor

191
Q

Factors that favour aim of total abstinence in rehab

A

> 40 years
Long standing alcohol problem
Severe/moderate dependence
Complications present
Impulsive personality
Poor social support
Ambivalence
Monitoring not possible

192
Q

What is Acamprosate?

A

Taurine derivative

Inhibits glutamatergic NMDA receptor function
Balances GABA-glutamate imbalance seen in alcohol dependence

193
Q

Odds ratio for abstinence with acamprosate vs placebo

A

1.73

194
Q

NNT for acamprosate

A

11

195
Q

Common SE of acamprosate

A

GI disturbances

196
Q

When is it recommended to start acamprosate?

A

Soon after detox

197
Q

How long can benefits of acamprosate continue for?

A

1-2 years after stopping drug

198
Q

What is naltrexone licensed for in the UK?

A

Ralapse prevention in alcohol dependence

199
Q

How does naltrexone work for alcohol dependence?

A

Reduces pleasurable effects of alcohol by blocking effects of opioids released by alcohol.
Results in reduced stimulation of mesolimbic dopamine reward system

200
Q

What has naltrexone been shown to be superior that placebo in?

A

Maintaining abstinence
Relapse rates
Time to first drink
Reduction in number of drinking days
Reduction in craving
Improvement in GGT

201
Q

NNT of naltrexone

A

9-11

202
Q

What is Nalmefene licensed for?

A

Reduction of alcohol consumption

203
Q

How can Nalmefene be px?

A

PRN with no need for LFT monitoring or withdrawal sx
Suitable for community settings

204
Q

How does Nalmefene work?

A

Opioid receptor modulator
Anatagonist at mu and delta receptors
Partial agonist at kappa receptors

205
Q

When is Nalmefene recommended?

A

To reduce alcohol consumption in dependent individuals with high drinking level risk after 2 weeks of initial assessment and without physical withdrawal sx and who do not require immediate detox

206
Q

What is the definition of high drinking risk level as per WHO?

A

> 60grams/day in men
40grams/day in women

207
Q

What must be px with Nalmefene?

A

Continuous psychosocial support focusing on treatment adherence and reducing alcohol consumption

208
Q

How does Disulfiram work?

A

Blocks aldehyde dehydrogenase resulting in accummulation of acetaldehyde if alcohol is taken

209
Q

Sx if patient on Disulfiram takes alcohol?

A

Flushing
Nausea/vomiting
Headache
Tachycardia
Palpitations

210
Q

What sx can occur if a patient on Disulfiram takes a large amount of EtOH?

A

HTN
Collapse

211
Q

What is important for the efficacy of Disulfiram?

A

Supervising the taking of the medication

212
Q

Effect of Disulfiram?

A

Reduces number of drinking days
Reduces quantity of alcohol consumed
Does not increase abstinence

213
Q

How long should Disulfiram be continued if initial beneficial effects?

A

3-6 months

214
Q

Contraindications of Disulfiram?

A

Impulsivity
Psychosis
Suicidality
Severe hepatic dysfunction
Peripheral neuropathies
Cardiac disease

215
Q

In whom can SSRIs be helpful for alcohol misuse?

A

Improve drinking outcomes in Type 1 alcoholism

216
Q

In whom can SSRIs be harmful for alcohol misuse?

A

Worsen outcomes in Type 2 Alcoholism

MRCPsych Part B (64 decks)

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