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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
How long does memory gap tend to last in alcoholic blackouts?
Hours
26
What types of alcoholic dementia are there?
``` Primary alcoholic dementia Wernickes/Korsakoffs Marchiafava-Bignami Hepato-cerebral degeneration Vitamin deficiency ```
27
What is primary alcoholic dementia?
Direct toxic effects of alcohol on the brain
28
What brain findings can be reversed on abstinence of alcohol?
Atrophy | Other alcohol-related brain changes
29
What are the sx of Wernickes?
Ohthalmoplegia Ataxia Global confusion
30
How many patients with Wernickes present with the triad of sx?
10%
31
What causes Wernickes?
Thiamine deficiency
32
What leads to thiamine deficiency?
Inadequate dietary intake Reduced GI absorption Decreased hepatic storage Impaired utilization
33
What factor increases risk of Wernickes?
Anormal thiamine-dependent transketolase
34
Brain findings in Wernickes
Gliosis and small haemorrhages in periventricular and periaqueductal structures - especially in mammillary bodies, hypothalamus, mediodorsal thalamic nucleus, colliculi and midbrain tegmentum
35
How many chronic alcoholics exhibit signs of Wernickes?
12.%
36
What is the most valuable diagnostic tool for Wernickes?
MRI
37
MRI sensitivity for Wernickes
53%
38
MRI specificity for Wernickes
93%
39
How many untreated patients with Wernickes go on to develop Korsakoffs?
84%
40
Mortality rate of untreated Wernickes?
20%
41
Why should Thiamine be given before glucose?
Glucose infusion exacerbates thiamine deficiency
42
How much PO thiamine should be given in low risk drinkers
300mg/day
43
How much thiamine should be given in high risk drinkers
250mg IM/IV OD for 3-5 days.
44
What does Pabrinex contain?
Thiamine Nicotinamide Vitamin B2 and B6 Vitamin C
45
How much thiamine should be given if Wernickes is suspected?
IM/IV of >500mg for 3-5 days
46
Which sx of Wernickes resolves with hours?
Ophthalmoplegia
47
Whatt characterises Korsakoffs?
Marked deficits in anterograde and retrograde episodic memory Apathy Intact sensorium Preservation of other intellectual abilities: attention, procedural memory, working memory
48
Physiological process of Korsakoffs
Storage of information in more permanent form (consolidation by transfer of information from primary to secondary memory) are affected
49
What does diagnosis of Korsakoffs correlate with?
Presence of lesions in dorsomedial thalamus
50
What correlates with memory dysfunction in Korsakoffs?
Lesions in mammillary bodies, mammilothalamic tract and anterior thalamus
51
What leads to confabulation in Korsakoffs?
Double lesion - frontal and diencephalic deficits
52
What leads to cerebellar degeneration in alcohol use?
Degeneration of Purkinje cells in cerebellar cortex due to alcohol-induced damage
53
How many chronic alcoholics have cerebellar degeneration?
40%
54
What characterises hepatic encephalopathy?
``` Altered sensorium Frontal release signs Metabolic flapping tremor Hyperreflexia Extensor plantar responses ```
55
What sx are noted in those who make a partial recovery from hepatic encephalopathy?
``` Tremor Choreoathetosis Dysarthria Gait ataxia Dementia ```
56
What is the name of the sx that occur in patients who make partial recovery from hepatic encephalopathy?
Hepatocerebral degenaration
57
Brain changes in hepatic encephalopathy?
Enlargement and proliferation of protoplasmic astrocytes in basal ganglia, thalamus, red nucleus, pons and cerebellum
58
Who first described Marchiafava-Bignami syndrome?
Carducci in 1898 in Italian red wine drinkers
59
Who expanded the description of Marchiafava-Bignami syndrome?
Marchiafava and Bignami in 1903
60
Who does Marchiafava-Bignami syndrome commonly occur in?
Malnourished alcoholics
61
M:F ratio of Marchiafava-Bignami syndrome
More in males
62
Pathology of Marchiafava-Bignami syndrome?
Demyelination of corpus callosum and adjacent subcortical white matter - extra-pontine myelinolysis
63
Sx of Marchiafava-Bignami syndrome
Dementia Spasticity Dysarthria Gait changes
64
Who described 2 clinical types of Marchiafava-Bignami syndrome
Heinrich, 2004
65
What is Type A of Marchiafava-Bignami syndrome
Predominant features of coma and stupor
66
What is Type A Marchiafava-Bignami syndrome associated with?
High prevalence of pyramidal rtact sx
67
Radiologic features of Type A Marchiafava-Bignami syndrome
Involvement of entire corpus callosum
68
What characterises Type B Marchiafava-Bignami syndrome?
Normal or mildly impaired mental status
69
Radiologic features of Type B Marchiafava-Bignami syndrome?
Partial or focal callosal lesions
70
Who first described central pontine myelinolysis?
Adams et al in 1959
71
What happens in central pontine myelinolysis?
Demyelination of central portion of base of pons
72
Sx of central pontine myelinolysis?
``` Pain sensation in limbs Bulbar palsy Quadriplegia Disordered eye movements VOmiting Confusion COma/locked-in syndrome ```
73
Which non-alcoholic diseases can result in central pontine myelinolysis?
``` Wilsons Malnutrition Anorexia Burns Cancer Addisons Severe hyponatraemia ```
74
What is alcoholic pancreatitis associated with?
Hypocalcaemia
75
Physiology underlying alcoholic pancreatitis?
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.
76
How can low Mg result in alcoholic pancreatitis?
Low albumin leads to reduced total serum calcium | If there is emesis or poor nutritional status, low Magnesium can make things worse
77
PTH levels in pancreatitis-induced hypocalcaemia?
Normal | Elevated if severe hypocalcaemia
78
Treatment of alcoholic pancreatitis?
Parenteral ca and Mg replacement | Vitamin D levels checked
79
What type of pancreatitis is associated with depression?
Chronic
80
Hallmark of amphetamine-induced psychosis?
Paranoia
81
What is the biological mechanism behind stimulant-induced psychosis?
Sensitisation
82
Features of stimulant-induced psychosis compared to schizophrenia?
``` Absence of negative sx Visual hallucinatinos Appropriate affect Hyperactivity Disinhibited sexual behaviour Confusion/incoherence No formal thought disorder ```
83
How can one diagnose stimulant-induced psychosis?
Positive finding in urine drug screen | Rapid resolution of sx in a few days
84
Treatment of stimulant-induced psychosis
Short-term use of antipsychotic such as Haloperidol
85
What is hemp insanity?
Florid psychosis after high doses of high potency cannabis use
86
Impact of cannabis on cognition
Long term use can cause impairment in memory, attention and integration of complex information
87
What is amotivational syndrome?
Lack of motivation in a task that requires prolonged attention or effort in those with long term heavy cannabis use
88
Findings in children born to mothers consuming cannabis during pregnancy
Mild attentional problems and impulsivity
89
What is a 'bad trip' in LSD use?
Acute panic reaction | Can produce psychotic sx
90
What is hallucinogen persisting perception disorder?
Long after ingesting a hallucinogen, person can experience a flashback of hallucinogenic sx
91
Which classification has the disorder of hallucinogen persisting perception disorder?
DSM V
92
What characterises hallucinogen persisting perception disorder?
``` Geometric hallucinations False perceptions of movement in peripheral visual fields Flashes/intensified colours Trails of images of moving objects Halos around objects ```
93
What can trigger hallucinogen persisting perception disorder?
Stress Sensory deprivation use of another psychoactive substance such as alcohol or cannabis
94
What can chronic inhalant use lead to?
Diffuse cerebral, cerebellar and brainstem atrophy with white matter disease
95
What is seen in CT and MRI of chronic inhalant users?
Leukoencephalopathy
96
Clinical effects of chronic inhalant use
``` Hearing loss Peripheral neuropathy Cerebellar signs Motor impairment Parkinsonism Memory loss Visuo-spatial dysfunction Impaired processing of linguistic material ```
97
What is the social learning model?
Views alcoholism as a maladaptive behaviour
98
What is the disease model?
Views issues as irreversible but reduces self-blame. | Loss of control is the primary concept
99
What sociocultural factors are linked with alcohol misuse?
Domestic Violence
100
How does family systems model consider the behaviour of family members in the impact of alcohol misuse behaviours?
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
What percentage of the general population has a FHx of alcoholism?
40%
102
How much of the population have multiple family members affected by alcoholism?
7-9%
103
How to calculate alcohol units based on ABV
Multiply ABV in % for a drink by the litres consumed.
104
How many units of alcohol in men is hazardous
21-49 in a week
105
How many units of alcohol in men is harmful
>49 in a week
106
How many units of alcohol in women is hazardous
14-35 in a week
107
How many units of alcohol in women is harmful?
>35 in a week
108
Which study estimated heritability of alcohol disorders?
Virginia Adult twin study of psychiatric and substance use disorders
109
Heritability of alcohol use disorders
0.51-0.66
110
Who calculated odds of alcohol dependence in families
Dawson et al 1992
111
Risk of alcohol dependence in individuals with both first and 2nd degree relative
4x increase
112
Risk of alcohol dependence in those with affected first degree relative
2x increase
113
Biomarkers found in impulsive problem drinkers
Low 5HT, 5HIAA and MAO
114
What biomarker is reduced in alcoholics?
P300 amplitude | Also reduced in their children
115
Physiological findings in men with FHx of alcoholism
Less physiological response (cortisol) when alcohol is ingested
116
Genetic loci linked to alcohol misuse
``` Chromosomes 4p13-12 (GABRB1) Chromosome 5q33-34 Chromosome 11q23.1 Chromosome 12q24.2 Chromosome 4q22 cluster ```
117
Role of GABRB1
GABA receptor subunits
118
Findings of GABRB1 and alcohol use
Linkage regions in association studies
119
Role of chromosome 11q23.1
Dopamine D2 receptor gene (DRD2)
120
What polymorphism occurs in the DRD2 gene?
Taq1
121
Role of chromosome 12q24.2
Aldehyde dehydrogenase variants
122
Findings of chromosome 12q24.2
Single base pair change in exon 12 of ALDH2 gene produces antabuse like reaction due to reduced ALDH activity.
123
Ethnic significance of chromosome 12q24.2
Homozygous in 12% of people of South East Asia/Chinese origin, conferring protection
124
Role of chromosome 4q22
Alcohol dehydrogenase polymorphism
125
Findings of chromosome 4q22
High-activity variants ADH2*1 and ADH3*1 significantly decreased in people with alcohol dependence in oriental population. They produce less acetaldehyde at slower pace.
126
Risk factors for smoking
Low school achievement Young among peer cohort Poor relationship with family Low household income
127
Risk factors for alcohol use
Disruption of family structure Social networks that use alcohol Recent immigration Small area deprivation
128
Risk factors for illicit substances
``` Peer drug use Single parenting Homelessness Poor educational attainment Neighbourhood disadvantage Unemployment ```
129
What domains of risk factors do public health bodies focus on?
``` Individual Family Peer group School Wider society ```
130
Risk factors for the individual in public health
Aggressive behaviour
131
Risk factors for the family in public health
Poor parenting | Dysfunctional attitudes towards substances
132
Risk factors in schools according to public health
Drug availability
133
Risk factors in wider society for public health
Poverty | Social deprivation
134
Preventive measures for the individual
Early identification | Targeted psychological intervention
135
Preventive measures for the family
Parental training | Family education
136
Preventive measures for peer groups
Academic competence | Legal policies
137
Preventive measures for schools
Legal policies | School-based educational interventions
138
Preventive measures for wider society
Promoting neighbourhood cohesion
139
Screening tools used for alcohol disorders
AUDIT CAGE MAST
140
What setting is AUDIT made for?
GP
141
Sensitivity of AUDIT
83% males | 65% females
142
How can AUDIT be carried out?
Brief structured interview or | self-report questionnaire
143
What subtype of AUDIT can be used in ED?
FAST - fast alcohol screening test
144
What is the most widely used alcohol screening tool?
CAGE
145
Disadvantages of CAGE
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
Who conducted a study into use of CAGE in GP?
Aertgeerts et al. 2001
147
Sensitivity of CAGE in primary care
62% males | 54% females
148
What does MAST stand for
Michigan Alcohol Screening test?
149
Who was MAST developed for?
Detecting dependent drinkers
150
Structure of MAST
25 questions related to respondents self-appraisal of problems associated with excessive drinking
151
Sensitivity of MAST
86-98%
152
Specificity of MAST
81-95%
153
Drawbacks of MAST
Focus is on lifetime rather than current occurrence of alcohol problems. Can therefore miss early stages of alcohol misuse
154
How long is alcohol present in urine?
Up to 12 hours
155
How long is amphetamine present in urine?
Up to 48 hours
156
How long are benzos present in urine?
Up to 3 days
157
How long is cannabis present in urine if occasional use?
Up to 3 days
158
How long is cannabis present in urine if heavy use?
Up to 4 weeks
159
How long is cocaine present in urine?
6-8 hours
160
How long is cocaine metabolite present in urine?
2-4 days
161
How long is codeine present in urine?
48 hours
162
How long is methadone present in urine?
3 days or more
163
How long is heroin present in urine?
1-3 days
164
How long is morphine present in urine?
2-3 days
165
How long is PCP present in urine?
3-8 days
166
How long is LSD present in urine?
<24 hours
167
False positive test producer of PCP
Dextromethorphan
168
False positive test producer of marijuana metabolites
Ibuprofen
169
False positive test producer of opiates?
Tonic water
170
False positive test producer of amphetamines
Phenylephrine decongestants
171
What are successive episodes of alcohol withdrawal associated with?
Increasing severity and complications
172
Goals of alcohol detox programmes
Symptom suppression Avoiding complications Completion of regime with subsequent abstinence
173
What does community-based detox involve?
Daily contact with a nurse to assess withdrawal and monitor for complication
174
Indications for inpatient alcohol detox
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
What can benzos help with in alcohol detox?
Reduce severity of withdrawal Reduce incidence of delirium and seizures Completion of regime and subsequent rehab
176
Which benzos are best in alcohol detox?
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
Which substances are suitable for patients in alcohol detox who have liver failure?
Substances which are eliminated without phase 1 metabolism e.g. lorazepam, oxazepam
178
Typical fixed regim for uncomplicated alcohol detox
20mg QDS CPZ, reduced over 7 days | PRN in first 2 days for titration
179
What is the front loading technique for alcohol detox?
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
What is the symptom triggered regime for alcohol detox?
CPZ used when clinical withdrawal rating scale such as CIWA shows significant sx scores
181
Advantages of symptom triggered regime for alcohol detox?
Faster control Fewer benzo doses needed Safer as avoid over-sedation and increased confusion
182
Problems with symptom triggered regime for alcohol detox?
Distress caused to patient may reduce their motivation to be abstinent
183
What drugs other than benzos can be used in alcohol detox?
Chlormethiazole Carbamazepine Anticonvulsants Haloperidol
184
Why should Chlormethiazole be avoided?
Risk of respiratory depression, especially when alcohol is consumed during detox
185
First-line alternative to benzos in alcohol detox?
Carbamazepine
186
Problems with Carbamazepine use in alcohol detox?
Limited evidence with respect to preventing DTs
187
Problem of using haloperidol for alcohol detox
Do not reduce risk of seizures or delirium
188
How many patients may have spontaneous abstinence of alcohol due to social changes
1 in 10
189
Goals of relapse prevention for alcohol
Controlled drinking or abstinence
190
Factors that favour aim of controlled drinking in rehab
``` 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
Factors that favour aim of total abstinence in rehab
``` >40 years Long standing alcohol problem Severe/moderate dependence Complications present Impulsive personality Poor social support Ambivalence Monitoring not possible ```
192
What is Acamprosate?
Taurine derivative Inhibits glutamatergic NMDA receptor function Balances GABA-glutamate imbalance seen in alcohol dependence
193
Odds ratio for abstinence with acamprosate vs placebo
1.73
194
NNT for acamprosate
11
195
Common SE of acamprosate
GI disturbances
196
When is it recommended to start acamprosate?
Soon after detox
197
How long can benefits of acamprosate continue for?
1-2 years after stopping drug
198
What is naltrexone licensed for in the UK?
Ralapse prevention in alcohol dependence
199
How does naltrexone work for alcohol dependence?
Reduces pleasurable effects of alcohol by blocking effects of opioids released by alcohol. Results in reduced stimulation of mesolimbic dopamine reward system
200
What has naltrexone been shown to be superior that placebo in?
``` Maintaining abstinence Relapse rates Time to first drink Reduction in number of drinking days Reduction in craving Improvement in GGT ```
201
NNT of naltrexone
9-11
202
What is Nalmefene licensed for?
Reduction of alcohol consumption
203
How can Nalmefene be px?
PRN with no need for LFT monitoring or withdrawal sx | Suitable for community settings
204
How does Nalmefene work?
Opioid receptor modulator Anatagonist at mu and delta receptors Partial agonist at kappa receptors
205
When is Nalmefene recommended?
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
What is the definition of high drinking risk level as per WHO?
>60grams/day in men | >40grams/day in women
207
What must be px with Nalmefene?
Continuous psychosocial support focusing on treatment adherence and reducing alcohol consumption
208
How does Disulfiram work?
Blocks aldehyde dehydrogenase resulting in accummulation of acetaldehyde if alcohol is taken
209
Sx if patient on Disulfiram takes alcohol?
``` Flushing Nausea/vomiting Headache Tachycardia Palpitations ```
210
What sx can occur if a patient on Disulfiram takes a large amount of EtOH?
HTN | Collapse
211
What is important for the efficacy of Disulfiram?
Supervising the taking of the medication
212
Effect of Disulfiram?
Reduces number of drinking days Reduces quantity of alcohol consumed Does not increase abstinence
213
How long should Disulfiram be continued if initial beneficial effects?
3-6 months
214
Contraindications of Disulfiram?
``` Impulsivity Psychosis Suicidality Severe hepatic dysfunction Peripheral neuropathies Cardiac disease ```
215
In whom can SSRIs be helpful for alcohol misuse?
Improve drinking outcomes in Type 1 alcoholism
216
In whom can SSRIs be harmful for alcohol misuse?
Worsen outcomes in Type 2 Alcoholism

MRCPsych Part B (64 decks)

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