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Week 3 Flashcards

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1
Q

What factors are important in determining the risk of alcoholic liver disease?

A

Amount
Type
Frequency

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2
Q

What are the main pathological features of hepatitis?

A

Liver cell necrosis
Inflammation
Mallory bodies
Fatty changes

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3
Q

What are the main pathological features of cirrhosis?

A

Fibrosis

Hyperplastic nodules

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4
Q

What are the main pathological features of liver steatosis?

A

Fatty changes

Perivenular fibrosis

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5
Q

What is the likelihood of heavy alcohol abusers developing hepatitis, cirrhosis and steatosis?

A

Hepatitis - 10-35%
Cirrhosis - 8-20%
Steatosis - 90-100%

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6
Q

What is the preferred route of alcohol metabolism in the liver?

A

Cytosolic pathway

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7
Q

Outline the cytosolic pathway of alcohol metabolism in the liver

A

Alcohol is oxidised by alcohol dehydrogenase to acetaldehyde which enters mitochondria and is oxidised by acetaldehyde dehydrogenase to acetate

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8
Q

What 3 pathways are involved in alcohol metabolism in the liver?

A

Microsomal ethanol oxidising system (MEOS)
Cytosolic
Peroxisomal

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9
Q

What enzyme is key in the MEOS pathway?

A

CYP2E1 (cytochrome P450 family)

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10
Q

What is the product of the MEOS pathway?

A

Reactive oxygen species

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11
Q

What enzyme is key in the peroxisomal pathway?

A

Catalase

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12
Q

What is the product of the peroxisomal pathway?

A

Reactive oxygen species

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13
Q

What is the difference between metabolism of acute and chronic alcohol consumption?

A

Acute - cytosolic pathway predominates

Chronic - cytosolic pathway flooded; MEOS and peroxisomal pathways used which produce ROS

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14
Q

How is the catalase enzyme affected by fasting alcohol intake?

A

More active

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15
Q

What is the consequence of too much acetaldehyde?

A

Immunogenic - binds to surface membrane proteins and labels them as foreign so they become attacked by immune system which causes collagen production by stellate cell activation

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16
Q

What are stellate cells?

A

Collagen fibre producing cells

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17
Q

What is the consequence of too much acetate?

A

Increased acetyl-CoA promotes inflammation by histone acetylation

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18
Q

What is the consequence of increased NADH/NAD ratio?

A

Increased fatty acid synthesis
Decreased fatty acid production
Overall promotion of steatosis

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19
Q

What is the consequence of non-oxidative metabolism of alcohol?

A

Fatty acid ethyl ester production which promotes steatosis

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20
Q

What is the consequence of production of hydrogen peroxide and superoxide in the liver?

A

Activate redox-sensitive transcription factors (e.g. NF-κB) → increased TNF-α production → promotion of lipid peroxidation → inflammation and damage to mitochondrial membranes → apoptosis

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21
Q

What is the role of TNF-α production in alcoholic liver disease?

A

Promotes apoptosis and necrosis
Activates stellate cells to produce collagen leading to fibrosis
Increases intestinal permeability

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22
Q

What is the consequence of increased intestinal permeability in alcoholic liver disease?

A

Portal circulation endotoxaemia

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23
Q

Explain how portal circulation endotoxaemia leads to Kupffer cell activation in alcoholic hepatitis

A

Translocation of gut bacteria and products (e.g. endotoxin) into portal venous system → blood from intestine towards the liver → liver exposed to chronic low grade infection/endotoxaemia → activation of Kupffer cells → promotion of liver injury by release of TNF-α

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24
Q

What are Kupffer cells?

A

Specialised stellate macrophages in the liver which line the walls of sinusoids

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25
Q

What does endotoxamemia target on Kupffer cells?

A

CD14

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26
Q

What are the effects of TNF-α and neutrophil activation on hepatocytes in alcoholic hepatitis?

A

TNF-α - interacts with ceramide, producing ROS

Neurophil activation - by IL-8 released from hepatocytes, contribute to ROS formation

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27
Q

What is apoptosis?

A

Controlled cell death

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28
Q

Outline the intrinsic apoptosis pathway

A

Initiated by oxidative stress and regulated by Bcl-2 proteins
Leak of proapoptotic factors from mitochondria (e.g. cytochrome-c) activates capsases which degrade the cell

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29
Q

By what 2 pathways is apoptosis mediated?

A

Intrinsic

Extrinsic

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30
Q

Outline the extrinsic apoptosis pathway

A

Initiated by TNF-α
TNF receptor binding activates caspases via FADD (fas-associated death domain) and TRADD (TNF receptor-associated death domain) proteins

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31
Q

What type of vesicle are cell components broken down into for degradation?

A

Apoptotic bodies

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32
Q

What is the difference between apoptosis and necrosis?

A

Apoptosis – natural cell death stimulated by cell signals, beneficial, produces cell fragments which are able to send signals that facilitate phagocytosis
Necrosis – traumatic cell damage stimulated by factors external to the cells, fatal, cannot send signals which leads to build up of dead tissue and cell debris

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33
Q

How is malnutrition associated with excessive alcohol consumption?

A

Drinking instead of eating causes deficiencies of:
Zinc - exacerbates ROS production and apoptosis
Vitamins - impaired methionine metabolism, reduced glutathione

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34
Q

Give 3 examples of mitochondrial survival factors

A

MnSOD
Bfl-1
Bcl-XL

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35
Q

Give 2 examples of anti-oxidants

A

Glutathione

α-tocopherol

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36
Q

Outline the metabolism of methionine

A

Methionine is metabolised to homocysteine → cysteine → glutathione
This process needs vitamins (folic acid, vitamin B12, vitamin B6, betaine)

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37
Q

What is the consequence of chronic alcohol consumption on methionine metabolism?

A

Loss of vitamins required for the process leads to accumulation of homocysteine which cannot be metabolised to methionine - high levels of S-adenosyl-homocysteine

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38
Q

What is the consequence of a reduced SAM:SAH ratio in methionine metabolism?

A

Decreased transmethylation (impaired gene expression)
Increased caspase 3/8 expression (apoptosis)
Increased TNF production (reduced IL-10 - inflammation)
Decreased cystathionine β-synthase activity

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39
Q

How is oxidative stress caused by dysfunctional methionine metabolism?

A

Decreased trans-sulfuration caused decreased glutathione which results in oxidative stress

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40
Q

What is lipodystrophy?

A

Group of genetic or acquired disorders in which the body is unable to produce and maintain healthy fat tissue - characterised by abnormal or degenerative conditions of the body’s adipose tissue

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41
Q

How does alcohol induce lipodystrophy?

A

Reduction in peripheral fat and increase in visceral fat
Induction of CYP2E1 by increased free fatty acids, insulin resistance and alcohol – increased ROS and further insulin resistance; metabolism of FFAs to ω-hydroxylated fatty acids

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42
Q

Which LFTs are cytosolic and mitochondrial?

A

Cytosolic - ALT

Mitochondrial - AST

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43
Q

What are the effects of alcohol on the liver exacerbated by?

A

Malnutrition

Obesity

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44
Q

What is the normal progression of alcoholic liver disease?

A

Normal → steatosis → steatohepatitis → fibrosis → cirrhosis → hepatocellular carcinoma

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45
Q

What are the histological features of steatosis?

A

Macrosteatosis in zone 2 and 3
‘Swiss cheese’ appearance
(Enlarged yellow liver)

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46
Q

What are the histological features of alcoholic hepatitis?

A 
Swollen hepatocytes
Giant mitochondria 
Steatosis 
Mallory's hyaline
Collagen in zone 3
Inflammatory infiltrate of neutrophils
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47
Q

What are the histological features of cirrhosis?

A

Degenerating micronodules with fibrotic tissue
May have evidence of hepatitis
(Deformed liver)

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48
Q

What zone of the liver is the predominant site of early disease and why?

A

Zone 3

Relatively ischaemic which renders it more susceptible to damage

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49
Q

How can the liver be assessed non-invasively?

A

FibroScan - transient elastography; stiffness measurement via sound pulse speed of return
Soft and spongy - slow return
Hard and firm - fast return

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50
Q

How is transient elastography used currently?

A

Offered to diagnose cirrhosis for men who drink over 50 units of alcohol per week and women who drink over 35 units of alcohol per week and have done so for several months

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51
Q

What are the clinical symptoms of alcoholic liver disease?

A

Malaise, nausea, hepatomegaly, fever, jaundice, susceptible to infection, sepsis, encephalopathy, ascites, renal failure, death
May be asymptomatic/non-specific

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52
Q

What would ALT and AST show in alcoholic liver disease?

A

Raised AST:ALT ratio - elevation of AST

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53
Q

What clinical symptoms may be seen in a newly jaundiced alcoholic liver disease patient?

A

Hepatomegaly, fever, leukocytosis, hepatic bruit

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54
Q

What are the essential features of newly jaundiced alcoholic liver disease?

A 
Recent excess alcohol
Bilirubin >80μmol/l
Exclusion of other liver disease
AST < 500 
AST:ALT ratio >1.5
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55
Q

What is the GAHS and how is it used?

A

Glasgow alcoholic hepatitis score
Score between 5 and 12; more than or equal to 9 is indicative of high mortality risk despite supportive medical care
Includes age, WCC, urea, PT ratio, bilirubin

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56
Q

What are the signs of chronic liver disease/portal hypertension?

A 
Ascites 
Spider naevi
Foetor hepaticus 
Encephalopathy 
Prothrombin time dysfunction 
Caput medusae
Splenomegaly
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57
Q

What is foetor hepaticus?

A

Also known as breath of the dead; condition seen in portal hypertension where portal-systemic shunting allows thiols to pass directly into the lungs (rich tea biscuit dipped in tea smell)

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58
Q

How is the severity of chronic liver disease assessed?

A 
Childs-Turcotte-Pugh score - encephalopathy, ascites, bilirubin, albumin, prothrombin prolongation  
Grade A (5-6) - mild, compensatory 
Grade B (7-9) - moderate
Grade C (10-15) - severe, decompensation
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59
Q

What is MELD?

A

Model for end-stage liver disease
Used in USA for liver donation allocation
Mild <10, moderate 10-15, severe >15

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60
Q

What are the effects of portal hypertension?

A

Resistance to flow of portal venous blood due to fibrosis
Blood passes through collaterals (shunting) which allows translocation of endotoxins etc.
Peripheral and splanchnic vasodilation spends more blood towards the intestine and therefore the portal system - vicious cycle which escalates over weeks/months)
Vasodilation causes circulating volume to decrease – body reacts by vasoconstricting and filling up (compensatory activation of RAAS and catecholamines) renal circulation potently vasoconsticted which causes kidneys to shut down - retention of salt and water causes ascites

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61
Q

What drug is used to treat ascites?

A

Spironolactone

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62
Q

What direct factors may influence adverse effects with recreational drugs?

A 
High dose
Speed of entry 
Individual sensitivity 
Chronic/repeated use
Interaction with other compounds in the drug/other drugs/pre-existing pathologies
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63
Q

What indirect factors may influence adverse effects with recreational drugs?

A

Effects from coma/fits
Infection risk
Lifestyle changes (e.g. alcoholism, homelessness)

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64
Q

What are the neurological effects of using recreational drugs?

A 
Neuropathy 
Botulism 
Guillain-Barre
Anterior cord syndrome 
Encephalopathy
Meningitis
Stroke
Intracerebral haemorrhage
Seizures
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65
Q

What recreational drugs work on the dopamine reward system?

A 
Heroin 
Cocaine
Methamphetamine 
Alcohol 
Phencyclidine
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66
Q

What recreational drugs work on the noradrenaline readiness system?

A

Cocaine

Methamphetamine

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67
Q

What recreational drugs work on the serotonin/acetylcholine/dopamine/tetrahydrocannabinol perception/association system?

A

Cannabis
LSD
Phencyclidine

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68
Q

What recreational drugs work on the GABA sedative system?

A

Heroin
Cannabis
Alcohol
Phencyclidine

69
Q

What is the effect of increased GABA?

A

Anxiolysis, ataxia

70
Q

What is the effect of increased GABA and decreased NMDA?

A

Sedation, amnesia

71
Q

At what blood alcohol level is euphoria experienced and what other effects occur?

A

0.08-0.09%

Impaired balance, speech, vision, hearing, muscle co-ordination

72
Q

At what blood alcohol level is unconsiousness experienced?

A

0.40-0.50%

73
Q

What is Wernicke-Korsakoff syndrome?

A

Condition affecting chronic alcoholics in which encephalopathy is combined with a thiamine (vitamin B1) deficiency

74
Q

What is the mechanism and action of stimulants?

A

Enhance catecholamine/dopamine/serotonin transmission
Increased motor activity, increased alertness, euphoria, confidence
Anxiety, insomnia, irritability

75
Q

What is a toxidrome?

A

A syndrome caused by a dangerous level of toxins in the body, often the consequence of an overdose

76
Q

What are the symptoms of stimulant toxidrome?

A 
Tachycardia 
Hypertension 
Risk of arrhythmia 
Sweaty 
Hallucination 
Agitation 
Dilated pupils 
Elevated temperature
77
Q

What is serotonin syndrome?

A

Triad of altered mental status (agitation, confusion, seizures), autonomic changes (hyperthermia, diaphoresis, diarrhoea, tachycardia, hypertension, salivation) and neuromuscular effects (myoclonus, clonus, hyperreflexia, tremor, rigidity)
Hallucinations also common with serotonergic activation
Seen in many causes of stimulant toxidromes

78
Q

How does cocaine work?

A

Blocks dopamine, noradrenaline and serotonin reuptake

79
Q

Outline the pharmokinetics/dynamics of cocaine/amphetamine

A

Quick onset (seconds/minutes)
Peak within 30 minutes
Rapid BBB penetration

80
Q

How long are amphetamines detectable in urine?

A

48 hours

81
Q

What are the acute neurological problems with stimulants?

A

Motor – tremor, myoclonus, rhabdomyolysis, movement disorders
Seizures
Neuropsychiatric – restlessness, irritability, violence, psychosis
Autonomic – hyperpyrexia

82
Q

What are the chronic neurological problems with stimulants?

A 
Anxiety 
Sleep deprivation 
Paranoia 
Aggression 
Paranoid psychosis (more with amphetamines) 
Cognitive dysfunction 
Simple negative feedback
83
Q

How do stimulants cause vasospasm?

A

Increased α-adrenergic stimulation causes ‘sticky’ blood due to increased platelet aggregation

84
Q

How do stimulants cause strokes?

A

Acute hypertension causes haemorrhagic/ischaemic stroke within 3 hours of use of cocaine and amphetamine

85
Q

How do opiates work?

A

Sedation - μ receptors

Dysphoria - k receptors and reduction of GABA release (which increases dopamine)

86
Q

Name 2 sedative recreational drugs

A

Opiates

GHB

87
Q

How does GHB work?

A

Dysphoria - stimulates dopamine release
Sedation - GABA receptor activation
Muscle twitching

88
Q

What are the symptoms of opiate toxidrome?

A 
Pinpoint pupils 
Respiratory depression 
Bradycardia 
Hypotension 
Hypothermia 
Pulmonary oedema 
Seizures
89
Q

What are the symptoms of sedative toxidrome?

A 
Ataxia 
Blurred vision 
Coma 
Confusion 
Delirium 
Sedation 
Pupils likely to be normal
90
Q

What are the neurological problems with sedatives?

A

Coma - compressive nerve palsies, anoxic brain injury
Complications of injection - embolic infarction, infective endocarditis, abscesses, discitis, meningitis, HIV related illness

91
Q

How can hallucinogens be described?

A

Psychedelics
Dissociative anaesthetics
Deliriants

92
Q

What is atropa belladonna?

A

Deadly nightshade

93
Q

What are the symptoms of cholinergic toxidrome?

A 
Defecation 
Urination 
Miosis (small pupils) 
Bronchoconstriction 
Bradycardia 
Emesis 
Lacrimation 
Salivation
94
Q

Outline the features of MDMA

A

Ecstasy
Structurally similar to serotonin - blocks serotonin and noradrenaline reuptake
Thermoregulatory problems, hallucinations, cardiovascular complications

95
Q

What are the neurological effects of hallucinogens?

A

Rare reports of stroke
Toxic psychosis
Dangerous behaviour
Wernicke’s type syndrome with phencyclidine

96
Q

Give examples of organic solvents and their effects

A

Toluene, hexane, benzene
Acute - lightheadedness, hallucinations
Chronic - cognitive impairment, ataxia, diplopia, nystagmus, coma, peripheral neuropathies

97
Q

Outline the features of marijuana

A

THC active component
Agonist at cannabinoid receptor; increases dopamine; modulates opioid receptors
Effects - psychosis, altered neural activity, cognitive effects

98
Q

What are legal highs?

A

Also known as new psychoactive substances (NPS) - designed to produce similar psychoactive effects to “traditional” illegal drugs but are structurally different in order to avoid being controlled under the Misuse of Drugs Act
UK Psychoactive Substances Act came into effect on the 26 May 2016 – makes it an offence to produce or supply a substance used to get high

99
Q

Give some examples of legal highs

A 
Stimulants - piperazines (e.g. BZP)
Cathinones (e.g. mephedrone)
Benzofurans and methiopropamine
Sedatives - benzodiazepine analogues (e.g. etizolam)
New synthetic opioids
Hallucinogenic drugs - NBOMes and alpha-methyltryptamine
Dissociatives - methoxetamine
Synthetic cannabinoids - 5F-AKB-48
100
Q

What is mephedrone?

A

4-methylephedrone
Bath salts, plant food
Stimulant effect like cocaine/MDMA - increased energy, euphoria, confidance, empathy
Available to buy online

101
Q

What is ivory wave?

A

Reduces dopamine reuptake, similar to cocaine
Long half-life
Prolonged agitation, hallucination, myoclonus

102
Q

Why is the relationship between substance misuse and psychiatric problems complex?

A

Mental disorder may be caused directly by substance misuse and clear with abstinence
Mental disorder may have been a pre-existing problem which contributed to the substance misuse
Both disorders may exist separately in the same person
Treatment is more difficult and outcomes are poorer when co-morbidities are present

103
Q

What psychological problems are associated with acute alcohol intoxication?

A 
Insomnia
Depression
Anxiety
Amnesia
Attempted Suicide
Suicide
104
Q

What psychological problems are associated with chronic alcohol intoxication?

A 
Same as acute plus:
Changes in personality
Delirium tremens
Alcohol hallucinosis
Dementia
Association with other addictions
105
Q

What are the 8 features of alcohol dependence?

A 
Compulsion
Control
Tolerance
Withdrawal
Persistence
Neglect
Repertoire Narrows
Reinstatement
106
Q

What are the effects of chronic excessive drinking on the CNS?

A 
Neuropathies
Cerebellar
degeneration
Dementia
Wernicke-Korsakoff’s
syndrome
107
Q

How much more common is suicide in those who are alcohol dependent than those who are not?

A

20-60 times

108
Q

What are the effects of alcohol withdrawal?

A

Generally the opposite of intoxication signs

109
Q

What is delirium tremens?

A

The most severe form of alcohol withdrawal manifested by altered mental status (global confusion) and sympathetic overdrive (autonomic hyperactivity), which can progress to respiratory failure and cardiac failure (death)

110
Q

What patients with delirium tremens are at highest risk of death?

A

Those with extreme fever, fluid and electrolyte imbalance or an intercurrent illness (e.g. occult
trauma, pneumonia, hepatitis, pancreatitis, alcoholic ketoacidosis, WernickeKorsakoff
syndrome)

111
Q

What drugs can interact with alcohol?

A

Illicit - cocaine, heroin
Prescription - benzodiazepines, metronidazole
Over the counter - acetaminophen

112
Q

What are the 2 major determinants of alcohol misuse?

A

Price of alcohol

Availability of alcohol

113
Q

What treatment is used to support withdrawal during an alcohol detoxification?

A

Benzodiazepines

Vitamin replacement

114
Q

What pharmacological treatments are there for alcohol dependence?

A

Disulfiram
Acamprosate
Naltrexone

115
Q

What non-pharmacological treatments are there for alcohol dependence?

A

Alcoholics anonymous

Motivationl/cognitive psychological therapies

116
Q

What are the psychiatric associations with cannabis?

A

Cannabis dependence
Cannabis and psychosis
Amotivational syndrome
Cognitive impairment in long term

117
Q

What are the psychiatric associations with opiate dependence?

A 
Depression 
Attempted Suicide/Suicide
Personality Disorder
PTSD
No evidence for increased psychosis
Polydrug dependence more likely
118
Q

What is the most common benzodiazepine to be dependent on?

A

Diazepam

119
Q

What are the psychiatric problems with stimulant drugs?

A

Anxiety
Depression
Antisocial Behaviours
Paranoid psychosis

120
Q

What are people with substance misuse disorders more likely to have?

A

Co-morbid psychiatric diagnosis

121
Q

What are important points when assessing for substance misuse?

A

Screen misuse for psychiatric and vice versa
Corroborative history
Repeat history when patient is not intoxicated/acutely unwell

122
Q

What features do psychiatric disorders and substance misuse have in common?

A

Chronic

Relapsing and remitting

123
Q

What features must be integrated into treatment for psychiatric disorders and substance misuse?

A 
Integrated 
Comprehensive 
Phase-specific 
Assertive 
Long-term
124
Q

What are the psychological problems associated with regular heavy drinking?

A 
Insomnia 
Depression
Anxiety
Attempted suicide/suicide
Changes in personality
Amnestic syndrome (formerly Korsakoff Syndrome)
Dementia
Delirium tremens
Alcohol hallucinosis
Association with other addictions
125
Q

What brain processes are affected in 50% of alcoholic adults?

A

Spatial skills
Planning
Learning and memory

126
Q

Give examples of alcohol related brain damage

A 
Neuropathies
Cerebellar degeneration
Dementia
Wernicke-Korsakoff/amnestic
syndrome
127
Q

What are the predisposing factors for neurotoxicity in alcohol induced brain damage?

A 
Genetic predisposition to alcohol induced
neurotoxicity
Quantity / frequency of alcohol use
Severity of dependence
Frequent episodes of acute intoxication
Withdrawal syndromes
Other drugs use
Concurrent liver damage
128
Q

What are the predisposing factors for nutritional/thiamine deficiency in alcohol induced brain damage?

A

Weight loss in the past year
Reduced Body Mass Index
High carbohydrate intake
Recurrent episodes of vomiting

129
Q

What is Wernicke’s encephalopathy and Korsakoff’s psychosis?

A

WE - acute medical illness
KP - chronic mental disorder
Caused by thiamine deficiency

130
Q

What is thiamine, what is the daily requirement and where is it found?

A

Vitamin B1
1-2mg
Whole grains, organ meats, lean pork, seeds/nuts, legumes

131
Q

What are the symptoms of Wernicke-Korsakoff syndrome?

A 
Confusion (global confusional state)
Memory disorder 
Eye symptoms - gaze paralysis, nystagmus 
Gait ataxia 
Neuropathological lesions
132
Q

What are the main brain areas affected in W-K syndrome?

A

Mamillary bodies
Mediodorsal thalamus
Cerebrum

133
Q

What is amnesic/Korsakoff syndrome?

A

Chronic prominent loss of recent memory while immediate recall is
preserved
Disturbance of time sense and ordering of events
Difficulties in learning new material.
Confabulation may be marked
Other cognitive functions usually well preserved

134
Q

What is confabulation?

A

A disturbance of memory defined as the production of fabricated, distorted, or misinterpreted memories about oneself or the world, without the conscious intention to deceive

135
Q

Is Korsakoff syndrome always preceded/associated with Wernicke’s encephalopathy?

A

No

136
Q

What are the features of dementia?

A

Memory loss plus 1 of:
Agnosia - cannot recognise familiar things
Aphasia - circumlocutions, cliches, circumstantiality
Apraxia - can understand what is asked and is able to physically do it but cannot
Loss of executive function - poor planning/organising/adaptability

137
Q

Why is MRI useful to image the brain?

A

Safe
No injection required
Shows small parts of the brain

138
Q

What physical changes are evident in the brain of alcoholics?

A

Increased ventricular space

Shrinkage of cerebellum

139
Q

What can cause irreversible cognitive impairment involving damage to cortical and subcortical structures?

A

Combination of alcohol neurotoxicity and thiamine depletion

140
Q

What is hepatic encephalopathy and how does it develop?

A

Decline in brain function as a result of severe liver disease
Impaired metabolism of nitrogen-containing compounds (e.g. ammonia) via the urea cycle which causes them to accumulate in the systemic circulation → ammonia crosses the BBB where it is metabolised by astrocytes in the cerebrum which use it to form glutamine from glutamate → astrocytes become swollen (osmotic pressure), leading to cytotoxic cerebral oedema

141
Q

What can be included in the differential diagnosis for hepatic encephalopathy?

A 
Metabolic encephalopathy 
Drugs/toxins 
Intracranial structural disorders 
Infection 
Seizures
Wernicke's encephalopathy 
Head injury
142
Q

What are the precipitating factors for hepatic encephalopathy?

A

Increased protein load (e.g. upper GI haemorrhage)
Decreased excretion of ammonia (e.g. renal failure)
Electrolyte disturbance, dehydration, paracentesis, creation of portacaval shunts, infection, drugs (e.g.
sedatives), superimposed acute liver injury

143
Q

What can be used to grade mental state in hepatic encephalopathy?

A

West Haven criteria

144
Q

How is hepatic encephalopathy treated?

A

Lactulose and dietary measures to reduce nitrogen load
Removal of precipitating factors
General supportive measures
Reduce/close shunts

145
Q

How is alcohol affected by ageing?

A

Increased blood alcohol level - decreased lean body mass and total body water, age-related decrease in gastric alcohol dehydrogenase, liver oxidation decreases with age, sensitivity of brain to alcohol increases with age

146
Q

What has been the impact of deinstitutionalisation and closure of long stay psychiatric wards?

A

Patients with alcohol related brain damage have been displaced from psychiatric care into residential and nursing care homes

147
Q

What services are available for ARBD patients?

A

Debate over who should provide - addiction, neurorehabilitation or both
ARBD team set up in Glasgow and specialist nursing home beds

148
Q

What is the prognosis for ARBD?

A

Poorer in sudden-onset
Better with global cognitive impairment than pure amnestic syndrome
Improved if abstinence is maintained

149
Q

What are the rehabilitative principles in ARBD?

A

Regular review in first year of diagnosis
Placement determined by multidisciplinary assessment
Mental Health Act, guardianship and Adults with Incapacity can be used if there is a safety concern
Environment and memory rehab important

150
Q

What is foetal alcohol syndrome?

A

A serious developmental disorder caused by prenatal alcohol exposure of the
foetus and characterised by - prenatal and/or postnatal growth retardation, CNS
dysfunction, characteristic craniofacial abnormalities

151
Q

What is the spectrum off effects alcohol can have on a foetus?

A

No effect
Foetal alcohol effects - alcohol related birth defects, alcohol related neurodevelopmental disorders
Foetal alcohol syndrome

152
Q

What are the main points to note about the effect of alcohol on the brain?

A 
Thinking problems
Tissue loss
Decreased blood flow
Altered brain response to task
Much recovery with abstinence
153
Q

Outline the process by which change occurs

A

Pre-contemplation → contemplation → preparation → action → maintenance → permanent change/relapse

154
Q

What are the key elements contributing to readiness to change?

A

Importance and confidence - I need to do this and I can do this

155
Q

What causes someone to move from precontemplation to contemplation?

A

Acknowledgement of their problems and experience of innter tension about their behaviour

156
Q

What happens when change is pushed too quickly?

A

Resistance

157
Q

What feeling is very common in health behaviours?

A

Ambivalence

158
Q

What are the stages of an alcohol brief intervention?

A

1 - raising the issue of alcohol
2 - screening and giving feedback
3 - listening for readiness to change
4 - selecting an approach

159
Q

What are the important things for a doctor to do during contemplation?

A

Acknowledge and accept the patient’s frustration
Emphasise small goals and progress
Talk about the patient’s independence

160
Q

What are the important things for a doctor to do during planning/action?

A

Give advice
Give a range of choices
Set goals with the patient
Build their confidence

161
Q

What are the important things for a doctor to do during relapse?

A

Help the patient to understand what happened

Emphasise successes

162
Q

What approach is used in precontemplation?

A

Information and advice

163
Q

What approach is used in contemplation?

A

Understanding and motivation

164
Q

What approach is used in preparation?

A

Menu of choices

165
Q

What approach is used in action?

A

Build confidence

166
Q

What approach is used in maintenance?

A

Coping strategies

167
Q

How is a motivational interview conducted?

A

Open questions/statements/non-verbal communication
Go with the patient’s opinion but be selective
Problem-oriented (not diagnosis)
Negotiate goals
Don’t push for a a quick decision
No dramatical consultations

168
Q

What is motivational interviewing useful for?

A

Helps patients think about whether to change - provides information and minimises resistance
Increases uptake, compliance and positive outcome of treatment

People and Illness (4 decks)

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