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Week 3 Flashcards

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
What does endotoxamemia target on Kupffer cells?
CD14
26
What are the effects of TNF-α and neutrophil activation on hepatocytes in alcoholic hepatitis?
TNF-α - interacts with ceramide, producing ROS | Neurophil activation - by IL-8 released from hepatocytes, contribute to ROS formation
27
What is apoptosis?
Controlled cell death
28
Outline the intrinsic apoptosis pathway
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
29
By what 2 pathways is apoptosis mediated?
Intrinsic | Extrinsic
30
Outline the extrinsic apoptosis pathway
Initiated by TNF-α TNF receptor binding activates caspases via FADD (fas-associated death domain) and TRADD (TNF receptor-associated death domain) proteins
31
What type of vesicle are cell components broken down into for degradation?
Apoptotic bodies
32
What is the difference between apoptosis and necrosis?
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
33
How is malnutrition associated with excessive alcohol consumption?
Drinking instead of eating causes deficiencies of: Zinc - exacerbates ROS production and apoptosis Vitamins - impaired methionine metabolism, reduced glutathione
34
Give 3 examples of mitochondrial survival factors
MnSOD Bfl-1 Bcl-XL
35
Give 2 examples of anti-oxidants
Glutathione | α-tocopherol
36
Outline the metabolism of methionine
Methionine is metabolised to homocysteine → cysteine → glutathione This process needs vitamins (folic acid, vitamin B12, vitamin B6, betaine)
37
What is the consequence of chronic alcohol consumption on methionine metabolism?
Loss of vitamins required for the process leads to accumulation of homocysteine which cannot be metabolised to methionine - high levels of S-adenosyl-homocysteine
38
What is the consequence of a reduced SAM:SAH ratio in methionine metabolism?
Decreased transmethylation (impaired gene expression) Increased caspase 3/8 expression (apoptosis) Increased TNF production (reduced IL-10 - inflammation) Decreased cystathionine β-synthase activity
39
How is oxidative stress caused by dysfunctional methionine metabolism?
Decreased trans-sulfuration caused decreased glutathione which results in oxidative stress
40
What is lipodystrophy?
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
41
How does alcohol induce lipodystrophy?
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
42
Which LFTs are cytosolic and mitochondrial?
Cytosolic - ALT | Mitochondrial - AST
43
What are the effects of alcohol on the liver exacerbated by?
Malnutrition | Obesity
44
What is the normal progression of alcoholic liver disease?
Normal → steatosis → steatohepatitis → fibrosis → cirrhosis → hepatocellular carcinoma
45
What are the histological features of steatosis?
Macrosteatosis in zone 2 and 3 'Swiss cheese' appearance (Enlarged yellow liver)
46
What are the histological features of alcoholic hepatitis?
``` Swollen hepatocytes Giant mitochondria Steatosis Mallory's hyaline Collagen in zone 3 Inflammatory infiltrate of neutrophils ```
47
What are the histological features of cirrhosis?
Degenerating micronodules with fibrotic tissue May have evidence of hepatitis (Deformed liver)
48
What zone of the liver is the predominant site of early disease and why?
Zone 3 | Relatively ischaemic which renders it more susceptible to damage
49
How can the liver be assessed non-invasively?
FibroScan - transient elastography; stiffness measurement via sound pulse speed of return Soft and spongy - slow return Hard and firm - fast return
50
How is transient elastography used currently?
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
51
What are the clinical symptoms of alcoholic liver disease?
Malaise, nausea, hepatomegaly, fever, jaundice, susceptible to infection, sepsis, encephalopathy, ascites, renal failure, death May be asymptomatic/non-specific
52
What would ALT and AST show in alcoholic liver disease?
Raised AST:ALT ratio - elevation of AST
53
What clinical symptoms may be seen in a newly jaundiced alcoholic liver disease patient?
Hepatomegaly, fever, leukocytosis, hepatic bruit
54
What are the essential features of newly jaundiced alcoholic liver disease?
``` Recent excess alcohol Bilirubin >80μmol/l Exclusion of other liver disease AST < 500 AST:ALT ratio >1.5 ```
55
What is the GAHS and how is it used?
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
56
What are the signs of chronic liver disease/portal hypertension?
``` Ascites Spider naevi Foetor hepaticus Encephalopathy Prothrombin time dysfunction Caput medusae Splenomegaly ```
57
What is foetor hepaticus?
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)
58
How is the severity of chronic liver disease assessed?
``` 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 ```
59
What is MELD?
Model for end-stage liver disease Used in USA for liver donation allocation Mild <10, moderate 10-15, severe >15
60
What are the effects of portal hypertension?
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
61
What drug is used to treat ascites?
Spironolactone
62
What direct factors may influence adverse effects with recreational drugs?
``` High dose Speed of entry Individual sensitivity Chronic/repeated use Interaction with other compounds in the drug/other drugs/pre-existing pathologies ```
63
What indirect factors may influence adverse effects with recreational drugs?
Effects from coma/fits Infection risk Lifestyle changes (e.g. alcoholism, homelessness)
64
What are the neurological effects of using recreational drugs?
``` Neuropathy Botulism Guillain-Barre Anterior cord syndrome Encephalopathy Meningitis Stroke Intracerebral haemorrhage Seizures ```
65
What recreational drugs work on the dopamine reward system?
``` Heroin Cocaine Methamphetamine Alcohol Phencyclidine ```
66
What recreational drugs work on the noradrenaline readiness system?
Cocaine | Methamphetamine
67
What recreational drugs work on the serotonin/acetylcholine/dopamine/tetrahydrocannabinol perception/association system?
Cannabis LSD Phencyclidine
68
What recreational drugs work on the GABA sedative system?
Heroin Cannabis Alcohol Phencyclidine
69
What is the effect of increased GABA?
Anxiolysis, ataxia
70
What is the effect of increased GABA and decreased NMDA?
Sedation, amnesia
71
At what blood alcohol level is euphoria experienced and what other effects occur?
0.08-0.09% | Impaired balance, speech, vision, hearing, muscle co-ordination
72
At what blood alcohol level is unconsiousness experienced?
0.40-0.50%
73
What is Wernicke-Korsakoff syndrome?
Condition affecting chronic alcoholics in which encephalopathy is combined with a thiamine (vitamin B1) deficiency
74
What is the mechanism and action of stimulants?
Enhance catecholamine/dopamine/serotonin transmission Increased motor activity, increased alertness, euphoria, confidence Anxiety, insomnia, irritability
75
What is a toxidrome?
A syndrome caused by a dangerous level of toxins in the body, often the consequence of an overdose
76
What are the symptoms of stimulant toxidrome?
``` Tachycardia Hypertension Risk of arrhythmia Sweaty Hallucination Agitation Dilated pupils Elevated temperature ```
77
What is serotonin syndrome?
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
How does cocaine work?
Blocks dopamine, noradrenaline and serotonin reuptake
79
Outline the pharmokinetics/dynamics of cocaine/amphetamine
Quick onset (seconds/minutes) Peak within 30 minutes Rapid BBB penetration
80
How long are amphetamines detectable in urine?
48 hours
81
What are the acute neurological problems with stimulants?
Motor – tremor, myoclonus, rhabdomyolysis, movement disorders Seizures Neuropsychiatric – restlessness, irritability, violence, psychosis Autonomic – hyperpyrexia
82
What are the chronic neurological problems with stimulants?
``` Anxiety Sleep deprivation Paranoia Aggression Paranoid psychosis (more with amphetamines) Cognitive dysfunction Simple negative feedback ```
83
How do stimulants cause vasospasm?
Increased α-adrenergic stimulation causes 'sticky' blood due to increased platelet aggregation
84
How do stimulants cause strokes?
Acute hypertension causes haemorrhagic/ischaemic stroke within 3 hours of use of cocaine and amphetamine
85
How do opiates work?
Sedation - μ receptors | Dysphoria - k receptors and reduction of GABA release (which increases dopamine)
86
Name 2 sedative recreational drugs
Opiates | GHB
87
How does GHB work?
Dysphoria - stimulates dopamine release Sedation - GABA receptor activation Muscle twitching
88
What are the symptoms of opiate toxidrome?
``` Pinpoint pupils Respiratory depression Bradycardia Hypotension Hypothermia Pulmonary oedema Seizures ```
89
What are the symptoms of sedative toxidrome?
``` Ataxia Blurred vision Coma Confusion Delirium Sedation Pupils likely to be normal ```
90
What are the neurological problems with sedatives?
Coma - compressive nerve palsies, anoxic brain injury Complications of injection - embolic infarction, infective endocarditis, abscesses, discitis, meningitis, HIV related illness
91
How can hallucinogens be described?
Psychedelics Dissociative anaesthetics Deliriants
92
What is atropa belladonna?
Deadly nightshade
93
What are the symptoms of cholinergic toxidrome?
``` Defecation Urination Miosis (small pupils) Bronchoconstriction Bradycardia Emesis Lacrimation Salivation ```
94
Outline the features of MDMA
Ecstasy Structurally similar to serotonin - blocks serotonin and noradrenaline reuptake Thermoregulatory problems, hallucinations, cardiovascular complications
95
What are the neurological effects of hallucinogens?
Rare reports of stroke Toxic psychosis Dangerous behaviour Wernicke’s type syndrome with phencyclidine
96
Give examples of organic solvents and their effects
Toluene, hexane, benzene Acute - lightheadedness, hallucinations Chronic - cognitive impairment, ataxia, diplopia, nystagmus, coma, peripheral neuropathies
97
Outline the features of marijuana
THC active component Agonist at cannabinoid receptor; increases dopamine; modulates opioid receptors Effects - psychosis, altered neural activity, cognitive effects
98
What are legal highs?
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
Give some examples of legal highs
``` 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
What is mephedrone?
4-methylephedrone Bath salts, plant food Stimulant effect like cocaine/MDMA - increased energy, euphoria, confidance, empathy Available to buy online
101
What is ivory wave?
Reduces dopamine reuptake, similar to cocaine Long half-life Prolonged agitation, hallucination, myoclonus
102
Why is the relationship between substance misuse and psychiatric problems complex?
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
What psychological problems are associated with acute alcohol intoxication?
``` Insomnia Depression Anxiety Amnesia Attempted Suicide Suicide ```
104
What psychological problems are associated with chronic alcohol intoxication?
``` Same as acute plus: Changes in personality Delirium tremens Alcohol hallucinosis Dementia Association with other addictions ```
105
What are the 8 features of alcohol dependence?
``` Compulsion Control Tolerance Withdrawal Persistence Neglect Repertoire Narrows Reinstatement ```
106
What are the effects of chronic excessive drinking on the CNS?
``` Neuropathies Cerebellar degeneration Dementia Wernicke-Korsakoff’s syndrome ```
107
How much more common is suicide in those who are alcohol dependent than those who are not?
20-60 times
108
What are the effects of alcohol withdrawal?
Generally the opposite of intoxication signs
109
What is delirium tremens?
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
What patients with delirium tremens are at highest risk of death?
Those with extreme fever, fluid and electrolyte imbalance or an intercurrent illness (e.g. occult trauma, pneumonia, hepatitis, pancreatitis, alcoholic ketoacidosis, WernickeKorsakoff syndrome)
111
What drugs can interact with alcohol?
Illicit - cocaine, heroin Prescription - benzodiazepines, metronidazole Over the counter - acetaminophen
112
What are the 2 major determinants of alcohol misuse?
Price of alcohol | Availability of alcohol
113
What treatment is used to support withdrawal during an alcohol detoxification?
Benzodiazepines | Vitamin replacement
114
What pharmacological treatments are there for alcohol dependence?
Disulfiram Acamprosate Naltrexone
115
What non-pharmacological treatments are there for alcohol dependence?
Alcoholics anonymous | Motivationl/cognitive psychological therapies
116
What are the psychiatric associations with cannabis?
Cannabis dependence Cannabis and psychosis Amotivational syndrome Cognitive impairment in long term
117
What are the psychiatric associations with opiate dependence?
``` Depression Attempted Suicide/Suicide Personality Disorder PTSD No evidence for increased psychosis Polydrug dependence more likely ```
118
What is the most common benzodiazepine to be dependent on?
Diazepam
119
What are the psychiatric problems with stimulant drugs?
Anxiety Depression Antisocial Behaviours Paranoid psychosis
120
What are people with substance misuse disorders more likely to have?
Co-morbid psychiatric diagnosis
121
What are important points when assessing for substance misuse?
Screen misuse for psychiatric and vice versa Corroborative history Repeat history when patient is not intoxicated/acutely unwell
122
What features do psychiatric disorders and substance misuse have in common?
Chronic | Relapsing and remitting
123
What features must be integrated into treatment for psychiatric disorders and substance misuse?
``` Integrated Comprehensive Phase-specific Assertive Long-term ```
124
What are the psychological problems associated with regular heavy drinking?
``` Insomnia Depression Anxiety Attempted suicide/suicide Changes in personality Amnestic syndrome (formerly Korsakoff Syndrome) Dementia Delirium tremens Alcohol hallucinosis Association with other addictions ```
125
What brain processes are affected in 50% of alcoholic adults?
Spatial skills Planning Learning and memory
126
Give examples of alcohol related brain damage
``` Neuropathies Cerebellar degeneration Dementia Wernicke-Korsakoff/amnestic syndrome ```
127
What are the predisposing factors for neurotoxicity in alcohol induced brain damage?
``` 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
What are the predisposing factors for nutritional/thiamine deficiency in alcohol induced brain damage?
Weight loss in the past year Reduced Body Mass Index High carbohydrate intake Recurrent episodes of vomiting
129
What is Wernicke's encephalopathy and Korsakoff's psychosis?
WE - acute medical illness KP - chronic mental disorder Caused by thiamine deficiency
130
What is thiamine, what is the daily requirement and where is it found?
Vitamin B1 1-2mg Whole grains, organ meats, lean pork, seeds/nuts, legumes
131
What are the symptoms of Wernicke-Korsakoff syndrome?
``` Confusion (global confusional state) Memory disorder Eye symptoms - gaze paralysis, nystagmus Gait ataxia Neuropathological lesions ```
132
What are the main brain areas affected in W-K syndrome?
Mamillary bodies Mediodorsal thalamus Cerebrum
133
What is amnesic/Korsakoff syndrome?
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
What is confabulation?
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
Is Korsakoff syndrome always preceded/associated with Wernicke's encephalopathy?
No
136
What are the features of dementia?
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
Why is MRI useful to image the brain?
Safe No injection required Shows small parts of the brain
138
What physical changes are evident in the brain of alcoholics?
Increased ventricular space | Shrinkage of cerebellum
139
What can cause irreversible cognitive impairment involving damage to cortical and subcortical structures?
Combination of alcohol neurotoxicity and thiamine depletion
140
What is hepatic encephalopathy and how does it develop?
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
What can be included in the differential diagnosis for hepatic encephalopathy?
``` Metabolic encephalopathy Drugs/toxins Intracranial structural disorders Infection Seizures Wernicke's encephalopathy Head injury ```
142
What are the precipitating factors for hepatic encephalopathy?
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
What can be used to grade mental state in hepatic encephalopathy?
West Haven criteria
144
How is hepatic encephalopathy treated?
Lactulose and dietary measures to reduce nitrogen load Removal of precipitating factors General supportive measures Reduce/close shunts
145
How is alcohol affected by ageing?
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
What has been the impact of deinstitutionalisation and closure of long stay psychiatric wards?
Patients with alcohol related brain damage have been displaced from psychiatric care into residential and nursing care homes
147
What services are available for ARBD patients?
Debate over who should provide - addiction, neurorehabilitation or both ARBD team set up in Glasgow and specialist nursing home beds
148
What is the prognosis for ARBD?
Poorer in sudden-onset Better with global cognitive impairment than pure amnestic syndrome Improved if abstinence is maintained
149
What are the rehabilitative principles in ARBD?
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
What is foetal alcohol syndrome?
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
What is the spectrum off effects alcohol can have on a foetus?
No effect Foetal alcohol effects - alcohol related birth defects, alcohol related neurodevelopmental disorders Foetal alcohol syndrome
152
What are the main points to note about the effect of alcohol on the brain?
``` Thinking problems Tissue loss Decreased blood flow Altered brain response to task Much recovery with abstinence ```
153
Outline the process by which change occurs
Pre-contemplation → contemplation → preparation → action → maintenance → permanent change/relapse
154
What are the key elements contributing to readiness to change?
Importance and confidence - I need to do this and I can do this
155
What causes someone to move from precontemplation to contemplation?
Acknowledgement of their problems and experience of innter tension about their behaviour
156
What happens when change is pushed too quickly?
Resistance
157
What feeling is very common in health behaviours?
Ambivalence
158
What are the stages of an alcohol brief intervention?
1 - raising the issue of alcohol 2 - screening and giving feedback 3 - listening for readiness to change 4 - selecting an approach
159
What are the important things for a doctor to do during contemplation?
Acknowledge and accept the patient's frustration Emphasise small goals and progress Talk about the patient's independence
160
What are the important things for a doctor to do during planning/action?
Give advice Give a range of choices Set goals with the patient Build their confidence
161
What are the important things for a doctor to do during relapse?
Help the patient to understand what happened | Emphasise successes
162
What approach is used in precontemplation?
Information and advice
163
What approach is used in contemplation?
Understanding and motivation
164
What approach is used in preparation?
Menu of choices
165
What approach is used in action?
Build confidence
166
What approach is used in maintenance?
Coping strategies
167
How is a motivational interview conducted?
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
What is motivational interviewing useful for?
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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