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Medicine Year 2 > People and Illness Week 3 > Flashcards

People and Illness Week 3 Flashcards

1
Q

What affect does alcohol consumption have on life expectancy?

A

Even below recommended limits (<12.5 units/per), alcohol consumption significantly decreases life expectancy

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2
Q

In the UK, how many grams of alcohol constitute a standard ‘unit’ of alcohol?

A

8g, percentage per litre is the number of units

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3
Q

Describe the trend of estimated deaths due to liver disease compared with the general population

A

Increasing

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4
Q

How does the risk of injury due to alcohol consumption vary depending on whether it is consumed alone or with meals?

A

Lower risk of injury if alcohol is consumed with meals

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5
Q

What factors affect the consumption of alcohol by a population?

A

Economic stability - disposable income

Availability of alcohol - licensing/legality

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6
Q

What is the peak admission age of patients with alcoholic liver disease?

A

Early/mid 50s

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7
Q

List the risk factors for alcoholic liver disease

A

The amount, the type and the frequency of alcohol consumption - daily drinking > binge
Alcohol abuse at a young age
Female
Overweight for at least 10 years

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8
Q

Explain the term ‘sick abstainers’

A

Those who abstain from alcohol who have previously abused alcohol, abstain due to health problems/fear of health problems in the future - makes some data appear as though those who abstain are at higher risk of developing disease, damage is already done in this group

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9
Q

What changes occur in the liver due to chronic excessive alcohol exposure?

A

Alcohol exposure leads to steatosis in 90-100% of heavy alcohol abusers, which can be reversed by abstinence.
Severe exposure will leads to hepatitis, which can develop from steatosis, hepatitis occurs in 10-35% of heavy alcohol abusers.
Abstinence can reverse hepatitis to steatosis.
Repeated attacks/continued exposure to alcohol can cause cirrhosis to develop from steatosis or hepatitis, which occurs in 8-20% of heavy alcohol abusers.

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10
Q

Describe the structural changes seen in the liver in steatosis

A

Fatty change
Perivenular fibrosis
Mactosteatosis in zone 2 and 3 - macrovesicular globules of fat
Enlarged liver, yellow colour due to fat accummulation

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11
Q

Describe the structural changes seen in the liver in hepatitis

A 
Liver cell necrosis
Inflammation - neutrophils infiltrate
Mallory bodies - hyaline
Fatty change
Swollen hepatocytes
Giant mitochondria
Steatosis
Collagen in zone 3
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12
Q

Describe the structural changes seen in the liver in cirrhosis

A

Fibrosis
Hyperplastic nodules - micronodular
Irregular nodular appearance

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13
Q

What is the final step in alcohol metabolism?

A

All processes produce acetaldehyde, which is oxidised to acetate by acetaldehyde dehydrogenase (in the mitochondria)

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14
Q

Describe the pathways involved in alcohol metabolism

A

Mostly oxidative metabolism in the cytosol by alcohol dehydrogenase
+ Microsomal ethanol oxidising system which uses cytochrome P4502E1 and produces reactive oxygen species
+ Catalase in perioxisomes which produces reactive oxygen species

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15
Q

How is alcohol metabolised in small/moderate amounts?

A

Oxidative metabolism in the cytosol by alcohol dehydrogenase to acetaldehyde then oxidation to acetate by acetaldehyde dehydrogenase in the mitochondria - other pathways only recruited in alcohol excess

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16
Q

What is the effect of chronic alcohol excess on alcohol metabolism?

A

Saturates normal pathway, induces recruitment of catalase and cytochrome P4502E1 (MEOS)
Increased production of acetaldehyde, acetate and reactive oxygen species

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17
Q

What are the consequences of alcohol metabolism on the body?

A

Acetaldehyde production - binds to proteins and DNA (immunogenic), stimulate collagen production by stellate cells

Acetate production - increased acetyl coA promotes inflammation by histone acetylation

Increased NADH/NAD ratio - increased fatty acid synthesis, reduced fatty acid oxidation (promotes steatosis)

Non-oxidative metabolism - fatty acid ethyl ester production (promotes steatosis)

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18
Q

Describe the conversion of NAD to NADH in alcohol metabolism

A

Cytosol oxidative metabolism -

NAD –> NADH

MEOS -

NADPH –> NADP

Mitochondrial conversion of acetaldehyde to acetate -

NAD –> NADH

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19
Q

What is the net change in NAD/NADH due to alcohol metabolism? What effect does this have?

A

Increasing NADH:NAD
Increasing NADH drives the electron transport chain - leaks electrons e.g. superoxide ions, hydrogen peroxide ions which are reactive

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20
Q

What produces reactive oxygen species in alcohol metabolism?

A

Largely through MEOS (especially CYP2E1) but catalase activity may contribute (especially in fasted state)

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21
Q

What are the effects of reactive oxygen species?

A

Activate redox-sensitive transcription factors such as NF-kapaB which leads to increased TNF-alpha production

Promotes lipid peroxidation which promotes inflammation and damages mitochondral membranes leading to apoptosis

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22
Q

What is the effect of TNF production?

A

Promotes apoptosis and necrosis, and activates stellate cells to produce collagen leading to fibrosis

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23
Q

What effect does alcohol have on the intestines?

A

Increases permeability, allows endotoxins to enter the portal circulation - portal circulation endotoxaemia.

This promotes activation of Kupffer cells which in turn promote liver injury - more proinflammatory cytokines (TNF-alpha) and reactive oxygen species.

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24
Q

Describe the changes which occur in hepatocytes following alcohol-related liver injury

A

Production of reactive oxygen species, activation of NF-kapaB, IL-8 and TNF recruition, neutrophil activation

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25
Q

How is the immune system changed in chronic alcohol excess?

A

Alcohol consumption stimulates the immune system to react to and damage the the liver

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26
Q

Describe the intrinsic apoptosis pathway

A

Intrinsic apoptosis (mitochondrial) pathway induced by oxidative stress - free-radicals, reactive oxygen species, toxins, radiation

Leads to leakage of pro-apoptotic factors from mitochondria (i.e. cytochrome-c), regulated by Bcl-2 proteins

Pro-apoptotic factors from mitochondria activate caspases leading to cell degradation

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27
Q

Describe the extrinsic apoptosis pathway

A

Initiated by TNF-alpha
Binding to TNF receptors leads to caspase activation via (Fas-associated death domain) and TRADD (TNF receptor-associated death domain) proteins

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28
Q

How does the process of apoptosis occur?

A

Proteolytic caspases degrade cellular organelles

Cell components broken down into vesicles (apoptotic bodies)

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29
Q

Compare apoptosis and necrosis

A 
Apoptosis:
Natural cell death 
Stimulated by cell signals
Beneficial
Produces cell fragments that are able to send signals that facilitate phagocytosis
Necrosis
Traumatic cell death
Stimulated by factors external to cells
Fatal 
Cannot send signals, leads to build up of dead tissue and cell debris
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30
Q

How does apoptosis contribute to liver injury in excessive alcohol consumption?

A

Apoptosis is usually a benign process, overstimulated in alcoholic liver injury = progressive damage without benefit

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31
Q

What factors may exacerbate the effect of excessive alcohol consumption on the liver?

A

Malnutrition - vitamin and trace element deficiencies

Obesity

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32
Q

Why are many alcoholics malnourished?

A

Drinking to excess, usually don’t eat adequately, can get 60-70% of calories from alcohol

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33
Q

How does malnutrition exacerbate liver injury?

A

Depletion of trace elements (i.e. zinc) may exacerbate ROS production and promote apoptosis

Vitamin deficiency may lead to impaired metabolism of methionine and reduction in gutathione

Mitochondria in chronic alcohol excess more susceptible to ROS, normally protected by mitochondrial survival factors (MnSOD, Bfl-1, Bcl-XL) and anti-oxidants (glutathione, alpha-tocopherol)
Depleted glutathione - alcohol induced cytotoxicity.

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34
Q

Which vitamin deficiencies increase susceptibility to cytotoxic damage in alcoholic liver disease?

A

Glutathione synthesis from methionine reduced by deficiency in folate, vitamin B6

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35
Q

How is glutathione synthesised?

A

Uses dietary sources of folic acid (e.g. leafy green vegetables), methionine to S-adenosyl-homocyteine to homocysteine to cryathionine to cysteine to gamma-glu-cysteine to glutathione

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36
Q

Which vitamins are needed for the production of glutathione?

A

Betaine (vitamin B)
Vitamin B6
Vitamin B12

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37
Q

What are the consequences of disrupted methionine metabolism?

A

Reduced S-adenosylmethionine:S-adenosylhomocysteine ratio:
Reduced transmethylation, impaired gene expression, increased caspase 3/8 expression

Apoptosis - increased TNF production (reduced IL-10)

Inflammation - reduced cystathionine beta-synthase activity

Reduced trans-sulfuration - reduced glutathione production (oxidative stress)

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38
Q

Describe the relationship between obesity and alcoholic liver disease

A

Alcohol induces a lipdystrophy - reduction in peripheral fat, increase in visceral fat

Induction of CYP2E1 by increased free fatty acids, insulin resistance and alcohol - increased ROS and further insulin resistance, metabolism of FFA to hydroxylated fatty acids

Obesity induced pro-inflammatory state - increased inflammatory mediators in response to endotoxaemia in obese patients

Obesity is a risk factor for alcoholic liver disease

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39
Q

Compare the features of non-alcoholic fatty liver disease and alcoholic liver disease

A

Similar histological features in both

Weight
NAFLD - elevated, ALD - variable

Fasting plasma glucose/HbA1c
NAFLD - often elevated, ALD - usually normal

AST/ALT ratio
NAFLD - <0.8 (more in advanced disease), ALD - >1.5

GGT
NAFLD - elevated or normal, ALD - markedly elevated

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40
Q

Explain the AST/ALT ratio in alcoholic liver disease compared with non-alcoholic fatty liver disease

A

AST in mitochondrial, ALT is cytoplasmic

Mitochondria remain intact in necrosis (predominant process in NAFLD)

Apoptosis breaks down mitochondrial membrane releasing AST (predominant process in ALD)

AST elevation also due to pyridoxine deficiency

AST not >500, ALT usually <300

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41
Q

Describe the pathological spectrum of alcoholic liver disease

A

Normal liver < steatosis < steatohepatitis < fibrosis < cirrhosis < hepatocellular carcinoma

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42
Q

Describe a non-invasive method of measuring the extent of liver disease

A

Fibroscan - transient elastography

Probe over rib cage measures the stiffness/firmness of the liver - soft/spongey = no fibrosis, hard/stiff = fibrosis

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43
Q

Which patient groups should be offered transient elastography?

A

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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44
Q

List the symptoms which develop as alcoholic liver disease progresses

A

Initially non-specific e.g. malaise, nausea

Progress to more clinical symptoms - hepatomegaly, fever, jaundice, sepsis, encephalopathy, ascites, renal failure

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45
Q

Why is fever a symptom of alcoholic liver disease?

A

Overstimulated immune system - many inflammatory mediators activated, active but dysfunctional so more susceptible to infection then sepsis

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46
Q

Describe the presentation of a patient with ‘clinically relevant’ alcoholic hepatitis

A

Newly jaundiced - bilirubin >80 umol/l (onset within 8 weeks)

Recent excess alcohol (within 8 weeks)

Exclusion of other liver diseases

AST < 500, AST:ALT ratio >1.5

Hepatomegaly, fever, leucocytosis, hepatic bruit - may feel well

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47
Q

What is the short-term mortality for a newly jaundiced patient with alcoholic liver disease?

A

Determined by the Glasgow alcoholic hepatitis score - takes age, white cell count, urea (renal function), prothrombin time ratio and bilirubin into account - score above 9 = 60% chance of death in the next 29 days if no medical therapy

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48
Q

How is acute hepatitis managed?

A

High dose prednisolone (corticosteroid) - reduces mortality, survival benefit greatest in patients with GAHS > 9

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49
Q

What volume of fluid can be held in the abdomen before ascites is clinically detectable?

A

5-6L - detected at lower volume with ultrasound

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50
Q

List the signs of chronic liver disease

A

Stigmata - spider naevi (from central arteriole, spread like the legs of spiders, only in distribution of venous drainage of vena cava), foetor encephalopathy
Synthetic dysfunction - tests of liver function e.g. prothrombin time, hypoalbuminuria

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51
Q

What is foetor?

A

Sweet smelling breath in advanced liver disease/portal hypertension

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52
Q

How can encephalopathy present clinically?

A

Spectrum - comatose/unarousable or ‘out of sorts’/not themselves

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53
Q

List the signs of portal hypertension

A

Caput medusae, hypersplenism (thrombocytopenia, pancytopenia)

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54
Q

What causes caput medusae?

A

After birth the vestigial ligament develops to separate the umbilicus from the systemic circulation.

Chronic increase in portal venous pressure means the a direct connection between the HPV and umbilicus envolves.

High blood pressure, blood is forced into superficial abdominal veins surrounding the umbilicus - gives prominent, wiggly vessels visible on surface.

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55
Q

How many spider naevi can be seen before clinical concern?

A

5

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56
Q

How can the severity of chronic liver disease be assessed?

A

Glasgow alcoholic hepatitis score

Childs-Tucotte-Pugh Score

Model for End-Stage Liver Disease - used to allocate donor organs in USA for liver transplant

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57
Q

What parameters are considered in the Childs-Turcotte-Pugh Score?

A

Encephalopathy, ascites, bilirubin, albumin, prothrombin time prolongation

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58
Q

Compare the clinical presentation of incidental and decompensated alcoholic cirrhosis

A

Incidental - no features of liver failure, ‘silent’, identified due to abnormal LFTs or abnormal imaging

Decompensation - presents with feature of advanced liver disease (variceal haemorrhage, hepatic encephalopathy, ascites/oedema, hepato-renal failure, hepatocellular carcinoma

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59
Q

What is the effect of cirrhosis on portal pressure?

A

Alcoholic cirrhosis leads to raised portal pressure, which causes porto-systemic shunting (anorectal, oesophageal, anterior abdominal wall)

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60
Q

How does portal hypertension lead to the complications of chronic liver disease?

A

Portal venous blood shunted back into the systemic circulation

Endotoxins in systemic circulation causes sepsis-like vasodilation (nitric oxide)

Dilation of blood vessels to gut means more blood to portal venous system and more portosystemic shunts

Shunts grow, eventually variceal haemorrhage - ammonia travels to brain causing encephalopathy

Vasodilation - BP down, reduced effective circulating volume, compensatory mechanisms (RAAS, catecholamines) cause sodium retention leading to ascites (use spironolactone to treat) and renal vasoconstriction leading to renal failure (hepatorenal syndrome)

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61
Q

Which drugs are commonly taken and by whom?

A

Mostly males

Cannabis in adolescents, cocaine in 20s, opiates in 30s

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62
Q

List common drugs and how they are taken

A

Heroin - oral, smoked, IV
Cannabis - oral, smoked
Cocaine - nasal, smoked, IV
Amphetamines (speed) - oral, nasal, smoked, IV
LSD (acid) - oral
Phencylidine/PCP (angel dust) - oral, nasal, smoked

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63
Q

Describe the factors which may influence adverse effects of recreational drugs

A

Directly due to drug -
Dose
Speed of entry
Individual sensitivity
Chronic/repeated use
Interaction with other compounds in the drug
Interaction with other drugs, including alcohol
Interaction with pre-existing pathologies

Indirectly due to drug -
Secondary effects of coma or fits
Infection risks
Accompanying lifestyle changes (homelessness, prostitution, trauma)

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64
Q

List the categories of common drugs

A 
Alcohol
Stimulants
Sedatives
Hallucinogens
Organic solvents
Performance enhancing drugs
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65
Q

Which neurochemical pathways does heroin act on?

A

Dopamine (reward), GABA/sedative activity

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66
Q

Which neurochemical pathways does cannabis act on?

A

Perception/association (serotonin/acetyl choline, THC/dopamine), GABA/sedative activity

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67
Q

Which neurochemical pathways does cocaine act on?

A

Dopamine (reward), noradrenaline (alertness)

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68
Q

Which neurochemical pathways do amphetamines act on?

A

Dopamine (reward), noradrenaline (alertness)

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69
Q

Which neurochemical pathways does alcohol act on?

A

Dopamine (reward)?, GABA/sedative activity

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70
Q

Which neurochemical pathways does LSD act on?

A

Perception/association (serotonin/acetyl choline/THC/dopamine)

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71
Q

Which neurochemical pathways does phencyclidine/PCP act on?

A

Dopamine (reward), GABA/sedative activity

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72
Q

Describe the sensations which alcohol gives and the transmitter/receptor which causes this

A

Euphoria/pleasure - dopamine, opiods
Anxiolysis/ataxia - increased GABA
Sedation/amnesia - increased GABA, decreased NMDA

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73
Q

How does increasing blood alcohol concentration change the effects of alcohol?

A
  1. 02-0.03% - mood elevation, muscle relaxation
  2. 05-0.06% - relaxation, increased reaction time/decreased fine muscle coordination
  3. 08-0.09% - euphoria, impaired balance, speech, vision, hearing, muscle coordination
  4. 14-0.15% - gross impairment of physical and mental control
  5. 20-0.30% - severely intoxicated, very little control of mind or body
  6. 40-0.50% - unconscious, death from respiratory depression
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74
Q

What are the physiological effects of alcohol?

A 
Wernicke-Korsakoff syndrome
Peripheral neuropathy
Cerebellar degeneration
Myopathy
Cognitive decline
Seizures
Withdrawal effects 
Injury/intracranial haemorrhage
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75
Q

Describe the action and effects of stimulants

A

Enhance transmission at the catecholaminergic/dopinergic/serotonergic synapses

Increase behavioural and motor activity
Increase alertness/disruption of sleep
Euphoria
Confidence

Central and peripheral sympatheomimetic effects
Side effects - anxiety, insomnia and irritability

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76
Q

Describe the toxidrome of stimulants

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

What is serotonergic syndrome?

A

Triad of:
Altered mental status - agitation/confusion/seizures
Autonomic changes - hyperthermia, diaphoresis, diarrhoea, tachycardia, hypertension, salivation
Neuromuscular effects - myoclonus, clonus, hyperreflexia, tremor, rigidity

Hallucinations also common with serotonergic activation

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78
Q

Describe the pharmacokinetics of cocaine

A

Quick onset of action - seconds to minutes
Peak levels - minutes to 30 minutes
Rapid BBB penetration - high brain concentrations
Half-life in plasma - 30-90 minutes (longer pharmacodynamic action)

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79
Q

Describe the pharmacodynamics of cocaine

A

Blocks dopamine, noradrenaline and serotonin re-uptake
Inhibitory effect on postsynaptic dopamine receptors
Blocks the presynaptic transporter protein for dopamine - dopaminergic pleasure effect, noradrenergic excess (readiness)

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80
Q

Describe the pharmacokinetics of amphetamines

A

Quick onset of action - seconds to minutes
Peak levels - minutes to 30 minutes
BBB penetration
Half-life in plasma - up to 12 hours for ICE

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81
Q

Describe the pharmacodynamics of amphetamines

A

Enhance release of dopamine and noradrenaline from pre-synaptic terminals - dopaminergic pleasure effect, noradrenergic excess (readiness)

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82
Q

For how long are amphetamines detectable in the system?

A

Detectable for 48 hours in urine

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83
Q

What are the acute neurological problems associated with stimulants?

A

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

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84
Q

What are the chronic neurological problems associated with stimulants?

A 
Anxiety
Sleep deprivation
Paranoia
Aggression
Paranoid psychosis (more with amphetamines)
Cognitive dysfunction
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85
Q

What physiological effect do stimulants have which can have serious circumstances?

A

Stimulants cause vasospasm, mediated by alpha-adrenergic stimulation (more alpha than beta signalling) - platelet aggregation is increased, evidence for accelerated atherosclerosis

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86
Q

How are stimulants associated with strokes?

A

Mostly haemorrhagic

Occurs soon after use - within 3 hours

More common if underlying pre-disposition

Infarcts more common with crack cocaine/methamphetamine - cocaine doubles the risk of ischaemic stoke

Outcomes same as patients with non-cocaine related stroke but patients are younger

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87
Q

List types of stimulants

A 
Cocaine
Amphetamines
Ephedrine
Pseudoephidrine
Phenylpropanolamine
Ephadra alkaloids
Methylphenidate (Ritalin)
MDMA
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88
Q

Describe the pharmacokinetics and pharmacodynamics of opiates

A

Sedation - u receptors

Dysphoria - kapa receptors/reduces GABA release (increases dopamine)

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89
Q

List common sedatives

A

Opiates - heroin

GHB

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90
Q

Describe the pharmacokinetics and pharmacodynamics of GHB

A

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

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91
Q

Describe the opiate toxidrome

A 
Pinpoint pupils
Respiratory depression
Bradycardia
Hypotension
Hypothermia
Pulmonary oedema
Seizures
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92
Q

Describe the sedative/hypnotic toxidrome

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

Causes include anticonvulsants, benzodiazepines, GNB, ethanol

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93
Q

What are the acute neurological problems associated with sedatives?

A

Typically indirect:
Coma
Compressive nerve palsies
Anoxic brain injury

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94
Q

What are the complications of intravenous drug used?

A 
Embolic infarction
Infective endocarditis
Abscesses
Discitis
Meningitis
HIV related illness
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95
Q

Describe the pharmacodynamics of hallucinogens

A

Serotoninergic
Noradrenergic
Cholinergic

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96
Q

Describe the effects of hallucinogens

A

Psychedelics
Dissociative anaesthetics
Deliriants

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97
Q

Describe the cholinergic toxidrome

A 
Defecation
Urination
Miosis (small pupils)
Bronchoconstriction
Bradycardia
Emesis
Lacrimation
Salivation
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98
Q

Describe the mechanism of action and effects of MDMA

A

3,4 methylenedioxymethamphetamine
Taken orally

Structurally similar to serotonin - blocks serotonin and noradrenaline reuptake

Stimulant toxidrome and perceptual effects - thermoregulatory problems, hallucinations, CV complications

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99
Q

What are the neurological effects of hallucinogens?

A

Rare reports of stroke
Toxic psychosis
Dangerous behaviour
Wernicke’s type syndrome - Angel dust

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100
Q

Give examples of organic solvents

A

Toluene, hexane, benzene

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101
Q

What are the acute effects of organic solvents?

A

Lightheadedness/hallucinations

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102
Q

What are the effects of prolonged organic solvent use?

A

Cognitive impairment
Diplopia, ataxia, nystagmus
Coma

Peripheral neuropathies can occur/some Guillain-Barre syndrome features

103
Q

What is the active component of marijuana?

A

THC - tetrahydrocannabinol

104
Q

What are the actions of marijuana?

A

Agonist at cannabinoid receptors - G protein linked receptors
Alters mood
Increases dopamine release
Modulates opioid receptors
Very lipid soluble, long T1/2 for metabolites

105
Q

What are the long-term effects of marijuana?

A

Hotly debated -
Psychosis
Altered neural connectivity on fMRI analysis
Cognitive effects

106
Q

What are ‘legal highs’?

A

New psychoactive substance, not controlled by the Misuse of Drugs act 1971

Contain substances which produce similar psychoactive effects to ‘traditional’ illegal drugs (e.g. cocaine)

107
Q

Give examples of legal highs

A

No officially agreed list of substances categorised as legal highs, e.g.
Stimulants such as cathionones e.g. mephedrone
Sedatives such as benzodiazepine analogues e.g. etizolam

108
Q

Describe the structure of mephedrone

A

Phenethylamine core with an alkyl group attached to the alpha carbon and a ketone group to the beta carbon

109
Q

Which groups experience highest mortality due to legal highs?

A

Males, age 20-29

110
Q

Describe the pharmacokinetics and pharmacodynamics of ivory wave (2-DPMP)

A

Reduces dopamine re-uptake (similar to cocaine)
Long half life
Prolonged agitation, hallucinations, myoclonus

111
Q

How have public health programmes attempted to control HIV transmission due to intravenous drug use?

A

Handing out clean needles to reduce needle sharing

HIV testing

112
Q

What is the relationship between alcohol and depressive illness?

A

Alcohol linked to higher risk of unipolar depressive disorders - high chance of suicide
Alcohol is strongest single predictor of suicide

Complex relationship - alcohol usually cause of depression rather than other way around, sometimes the mental disorder pre-dates the substance misuse and may have directly contributed to the development of the substance misuse (secondary alcohol misuse/dependence)
The two disorders may exist coincidentally in the same individual e.g. schizophrenia and alcohol dependence - treatment more difficult and outcomes poorer

113
Q

Why is life expectancy falling in some deprived areas of the UK?

A

Smoking, drinking, poor diet

114
Q

What are the acute effects of alcohol?

A

CNS - accidents (e.g. road traffic accidents)
Gastrointestinal
Respiratory - overdose

115
Q

What are the psychological problems with acute intoxication with alcohol?

A 
Insomnia
Depression
Anxiety
Amnesia
Attempted suicide
Suicide
116
Q

What are the psychological problems associated with regular heavy drinking?

A 
Insomnia
Depression
Anxiety
Attempted suicide/suicide
Changes in personality
Amnesia
Delirium tremens
Alcohol hallucinosis
Dementia
Association with other addictions

Usually greatly improved by detoxification and abstinence from alcohol

117
Q

Describe the features of alcohol dependence syndrome

A 
Compulsion (to drink)
Control 
Tolerance
Withdrawal
Persistance
Neglect
Repertoire narrows - less variation in drinks of choice
Reinstatement - negative reinforcement (drinking makes you feel better/stops negative feelings, reinforces the drinking behaviour)
118
Q

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

A

Neuropathies
Cerebellar degeneration
Dementia
Wernicke-Korsakoff’s syndrome

119
Q

Describe alcohol withdrawal

A 
Withdrawal effects are opposite of intoxication symptoms/signs -
Dilated pupils
Sweating
Delirium
Can't sit still
Confused disorientation
Delusions of persecution
120
Q

Describe the features of delirium tremens

A

Rapid onset confusion cause by withdrawal of alcohol, onset 3 days after stopping drinking, lasts for 2-3 days

Physical effects:
Shaking, shivering, irregular heart rate, sweating, visual hallucinations, auditory hallucinations, disorientation, convulsions

121
Q

Describe the mortality associated with delirium tremens

A

Current mortality - 5-15%
Most common conditions leading to death are respiratory failure and cardiac arrhythmias
Those at greatest risk are those with extreme fever, fluid and electrolyte imbalance or an intercurrent illness e.g. occult trauma, pneumonia, hepatitis, pancreatitis, alcoholic ketoacidosis or Wernicke-Korsakoff syndrome

122
Q

What causes alcohol problems?

A

Price and availability of alcohol
Biological factors
Cultural influences
Socio-economic factors

123
Q

Describe the treatment of alcohol dependence

A

Assistance for withdrawal - home detox, daypatient detox, inpatient detox, benzodiazepines and vitamin replacement

Psychological therapies based on motivational and cognitive models

Treatment goal varies with misuse and dependence and associated comorbidity

Non-statutory agencies e.g. alcoholics anonymous

Pharmacotherapy - disulfiram, acomprosate, naltrexone

Treatment of physical and psychiatric comorbidity

124
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

Stabilisation on methadone improves mental health scores

125
Q

Describe benzodiazepine dependence and treatment

A

Specific and prolonged abstinence syndrome after only a short period of regular use in some individuals

Long-term use - management with specialist advice
Differing patterns of use for prescribed and non-prescribed misuse

126
Q

Describe the psychiatric problems associated with use of stimulant drugs

A

Anxiety
Depression
Antisocial behaviours
Paranoid psychosis

127
Q

Describe the assessment of patients with substance use problems

A

Screen all substance misuse patients for psychiatric symptoms, and all patients presenting with psychiatric symptoms for substance misuse
History taking may be difficult in patients with acute psychiatric presentations
Seek corroborative history
Repeat substance use history when patient not intoxicated or acutely unwell
Repeat psychiatric history when patient not intoxicated or withdrawing

128
Q

Describe the principles of management of substance misuse/psychiatric problems

A

Both are chronic relapsing and remitting conditions, long-term treatment approaches required
Treatment needs to be - integrated, comprehensive, phase-specific, assertive, long-term

129
Q

What is a mental state examination?

A

An assessment of a person’s current state of mind, describes a snapshot of their presentation during interaction with them
Carried out while taking a psychiatric history
Includes observations and their answers to specific questions

130
Q

What is a mental state examination used for?

A

Records current symptoms and severity, as well as negative findings
Used alongside the psychiatric history in assessment and diagnosis
Used to assess progress during/after treatment

131
Q

Describe the format of a mental state examination

A 
Appearance and behaviour
Speech
Mood and affect
Thought form and content
Perception
Cognition
Insight
132
Q

What factors could be mentioned when assessing appearance in a mental state examination?

A 
How the person looks:
Ethnicity, build, hair colour, clothing
Biological vs chronological age
Are they well kempt?
Is there evidence of self-neglect?
Do they appear physically unwell or intoxicated?
Any distinguishing features
133
Q

What areas of behaviour are assessed in a mental state examination?

A

How the person acts:
Level of motor activity (e.g. agitation or motor retardation)
Eye contact
Rapport and engagement with interview
Body language and posture
Any unusual or socially inappropriate behaviour

134
Q

What aspects of speech are assessed in a mental state examination?

A 
How the person talks:
Rate and quantity of speech
Rhythm
Volume
Tone 
Spontaneity
135
Q

Define mood and affect

A

Mood - a person’s emotional state overall

Affect - changes in the persons emotions that you observe moment-to-moment during the interview

136
Q

What aspects of mood are assessed in a mental state examination?

A

Subjective - how the person tells you they feel in their own words
Objective - your impression of the person’s mood during the interview - euthymic (normal), elevated/elated, low/depressed, anxious

137
Q

Give examples of types of affect which may be identified during a mental state examination

A

Reactive - appropriate reaction to the situation or topic being discussed
Flattened - limited emotional reaction
Blunted - no observed emotional reactions (specifically associated with psychosis)
Labile - excessive emotional fluctuations

138
Q

What is thought form and how is it assessed in a mental state examination?

A

The pattern of the person’s thoughts
Are there logical connections between the things they are saying?
‘No formal thought disorder’ - the flow of their thoughts seems normal
Include specific quotes if possible
Lots of descriptive terms that can be used, for example - fight of ideas, loosening of associations/knight’s move thinking

139
Q

What is flight of ideas?

A

Rapid flow of speech, moving from topic to topic with logical connections (mania)

140
Q

What is knight’s move thinking?

A

Little or no logical connections between thoughts (schizophrenia)

141
Q

What is thought content and how is it assessed during a mental state examination?

A

What the person is saying, any topics discussed more than others
Delusions, obsessions, fixed ideas, risk (any thoughts of harm to self or others, including the degree of planning and intent)

142
Q

What is a delusion?

A

A fixed, false belief that is out of keeping with the person’s religious and cultural background e.g. psychosis

143
Q

Give examples of types of delusions

A

Paranoid - perceived threat from others
Grandiose - considerable overestimate of abilities or possession of special powers
Nihilistic - belief that they are dead or do not exist
Delusions of reference - belief that external events/objects are directly related to them e.g. TV programmes
Thought interference - insertion, withdrawal or broadcast

144
Q

What is an over-valued idea?

A

A false belief, not totally fixed but causing great disability e.g. anorexia, hypochondriasis

145
Q

What is an obsession?

A

Recurrent, intrusive, distressing ideas, impulses or images that the patient recognises as their own (e.g. OCD)

146
Q

What aspects of perception may be documented in a mental state examination?

A

What the patient tells you and what you observe,
Hallucinations - perception without external stimulus
Can occur in any sensory modality - auditory (associated with psychosis), visual, olfactory, gustatory, tactile - more often with organic states
Illusion - false perception of a real stimulus e.g. seeing a person in a shadow (can be normal)

147
Q

What aspects of cognition can be assessed in a mental state examination?

A

Is the person alert (fully awake) and orientated (to time, place and person)?
How is their concentration and memory? Are they able to maintain focus during the interview, are they easily distracted?
Memory - tell them 3 objects, ask them to repeat until they are correct, continue with history then ask again after a few minutes.
If relevant, use a specific assessment tool such as the Mini Mental State Examination (MMSE)

148
Q

How is insight assessed in a mental state examination?

A

The patient’s understanding of their presentation and their need for treatment

Complex, not just present or absent -
Do they believe their experience is unusual?
Is it part of an illness? A mental illness?
Do they require treatment?
What type of treatment?
Do they need to be admitted to hospital?

149
Q

What neurological signs are often seen in chronically heavy drinkers?

A

50% alcoholic adults show problems with:
Spatial skills
Planning
Learning and memory - memories retained but difficult to access (can remember with prompting)

150
Q

What neurological skills are often retained even in alcoholic brain damage?

A

IQ and language

151
Q

Describe the ability of the alcoholic brain to recover

A

Abstinence - much recovery in first month, more in 1st year if sober

152
Q

What is the neurological effect of chronic heavy drinking and associated malnutrition?

A

Alcohol related brain damage - neuropathies (including peripheral), cerebellar degeneration, dementia, Wernick-Korsakoff syndrome/amnesitc syndrome

153
Q

List the factors which predispose to alcohol induced brain damage

A

Neurotoxicity -
genetic predisposition to alcohol induced neurotoxicity, quantity/frequency of alcohol use, severity of dependence, frequent episodes of acute intoxication, withdrawal syndrome (Kindling effect), other drugs used (often tobacco), concurrent liver damage

Nutritional/thiamine deficiency - weight loss in the past year, reduced body mass index, high carbohydrate intake, recurrent episodes of vomiting

154
Q

How much thiamine is required by the body daily?

A

1-2mg
Men - 1.4
Women 1.0

155
Q

How much thiamine is stored in the body? What are the consequences of this?

A

Stores are small
Liver - 3-4mg
Total body ?30mg

Depletion soon reflected in reduced circulating levels and reduced stores

156
Q

Define Wernicke-Korsakoff’s syndrome

A

Two syndromes - Wernicke’s encephalopathy and Korsakoff’s psychosis

Wernicke’s is a serious acute medical illness, Korsakoff’s is a psychosis, two syndromes described separately but usually stages of the same disorder

Linked with alcoholism and due to a deficiency of Vitamin B1 or thiamine

157
Q

What constitutes one unit of alcohol?

A 
1 unit = 86/10ml ethanol
1/2 pint of ordinary strength beer (ABV 3-4%)
A small (125ml) glass of wine (ABV 13%)
A single (25ml) shot of spirits (ABV 40%)
158
Q

How can the number of units in an alcoholic drink be calculated?

A

Number of units in drink = ABV (%) x volume (ml)/1000

%ABV x 0.78 = g alcohol/100ml

159
Q

Why is the unit system difficult to apply to real life?

A

Beers, lagers and ciders have very different alcohol contents and containers vary in size

Wines vary in strength, no standard glass measure

Mixed drinks containing more than one alcoholic beverage have non-standard composition

Drinks poured at home are usually larger than those served outside

160
Q

Describe the recommended low risk guidelines for alcohol consumption

A

Low risk - unlikely to be associated with the development of alcohol related harm if spread over 7 days
Per week:
No more than 14 units of alcohol per week for men and women
2-3 days per week should be alcohol free
The amount of alcohol drunk on any single occasion should be limited
Alcohol taken in any amount increases the risk of injury

161
Q

What constitutes hazardous drinking?

A

Hazardous drinking = intake likely to increase the risk of developing alcohol related harm
Male = 22-50 units per week
Female = 15-35 units per week

162
Q

What constitutes harmful drinking?

A

Alcohol misuse - a pattern of drinking associated with the development of alcohol-related harm
Male = >50 units per week
Female = >35 units per week

163
Q

Define alcohol dependence

A

Syndrome characterised by 3 or more of the following:

A strong desire or compulsion to drink
Difficulty in controlling the onset or termination of drinking or the levels of alcohol use
A physiological withdrawal state on cessation of alcohol or its use to avoid withdrawal symptoms
Increasing tolerance to alcohol so that increased amounts are needed in order to achieve similar effects to those produced originally by smaller amounts
Progressive neglect of other interests
Persisting use of alcohol despite clear evidence and an awareness of the nature and extent of the harm it is causing

164
Q

Define a problem-drinker

A

An individual who is experiencing alcohol-related harm

165
Q

Describe the drink-driving limits in Scotland

A

Maximum alcohol limit is:
22 micrograms of alcohol in 100ml of breath
50mg of alcohol in 100ml of blood
67mg of alcohol in 100ml of urine

166
Q

List the factors which affect blood alcohol content

A

Volume/strength of alcohol consumed
Speed at which alcohol is consumed
Gender - females have less body water content than males, will have higher BAC
Weight - higher weight, lower BAC
Alcohol metabolism - heavy drinkers have more active livers, so will metabolise the same volume/strength of alcohol more quickly
Medication and what they have eaten
Age - young tend to metabolise alcohol more quickly than old

167
Q

How are drink drivers assessed for suitability to drive?

A

Have to satisfy the DVLA of their fitness to drive by attending an independent medical examination with a DVLA appointed doctor before a driving license will be issued to them, consists of examination, serum carbohydrate deficient transferrin (CDT) and a questionnaire

168
Q

What does carbohydrate deficient transferrin indicate about drinking habits?

A
  1. 1% or less indicates no excessive alcohol intake
  2. 2-2.9% indicates a possible problematic alcohol consumption (may drink to excess of binge drinks regularly)

3% or more indicates alcohol consumption in a dependent manner, driving license refused

169
Q

Define binge drinking

A

8 units of alcohol in a single session for men

6 units of alcohol in a single session for women

170
Q

What is the recommended drinking advice for pregnant women?

A

Abstinence for the first trimester then no more than 1-2 units once or twice weekly, 2-4 units in a week at most

171
Q

What concentration of alcohol produces intoxication?

A

In non-habitual drinkers, blood ethanol concentrations between 30-70mg/100ml can lead to definite cognitive impairment, motor co-ordination and sensory perception, concentrations of 150-250mg/100ml are associated with obvious intoxication

BAC at which death occurs varies, concentrations >450mg/100ml are often fatal, >700mg/ml has been recorded in habitual drinkers

Habitual drinkers can sustain BAC of 300mg/100ml or more without signs of intoxication

172
Q

Describe behaviour in early stages of intoxication

A

Dependent on individual’s personality and environment - in social situation will be happy/excited, solitary drinking can lead to to feelings of depression and social isolation

173
Q

Describe the effects of advancing intoxication

A

Speech slurred
Unsteadiness and drowsiness
Autonomic effects e.g. flushing of skin, dilation of pupils, tachycardia
Reasoning and judgement impaired
Perception reduced
Increasingly distractible
Reduced motor and intellectual performance conflicting with feelings of enhanced ability
Loss of emotional restraint - excessively/inappropriately jocular, aggressive and occasionally paranoid/self-pitying
More severe intoxication - increasing drowsiness and coma, depressed tendon reflexes, hypotension and hypothermia, respiration shallow and stertorous (gasping)
Death may result from respiratory depression or following inhalation of vomitus

174
Q

What are the acute physical effects of alcohol misuse?

A 
Accidents and injury
Acute alcohol poisoning
Aspiration pneumonia
Oesophagitis
Mallory-Weiss syndrome
Gastritis
Pancreatitis 
Cardiac arrhythmias
Cerebrovascular accidents
Neuropraxia
Myopathy/rhabdomyolysis
Hypoglycaemia
175
Q

List the systemic effects of chronic alcohol excess

A 
Oesophagitis
Gastritis
Malabsorption
Malnutrition
Pancreatitis
Liver damage - fatty change, hepatitis, cirrhosis
Systemic hypertension
Cardiomyopathy
Coronary heart disease
Cerebrovascular accidents
Brain damage - dementia, Wernicke-Korsakoff syndrome, cerebellar atrophy, Marchiafava-Bignami syndrome, central pontine myelinosis
Peripheral neuropathy
Myopathy
Osteoporosis
Skin disorders
Sexual dysfunction
Infertility
Foetal damage
176
Q

How does alcohol cause systemic disease?

A

Negative effects caused by alcohol, its metabolites or the consequences of alcohol metabolism - gut-derived endotoxins, oxidative stress and immune response

177
Q

List external signs of alcohol misuse

A

Spider naevi - only found in distribution of superior vena cava, most common on face and anterior chest wall, large central arteriole, vessels radiate
Telangiectasia - broken veins, commonly on face
Facial mooning - rounded or moon-shaped face, puffy eyelids
Parotid/submandibular hypertrophy - contributes to roundness of face
Palmar erythema
Dupuytren’s contracture - fibrous change in the palmar fascia which inserts into the flexor tendons on the palm of the hand, ring finger most commonly affected
Gynaecomastia - enlargement of the breast tissue in men, bilaterally or unilaterally

178
Q

What are the effects of chronic alcohol consumption on the oesophagus?

A

Ingestion of large amounts of alcohol in short period of time = vomiting, development of a Mallory-Weiss tear in the mucosa of the cardio-oesophageal junction, resultant often profuse GI bleeding

Reduces the upper and lower oesophageal sphincter pressure and impedes oesophageal peristalsis - may lead to development of gastroesophageal reflux - oesophagitis, distal mucosal ulceration - Barrett’s oesoophagus (pre-malignant) - carcinoma of the oesophagus, especially in heavy smokers

179
Q

What are the effects of chronic alcohol consumption on the stomach?

A

Acute gastritis - nausea, vomiting, epigastric pain, symptoms settle after 48-72 hours abstinence
Habitual drinking - chronic gastritis, asymptomatic or non-specific digestive symptoms
Not associated with increased prevalence of peptic ulceration, tend to have lower prevalence of H. Pylori infection

180
Q

What are the effects of chronic alcohol consumption on the small intestine?

A

Acute or chronic - diarrhoea, changes in SI permeability and motor activity
Habitual use - defective absorption of glucose, amino acids, vitamins and minerals - little clinical consequence

181
Q

What structural changes occur in the pancreas following chronic alcohol exposure?

A

Inflammation, acinar atrophy, fibrosis - significant exocrine and endocrine insufficiency

182
Q

What group are particularly affected by pancreatitis following chronic alcohol exposure?

A

30-50 year old men

183
Q

Describe the acute presentation of alcohol induced pancreatitis

A

Abdominal pain
Nausea/vomiting
Profound metabolic abnormalities
Circulatory collapse

184
Q

List the complications of acute pancreatitis due to chronic alcohol exposure

A

Obstruction of bile duct, localised leakage of pancreatic fluid, pancreatic exocrine and endocrine insufficiency - jaundice, pseudocystic formation, malabsorption and diabetes

185
Q

How is pancreatitis due to chronic alcohol dependency diagnosed?

A

History of alcohol misuse, suggestive clinical features, imaging to determine pancreatic structure and assessments of pancreatic endocrine/exocrine function
X-Ray may show calcification
CT/MRI may show calcification and gland distortion
ERCP identify the typical irregular and attenuated ductal system

186
Q

What electrophysiological effects does alcohol have on the cardiovascular system?

A

Acute ingestion associated with depression of LV function, development of ventricular premature beats
More significant cardiac arrhythmias e.g. atrial fibrillation with more significant quantities
Worse if pre-existing heart disease

187
Q

What effect does chronic excessive alcohol consumption have on blood pressure?

A

Increased systolic and diastolic BP

188
Q

What effect does chronic excessive alcohol consumption have on heart muscle?

A

Alcoholic cardiomyopathy occurs in those consuming >60g daily for 10 years
May be asymptomatic, may present with non-specific e.g. fatigue, palpitations, breathlessness or frank heart failure e.g. arrhythmias, raised central venous pressure, cardiomegaly, pulmonary and/or peripheral oedema

189
Q

What is the treatment for alcoholic cardiomyopathy?

A

Abstinence from alcohol, diuretics, anti-arrhythmic agents

190
Q

Describe the relationship between alcohol consumption and coronary heart disease

A

Daily alcohol intakes of 1-3 units protect middle-aged men from coronary heart disease, 1-2 may protect post-menopausal women - increased HDL, decreased LDL, prevention of clot formation, reduction in platelet aggregation, lowering of plasma adipolipoproteins - inhibits atheroma formation and blood coagulation

191
Q

Describe the relationship between alcohol consumption and cerebrovascular disease

A

Acute and chronic use increase the risk of stroke - acute of all stokes, chronic of haemorrhagic strokes specifically
Also risk of subarachnoid haemorrhage
Increased risk of head injuries - subdural and extradural haematoma risk

192
Q

How does alcohol damage the nervous system?

A

Central and peripheral, direct or indirect as result of thiamine deficiency

193
Q

List the disorders of the nervous system caused by chronic alcohol dependence

A 
Alcohol related dementia
Wernicke-Korsakoff's syndrome
Cerebellar atrophy
Marchiafava-Bignami syndrome
Central pontine myelinosis
194
Q

Describe alcohol related dementia

A

Specific cognitive deficits and mild non-progressive impairment of intellectual capacity
Cortical atrophy, reduction in volume of cerebral white matter
Reversible to a variable degree with prolonged abstinence

195
Q

Describe the clinical features of Wernicke’s encephalopathy

A

Acute neuropsychiatric condition characterised by global confusion, eye signs and ataxia (trunk and lower limbs), apathy, disorientation, disturbed memory
Eye signs - nystagmus, gaze palsies, ophthalmoplegia

196
Q

Describe the clinical features of Korsakoff’s psychosis

A

Amnesic state, profound impairment of retrograde and anterograde memory, relative preservation of other intellectual abilities in a setting of clear consciousness, sometimes confabulation (unconsciously lying to fill gap in memory)

197
Q

Describe the usual natural progression of Wernicke-Korsakoff’s syndrome?

A

Korsakoff’s psychosis usually develops after an acute episode of Wernicke’s encephalopathy, some patients develop a combined syndrome from the outset - memory loss, eye signs, unsteadiness, no confusion

198
Q

Describe the neuropathology of Wernicke-Korsakoff’s syndrome

A 
Neuronal loss in paraventricular and periaqueductal grey matter, thalamus (mediodorsal thalamic nucleus) and mammillary bodies, inferior colliculus in midbrain, vestibular nuclei and olivary complex in the brainstem
Mammillary bodies, mammillo-thalamic tract and anterior thalamus = memory loss
Cortical atrophy (frontal lobes) and cerebellar atrophy
199
Q

What is the treatment for Wernicke-Korsakoff’s syndrome?

A

High dose thiamine (Pabrinex), IV or IM - IM not suitable for patients with liver disease and associated defective blood clotting

Give thiamine prophylactically to all consuming alcohol at risk of developing Wernicke-Korsakoff’s syndrome

Wernicke’s encephalopathy resolves rapidly following treatment, Korsakoff’s psychosis less predictable

200
Q

Which areas of the brain are affected in cerebellar atrophy? What effect does this have on function?

A

Atrophy in anterior and superior vermis
Causes ataxia predominantly affecting trunk and lower limbs
Improves with prolonged abstinence, some degree of residual deficit common

201
Q

What is Marchiafava-Bignami syndrome?

A

Demyelination of corpus callosum
Rare
Presentation - dementia, spasticity, dysarthria, inability to walk
No treatment, may deteriorate very quickly, lapse into coma and die or survive severely demented, occasionally completely recover

202
Q

Describe central pontine myelinosis

A

Rare demyelinating disorder of cerebral white matter, often rapidly fatal
Progressive quadriplegia, pseudobulbar palsy and paresis or paralysis of horizontal eye movements
Cause - electrolyte abnormalities?
Characteristic lesion in mid pons which crosses midline

203
Q

Describe peripheral neuropathies caused by chronic alcohol dependence

A

Focal peripheral nerve lesions common - compression when sleeping

Somatic and autonomic -
Symptoms - mainly sensory e.g. numbness, painful cramps, burning and hyperaesthesia in ‘glove and stocking’ distribution, motor e.g. distal weakness, muscle loss, diminished or absent tendon reflexes

Autonomic - postural hypotention, changes in GI transit time, erectile dysfunction

204
Q

How are alcohol induced peripheral neuropathies treated?

A

Improvements with abstinence, thiamine supplementation, muscle cramps response to amitriptyline

205
Q

Describe myopathies associated with alcohol misuse

A

Acute myopathy - develops in association with acute intoxication
Rhambdomyolosis and myoglobinuria
Typical presentation - myalgia or muscle pain around hip and shoulders girdles, calves, muscle swelling, progressive weakness in legs
Symptoms resolve in days-weeks with abstinence

Chronic myopathy
Selective atrophy of type 2 fibres, progressive and usually painless wasting and weakness of proximal limb muscles - difficulty climbing stairs, lifting arms
Associated with frequent falls and osteopenia
Abstinence - improves in 2-12 months

206
Q

What effect does chronic alcohol misuse have on bone?

A

Increased risk of osteoporosis and osteoporotic fractures - direct effect of alcohol on bone remodelling and mineralisation as well as nutritional deficiencies and smoking etc.
Abstinence can reverse to some extent, treated with Vitamin D, calcium, bisphosphonates

207
Q

What effect does chronic alcohol misuse have on skin?

A

Spider naevi, telangiectasia
Discoid eczema and acne rosacea
Precipitate development of psoriasis in genetically susceptible or exacerbate existing lesions
Seborrheic dermatitis and bacterial and fungal infections

208
Q

What is the relationship between chronic alcohol misuse and malignancies?

A

Causal link between alcohol and development of cancers of mouth, pharynx, larynx, oesophagus, colon and rectum and breast in women
Suspected association with pancreas, lung and kidney
Exacerbated by smoking

209
Q

How does chronic alcohol misuse contribute to development of malignancies?

A

Damaging effect of acetaldehyde on DNA
Production of reactive oxygen and nitrogen species
Reduction of immune surveillance
Increased oestrogen secretion - breast cancer

210
Q

What is the relationship between chronic alcohol misuse and sexual dysfunction/infertility?

A

Sexual function and reproduction affected in men and women
4-6 units per day can reduce sperm count, abstinence = restoration in fertility
Women - 3+ units per day may be sub-fertile (reversibility?)

211
Q

What is the effect of alcohol consumption in pregnancy?

A

Alcohol is teratoxitc and foetotoxic when consumed during pregnancy

Factor in spontaneous abortion in first and second trimesters - drinking 80-112g per week gives 4x risk of spontaneous abortion first trimester, 2x second trimester

If retain pregnancy but continue to drink, risk damaging foetus, other factors e.g. smoking and malnutrition may contribute, most vulnerable period is 4-10 weeks but may occur at any time, leads to foetal alcohol syndrome (first trimester - organ and craniofacial development, third trimester - growth)

212
Q

Define foetal alcohol syndrome

A

Broad spectrum of abnormalities which arise as a consequence of maternal drinking during pregnancy

213
Q

What is the advice given to pregnant women/women wishing to conceive on alcohol consumption?

A

Should avoid alcohol, especially in the first trimester

If they choose to drink it should be limited to 1-2 units once or twice per week and they should not get drunk

214
Q

Describe the aspects of foetal alcohol syndrome

A

Growth retardation
Mental and behavioural abnormalities - attention deficits, problems with impulse control, aggression and other features of executive function, hyperactivity, incoordination and neurophysical impairment

215
Q

List the CNS abnormalities associated with foetal alcohol syndrome

A 
Microcephaly
Agenesis of the corpus callosum 
Cerebellar hypoplasia
Mental retardation
Irritability
Hypotonia
Incoordination
Hyperactivity
216
Q

List the craniofacial abnormalities associated with foetal alcohol syndrome

A 
Short palpebral fissure
Epicanthic folds
Smooth philtrum
Thin upper lip
Mid-facial hypoplasia
Lower jaw hypoplasia
Short upturned nose
Minor ear abnormalities
Ptosis
Strabismus
217
Q

Which body systems are affected by foetal alcohol syndrome?

A 
Cardiovascular
Skeletal
Genitourinary 
Ocular
Auditory
CNS
218
Q

Describe the epidemiology of foetal alcohol syndrome

A

Most common cause of developmental disability and birth defects in the western world

219
Q

List the areas of investigation when taking a history for alcohol dependency

A

How much they currently drink (drinking diary may be useful?)

Previous heavy drinking?

Drinking habits of partner and family members

If binging - length of binge, time between binges, precipitating factors for binging

Evidence of physical dependence - early morning retching, tremor, anxiety, irritability, ingestion of alcohol before midday, amnesia and blackouts

Previous advice, counselling, treatments

Domestic, social, financial and employment history

Current psychological status - anxiety, panic, depression, suicidal, previous psychiatric illness

Repeat history is intoxicated or acutely unwell due to withdrawal

220
Q

What should be assessed when doing a physical examination for alcohol dependence?

A

Evidence of recent alcohol consumption - smell alcohol on breath, flushed with bloodshot eyes, excited/tremulous, intoxicated

Symptomatic of chronic alcohol use - spider naevia, cutaneous talengiectasia, palmar erythema, Dupuytren’s contracture, facial mooning, parotid enlargement, gynaecomastia, hepatomegaly

221
Q

What laboratory investigations should be done in suspected alcohol dependence?

A

AST/GGT, erythrocyte mean corpuscular volume (MSV) - not sensitive or specific enough to be used in isolation to diagnose alcohol dependence
Carbohydrate deficient transferrin (CDT)
Organ damage specific markers e.g. liver - hyperbilirubinaemia, hypoalbuminuria, prolonged prothrombin time, pancreas - hyperamylasaemia

222
Q

Give an example of screening questionnaires used to diagnose alcohol dependence

A

CAGE:
Have you ever felt that you ought to Cut down on your drinking?
Have people ever Annoyed you by asking about your drinking?
Have you ever felt bad or Guilty about your drinking?
Have you ever had a drink first thing in the morning (Eye-opener) to steady your nerves or get rid of a hangover?

Michigan alcohol screening test
Alcohol Use Dependency Identification Test

223
Q

How is hazardous drinking managed?

A

Alcohol brief intervention - advice in primary care

Empathetic, non-judgemental and understandable

224
Q

How is harmful drinking managed?

A

Self help groups e.g. Alcoholics Anonymous or local alcohol advice services
Community alcohol team, referred by primary physician
Severe dependence and co-morbid physical and psychiatric morbidity - referral for specialist consultant care, mostly as out-patients, in-patient for minority to allow controlled withdrawal and further assessment
Cognitive behavioural therapy
Pharmacotherapy

225
Q

What is the management goal of most alcoholics? Is this achieved in practice?

A

Most hope to regain controlled social drinking

Abstinence preferred in older, those who have exhibited serious physical dependency on alcohol, those with significant alcohol-related physical harm and those who have previously failed to modify their drinking behaviour or are in an environment where relapse seems likely

226
Q

List the barriers to change in alcohol dependence

A

Dependence- physical or psychological (physical needs to be carefully withdrawn)
Stress - many use alcohol to deal with difficult situations in life (manage with counselling and CBT, self-help manuals)
Environment - occupation, social life
Habit - identify dangerous times/situations to avoid
Used as self-medication to cope with psychiatric or physical illness
Influence of others - can be positive or negative (rehearse how to refuse drinks)
Sense of hopelessness/pessimism

227
Q

Describe the types of goals which should be set with an alcohol dependent patient

A

Specific, attainable, short-term, immediately rewarding

228
Q

Describe the use of cognitive behavioural therapy in alcohol dependence management

A

Solution focused relapse prevention therapy
Stress management and relaxation training
Counselling
Family/couples therapy

229
Q

Describe the use of pharmacotherapy in alcohol dependence management

A

Alcohol sensitising agent - disulfiram (Antabuse), inhibitor of hepatic ALDH
Opiate receptor antagonist - naltrexone
Functional glutamate antagonist Acamprosate (calcium acetylhomotaurinate) - just before withdrawing alcohol

230
Q

What effect does an alcohol sensitising agent have when alcohol is consumed?

A

Flushing reaction, nausea, vomiting, tachycardia, hypotension, dyspnoea, dizziness, headache, can have severe/fatal reaction

231
Q

Which groups have special needs when managing alcohol dependence?

A

Ethnic minority - stigma within community
Young people, particularly adolescents
Older problem drinkers - frailty, sleep problems, social isolation, depression, loss of mental acuity and mobility
Prison population - offered help on release to avoid relapse

232
Q

Describe withdrawal from alcohol

A

40% of those who misuse alcohol will develop an acute withdrawal syndrome when they abruptly stop or substantially reduce their alcohol intake

Minor symptoms complex or syndrome - generalised hyperactivity, anxiety, tremor, sweating, nausea, retching, tachycardia, hypertension, mild pyrexia

Symptoms peak between 1-30 hours and subside by 40-50 hours

Rare - fits, auditory and visual hallucinations

Delirium tremens

233
Q

Describe delirium tremens

A

Uncommon, 5%
Starts 48-72 hours after cessation - coarse tremor, agitation, fever, tachycardia, profound confusion, delusions and hallucinations
May have convulsions, hyperpyrexia, ketoacidosis and profound circulatory collapse

234
Q

When should alcohol dependent patients withdraw as in-patients?

A

Most can withdraw as outpatients, some best withdrawn in hospital - experience severe withdrawal in the past, history of fitting, significant co-morbidities or complex social needs

235
Q

How should moderate to severe withdrawal symptoms be managed?

A

Sedation - benzodiazepines and chlormethiazole

236
Q

Describe alcoholic dementia

A

Decline from previous level

Memory loss

At least one of:
Agnosia - cannot recognise familiar things
Aphasia - circumlocutions, cliches, circumstantiality
Apraxia - senses intact, understand what asked, physically able to do it but still can’t do it

Loss of executive functioning - poor planning and organisation of simple actions into more complicated sequences of action (like dressing), and very poor adaptability, ok in familiar place but cannot cope with change in circumstance on surroundings

237
Q

Describe the brain changes caused by chronic alcohol misuse

A

Shrinking of cortex, dilation of ventricles

Shrinkage of cerebellum

Volume returns to normal with abstinence

238
Q

How can Wernicke-Korsakoff’s syndrome occur in non-alcohol related cases?

A

Thiamine depletion alone - malnutrition, starvation

Usually show full recovery, less likely to progress from Wernicke’s encephalopathy to Korsakoff’s psychosis

239
Q

Which factors contribute to the development of cognitive impairment with alcohol misuse?

A 
Intoxication
Seizures
Alcohol neurotoxicity
Vitamine deficiency - particularly vitamin B1/thiamine
Hypoglycaemia
Head injury
Cerebrovascular accidents
Withdrawal delirium
Hepatic encephalopathy
Hypoxia
Non-alcohol related cerebral pathology in older people
240
Q

Describe the pathogenesis of hepatic encephalopathy

A

Hepatic function impaired, ammonia metabolism dysfunctional - high ammonia
Blood brain barrier more permeable to ammonia due to down-regulation of glutamate receptors and uptake - increase in astrocyte glutamine and osmotic stress

241
Q

List the differential diagnosis of hepatic encephalopathy

A

Metabolic encephalopathies - drugs/toxins
Intracranial structural disorders - infection
Seizures - Wernicke’s encephalopathy
Head injury

242
Q

Describe precipitating factors for hepatic encephalopathy

A

Increased protein load e.g. upper GI haemorrhage
Decreased excretion of ammonia e.g. renal failure
Others - electrolyte disturbance, dehydration, paracentesis, creation of portocaval shunts, infection, drugs e.g. sedatives, superimposed acute liver injury

243
Q

How is hepatic encephalopathy treated?

A

Lactulose and dietary measures to reduce nitrogen load, removal of precipitants, general supportive measures, reduction or closure of shunts

244
Q

How is hepatic encephalopathy diagnosed?

A

Various assessment tools e.g. West Haven criteria for grading mental state in hepatic encephalopathy

245
Q

How does the physiological response to alcohol change with age?

A

Decreased lean body mass and total body water increase BAC
Age-related decrease in gastric alcohol dehydrogenase
Liver oxidation decreases with age, increases BAC
Sensitivity of brain to alcohol increases with age

246
Q

Describe the prognosis of alcohol related brain damage

A

Poorer in sudden-onset than in insidious onset cases
Better with more global cognitive impairment than in purer amnestic syndrome (provided there is abstinence from alcohol)
Improved if abstinence from alcohol is maintained in milder cases

247
Q

Describe the rehabilitative aspect of management of alcohol related brain damage

A

Regular review in first year after diagnosis
Eventual placement determined by careful multidisciplinary assessment
If patient not capable of independent living then provisions of Mental Health Act, guardianship and Adults with Incapacity act can be used to ensure safety
Design of environment and use of memory rehabilitation techniques important

248
Q

Describe the cycle of change

A
  1. Precontemplation - doesn’t think they have a problem, at the back of their mind
  2. Contemplation - thinking about it
  3. Preparation - getting ready to do something
  4. Action - doing something
  5. Maintenance - keeping it going (» permanent change?)
  6. Relapse (» back to 1)
249
Q

What ideas contribute to readiness to change?

A

Importance - ‘I need to do this’

Self-efficacy/confidence - ‘I can do this’

250
Q

List the stages of an alcohol brief intervention

A

Stage 1 - Raising the issue of alcohol
Stage 2 - Screening and giving feedback
Stage 3 - Listening for readiness to change
Stage 4 - Selecting an approach

251
Q

Describe the approach which should be used to help patients in each stage of the change cycle

A

Precontemplation - information and advice
Contemplation - understanding and motivation
Preparation - menu of choices
Action - build confidence
Maintenance - coping strategies

252
Q

List the sections of the MMSE

A 
Orientation to time
Orientation to place
Registration - 3 words
Attention and calculation (serial 7s, spell world forwards and backwards)
Recall 
Naming
Repetition 
Comprehension
Reading
Writing
Drawing
Assessment of level of consciousness
253
Q

How is the MMSE scored?

A

Out of maximum 30
Score greater than or equal to 24 indicates normal cognition
Mild cognitive impairment - 19-23
Moderate cognitive impairment - 10-18
Severe cognitive impairment - less than 9

254
Q

How is the MMSE used in diagnosis of dementia?

A

Impaired cognition as indicated by score below 24 is not necessarily indicative of dementia - used as screening tool

Score may be effected by sensory or motor impairment, anxiety/stress

Medicine Year 2 (41 decks)

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