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module 104 - theme 2 > alcohol symposium > Flashcards

alcohol symposium Flashcards

1
Q

what intake of alcohol counts as low risk?

A

less than 14 units a week over 3 or more days

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2
Q

what intake of alcohol counts as increased risk?

A
  • men 14 - 50 units

- women 14 - 35 units

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3
Q

what intake of alcohol counts as higher risk?

A
  • men over 50 units a week

- women over 35 units a week

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4
Q

in Brighton and Hove how many adults drink over 14 units of alcohol a week?

A

2 in 5 people

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5
Q

nationally how many adults drink over 14 units of alcohol a week?

A

1 in 5

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6
Q

what factors are associated with having a drink in the last week?

A
  • parents don’t discourage drinking
  • older pupils
  • recent drug use
  • drinkers at home
  • smoking
  • white ethnicity
  • playing truant
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7
Q

what percentage of adults don’t drink at all?

A

20%

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8
Q

globally how many deaths a year does alcohol misuse contribute to?

A

2.5 million deaths

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9
Q

what fraction of domestic violence is due to alcohol?

A

1/3

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10
Q

how many people are killed in road traffic accidents due to alcohol?

A

1 in 7

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11
Q

how many calls to Childline are related to parent’s alcohol consumption?

A

1/5

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12
Q

what factors influence alcohol consumption?

A
  • individual factors (age, gender, health…)
  • family
  • culture and community
  • socioeconomics
  • religion
  • country and laws
  • taxes
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13
Q

how do we estimate alcohol consumption?

A
  • reported consumption (surveys)

- taxation data from HMRC

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14
Q

what fraction of the UK population drink about hazardous levels?

A

1/3

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15
Q

what policies limit consumption of alcohol to reduce harm?

A
  • taxation: limit affordability and raise revenue

- regulation and legislation: alcohol promotion and marketing, price and drink driving

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16
Q

how much ethanol is lost through breath/urine?

A

10%

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17
Q

what happens to the rest of ethanol that isn’t lost via breath/urine?

A

it is metabolised

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18
Q

what enzyme breaks down alcohol?

A

alcohol dehydrogenase

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19
Q

what effect does alcohol and aldehyde dehydrogenase have on the redox state?

A
  • they both reduce NAD to NADH
  • they increase lactate:pyruvate ratio and the beta-hydroxybutyrate:acetoacetate ratio
  • they inhibit: glycolysis, citric acid cycle, fatty acid oxidation, gluconeogenesis
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20
Q

what toxic and metabolic effects does alcohol have?

A
  • oxidant stress
  • lipid peroxidation which is associated with both acute tissue damage and fibrosis
  • free radicals attack cellular and mitochondrial DNA causing deletions and mutations
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21
Q

what are the stages of methanol metabolism?

A

1) methanol
2) formaldehyde
3) formic acid
4) CO2 + H20

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22
Q

how much pure alcohol is in one unit?

A

10mL or 8g

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23
Q

what is the legal limit of blood ethanol for driving?

A

<80mg/dL

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24
Q

what is the legal limits of alcohol for driving?

A
  • 2-3 units in females

- 3-4 units in men

25
Q

why shouldn’t pregnant women drink alcohol?

A

ethanol crosses the placenta and can seriously affect foetal development (foetal alcohol syndrome)

26
Q

when blood ethanol levels are 50-100mg/dL what are the symptoms of sporadic and chronic drinkers?

A
  • sporadic drinkers: euphoria, incoordination

- chronic drinkers: minimal or no effect

27
Q

when blood ethanol levels are 100-200mg/dL what are the symptoms of sporadic and chronic drinkers?

A
  • sporadic drinkers: slurred speech, ataxia, labile mood, drowsiness, nausea
  • chronic drinkers: sobriety, incoordination, euphoria
28
Q

when blood ethanol levels are 200-300mg/dL what are the symptoms of sporadic and chronic drinkers?

A
  • sporadic drinkers: lethargy, combativeness, stupor, incoherent, speech, vomiting
  • chronic drinkers: mild emotional and motor changes
29
Q

when blood ethanol levels are 300-400mg/dL what are the symptoms of sporadic and chronic drinkers?

A
  • sporadic drinkers: coma

- chronic drinkers: drowsiness

30
Q

when blood ethanol levels are >500mg/dL what are the symptoms of sporadic and chronic drinkers?

A
  • sporadic drinkers: respiratory depression, death

- chronic drinkers: lethargy, stupor, coma

31
Q

what is alcoholic ketoacidosis?

A

metabolic acidosis with and increased anion gap that typically occurs in chronic alcoholics who binge with little nutritional intake

32
Q

what is the pathophysiology of alcoholic ketoacidosis?

A
  • glycogen depletion/inhibited gluconeogenesis
  • lipolysis ad ketones increases
  • insulin suppressed
  • extracellular volume depletion/dehydration/stress-increase counter regulatory hormones further supressing insulin
33
Q

how does ethanol cause hypoglycaemia?

A
  • decreased intake of glucose
  • depletion of glycogen
  • blockade of gluconeogenesis
34
Q

how do you treat hypoglycaemia?

A
  • prompt treatment with glucose

- need to give parental thiamine as well as to prevent CNS damage in case there is also thiamine deficiency

35
Q

what are the endocrine effects of alcohol?

A
  • decreased testosterone
  • Pseudo Cushings
  • metabolic syndrome and dyslipidaemia
36
Q

what are the general nutritional issues of alcohol?

A
  • low calciun
  • low phosphate
  • low Mg, K
37
Q

what are the typical liver function tests?

A
  • gamma glutamyl transferase (GGT) increased by liver enzyme induction
  • transaminases increased by hepatocellular damage
  • globulin increased cirrhosis
  • bilirubin and INR increased and albumin decreased by liver failure
38
Q

what are the causes of thiamine deficiency?

A
  • ethanol interferes with GI absorption
  • hepatic dysfunction which hinders storage and activation
  • malnourishment
39
Q

what are relevant blood tests related to alcohol?

A
  • macrocytosis: raised MCV in full blood count
  • raised serum ferritin concentration
  • hyperuricaemia
  • hypertriglyceridaemia
  • increased carbohydrate-deficient transferring or CDT
40
Q

what are the possible mechanisms linking alcohol and hypertension?

A
  • impairment of the baroreceptors
  • increase of sympathetic activity
  • stimulation of the renin-angiotensin-aldosterone system
  • increase in plasma cortisol
  • increase of intracellular calcium with subsequent increase in vascular reactivity
  • endothelial
41
Q

on a liver biopsy what are the signs of increased risk of progression?

A
  • microvesicular fatty change
  • extend of fibrosis
  • amount of MD bodies
  • intrahepatic cholestasis
42
Q

what is shown with steatohepatitis?

A
  • ballooning of hepatocytes
  • inflammation: neutrophils
  • necrosis of hepatocytes
  • Mallory Denk bodies
43
Q

what are the fibrosis/cirrhosis mechanisms?

A
  • inflammation and necrosis cause increase in cytokines and growth factors that activate fibroblasts/myofibroblasts to deposit collagen
  • centrilobular fibrosis - reversible
  • septal fibrosis - increasingly irreversible
44
Q

what are the portal hypertension consequences?

A
  • impaired intestinal function and malabsorption
  • splenomegaly with anaemia and thrombocytopenia
  • portal bypass circulations: haemorrhoids, caput medusae, oesophageal veins
  • vasodilation and compensatory increase in cardiac output
  • toxic metabolised bypass the liver and may cause portosystemic encephalopathy
45
Q

what are the symptoms of withdrawal?

A
  • tremor/shaking
  • sweating
  • tachycardia
  • nausea
  • agitation
  • seizures
  • visual hallu
46
Q

how do you manage alcohol withdrawal?

A
  • chlordiazepoxide

- diazepam

47
Q

what are the potential hazards with managing alcohol withdrawal?

A
  • severe liver disease: precipitation of hepatic encephalopathy
  • respiratory depression
  • reluctance to prescribe more
  • concomitant alcohol consumption
48
Q

what are the core features of delirium?

A
  • disturbance of consciousness
  • change in condition or a perceptual disturbance
  • tendency to fluctuate
  • behaviour overactive or under active
  • other features: disorganised thinking, poor memory, delusions and moof liability
49
Q

what are the other causes of delirium?

A
  • any infection
  • drug side effect
  • hypoxia
  • drug overdose
  • alcohol intoxication
  • Wenicke encephalopathy
  • hypoglycaemia
  • meningitis/encephalitis
  • psychiatric illness
  • head injury
  • constipation
  • hepatic encephalopathy
50
Q

what are the dietary sources of thiamine?

A
  • wheat
  • yeast
  • nuts
  • oatmeal
  • potatoes
  • pork
  • marmite
51
Q

what does the thiamine coenzyme do?

A
  • glucose and lipid metabolism
  • production of amino acids
  • production of glucose derived neurotransmitters
52
Q

what are the causes of thiamine deficiency?

A
  • alcoholism
  • chronic vomiting
  • famine
53
Q

what is the classic triad of Wernicke’s encephalopathy?

A
  • confusion
  • eye signs (ophthalmoplegia and nystagmus)
  • ataxia
54
Q

what is Korsakoff’s psychosis?

A
  • permanent brain damage
  • severe short term memory loss
  • confabulation
55
Q

what happens with Wernicke-Korsakoff syndrome?

A

any available thiamine in brain is utilised in the metabolism of glucose leading to sudden complete deficiency

56
Q

how do you treat Wernicke-Korsakoff syndrome?

A
  • always check glucose levels first
  • give parental thiamine before dextrose or nutrition
  • give pabrinex (thiamine 250mg and others)
57
Q

what are the 4 categories for the reasons people drink?

A

1) enhancement: to feel better, to do things otherwise impossible
2) social: to be sociable, to celebrate at parties
3) conformity: because others do, to fit in
4) coping: because it helps you forget about your problems

58
Q

why do people not drink?

A
  • short term harm
  • long term harm
  • hangovers
  • aldehyde dehydrogenase 2 deficiency
  • religion/culture
59
Q

what are the 3 things people must have to adhere to guidelines?

A

1) information
2) motivation
3) behavioural skills

module 104 - theme 2 (18 decks)

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