Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

104-theme 2-the liver and regulation of metabolism > alcohol symposium > Flashcards

alcohol symposium Flashcards

1
Q

what is the CMO guidance for alcohol consumption? 3

A
  • low risk: less than 14 units a week, spread over 3 or more days
  • Increased risk: men 14-50 units a week, women 14-35 units a week
  • High risk: men over 50 units a week, women over 35 units a week, risk or alcohol related problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the proportions of people who drink in Brighton and Hove? 2

A
  • 1/5 adults drink over 14 units of alcohol nationally

- 2/5 in Brighton and Hove

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what factors are associated with children having a drink in the last week? 7

A
  • Parents don’t discourage drinking
  • Older pupils
  • Recent drug use
  • Drinkers at home
  • Smoking
  • White ethnicity
  • Playing truant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe the statistics for children in Brighton and Hove? 5

A
  • 73% of 15 year olds in the UK have drunk alcohol
  • 15% of 11 year olds
  • 11% of 15 years olds in Brighton and Hove drink regularly

-24% of 15-year-olds in Brighton and Hove have tried cannabis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe the statistics around death with alcohol? 6

A
  • Alcohol misuse is the biggest factor for early death in England in adults under 50
  • It can lead to cardiovascular disease, liver disease and more
  • Globally there are 2.5 million deaths a year, 5.1% of the global burden of disease and injury is attributable to alcohol
  • 1/3 cases of domestic violence are alcohol related
  • 1/7 RTA are due to alcohol
  • 1/5 of all calls to ChildLine are related to parents’ alcohol consumption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

who can influence alcohol consumption? 7

A
  • Individual factors
  • Family
  • Culture and community
  • Socioeconomics
  • Religion
  • Country/laws
  • Taxes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

name some policies to limit consumption and reduce harm? 2

A
  • Taxation to limit affordability and raise revenue

- Regulation and legislation- alcohol promotion and marketing, price, drink driving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe minimum unit pricing? 4

A
  • 50p minimum price per unit
  • Increases the price of cheap high alcohol drinks
  • Reduces harm
  • Not a tax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe sensible on strength? 7

A
  • Licensed businesses voluntarily stop selling super strength beer, lager and cider about 6% refusals systems, CCTV, documented training
  • Tackle anti-social behaviours
  • Improve health for vulnerable drinkers
  • Identify problem areas in the city
  • Reduces crime and disorder
  • Reduced intimidation and violence to staff
  • Not an anti-alcohol scheme
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe views on drinking with different cultures? 2

A
  • In wet drinking cultures, there is integration of alcohol into daily life, as a consumer commodity like any other
  • In dry drinking cultures, alcohol is marginalised as an especially powerful and hazardous commodity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

why do people drink? 4

A
  • Various reasons
  • Enhancement- to feel better, to do things otherwise impossible
  • Social- to be sociable, to celebrate parties
  • Conformity- because other do, to fit in coping- because it helps you forget about problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why don’t some people drink? 5

A
  • Short term harm= alcohol poisoning, accidents and injury, violence, antisocial behaviours
  • Long term harm= cirrhosis, cancers, stroke, premature death and suicide
  • Hangovers
  • Aldehyde dehydrogenase 2 (ALDH-2) deficiency
  • Religion/ culture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

can we change how people drink? 2

A
  • Efforts must focus on motives for drinking and not drinking
  • Messages may be gained-framed or loss-framed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what do people need to adhere to guidelines? 3

A
  • Information= be exposed to and understand the guidelines
  • Motivation= consider the guidelines to be meaningful/ relevant
  • Behavioural skills= know how to apply the guidelines to own behaviour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe awareness/ screening/ brief intervention? 5

A
  • People tend to have poor knowledge and lack the requisite skills
  • Personalised feedback on drink pouring:
  • Improved knowledge
  • Enhances behavioural skills
  • Reduces alcohol intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe the outcomes of dry January? 3

A
  • Abstinence challenges allows people to perform behavioural experiments, boot motivation and enhance behavioural skills
  • Benefits of not drinking- majority report better sleep, concentration, saving money and a minority report weight loss
  • Enduring effects- 40% drink less 6 months later and have a greater sense of control over drinking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

why is a psychosocial approach required? 5

A
  • Qualitative studies show the importance of social context and social factors
  • Interventions and attempts to motivate people must acknowledge this
  • Concerns about health
  • Concerns about fitting in
  • Concerns about reputation, image, weight
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is alcohol dehydrogenase polymorphism? 2

A
  • Several isoforms of this enzyme are present, with variable activity in individuals depending on genetic makeup and other factors
  • Individuals of Asian descent who have the B2 ADH isoform, metabolise ethanol 20% faster than northern Europeans who possess the B1 ADH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe the effect of alcohol dehydrogenase polymorphism on the redox state? 3

A
  • Both alcohol dehydrogenase and aldehyde dehydrogenase reactions reduce NAD to NADH
  • Increases= lactate: pyruvate ratio, beta-hydroxybutyrate: acetoacetate ratio
  • Inhibits: glycolysis, citric acid cycle (ketogenesis), fatty acid production, gluconeogenesis
20
Q

describe the toxic and metabolic effects of alcohol dehydrogenase polymorphism? 2

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

describe methanol metabolism? 7

A 
- methanol 
\+alcohol dehydrogensase
-formaldehyde
\+aldehyde dehydrogenase
- formic acid 
\+ folate
- Co2 + H2O
22
Q

describe ethylene glycol (antifreeze) poisoning? 8

A 
- ethylkene glycol
\+alcohol dehydrogenase
- glycoaldehyde 
\+ aldehyde dehydrogenase
- glycolic acid
\+lactate dehydrogenase and glycolic acid oxidase
- glyoxylic acid
- glycine, oxalate acid, formic acid, alpha-hydroxy-beta-ketoadipate
23
Q

what is one unit of alcohol?

A

10ml or 8g of pure alcohol

24
Q

describe ethanol and driving? 5

A
  • Legal limit for driving in the UK is blood ethanol <80mg/dl
  • <2-3 units in females
  • <3-4 units in men
  • Drinking any alcohol can still be too much if you are going to drive, operate machinery, swim or do strenuous physical activity
  • Pregnant women or women trying to conceive should not drink alcohol as ethanol crosses the placenta and alcohol can seriously affect foetal development (foetal alcohol syndrome)
25
Q

what is alcoholic ketoacidosis? 6

A
  • Metabolic acidosis with increased anion gap
  • Typically occurs in chronic alcoholics who binge with little nutrition intake:Pathophysiology:
  • glycogen depletion/ inhibited gluconeogenesis
  • lipolysis and ketones increased (beta hydroxybutyrate)
  • insulin suppressed
  • extracellular volumes depletion/ dehydration/ stress- increase counter regulatory hormones further supressing insulin
26
Q

describe hypoglycaemia? 6

A
  • ethanol causes hypoglycaemia through:
  • decreased intake of glucose (CHO)
  • depletion of glycogen
  • blockade of gluconeogenesis
  • .
  • Prompt treatment with glucose is lifesaving
  • Need to give parenteral thiamine as well to prevent CNS damage in case there is also thiamine deficiency
27
Q

name some typical liver function tests? 4

A
  • Gamma glutamyl transferase (GGT) increased by liver enzyme function
  • Transaminases (ALT and AST) increased by hepatocellular damage
  • Globulin increased in cirrhosis
  • Bilirubin and INR increased, and albumin decreased by liver failure
28
Q

what can cause a thiamine deficiency? 3

A
  • Ethanol interferes with Gi absorption
  • Hepatic dysfunction, which hinders storage and activation
  • Malnourishment
29
Q

name some other relevant blood tests for alcohol related issues? 5

A
  • Macrocytosis- raised MCV in a full blood count
  • Raised serum ferritin concentration
  • Hyperuricaemia
  • Hypertriglyceridemia
  • Increased carbohydrate-deficient transferrin of CDT
30
Q

describe alcohol and hypertension? 6

A
  • Impairment of the baroreceptors (which sense blood pressure)
  • Increase of sympathetic activity
  • Stimulation of the renin-angiotensin-aldosterone system
  • An increase in plasma control
  • An increase of intracellular calcium with subsequent increase in vascular reactivity
  • Endothelial (inhibition of endothelium-dependent nitric oxide production
31
Q

why do we do liver biopsies? 9

A
  • To make a diagnosis
  • Stage and grade the disease
  • To monitor treatment
  • To inform prognosis
  • Increased risk of progression
  • Micro vesicular fatty change
  • Extend of fibrosis
  • Amount of MD bodies
  • Intrahepatic cholestasis
32
Q

describe the symptoms of alcoholic liver disease? 12

A
  • Steatosis.
  • Macrovesicular
  • Microvesicular
  • .
  • Steatohepatitis;
  • Ballooning of hepatocytes
  • Inflammation of neutrophils
  • Necrosis of hepatocytes
  • Mallory denk bodies
  • .
  • Fibrosis/ cirrhosis
  • Inflammation and necrosis cause an increase in cytokines and growth factors (TGF-beta, MCP-1) that activate fibroblasts/ myofibroblasts to deposit collagen (disse’s space)
  • Cellular fibrosis- reversible
  • Septal fibrosis- increasingly irreversible
33
Q

portal hypertension consequences? 8

A
  • Impaired intestinal function and malabsorption
  • Splenomegaly with anaemia and thrombocytopaenia
  • Portal bypass circulations:
  • Haemorrhoids
  • Caput medusae
  • Oesophageal veins
  • .
  • Vasodilation and compensatory increase in cardiac output
  • Toxic metabolites (NH3, fatty acids, biogenic amines) bypass the liver and may cause portosystemic (hepatic) encephalopathy
34
Q

describe alcohol withdrawal? 3

A
  • Physiological dependence
  • The need to drink to avoid unpleasant symptoms- relief drinking
  • Delirium tremens
35
Q

what are the symptoms of alcohol withdrawal? 7

A
  • Tremor/shaki
  • Sweating
  • Tachycardia
  • Nausea
  • Agitation
  • Seizures
  • Visual hallu
36
Q

describe planned and unplanned alcohol withdrawal? 4

A

Planned:

  • In community
  • In hospital/ detox facility

Unplanned:

  • Known alcohol problems and another medical problem
  • Alcohol history not known in patient presenting with a separate problem
37
Q

describe alcohol withdrawal managements? 2

describe the potential hazards of management? 4

A
  • Chlordiazepoxide- used at RSCH and PRH
  • Diazepam

Potential hazards of management:

  • Severe liver disease- precipitation of hepatic encephalopathy
  • Respiratory depression
  • Reluctance to prescribe more
  • Concomitant alcohol consumption
38
Q

what is delirium? 8

A
  • Disturbances of consciousness
  • Change in cognition or a perceptual disturbance (hallucination)
  • Tendency to fluctuate
  • Behaviour overactive or underactive
  • Disorganised thinking
  • Poor memory
  • Delusions
  • Mood lability
39
Q

name some other causes of delirium? 12

A
  • Any infection
  • Drug side effect
  • Hypoxia
  • Drug overdose
  • Alcohol intoxication
  • Wernicke encephalopathy
  • Hypoglycaemia
  • Meningitis/ encephalitis
  • Psychiatric illness
  • Head injury
  • Constipation
  • Hepatic encephalopathy
40
Q

describe Wernicke’s encephalopathy? 2

A
  • Brain damaged: multiple small haemorrhages especially in upper brainstem, hypothalamus and thalamus, mamillary bodies
  • 20% mortality if untreated
41
Q

describe Korsakoff’s psychosis? 3

A
  • Permanent brain damage
  • Sever short term memory loss
  • Confabulation
42
Q

what is the importance of thiamine?

A
  • Confusion
  • Eye signs
  • Ataxia
  • Only seen in 10% of cases
  • Underdiagnosed
43
Q

describe Wernicke-Korsakoff syndrome? 4

A
  • Can be precipitated and rapidly worsened with introduction of nutrition or administration of IV 5% dextrose
  • Any available thiamine in the brain is utilised in the metabolism of glucose leading to sudden complete deficiency
  • Give parenteral thiamine before dextrose of nutrition
  • Always check glucose level first
44
Q

what is the treatment for Wernicke-Korsakoff syndrome? 4

A
  • PABRINEX= thiamine 250mg and others
  • Give IV for 25 days depending on response
  • Rarely causes anaphylaxis
  • Continue oral thiamine and other vitamins after initial treatment
45
Q

describe thiamine? 3
coenzyme? 3
causes of deficiency? 3

A
  • Vitamin B1
  • Wheat, yeast, nuts, oatmeal, potatoes, pork, marmite
  • Deficiency starts a month after a thiamine free diet

Co-enzyme:

  • Glucose and lipid metabolism
  • Production of amino acids
  • Production of glucose derived neurotransmitters

Causes of thiamine deficiency:

  • Alcoholism is the commonest cause
  • Chronic vomiting
  • famine

104-theme 2-the liver and regulation of metabolism (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions