alcohol and liver disease Flashcards

1
Q

hazardous vs harmful drinking

A

hazardous - drinking more than the recommended weekly allowance or in a risky manor
harmful - hazardous drinking with health/social problems directly related to alcohol

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2
Q

what is dependent drinking

A

when a pt feels that they cannot function without drink

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3
Q

signs of dependent drinking (5)

A
  1. alcohol tolerance
  2. withdrawal symptoms
  3. unsuccessful attempts to cut drinking
  4. loss of social/occupational pursuits
  5. use despite knowledge of harm
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4
Q

what is the major breakdown pathway for low levels of alcohol

A

ethanol –(alcohol dehydrogenase)–> acetaldehyde –(aldehyde dhydrogenase)–> acetate

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5
Q

what is the major breakdown pathway for high serum levels of alcohol

A

microsomal ethanol oxidising system:
ethanol –(cytochrome P450 2E1)–> acetaldehyde –(aldehyde dehydrogenase)–> acetate

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6
Q

what is a by product of the microsomal ethanol oxidising system that can cause harm to the liver

A

ROS

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7
Q

what cells does the microsomal ethanol oxidising system take place in

A

hepatocytes and Kupfer cells (after chronic exposure)

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8
Q

can people be genetically susceptible to alcholism/ALD

A

yes - defects in main alcohol metabolising receptors (e.g. CYPE2, alcohol dehydrogenase etc.) can lead to greater susceptibilty

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9
Q

risk factors for alcohol liver disease

A
  1. gender - being female increases risk)
  2. genetic variability
  3. nutrition
  4. hepatitis virus
  5. co-exposure to drugs/toxins
  6. immunological derangement - MCH1/ DR2 antigens
  7. development of antibodies to neo-antigens
  8. haematochomatosis/alpha anti-tripsin 1
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10
Q

why are women at a higher risk of alcohol liver disease (2)

A
  1. lower levels of mucosal alcohol dehydrogenase
  2. oestrogen levels correlate to liver damage
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11
Q

why do alcohol withdrawal symptoms happen (biochem)

A

alcohol enhances the effect of GABA on GABA-A neuroreceptors, resulting in decreased overall brain excitability -> Chronic exposure to alcohol results in a compensatory decrease of GABA-A neuroreceptor response to GABA (evidenced by increasing tolerance of the effects of alcohol) -> Abrupt cessation of alcohol exposure results in brain hyperexcitability, because receptors previously inhibited by alcohol are no longer inhibited -> Brain hyperexcitability manifests clinically as anxiety, irritability, agitation, and tremors

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12
Q

alcohol withrawal timeline stages (3)

A
  1. anxiety, insomnia, nausea, abdominal pain (first 8hrs)
  2. high blood pressure, increased body temp (1-3 days)
  3. hallucinations, fever, seizures, agitation (1 wk)
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13
Q

what nutrition deficiencies are associated w alcoholic liver disease

A
  1. B complex vitamin deficiencies
  2. vitamin A, D deficiencies
  3. vit C deficiency
  4. micronutrients (Se, Zn)
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14
Q

is alcoholic liver disease treateble

A

yes - it is reversible with abstinence

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15
Q

what other factors are essential for treating alcoholic liver disease other than abstience

A
  1. good nutritional support
  2. good psychological support/drugs support
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