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X Understanding Disease > Alcohol Metabolism and Alcohol-Induced Liver Disease > Flashcards

Alcohol Metabolism and Alcohol-Induced Liver Disease Flashcards

1
Q

how is ethanol usually metabolised?

A

Ethanol (alcohol dehydrogenase) -> Acetaldehyde
NAD+ -> NADH

Acetaldehyde (aldehyde dehydrogenase) -> Acetate
NAD+ -> NADH

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2
Q

what happens to acetate after metabolism?

A

doesn’t stay in the blood - fuel, especially in heart & skeletal muscle

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3
Q

what is the outline of glucose metabolism in the liver?

A

Glucose -> pyruvate -> acetyl CoA

  • > fatty acids
  • > TCA cycle -> Co2 and water
glycolsis = glucose -> Co2 and water
gluconeogenesis = Co2 and water -> glucose
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4
Q

what is the outline of liver fatty acid catabolism?

A

Fatty acid release from triacylglycerol
in adipose tissue -> Transport to liver -> Fatty acid oxidation (β-oxidation) -> Acetyl CoA -> TCA Cycle -> Carbon Dioxide + Water

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5
Q

what is the outline of liver fatty acid synthesis?

A

Acetyl CoA -> Fatty acid synthesis -> Triacylglycerol synthesis -> Release as part of VLDL

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6
Q

what are the consequences for metabolising a lot of ethanol?

A

NAD+ used up & NADH accumulates

Inhibition of all other reactions that use NAD+ as hydrogen atom/electron acceptor

Inhibition of pathways that contain these reactions

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7
Q

what pathways are affected by extensive ethanol metabolism?

A

TCA Cycle

β-Oxidation

Gluconeogenesis

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8
Q

what happens when β-Oxidation is inhibited?

A

Uses nad+ as electron acceptor – production of fatty acids slows down

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9
Q

what 3 mechanisms is blood glucose levels maintained by?

A

Diet

Breakdown of stored glucose (glycogen)

Gluconeogenesis

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10
Q

how is alcohol-induced hypoglycaemia caused?

A

Inhibition of gluconeogenesis – increases risk of being unable to maintain blood glucose concentration – risk of hypoglycaemia

Alcohol takes gluconeogenesis – diet and glycogen stand. If they don’t = alcohol-induced hypoglycaemia

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11
Q

who is at risk of alcohol-induced hypoglycaemia?

A

Alcohol abusers – chronic under nourishment

Those who exercise vigorously & fail to eat before consuming alcohol

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12
Q

if well-nourished, what is the fuel source?

A

glucose

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13
Q

if under-nourished, what is the fuel source?

A

fatty acids

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14
Q

what occurs in well-nourished fat metabolism?

A

Liver converts glucose to acetyl CoA as normal, but acetyl CoA then converted into fatty acids because TCA cycle inhibited

Fatty acids incorporated into triacylglycerol & exported into blood on VLDL -> hypertriacylglyerolaemia

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15
Q

what occurs in under-nourished/fasting fat metabolism?

A

Fatty acids arriving at liver unable to be used as fuel due to decrease in β-oxidation = incorporated into triacylglycerol instead

Excess triacylglycerol tends to accumulate in liver as under nutrition also problems with export mechanism

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16
Q

when does acetaldehyde toxicity occur?

A

if substantial ethanol concentration achieved or if aldehyde dehydrogenase activity low

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17
Q

what are the consequences of acetaldehyde toxicity?

A

Catecholamine release in heart rate & facial flushing
Reaction of acetaldehyde with proteins
dysfunction

18
Q

what does MEOS stand for?

A

Microsomal Ethanol Oxidising System

19
Q

what does MEOS do?

A

Oxidises ethanol to acetaldehyde

Can generate ROS

20
Q

what is MEOS induced by?

A

ethanol

21
Q

in what situations is MEOS Likely to Catalyse Oxidation of a Significant Amount of Alcohol?

A

Binge drinking – normal pathway saturated

Alcohol abusers – higher levels of MEOS because induced by ethanol

22
Q

what other enzymes are involved in ethanol metabolism?

A

Aldehyde Oxidase & Xanthine Oxidase

23
Q

what do Aldehyde Oxidase & Xanthine Oxidase do?

A

Oxidise acetaldehyde to acetate

Can generate ROS

24
Q

when are Aldehyde Oxidase & Xanthine Oxidase significant?

A

Only of significance in individuals with low aldehyde dehydrogenase activity

25
Q

what nutritional issues are there about carbohydrates?

A

ethanol metabolised less efficiently than carbohydrate

carbohydrate content highly variable, and most alcoholic drinks except beer very low in protein and vitamins

26
Q

what nutritional issues are there about iron content?

A

iron content can be high, especially in wine

27
Q

what nutritional issues are there about vitamins and calcium?

A

intakes of various vitamins and of calcium, iron and fibre tend to be low in alcoholics

28
Q

what nutritional issues are there about absorption transport?

A

absorption transport, storage and/or metabolism of vitamins and minerals can be altered, especially in alcohol-induced liver diease

29
Q

what digestive problems are associated?

A 
•	acute gastritis and duodenitis
•	diarrhoea
•	malabsorption
•	fibrosis of parotid glands  decrease in salivary flow*
•	lack of bile salts*
*seen in cirrhosis
30
Q

what are the stages of alcohol-induced liver disease?

A

Stage I Fatty liver
Stage II Steatohepatitis
Stage III Cirrhosis

31
Q

what is stage 1 alcohol-induced liver disease?

A

Characterised by fatty deposits - triacylglycerol form

32
Q

what is stage 2 alcohol-induced liver disease?

A

fatty liver and inflammation
characterised by disruption of liver architecture, swelling and death of liver cells and accumulation of lymphocytes and phagocytes

33
Q

what is stage 3 alcohol-induced liver disease?

A

characterised by fibrosis (scarring) of the liver
entire liver affected and architecture disrupted
fibres divide the liver into nodules
in alcoholic cirrhosis, nodules relatively smaller and more numerous than in other types of cirrhosis

34
Q

what are the risk factors for alcohol-induced liver disease?

A
  • excessive ethanol consumption >160g (16 units)/day for at least 5 years
  • female sex – females achieve a higher blood ethanol concentration following ingestion of a defined ingested dose

•genetics
−>1 gene involved
−associations with genes encoding alcohol-metabolising enzymes and proteins that control collagen synthesis

•Nutrition
−Increased susceptibility if deficient in protein and/or calories

•Hepatitis B or C infection – predispose to alcohol causing problems

35
Q

what are presenting signs and symptoms of alcohol-induced liver disease?

A
  • Non specific digestive problems e.g. anorexia, diarrhoea, vague upper right quadrant abdominal pain
  • Concern about effect of alcoholism, e.g. depression, poor work performance
  • Physical signs, e.g. tender hepatomegaly tremors and other features of alcoholism
36
Q

what are typical lab findings of alcohol-induced liver disease?

A
  • Increase in mean red cell volume
  • Due to folate deficiency or toxic effect of acetaldehyde on bone marrow
  • Increase in serum activities of gamma glutamyl transferase (GGT), alanine transferase (ALT) and aspartate aminotransferase (AST)
  • GGT induced by ethanol
  • ALT and AST indicate cellular damage
  • ALT>AST
  • ^ in serum procollagen III peptide
37
Q

how is ROS produced from ethanol metabolism?

A

production of hydrogen peroxide via MEOS action on ethanol, or aldehyde oxidase/xanthine oxidase action on acetaldehyde

38
Q

what are the consequence of ROS production from ethanol metabolism?

A

ROS inhibit lipid export from liver - may contribute to lipid accumulation

Lipid peroxides alter membrane properties - may contribute to cell lysis

Some evidence that lipid peroxides induce collagen production - may contribute to fibrogenesis

39
Q

what evidence is there that ROS production is linked to alcohol-induced liver disease?

A

Susceptibility of rats to alcohol-induced liver damage increased by feeding diet rich in polyunsaturated fatty acids

Lipid peroxidation products in serum & red cells of cirrhotic alcoholics correlated with ethanol intake & extent of liver damage

Alcoholics exhibit early in plasma concentrations of antioxidant vitamins with onset of cirrhosis

decrease in hepatic antioxidants concentrations in subjects with alcohol-induced liver injury

Toxic effect of carbon tetrachloride in rat liver enhanced by chronic ethanol feeding

Alcohol-induced damage reduced by drugs that protect liver against toxins which generate ROS

40
Q

what is the role of MEOS in alcohol-induced liver disease?

A

Hepatic distribution of enzyme & tissue damage correlated

Susceptibility of rats to alcohol-induced liver damage correlated with inducibility of this enzyme

X Understanding Disease (10 decks)

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