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Biochem BLOCK 3 > Ethanol Metabolism > Flashcards

Ethanol Metabolism Flashcards

1
Q

What is the 4th major nutrient that provides a significant amount of energy in many people?

A

Ethanol

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2
Q

How many kcal/g in alcohol?

A

7

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3
Q

Calories of alcohol

A

A lot of calories, although they are empty calories because they have no nutritional value

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4
Q

How many grams of alcohol does the “standard drink” have?

A

14 grams

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5
Q

What is the estimated calories in a drink (minus the mixers used)

A

98

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6
Q

What is the 3rd leading preventable cause of death?

A

Alcoholism

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7
Q

What percentage of men meet the criteria for alcoholism?

A

17%

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8
Q

What percentage of women meet the criteria for alcoholism?

A

8%

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9
Q

Affects of over drinking on brain?

A

Interferes with the brain’s communication pathways

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10
Q

Affect of drinking on heart

A

Can damage the heart leading to cardiomyopathy, arrhythmias, stoke, high blood pressure

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11
Q

Drinking affects on liver

A

Steatosis, alcoholic hepatitis, fibrosis, cirrhosis

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12
Q

What is the 1st severely damaged organ from drinking?

A

Liver

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13
Q

Affects of drinking on pancreas

A

Produces toxic substances that can lead to pancreatitis

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14
Q

Affects of drinking on eyes

A

Short and long term vision problems

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15
Q

What is over consumption of alcohol a risk factor for?

A

Many cancers

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16
Q

What does over consumption of alcohol interfere with?

A

Proper function of the immune system therefore decrease the body’s ability to fight infections

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17
Q

Solubility of ethanol

A

Both water and fat soluble

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18
Q

Absorption of alcohol into the intestine

A

Very easily absorbed by the intestine and readily enters the blood stream because of the fat and water soluble characteristics of ethanol

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19
Q

Where can a small amount of ethanol be metabolized?

A

By cells in the upper GI tract

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20
Q

What happen to a small amount of ethanol?

A

Lost through the lungs and kidneys

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21
Q

Where is the majority of ethanol processed?

A

In the liver via 2 pathways

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22
Q

What are the two pathways that liver can process ethanol?

A
  1. Involves alcohol dehydrogenase (ADH)

2. Uses the microsomal ethanol oxidizing systems (MEOS) relying on cytochrome P450 enzymes

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23
Q

What do we even have enzymes to process alcohol?

A

Intestinal bacteria will produce ethanol via fermentation, that’s why we have the enzyme to break it down

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24
Q

Where does ethanol metabolism predominantly happen?

A

Liver

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25
Q

Ethanol metabolism via MEOS

A

10-20%

Extremely upregulated

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26
Q

Ethanol metabolism via ADH system

A
  • 80-90%

- uses ADH and ALDH

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27
Q

What is the damaging molecule of excessive drinking?

A

Acetaldehyde H3C-CHO

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28
Q

What does ADH do to ethanol?

A

Converts it to acetaldehyde

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29
Q

What is the rate limiting step in ethanol metabolism?

A

ADH and the availability of NAD+

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30
Q

What is another limiting factor for alcohol metabolism other than ADH?

A

Availability of NAD+

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31
Q

What is the Km of ADH for ethanol?

A

Near 1 mmol/L

32
Q

When does the enzyme get saturated when drinking alcohol?

A

ADH gets saturated essentially after one drink, and alcohol metabolism follows zero order kinetics

33
Q

What kind of kinetics does alcohol metabolism follow?

A

Zero order kinetics

34
Q

What happens when ADH is saturated?

A

Additional ethanol circulates in blood until active site opens up

35
Q

How much alcohol does a person metabolize per hour?

A

About 10g of alcohol per hour

36
Q

How does the blood alcohol level decrease per hour?

A

By about 0.15g/L every hour. Important calculations after car accidents

37
Q

ALDH in east asians

A

Atypical with a single amino acid substitution

Glu—Lys

38
Q

Dominant negative mutation of ALDH

A
  • Single amino acid mutation of ALDH of glu—lys
  • -even heterozygotes, who still produce the normal enzyme in addition to the defective one, have near zero enzyme activity
39
Q

What happens to someone with atypical ALDH when they drink?

A

The toxic acetaldehyde accumulates to high levels after only one or two drinks

40
Q

Oriental flush response

A
  • asians typically have atypical ALDH

- causes vasodilation, facial flushing, tachycardia

41
Q

Rate of alcoholism in asians

A

Barely any. Oriental flush response is so unpleasant that no one wants to drink

42
Q

What percentage of asians have atypical ADH?

A

30-40%

43
Q

What is one symptom of acetaldehyde toxicity?

A

Flushing of the face and nausea

44
Q

This inhibits aldehyde dehydrogenase, which will result in the accumulation of acetaldehyde after ingestion of alcohol.

A

Disulfiram

45
Q

What is disulfiram used for?

A

As a deterrent from drinking from the sickness that will result

46
Q

What happens if a person is on disulfiram and still drinks?

A

The damage caused by acetaldehyde that is seen in long time alcoholics will be accelerated

47
Q

What is another compound that will have a more immediate affect on ethanol metabolism?

A

NADH

48
Q

What does the processing of alcohol in the liver produce?

A

Large quantities of NADH in the liver

49
Q

Drinking only a moderate amount of alcohol and NADH in liver

A

Likely that it will not result in significant changes (unless fasting)

50
Q

Large amount of NADH building up

A

Alter many metabolic processes

51
Q

When are significant effects of NADH build up seen?

A

Found mainly in heavy drinkers, or occasional drinkers that binge

52
Q

Large build up of NADH in well fed state

A

When the liver is taking up glucose and performing glycolysis producing NADH and pyruvate, high levels of NADH will inhibit PDH complex and cause pyruvate to be converted into lactate resulting in lactic acidosis

53
Q

Secondary effect of lactic acidosis

A

Will be the underexcretion of uric acid, resulting in hyperurecima

54
Q

Build up of large amounts of NADH in fasting state

A

Liver will try to perform gluconeogensis
HOWEVER
-precursors will be diverted at pyruvate to the production of lactate
-if liver glycogen stores depleted, this can result in hypolycemia

55
Q

Hypoglycemic effect of fasting and drinking

A

Can happen to even occasional drinkers, if they happen to drink when their glycogen stores are depleted

56
Q

Is alcohol a substrate for gluconeogensis?

A

Nom it is ketogenic but not glucogenic

57
Q

What do high levels of NADH inhibit?

A

Oxidation of fatty acids

58
Q

Net result of inhibition of oxidation of fatty acids due to high levels of NADH

A

Accumulation of TAG as lipid droplets leading to fatty liver disease, some of the fat is released into the blood stream as VLDLs, which causes hyperlipidemia

59
Q

The acetyl CoA that is produced from acetate that results from ethanol breakdown

A

Can not be used in the TCA cycle because of the build up of NADHq

60
Q

High ratio of acetyl CoA and NADH

A

Causes the conversion of oxaloacetate back into malate to regenerate NAD+, but since there is already too much fat, that pathway will be inhibited too

61
Q

What happens to acetyl CoA in ethanol consumption

A

Tends to get forced into the pathway for ketone syntheiss and ketoacidosis can result

62
Q

Ethanol effects on nitrogen metabolism

A

Hyperammonemia and hyperbilirubinemia will result from liver failure

63
Q

Cytochrome P450 in ethanol metabolism

A

The induction of cytochrome P450 enzymes and their increased role in ethanol metabolism results in a side effect of free radical production

64
Q

Acetaldehyde and free radicals

A

It is a reactive compound that can bind glutathione, depleting glutathione supplies and reducing the cells ability to neutralize free radicals

65
Q

Free radical mediated damage to the liver

A

Results in cirrhosis and eventually destruction of the liver

66
Q

Why do alcoholics suffer from malnutrition?

A
  • alcohol will provide significant calories while providing very little (or no) other nutrients
  • the negative effects on the liver, pancreas, and GI tract further increase nutritional deficiencies
67
Q

What are the two vitamin deficiencies prevalent in alcoholics

A
  • folate deficiency

- thiamine deficiency

68
Q

Folate deficiency in alcoholics

A

Results in megaloblastic anemia

69
Q

Thiamine deficiency in alcoholics

A

Due to alcohol abuse and causes Wenicke-Korsakoff syndrome divided into two conditions

70
Q

Wernickes encephalopathy

A

Reversible early stage of thiamine deficiency

71
Q

Karsakoff syndrome

A

Thiamine deficiency

-end stage, brain damage and death

72
Q

FASD

A

Any physical or developmental disorders causes by prenatal alcohol exposure

73
Q

When is the time frame that the most vital organs can be especially damaged in babies?

A

First 3 months of pregnancy

74
Q

Alcohol metabolism of pregnant women

A

Much more depressed compared with that of a non pregnant woman, as estrogen largely inhibit the activity of ADH

75
Q

What hormone largely inhibits the activity of ADH?

A

Estrogen

Biochem BLOCK 3 (12 decks)

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