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Biochemistry II > Chapter 68: Ethanol Metabolism > Flashcards

Chapter 68: Ethanol Metabolism Flashcards

1
Q

Functional definition of alcoholism

A
  • Consumption of alcohol to the point where normal social, sexual or vocational functioning is significantly impaired
  • Usually 50% of caloric intake is in the form of alcohol
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2
Q

Quantitative definition of alcoholism (WHO)

A
  • Daily consumption of more than 120 grams (4.2 oz.) of pure alcohol per day
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3
Q

Ethanol absorption

A
  • Rapidly and without modification

- 20% stomach, 80% in intestines

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4
Q

Blood alcohol content

A
  • Detectable within five minutes of consumption

- Peaks in 30 to 45 minutes

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5
Q

Blood alcohol concentration curve

A
  • Estimates time needed to absorb and metabolize alcohol
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6
Q

After absorption alcohol is distributed to the tissues of the body

A
  • Direct proportion to blood flow
  • Small amount not metabolized (excreted via sweat, saliva, urine, breath)
  • None is stored
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7
Q

BAC vs. time

A
  • 100 mg/dL = legal intoxication

- 50 mg/dL = driving impaired

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8
Q

Alcohol metabolism rates

A
  • Metabolized slower than absorbed

- Accumulation = intoxication

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9
Q

Oxidative breakdown of alcohol

A
  • Occurs in liver

- Broken down to acetaldehyde (via ADh) –> acetate + acetyl CoA –> CO2 + H2O (via the CAC)

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10
Q

Ethanol (alcohol) is metabolized by

A
  • Catalase
  • Cytochrome P450
  • Alcohol dehydrogenase
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11
Q

First pass metabolism of alcohol is reduced by

A
  • Aspirin
  • Cimetidine
  • Ranitidine
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12
Q

Ethanol metabolism generates

A
  • NADH

- Inhibits gluconeogenesis + FA metabolism

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13
Q

Gluconeogenic/FA metabolism enzymes inhibited by NADH from ethanol metabolism

A
  • Pyruvate carboxylase

- Malate dehydrogenase

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14
Q

NADH produced from the oxidation of ethanol can be used to

A
  • Generate ATP
  • Fat deposits observed in the liver (even after one night)
  • Liver develops a decreased capacity to burn fat
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15
Q

Excess NADH shifts the equilibrium of

A
  • Lactate dehydrogenase reaction

- Accumulation of lactate predisposes to gout

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16
Q

Minor pathway of alcohol metabolism

A
  • Isoenzymes of microsomal enzyme cytochrome P 450 (CYP2EI)
17
Q

Isoenzymes of cytochrome P 450 (CYP2EI)

A
  • May be increased after chronic drinking

- Important in accelerated ethanol metabolism (associated with tolerance)

18
Q

Small quantity of alcohol that remains unmetabolized permits

A
  • Measurement of alcohol concentration in breath and urine
19
Q

Food influences alcohol

A
  • More dietary fat = longer absorption
20
Q

Age influences alcohol

A
  • Older = less body water, loss of muscle tissue, decreased metabolism
21
Q

Gender influences alcohol

A
  • Women = higher BACs
  • Less body water (and higher body fat) = concentrates alcohol
  • Lower activity of gastric/liver alcohol dehydrogenase
22
Q

Body weight influences alcohol

A
  • Doesn’t always result in increased body weight (despite 7.1 kcal/g high caloric value)
23
Q

Medication influences alcohol

A
  • Chronic heavy drinking = activates cytochrome P450

- Acetaminophen pain relievers (e.g Tylenol) can increase risk of kidney/liver disease

24
Q

Short term alcohol related damage

A
  • Inhibition of microsomal hydroxylase system
  • CNS effects (sociability & elation)
  • Hepatic effects (fat deposition/steatosis, necrosis
  • Mitochondrial swelling
25
Q

Long term alcohol related damage

A
  • Induction of cytochrome P450 system
  • Excess NADH production and NAD utilization
  • Alcoholic hepatitis (acute or chronic; may be reversible)
  • Increases susceptibility of liver to other drugs
26
Q

Long term effects of excess NADH production and NAD utilization

A
  • Inhibition of gluconeogenesis

- Alcohol-induced hypoglycemia

27
Q

Alcohol decreases synthesis of liver proteins, causing

A
  • Extended prothrombin time (blood thinning)
28
Q

Alcohol decreases hepatic activation of

A
  • Vitamins
29
Q

Acetaldehyde effects due to alcohol consumption

A
  • Carcinogenic

- Released into the blood, so effects are widespread

30
Q

Chronic alcoholism in men can cause

A
  • Gynecomastia

- Hypotrophy of testes

31
Q

Cirrhosis

A
  • Replacement of liver tissue with fibrous tissue
  • Causes irreversible loss of liver function
  • 10-15% of alcoholics have cirrhosis at time of death
32
Q

Production of cirrhosis

A
  • Takes 5-25 years of heavy drinking

- Recall that AST/ALT ratio > 2 in alcoholic liver disease

33
Q

Cirrhosis symptom development

A
  • About 60% of liver tissue can be destroyed before symptoms appear
34
Q

Common symptoms of cirrhosis

A
  • Jaundice
  • Ascites
  • Edema
35
Q

Portal hypertension as a result of cirrhosis

A
  • Due to fibrotic build up, blood flow through the liver is impeded
  • Causes formation of esophageal varices
36
Q

Portal hypertension may be worsened by

A
  • Inadequate prothrombin production by the liver

- Contributes to bleeding esophageal varices common in alcoholics

37
Q

“Advantages” of light alcohol ingestion

A
  • Potential reduced incidence of heart disease
  • Increasing HDL circulating levels (“good” cholesterol)
  • Antioxidant effects of various compounds
  • Antioxidant potential
38
Q

Heme-containing cytochrome P450 2E1 (AKA CYP2E1)

A
  • Also metabolizes ethanol in the liver
  • Inducible enzyme
  • Higher Km for ethanol than alcohol dehydrogenase
  • More significant at increased ethanol consumption

Biochemistry II (5 decks)

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