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Biochemistry I/II > Lecture 24: Alcohol Metabolism > Flashcards

Lecture 24: Alcohol Metabolism Flashcards

1
Q

When present, alcohol becomes the ___ fuel, displacing other fuels

A

preferred

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2
Q

Alcohol is absorbed ___ and metabolized ___

A

fast; slowly

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3
Q

Where is ETOH mostly oxidized?

A

Liver (some in stomach)

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4
Q

What are the two main pathways for ethanol metabolism?

A

1) ADH pathway of the cytosol (stomach/liver)
2) Microsomal Ethanol Oxidizing System (MEOS) - endoplasmic reticulum of liver

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5
Q

Both pathways result in the production of ___, a highly toxic metabolite

A

Acetylaldehyde

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6
Q

First pass metabolism of alcohol occurs in the ___

A

stomach

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7
Q

ADH comprises a family of enzymes that catalyze the conversion of ethanol to ___

A

acetaldehyde

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8
Q

Even the ____ form of ADH is activated after alcohol ingestion due to high gastric ethanol concentration

A

high Km

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9
Q

First pass metabolism ___ bioavailability of ethanol

A

decreases

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10
Q

_____ is a protect barrier against systemic effects of alcohol, which is commonly lost in individuals who suffer from alcohol abuse disorder

A

First pass metabolism

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11
Q

True or False: For a given amount of alcohol consumed, blood levels are higher in men than women. Why or why not?

A

False - blood levels are higher in women than men

-Women are smaller, have more fat, and less gastric ADH

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12
Q

How is moderate drinking defined?

A

Men: Not more than 2 drinks per day
Women: One drink per day

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13
Q

Alcohol + NAD is => acetaldehyde+NADH as a result of what enzyme?

A

Alcohol Dehydrogenase

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14
Q

What compound overwhelms the liver’s capacity to maintain redox homeostasis?

A

NADH

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15
Q

Normally, is there greater NAD+ or NADH in the liver? How is this balance shifted?

A

Typically there is higher NAD+/NADH
-The balance is shifted with alcohol

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16
Q

The inability of the liver to maintain ___ homeostasis is the reason for the metabolic derangement seen when ETOH is consumed

A

redox

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17
Q

Ethanol is converted to ___ and ___. As a result, what products are made?

A

acetaldehyde ; acetate
x2 NADH

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18
Q

NADH feeds the ETC, causing the TCA to ___, increased levels of ___ and ___

A

slow; ATP; acetyl CoA

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19
Q

As a result of ethanol intake (conversion froom acetylaldehyde to acetate) there is elevated acetyl CoA, which can cause synthesis of ____ ____, leading to a disorder known as ____

A

fatty acids; fatty liver

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20
Q

Ethanol oxidation causes NADH to be made. NADH + pyruvate can make lactate using LDH. Lactic acid build up can lead to?

A

Hyperlactacidemia
Renal acidosis
Uricacidemia
Gout

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21
Q

When alcohol oxidation occurs, you can convert ___ to ___ but not vice versa. Therefore, you can not undergo gluconeogenesis and, as a result, can develop ______

A

pryuvate; lactate
-Hypoglycemia

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22
Q

If you are unable to convert lactate to pyruvate, you cannot undergo _____

A

gluconeogenesis

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23
Q

Lactic acidosis can lead to reduced excretion of ______

A

Uric Acid

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24
Q

Mitochondria use ____ originating from ethanol rather than those derived from oxidation of fatty acids that normally serve as the main energy source of the liver

A

hydrogen

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25
Q

An early manifestation of alcohol consumption is the excessive accumulation of fat in the liver, resulting in a condition known as _______

A

fatty liver

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26
Q

How will increased alcohol consumption affect levels of MEOS (microsomal ethanol oxidizing system)?

A

Increased MEOS expression and synthesis

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27
Q

____ ____ are the sites for adaptive system of ethanol oxidation named microsomal ethanol oxidizing system

A

Liver microsomes

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28
Q

MEOS belongs to a class of cytochrome p450 oxidases and oxidation of alcohol involves a specific form of cytochrome P450 oxidase called ____

A

2E1

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29
Q

____ is highly induced after chronic alcohol consumption

A

2E1 (CYP2E1)

30
Q

True or False: 2E1 is highly induced after chronic alcohol consumption whereas hepatic ADH is not inducible

A

True

31
Q

The fact that CYP 2E1 is highly induced after chronic alcohol consumption contributes to the metabolic ___ that develops in individuals with alcohol dependence disorders

A

tolerance

32
Q

When ethanol is converted to acetylaldehyde, what substrate is used? Product?

A

NADPH
-NADP+

33
Q

Which has a higher affinity for alcohol: ADH or P4502E1?

A

ADH

34
Q

Under what conditions is P4502E1 most effective?

A

When large amounts of ETOH are consumed

35
Q

In what individuals is P4502E1 most effective?

A

Individuals with ETOH dependence

36
Q

In social drinkers who also are taking a prescription medication, they will have elevated ETOH blood levels and retain the drug in their system longer. Why?

A

-Drugs inhibit alcohol oxidation in stomach, leading to elevated alcohol levels
-The alcohol will be down in the liver, but only after the drug does

37
Q

In alcohol dependent individuals on prescription medications, drugs get broken down in the liver ____, which could lead to less drug in the system and less action of the drug itself. Alcohol also gets broken down in the liver

A

very fast

38
Q

In alcohol dependent individuals on prescription medications, alcohol oxidation in the stomach is ___

A

inhibited

39
Q

In the non-alcoholic, alcohol is metabolized by __, an enzyme. Drugs, however, are metabolized by the ____ in the lvier

A

ADH; microsomal cytochrome P450

40
Q

In the non-alcoholic, how will an increased in alcohol concentration affect drug metabolism in the liver and ADH in the stomach?

A

In the non-alcoholic, an increase in alcohol concentration will inhibit drug metabolism/ADH in stomach

41
Q

With chronic drinking, gastric ADH ___ resulting in decreased _______ in the stomach

A

decreases; ethanol metabolism

42
Q

In chronic drinkers, liver MEOS is highly ___

A

induced

43
Q

True or False: Inducation of MEOS produces other related toxicities. In other words: cytochrome oxidases can convert many exogenous compounds to toxic metabolites

A

True

44
Q

Many endogenous and xenobiotic compounds (including: ETOH) are substrates for ___

A

CYP2E1

45
Q

Activation of CYP2E1/NADPH can lead to production of _____, activation of ___/____

A

free radicals; toxins/carcinogens

46
Q

True or False:
An effect of the induction of the MEOS is the enhanced metabolism of various other drugs (prescribed drugs and OTC meds)? Why is this?

A

True
-substrate for/inducers of: 2E1

47
Q

True or False:
On many occasions, metabolites produced in the microsomes are more toxic than the precursor compounds

A

True

48
Q

Phase I of Acetaminophen metabolism produces ____, which is highly toxic

A

NAPQ1

49
Q

Alcohol reduces glutathioine levels, resulting in increase _____-mediated damage because you make more ___

A

free radical; NAPQ1

50
Q

When is NAPQ1 produced in large quantities?

A

When 2E1 is highly induced

51
Q

Increase in P4502E1 may partially account for the increase incidence of ___ among persons with ETOH abuse disorder

A

cancer

52
Q

Testicular atrophy and gynecomastia are common seen in _____

A

ETOH abuse

53
Q

Ethanol is converted to ___ and ___

A

acetylaldehyde and acetate

54
Q

Conversion of acetylaldehyde to acetate occurs via what enzyme?

(acetylaldehyde+NAD+ -> acetate + NADH)

A

ALDL (aldehyde dehydrogenase)

55
Q

When is the activity of ALDL reduced? What occurs as a result?

A

Chronic alcohol consumption
-Acetylaldehyde becomes the major end product accumulating in tissues and blood

56
Q

Acetylaldehyde reacts with cellular constituents like proteins and other macromolecules to cause ____ damage

A

Free-radical mediated oxidative

57
Q

Alcohol is energy ___ and individuals with alcohol dependence obtain large proportion of their energy from ethanol, which typically result in decreased intake of non-alcoholic foods containing essential nutrients

A

dense

58
Q

The intrinsic toxicity of alcohol can be responsible for some of the nutritional ___ seen in individuals with ETOH abuse

A

deficiency

59
Q

What 2 factors contribute to malnutrition in alcohol abuse?

A

1) maldigestion/malabsorption
2) impaired utilization

60
Q

What is secondary malnutrition a result of?

A

Maldigestion and malabsorption

61
Q

True or False:
Alcohol abuse can alter the GI tract and directly interfere with absorption of certain nutrients

A

True

62
Q

Severe liver damage interferes directly with ___, ___, and ___ of certain nutrients

A

storage, activation, degradation

63
Q

What causes thiamin deficiency?

A

Impaired absorption

64
Q

______ Syndrome is commonly seen in alcoholics due to severe thiamin deficiency

A

Wenicke-Korsakoff Syndrome

65
Q

People with ETOH abuse disorder show folic acid/pyridoxine deficiency due to ____ as well as Vitamin A deficiency due to ____

A

malabsorption; degradation of stored vitamin

66
Q

Alcoholic Cirrhosis is a result of both ___ and _____

A

Malnutrition and direct toxic effects of alcohol

67
Q

Disulfiram (antabuse) causes accumulation of ____, resulting in flushing, tachy, nausea, and hyperventilation. It is commonly used to help individuals stop abusing ETOH.

A

acetylaldehyde

68
Q

___ accumulation results in reduced conversion of ___ to ___. This results in impaired gluconeogenesis. Increased lactate causes ____

A

NADH; lactate; pyruvate; acidosis

69
Q

Lactic acidosis can lead to a reduction in excretion of _____

A

Uric acid

70
Q

In addition to
tolerance to ethanol,
individuals with
alcohol dependence
tend to display
tolerance to various
other ___

A

Drugs

Biochemistry I/II (23 decks)

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