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USMLE Biochemistry > Ethanol > Flashcards

Ethanol Flashcards

1
Q

What are the 2 steps of ethanol metabolism?

A
  • Ethanol -> Acetaldehyde
    NAD+ -> NADH
    (Alcohol dehydrogenase)
  • Acetaldehyde -> Acetate
    NAD+ -> NADH
    (Aldehyde dehydrogenase)
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2
Q

Where does the first step of ethanol metabolism occur?

A

Cytosol

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3
Q

Where does the second step of ethanol metabolism occur?

A

Mitochondria

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4
Q

What are some problems caused by excessive ethanol consumption?

A
  • CNS depressant - coma
  • Hypoglycemia
  • Ketone body formation (ketosis)
  • Lactic acidosis
  • Accumulation of fatty acids
  • Hyperuricemia
  • Hepatitis and cirrhosis
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5
Q

What is the trigger for practically all biochemical problems associated with alcohol?

A

Increased NADH: NAD+ ratio

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6
Q

What 2 enzymes can NADH inhibit in the TCA cycle?

A
  • Isocitrate Dehydrogenase (Isocitrate -> a-ketoglutarate)
  • Alpha-KG Dehydrogenase
    a-KG -> Succinyl-CoA
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7
Q

What does NADH shunt oxaloacetate to?

A

Malate (generates NAD+)

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8
Q

What enzyme converts Oxaloacetate to Malate?

A

Malate dehydrogenase (reversible)

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9
Q

How does the shunting of Oxaloacetate to Malate generate ketones|?

A

Acetyl-CoA cannot bind with oxaloacetate to create citrate

  • Shunted away from TCA cycle
  • Instead Acetyl-CoA converted to ketones
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10
Q

Describe how alcoholics get hypoglycemia?

A
  • Oxaloacetate depleted (shunted to malate) which is involved in gluconeogenesis
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11
Q

When is hypoglycemia posssible after drinking?

A

When glycogen stores are low as this is an important source of fasting glucose
- Drinking w/o eating
- Drinking after running
As these deplete glycogen stores

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12
Q

What is acetate converted into in the liver?

A

Acetyl-CoA

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13
Q

What other than acetate is converted to acetyl coA (and subsequently ketones, if NADH/NAD ratio is high)?

A
  • Glucose
  • Amino acids
  • Fatty acids
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14
Q

What enzyme leads pyruvate towards the TCA cycle and is inhibited by NADH?

A

Pyruvate dehydrogenase

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15
Q

What does the conversion of pyruvate to lactate produce, why is this important in the context of alcohol?

A

Pyruvate -> Lactate

  • Generates NAD+ (from NADH)
  • Increased NAD+ which is depleted in ethanol metabolism
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16
Q

How does alcohol cause an accumulation of fatty acids in the liver?

A

High levels of NADH stall Beta oxidation

  • Beta oxidation generates NADH (like TCA cycle)
  • Requires NAD+
  • Inhibited when NADH is high
  • Therefore decreased FA breakdown
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17
Q

What molecule in the TCA cycle builds up in alcholol and can then be converted to fatty acids?

A

Citrate

  • Will migrate from mitochondria to cytosol
  • Can then be converted to fatty acids
18
Q

What is the rate limiting step/enzyme of fatty acid synthesis?

A

Acetyl-CoA Carboxylase (biotin cofactor)

Acetyl-CoA -> Malonyl-CoA

19
Q

What molecule enhnces Acetyl-CoA carboxylase?(rate-limiting enzyme of FA synthesis)

A

Citrate (slow TCA cycle)

20
Q

What molecule in fattty acid synthesis will inhibit Beta-oxidation?

A

Malonyl-CoA

21
Q

What will Malic enzyme generate (from malate)?

A

NADPH and Pyruvate

22
Q

What does NADPH favor?

A

Fatty acid synthesis (NADPH generated in alcoholism)

23
Q

What does fatty acid synthase require (generated from malate/malic acid synthase)?

A

NADPH

24
Q

What is palmitate generated from?

A

Acetyl CoA and malonyl CoA

  • Requires NADPH
  • Enzyme: Fatty acid synthase
25
Q

What does glycerol-3-Phosphate require to be converted into Dihydroxyacetone Phosphate?

A

NAD+ (depleted with alcohol)

- Enzyme: Glycerol-3-Phosphate Dehydrogenase

26
Q

What will a depletion of NAD+ cause to glycerol-e-phosphate levels?

A

Will increase G3P

  • Increased triglycerides
  • Fatty liver
27
Q

How can alcohol trigger gout?

A
  • Urate and lactate compete for excretion in PCT

- Increased lactate results in decreased urate excretion

28
Q

What substance is toxic to liver cells and leads to alcoholic inflammation, hepatitis and cirrhosis?

A

Acetaldehyde

  • High NADH will slow its metabolsim to acetate
  • Build up occurs in alcoholics
29
Q

What substance leads to catecholamine release, fluching, palpitations, N/V?

A

Acetaldehyde

30
Q

What inhibits aldehyde dehydrogenase (builds up acetaldehyde)?

A

Disulfiram (antabuse)

31
Q

What deficiency causes alcoholic flushing?

A

Aldehyde dehydrogenase 2 (ALDH2)

32
Q

What cancers are at incr risk in Aldehyde dehydrogenase 2 (ALDH2) deficiency (asian flush)?

A
  • Esophageal cancer

- Oropharyngeal cancer

33
Q

Wha substance inhibits alcohol dehydrogenase?

A

Fomepizol (antizol)

34
Q

What is Fomepizol used in?

A
  • Methanol and ethylene glycol intoxication
35
Q

What toxic substances does alcohol dehydrogenase convert methnol and ethylene glycol into? (hence the use of feompeizol)

A
  • Methanol - Formaldehyde

- Ethylene glycol - Glycoaldehyde

36
Q

What other metabolic pathway can lead to hepatitis and cirrhosis (not acetaldehyde buil-up)?

A

Microsomal ethanol-oxidising system (MEOS)

- Normally metabolises samll amount of ethanol but becomes important w. excessive consumption

37
Q

What molecules does Microsomal ethanol-oxidising system (MEOS) pathway consume?

A
  • NADPH

- Oxygen

38
Q

What does Microsomal ethanol-oxidising system (MEOS) generate?

A
  • Acetaldehyde
  • Acetate
  • Free radicals from oxygen consumption -> damage
39
Q

What does the consumption of NADPH from the Microsomal ethanol-oxidising system (MEOS) cause?

A

Glutathione which cannot be regenrated

- Loss of protection from oxidative stress -> liver hepatitis and cirrhosis

40
Q

What enzyme is Microsomal ethanol-oxidising system (MEOS) dependant on?

A

CYP450

USMLE Biochemistry (44 decks)

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