lecture 34 - alcohol metabolism Flashcards

1
Q

What receptor does alcohol act as an agonist of?

A

GABA A receptor

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2
Q

How does alcohol affect the nervous system?

A

Acts as an agonist of the GABA A receptor causing an increase in the inhibitory effect on neurotransmission.

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3
Q

What type of receptor is the GABA A receptor?

A

Membrane bound ligand-gated chloride channel

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4
Q

What happens when the GABA A receptor is activated?

A

Selectively conducts Cl- ions causing an inhibitory effect on neurotransmission by reducing the chance of a successful action potential.

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5
Q

Does alcohol amplify or dampen the effects of a GABA A receptor?

A

Amplifies, as it is an agonist, increasing the number of chloride molecules that cab pass through

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6
Q

What is the chemical we know as alcohol?

A

Ethanol

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7
Q

Why is alcohol rapidly absorbed into the blood?

A

Small molecule that does not require enzymatic digestion, so will be readily absorbed and then metabolised.

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8
Q

What is alcohol/ethanol converted to when it first enters the body?

A

Acetaldehyde

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9
Q

What enzyme is needed to convert ethanol to acetaldehyde?

A

Alcohol dehydrogenase

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10
Q

What is alcohol dehydrogenase coupled to when forming acetaldehyde from ethanol?

A

NAD+ is converted to NADH and H+

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11
Q

What is acetaldehyde converted to by aldehyde dehydrogenase?

A

Acetate

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12
Q

What enzyme is used to convert acetaldehyde to acetate?

A

Aldehyde dehydrogenase

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13
Q

What is the acetaldehyde to acetate reaction coupled to?

A

The conversion of NAD+ to NADH and H+

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14
Q

How does acetate form Acetyl CoA?

A

Using Acetyl CoA synthetase enzyme. CoA and ATP are fed into the reaction, AMP and PPi produced

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15
Q

What are the consequences of alcohol metabolism on the citric acid cycle and electron transport chain?

A

Slows CAC and ETC by increasing the NADH to NAD+ ratio

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16
Q

What is the effect of alcohol metabolism on fatty acids?

A

They are esterified to TAG, which can cause a build up in the liver - ‘fatty liver’ as well as high blood cholesterol and TAG concentrations

17
Q

What is the consequence of alcohol metabolism on pyruvate?

A

Increases the NADH to NAD+ ratio, which causes the pyruvate to lactate reaction, which decreases the pH of the liver.

18
Q

What is the consequence of alcohol metabolism on gluconeogenesis?

A

Increases [NADH], which inhibits gluconeogenis which can lead to low blood glucose between meals.

19
Q

What happens to the ratio of NADH to NAD+ when alcohol is metabolised?

A

Increased NADH, decreased NAD+. Increased NADH/NAD+

20
Q

Where is the majority of ethanol metabolised?

A

The liver

21
Q

What system metabolises alcohol when it is treated as a toxin?

A

The microsomes ethanol oxidising system

22
Q

What product of ethanol metabolism is toxic?

A

Acetaldehyde

23
Q

What can the oxidase in ethanol metabolism give rise to?

A

Reactive oxygen species

24
Q

What is the outcome of chronic fatty liver and inflammation?

A

Alcoholic hepatitis

25
Q

What are the outcomes of alcoholic hepatitis?

A

necrosis, cirrhosis, then coma and death

26
Q

What builds up in liver dysfunction?

A

NH3

27
Q

What limits the rate of alcohol metabolism?

A

Alcohol dehydrogenase becomes saturated after a couple of drinks, meaning it can only catalyse the reaction to acetaldehyde at a limited rate.

28
Q

What is the impact of alcohol metabolism on citrate levels?

A

By limiting the CAC and ETC, citrate builds up

29
Q

What is the mechanism by which fatty liver occurs?

A

Excess alcohol intake causes reduced fatty acid metabolism due to a depletion in NAD+. Fatty acids are instead converted to TAGs, which build up in the liver.