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MEH > Alcohol Metabolism > Flashcards

Alcohol Metabolism Flashcards

1
Q

Where is most of alcohol metabolised?

A

The liver

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2
Q

What happens to the alcohol that is not metabolised?

A

Excreted in urine and breath

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3
Q

What oxidises alcohol?
Into what?

A

Alcohol dehydrogenase
Acetaldehyde

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4
Q

What oxidises acetaldehyde?
Into what?

A

Aldehyde dehydrogenase
Acetate

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5
Q

What is acetate converted into?

A

Acetyl CoA

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6
Q

What is acetyl CoA used in? (2)

A

TCA cycle
Fatty acid synthesis

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7
Q

If alcohol isn’t oxidised by alcohol dehydrogenase what can it be oxidised by?

A

Catalase in the brain
Cytochrome P450 2E1

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8
Q

What is the recommended alcohol consumption?

A

14 units
Spread over at least three days

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9
Q

What is the rate of alcohol elimination?

A

7g per hour

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10
Q

How many grams is one unit of alcohol?

A

8g

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11
Q

What causes a hangover as well as dehydration?

A

Accumulation of acetaldehyde - which is toxic

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12
Q

What enzyme controls the levels of acetaldehyde?
How?

A

Aldehyde dehydrogenase
Has a low Km for acetaldehyde - high affinity

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13
Q

What is the primary cause of liver damage?

A

Prolonged and excessive alcohol consumption
Acetaldehyde accumulation

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14
Q

What causes changes in liver metabolism?

A

Excess NADH
Excess Acetyl CoA

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15
Q

Three key conditions that effect the liver, caused by excessive alcohol consumption

A

Fatty liver
Alcohol hepatitis - inflammation of the liver
Alcohol cirrhosis - the liver has become significantly scarred

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16
Q

What drug is used in the treatment of alcohol dependence?

A

Disulfiram

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17
Q

How does disulfiram work?

A

Inhibits aldehyde dehydrogenase
Acetaldehyde accumulates if alcohol drunk - causing nausea

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18
Q

Explain how increased NADH effects liver metabolism (3)

A
  1. NAD+ levels inadequate for fatty acid oxidation
  2. Less lactate converted to pyruvate
  3. Lactate accumulate in the blood
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19
Q

How is the electron transport chain a source of ROS?

A

E- can escape the chain and react with dissolved O2
To form superoxide

20
Q

What are the three types of NOS?
What do they all do?

A

INOS - inducible - produces high NO conc in phagocytes for direct toxic effect
ENOS - endothelial - signalling
NNOS - neuronal - signalling

21
Q

What is NOS?

A

Nitric oxide synthase

22
Q

Toxicity of NO* (nitric oxide)

A

Toxic at high levels

23
Q

Role of NO* (2)

A

Vasodilation
Neurotransmission

24
Q

What occurs in respiratory burst? (2)

A
  1. Rapid production of superoxide and H2O2 - from phagocytic cells
  2. The bacteria around the cell are destroyed (sometimes the phagocytic cells are too)
25
Q

What enzyme is required in respiratory burst?
Where is it found?
What does it do?

A

NADPH oxidase
Present in membrane of phagosomes
Transfers e- from NADPH to O2 - to make superoxide radicals

26
Q

Link defect in respiratory burst process to a disease

A

Genetic defect in NADPH oxidase
Enhanced susceptibility to bacterial infects
(Pneumonia, abscesses…)

27
Q

What are two enzymes in cellular defence against ROS and RNS

A

Superoxide dismutase
Catalase

28
Q

How does superoxide dismutase work?

A

Converts superoxide (O2*-) to H2O2 and O2

29
Q

How does catalase work (in defences against oxidative stress)?
What type of cells are they prominent in?

A

Converts H2O2 to H2O and O2
Immune cells

30
Q

What is another cellular defence of a cellular defence?

A

Glutathione (GSH)

31
Q

How does glutathione act as a cellular defence?

A

The structure is GLY-CYS-GLU
The thiol group of Cys donates e- to ROS + reacts with another GSH to form a disulphide bond - now GSSG

32
Q

What enzyme is required in the bonding of two Cys molecules during glutathione cellular defence?
What does it require?

A

Glutathione peroxidase
Selenium

33
Q

What is required to reduce GSSG back to GSH?
How does it work?

A

Glutathione reductase

Catalyses the transfer of e- from NADPH to disulphide bond of GSSG
Resulting in GSH

34
Q

What is the main source of NADPH?

A

Pentose phosphate pathway

35
Q

Name two free radical scavengers
Name their solubilities
Where they are important

A

Vitamin E - lipid soluble, protection against lipid peroxidation

Vitamin C - water soluble, regenerate reduced form of vitamin E!

36
Q

How do free radical scavengers work?

A

Reduce free radical damage

Donate H atom and its electron to free radicals in non enzymatic reactions

37
Q

Name the ROS and RNS

A

O2*- superoxide
H2O2 hydrogen peroxide
*OH hydroxyl radical

NO* nitric oxide
ONOO- peroxynitrite

38
Q

How do Heinz bodies form?

A

G6PDH deficiency
Less NADPH produced in Pentose phosphate pathway
Less GSH reformed
Haemolysis - cross linked haemoglobin form Heinz bodies

39
Q

What is a clinical sign of G6PDH deficiency?

A

Heinz bodies

40
Q

What do Heinz bodies do?

A

Bind to membrane
Altering structure of RBC
RBC can’t fit through small capillaries

41
Q

How do anti-malarials effect ROS?

A

Deplete NADPH
GSH not reformed

42
Q

Why are RBC more susceptible to oxidative stress?

A

In RBC the only way of getting NADPH is through pentose phosphate pathway

43
Q

What can small amounts of alcohol be metabolised by?

A

P450 enzymes
Catalase in the brain

44
Q

What is the rate of alcohol metabolism?

A

7g/hr

45
Q

What processes would increase in chronic excessive alcohol consumption?

A

Synthesis of fatty acids and ketone bodies

MEH (10 decks)

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