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MCB II Block 2 > Ethanol metabolism > Flashcards

Ethanol metabolism Flashcards

1
Q

alcohol dehydrogenase does what

A

makes ethanol go to acetaldehyde

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2
Q

if acetaldehyde is not metabolismed it is what to liver

A

toxic

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3
Q

ADH1B1 has what Km for ethanol

A

.05 - caucasians

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4
Q

ADH1B2 has what Km for ethanol

A

.9 - asians!

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5
Q

what is Vmax of ADH1B*2

A

high

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6
Q

why do asians have lower risk of alcholism

A

they get sick way more easily from alcohol which protects them from alcoholism

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7
Q

ALDH2*2 what is Vmax

A

low

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8
Q

what does ALDH2*2 with low Vmax mean

A

acetaldehyde toxicity increased

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9
Q

why are women more susceptible to ethanol

A

women have more fat and less water than men, b/c there is less water, the alcohol is more concentrated.

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10
Q

aldehyde dehydrogenase is where

A

mitochondria

cytosol

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11
Q

what is normal version of aldehyde dehydrogenase

A

ALDH2

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12
Q

what is Km and Vmax of ALDH2

A

(Km ~ 0.2μM, Vmax 0.60 units/mg)

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13
Q

ALDH1 is found where

A

cytosol

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14
Q

accumulation of acetaldehyde causes

A

nausea and vomiting

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15
Q

ALDH2*2 what is Km and Vmax

A

Km 46μM, Vmax 0.017 units/mg

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16
Q

if a person is ALDH2*2 what are the chances they will be alcoholic

A

0 - so far none has been found

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17
Q

Disulphiram promotes alcohol avoidance, how?

A

inhibiting ALDH

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18
Q

ADH1B*2 is common in

A

asians

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19
Q

what does liver do to acetate

A

Acetyl CoA

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20
Q

what enzyme turns acetate into acetyl CoA

A

acetyl CoA synthetase

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21
Q

acetyl CoA is used to make

A

fat

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22
Q

how does a lot of alchol cause damage to liver

A

one way: Liver – ACS-I in cytosol generates acetyl CoA for cholesterol & fatty acid synthesis

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23
Q

cytochrome p450 is where

A

ER

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24
Q

draw the flow chart from ethanol to acetate

A

pg 4

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25
Q

ethanol ingestion, where does it all go

A

pg 4

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26
Q

ADH1 has high affinity for

A

EtOH

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27
Q

ADH4 activity in GI may be related to what

A

increased cancer risk

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28
Q

describe how asians with ADH1B*2 mutation process alcohol

A

They have a higher Km than cauasians so they have lower affinity for binding ethanol to alcohol dehydrogenase. however, they have a higher vmax so they process it more quickly

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29
Q

describe why hapa’s get the asian flush

A

pg 8

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30
Q

alcohol is mainly metabolized in cytosol by what

A

alcohol dehydrogenase

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31
Q

when alcohol is processed by alcohol dehydrogenase it becomes what

A

acetaldehyde

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32
Q

if there is a LOT of drinking, what enzyme becomes active

A

P450 2E1

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33
Q

what is function of P450 2E1

A

metabolizes alcohol to acetaldehyde

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34
Q

beside cytosol, where are two minor places ethanol is metabolized

A

peroxisome

mitochondria

35
Q

what does MEOS stand for

A

Microsomal ethanol oxidising system

36
Q

what is function of cytochrome P450 reductase

A

transfers electrons from NADPH to cytochrome P450 which binds substrate and O2

37
Q

draw out MEOS and function

A

pg 11

38
Q

if there is too much alcohol consumption, what happens regarding MEOS

A

consumption initiates MEOS with consequences of acetaldehyde and free radical injury

39
Q

If there is a lot of drinking and therefore more use of ADH & ADLH, what is consequence

A

ADH & ALDH generates NADH increasing NADH/NAD+ ratio and disrupting cellular metabolism

40
Q

if there is chronic alcohol abuse what happens to liver

A

90% fatty liver - inhibition of fatty acid oxidation

41
Q

alcohol toxicity comes from

A

NADH/NAD+

42
Q

aldehyde dehydrogenase is found in

A

mitochondria

43
Q

what happens to acetaldehyde with alcohol consumption

A

increased production of it

44
Q

what are properties of acetaldehyde

A

reactive

45
Q

alcohol consumption leads to deficiency of what vitamin

A

vitamin B1

46
Q

by increasing NADH/NAD+ ratio, it leads to what

A

mitochondria are damaged by acetaldehyde and free radicals

47
Q

what does NADH/NAD+ ratio increase do to fatty acids

A

inhibits oxidation of fatty acids

48
Q

NADH/NAD+ inhibits

A

TCA cycle

reverses malate and oxaloacetate so there will not be substrate for citrate synthase

49
Q

how does alcohol consumption cause gout

A

elevate uric acid in blood

uric acid in blood b/c it’s not excreted as much

50
Q

if there is insufficient diet and too much drinking, what happens

A

there is insufficient glucose

induces glucogenesis which relies on pyruvate from lactate, Ala & Leu

51
Q

increased lactate in kidney, what will it do

A

kidney excrete uric acid, if there is too much lactic acid it will take lactate and put in lumen and rescue uric acid. therefore the people will be internalizing uric acid and develop gout

52
Q

what is affinity of CYPE2E1 for alcohol

A

low

53
Q

when you use CYP2E1, it is stabilized by

A

alcohol

54
Q

CYP2E1 is involved in production of

A

more P450s

55
Q

P450 is involved in what

A

drug metabolism

56
Q

cytochrome P450 is used to do what

A

detoxify molecueles. tags oxygen.

57
Q

cytochrome P450 is part of

A

MEOS

58
Q

many drugs are metabolised by

A

cytochrom P450

59
Q

Acetaminophen is active ingredient in

A

tylenol

60
Q

what happens to acetaminophen in liver

A

add glucuronate or SO4 (Pg 17)

61
Q

alcohol induced hepattiis

A

formation of aducts with AAs ↓ hepatic protein synthesis esp. calmodulin, ribonuclease, tubulin

62
Q

how does alcohol induced hepatitis affect tubulin

A

tubulin adducts inhibit secretion of serum proteins & VLDL, accumulation draws in H2O -> swelling -> portal hypertension -> disruption of architecture

63
Q

WKS (Wernicke–Korsakoff syndrome)

A

drinking alcohol and causing vitamin B1 deficiency

64
Q

what are symptoms of WKS

A

Apathy, memory loss, ataxia, nystagmus

65
Q

when you have B1 deficiency you affect key enzymes where

A

affect key enzymes in cardiovascular and nervous system

66
Q

ehtanol via cytochrom P450 will produce

A

acetylaldehyde

67
Q

aldehyde dehydrogenase produces a lot of NADH and interferes with

A

TCA cycle

68
Q

ethanol processed in liver via

A

ADH

69
Q

if you drink too much you get what to com ein in lvier

A

MEOS

70
Q

acetaldehyde can do what negative things in liver

A

modify aa
bind to microtubules
bind to glutathione (need for reactive oxygen species)

71
Q

Hepatic cirrhosis, describe

A

liver can be so fatty the belly is fatty
Liver injury is irreversible once cirrhosis develops
enlarged, fatty, fibrotic
as liver function ↓, liver may shrink (Laennec cirrhosis)

Loss of normal liver function
synthesis of albumin, clotting factors etc ↓
urea synthesis ↓, so blood ammonia ↑
bilirubin conjugation & excretion ↓ so deposited in skin, sclera & mucosa -> jaundice

72
Q

if you damage liver what will liver have problems processing

A

bilirubin - get jaundice, pt has yellow skin/eyes

73
Q

↑NADH/NAD+ ratio turns pyruvate into

A

lactate

74
Q

↑NADH/NAD+ → lactic acidosis, this means lactate isn’t availble for gluconeogenesis, therefore what happens

A

hypoglycaemia

75
Q

what is CYP2E1 affinity for ethanol

A

low

76
Q

what becomes involved with higher levels of ethanol consumption

A

CYP2E1 & MEOS

77
Q

CYP2E1 is stabilized by

A

alcohol

78
Q

MEOS produces more acetaldehyde than can be

A

metabolised by ALDH

79
Q

MEOS activity produces more acetaldehyde than can be metabolised by ALDH: what does this lead to?

A

hepatic injury, tissue damage

80
Q

what happens if drugs are taken with a lot of alcohol consumption

A

the ethanol can inhibit the metabolism of the drugs, leading to drug toxicity. ex: tylenol.

81
Q

Acetaminophen toxicity can be treated with

A

N-acetyl cysteine to increase GSH production

82
Q

excess acetaminophen is oxidised by

A

CYP2E1

83
Q

when excess acetaminophen is oxidised by CYP2E1 what toxic product results

A

NAPQI

84
Q

NAPQI is metabolised by what

A

GSH

MCB II Block 2 (10 decks)

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