Alcohol Flashcards

exam 2

1
Q

what to happens after eating a heavy fatty meal?

A

slows gastric transport and absorption

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2
Q

First step of alcohol metabolism

A

oxidation of ethanol to acetaldehyde

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3
Q

enzyme of the first step of alcohol metabolism

A

alcohol DH

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4
Q

what do you nee for the oxidation step from ethanol to acetaldehyde?

A

NAD+

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5
Q

what do you nee for the oxidation step from ethanol to acetaldehyde?

A

NAD+

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6
Q

ADH1B*2

A

allele found majorly in the asian population and it allows for a quicker metabolism of alcohol of the first step

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7
Q

what is activated under chronic alcohol consumption?

A

MEOS: microsomal ethanol oxidizing system

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8
Q

second step of alcohol metabolism

A

oxidation of acetaldehyde to acetate

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9
Q

enzyme of the second step of alcohol metabolism

A

aldehyel DHII

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10
Q

Aldehyde DHII is inhibited by

A

disulfiram (antabuse)

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11
Q

what do you nee for the oxidation step from acetaldehyde to acetate?

A

NAD+

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12
Q

What is a common feature of reduced activity of aldehyde DHII?

A

red face

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13
Q

E487K is a mutation in

A

Aldehyed DHII; reduced activity

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14
Q

why is a mutation that reduces the activity of ADHII so bad?

A

acetaldehyde is a carcinogen and the longer it takes to get it oxidized the higher the risk of developing esophogeal cancer

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15
Q

How can we convert acetate to acetyl-CoA?

A

with AcetylCoA synthetase and ATP

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16
Q

production of NADH inhibits

A

Gluconegensis by reducing Oxaloacetate

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17
Q

A fraternity (sorority?) pledge arrives at the ER confused, hypoglycemic and with a high liver NADH. This person:
A. Will show cocaine in the urine
B. Is a type II diabetic
C. Takes amitryptyline
D. Has been consuming alcohol
E. Has been exposed to infected bodily fluids

A

D. Has been consuming alcohol

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18
Q

Production of NADH stimulates

A

triglyceride formation

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19
Q

what role does acetaldehyde play in fatty liver disease?

A

it increases transcription factors driving FA synthesis and inhibits transcription factors supporting FA oxidation

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20
Q

Alcoholics are often _____ deficient

A

thiamine

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21
Q

thiamine deficiency leads to (2) possible dx.

A

(1) Wernicke’s

(2) Korsakoff’s

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22
Q

Wernicke’s encephalopathy is what phase?

A

Acute

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23
Q

Wernicke’s encephalopathy acronym

A

COAT

24
Q

Korsakoff’s psychosis is what phase

A

chronic

25
Q

Korsakoff’s psychosis acronym

A

RACK

26
Q

COAT

A

C- confusion
O- ophthalmoplegia
A- ataxia
T- thiamine Tx.

27
Q

RACK

A

R- retrograde amnesia (lose old)
A- anterograde amnesia (no new)
C- confabulation
K- korsakoff’s psychosis

28
Q

ethanol vs methanol

A

ethanol has higher affinity to alcohol DH

29
Q

Methanol forms

A

formate

30
Q

formate leads to

A

tissue damage (eye), acidosis

31
Q

anti-freeze

A

glycols

32
Q

glycols forms

A

glycolic acid

33
Q

glycolic acid leads to

A

acidosis (kidney failure)

34
Q

where is ethanol absorbed

A
  • 20% stomach

- 80% intestine

35
Q

clearance of alcohol is a relatively

A

slow process

36
Q

Disulfuram is an inhibitor of

A

ALDH2

37
Q

Habitual drinkers activate a

A

cytochrome p450

38
Q

what does MEOS do?

A

clears alocohol faster than normal

39
Q

fomepizole is a pharmacologic inhibitor of

A

ADH

40
Q

if women typically have more fat what happens with alcohol?

A

they experience higher blood ethanol levels

41
Q

alochol is

A

water-soluble

42
Q

NAD+ is an ______ and thus gets

A

NAD+ is an oxidizing agent and thus gets reduced

43
Q

ADH1B*2 has a _____ km and ______ vmax

A

higher

44
Q

MEOS leads to what being reduced?

A

NACP+ reduced to NADPH

45
Q

ALDH2 is a ______ and has a _______ effect

A

ALDH2 is a tetramer and has a dominant-negative effect

46
Q

acetate is either converted ______ or released _______

A

acetate is either converted to acetyl-CoA or released as acetic acid

47
Q

OAA is a precursor to _____ thus inhibits_______ leading to ________

A

OAA is a precursor to Glucose thus inhibits Gluconeogenesis leading to hypoglycemia

48
Q

increased NADH concentration affects___________ by inhibiting the oxidation of ________ to acetyl-CoA

A

fatty acid metabolism by inhibiting the oxidation of fatty acids to acetyl-CoA

49
Q

Glycerol-3-phosphate serves as a precursor molecule to

A

triglyceride

50
Q

alocholics are often

A

thiamine deficient

51
Q

Moonshine

A

ADH to formaldehyde

52
Q

formaldehyde is converted to formate via

A

ADH2

53
Q

what can be used as competitive inhibitors of ADH?

A

fomepizole/ethanol

54
Q

formate causes

A

tissue damage and acidosis

55
Q

Glycol cause severe ____ but can also be tx with _____

A

causes severe acidosis but can be tx. with alcohol