3.6-ALCOHOL!!! Flashcards

1
Q

Since the two main reactions involving alcohol use dehydrogenase’s…WHAT by product are we making a lot of?

A

NADH!! We are taking H’s off things, and filling up all of our taxi cabs! It explains all of the problems w/ EtOH consumption.

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2
Q

What is the general legal limit for DUI?

A

80mg/dL or .08g/dL

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3
Q

What two features allow EtOH to be absorbed EVERYWHERE in the body? What is its method of absorption?

A

Polar AND hydrophobic. Best of both worlds!…. Diffusion

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4
Q

Where is 80% of EtOH absorbed? What about the other 20%? Where is it mostly OXIDIZED (dehydrogenated!)

A

80% in s.i. and 20% in liver…Mostly oxidized in the Liver (some in stomach and si)

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5
Q

About how much EtOH goes unabsorbed and expelled through sweat, urine, feces, breath, saliva, and milk?

A

10%

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6
Q

What is the product of the first reaction of EtOH oxidation? REGARDLESS of route taken..(there are 4 routes)

A

Acetaldehyde=freaking toxic

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7
Q

Which EtOH oxidation pathway begins in the cytosol and is for naive drinkers?

A

Alcohol Dehydrogenase

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8
Q

Which EtOH oxidation pathway is inducible (for habitual drinkers) and occurs in the Smooth ER? What is the main enzyme in this system? (Dr.T would be upset if I get this wrong)

A

the Cytochrome P450 system MEOS (microsomal-EtOH-Oxidating-System)…. Main enzyme: Cytochrome-Y-2-E-1

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9
Q

What is the major EtOH oxidation rxn in the Brain/CNS happening in peroxisomes?

A

Catalase Dependent Oxidation

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10
Q

What is “first pass” EtOH oxidation? (its the same rxn as ADH, this is unique c/o location)

A

Gastric Oxidiation

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11
Q

What is the easiest enzyme to become saturated? Where is the enzyme housed? What is the hardest?

A

Alcohol Dehydrogenase in the mitochondria….vs MEOS a 1000x difference!!

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12
Q

What is the second reaction of EtOH oxidation? What is the enzyme?

A

Acetaldehyde–>Acetate using Acetaldehyde Dehydrogenase 2

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13
Q

What are the two ways the end product of Acetakdehyde dehydrogenase can be used?

A

Acetate can then be used to build stuff (acetate—>acetyl-CoA—>fat) or used for energy 30kJ/g

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14
Q

What are the three NEGATIVE outcomes of EtOH metabolism?

A

1.Acetaldehyde is an adduct (clingy and disruptive) 2. Increases ROS (reactive oxygen species) 3. Fills up all the taxi cabs (high NADH/NAD+ ratio)

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15
Q

What might be the leading cause for the almighty HANGOVER?

A

the build up of Acetaldehyde (very close to formaldehyde=toxic!!)

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16
Q

WHERE is the second step (acetaldehyde dehydrogenase) occurring?

A

In the mitochondria (weird, more breaking down in mitochondria)

17
Q

What are the two main structural features of Alcohol Dehydrogenase?

A

Its a DIMER and it has ZINC in it!

18
Q

What is the general name for the different classes of ADH? What is the main class of these?

A

Isozymes=iso enzymes…Class I most important

19
Q

Rank the effectiveness of the ALDH2s: 1/1, 1/2, & 2/2 (converting acetaldehyde to acetate)

A

1/1 > 1/2 > 2/2.. I’d definitely a 2/2

20
Q

What is the ONE main reason for ALL the negative effects of Alcohol in the body? Hyperlactacidemia, hyperuricemia, hypoglycemia, ketosis, hyperlipemia, fatty liver, adducts, abnormal protein trafficking….

A

DECREASED NAD+/NADH ratio

21
Q

Why in the world would alcohol cause hypoglycemia?!

A

GNG gets suppressed because excess NADH goes towards making more MALATE and LACTATE instead of glucose

22
Q

What does EtOH do to ADH to cause dehydration?

A

EtOH inhibits AntiDiureticHormone, so you pee out more becoming dehydrated!

23
Q

What is the build up of lactate called coupled with dehydration?

A

Lactic Acidemia

24
Q

What is the result of a build up of acetyl-CoA when glycogen stores are depleted and GNG is suppressed?

A

Ketonemia!

25
Q

What is the result of increased ketones and lactate competing with uric acid for the renal pump? AND you have increased breakdown of purines in muscle…

A

HyperUricemia

26
Q

What is the result of acetaldehyde adducts to tubilin causing impaired microtubule function in the liver?

A

Fatty liver

27
Q

How does EtOH affect the N.T. Gluatmate?

A

Glutamate is a major Exititory NT and EtOH INHIBITS Glutamate RECEPTOR function

28
Q

How does EtOH affect the NT GABA?

A

GABA is a major inhibitory NT and EtOH ENHANCES GABA RECEPTOR function

29
Q

What does EtOH do to the NT dopamine?

A

Increases Dopamine (excitement and stimulation)

30
Q

What does EtOH do to the NTs Endorphins?

A

Increases endorphins (pain reduction/feeling high)

31
Q

Alcohol consumption leads to weight _____ in occasional drinkers and weight _____ in alcoholics.

A

Gain in occasional, loss in alcoholics…GO FIGURE!

32
Q

Alcohol Vitamin deficiency: this syndrome is the cause of low thiamin (B1) levels..

A

Wernicke-Korsakoff syndrome

33
Q

What is the result of low folic acid (B9) levels due to EtOH?

A

Anemia

34
Q

What degrades Vit A (Retinol) in EtOH metabolism? This can cause blindness YO!

A

the MEOS pathway

35
Q

What are the four reasons alcohol might have a bigger effect on women then men?

A
  1. Less total body water 2. ADH less affective in stomach 3.Menstral cycle 4. Chronic abuse not handled well