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3.1 cards > Alcohol Metabolism > Flashcards

Alcohol Metabolism Flashcards

1
Q

Why does oral ingestion lead to lower blood ethanol level than IV

A

First pass metabolism in the stomach but mostly in the liver (80-85%)

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2
Q

Excretion of unmetabolised alcohol

A

3-10% breath, urine and sweat

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3
Q

BAC

A

detectable within 5 mins and max after 30-90 mins.

effect of -Oh = concentration and duration of exposure

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4
Q

Three alcohol metabolism pathway

A

Main = ADH
Peroxisome pathway by catalase
Microsomes pathway with CYP2E1
ALDH2 = second, common pathway

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5
Q

ADH pathway details

A

Alcohol –> acetaldehyde (via ADH) and then Acetaldehyde to Acetate (via ALDH)

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6
Q

Expressive drinking is accumulation of

A

toxic acetaldehyde

because 3 pathway leading to this stage but then only one ahead

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7
Q

ADH class mainly responsible for alcohol metabolism

A

Class I ADH in liver

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8
Q

Class of ADH recruited in chronic or heavy drinkers

A

Class III ADH

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9
Q

Class of ADH in gastric mucosa

A

Class IV

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10
Q

Acetaldehyde metabolism

A

predominantly ALDH2

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11
Q

Asian flush

A

ALDH 2*2 genetic polymorphism - reduce rate of metabolism

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12
Q

Microsomal Ethanol Oxidizing system (MEOS)

A

Ethanol + NADPH + H + O –> acetaldehyde + NADP + water
catalysed by microsomal cytochrme P450 2E1
increased 4-10 folds in chronic or large -OH consumption

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13
Q

significance of CYP 450 use in chronic and large alcohol consumption

A

used for drug metabolism, increased actitivty = beneficial for detoxification but also harmful because you get heptotoxicity from drugs

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14
Q

When is MEOS pathway utilised

A

large/chronic -OH consumption.
low affinity to ethanol vs high affinity hepatic ADH.
Can occur in Brain

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15
Q

Catalase-mediated alcohol oxidation

A

Marginal pathway in liver except fasted state
fatty acids –> hydrogen peroxide, then thats used with catalase to make acetaladehyde
MAJOR IN BRAIN (b/c ADH not physiologically active in brain)

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16
Q

Non-oxidative pathway

A

high BAC
Fatty acid ethyl ester (FAEE) in chronic alcohol abuse –> steatosis –> alcoholic pancreatitis (in pancreas, low ADH so use non-oxidative pathway more)

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17
Q

Mechanism for beneficial effect of alcohol consumptions

A

Resveratrol

  • anti-oxidant
  • anti-thrombotic : inhibit thromboxane synthesis and platelet aggregation, increase vasodilatory prostacyclin synthesis
  • inhibit oxidation of LAL cholestrol and increase HDL cholestrol
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18
Q

Tissue damage in excessive drinking caused by

A

Acetaldehyde

19
Q

Physiological effects of excess acetaldehyde

A

“alcohol sensitivity” in periphery

  • facial flushing, throbbing in head and neck
  • headache, nausea, vomiting
  • sweating, thrist, chest pain, palpitation
  • dyspnea, hyperventilation, tachycardia
  • hypotension, syncope, marked uneasiness
  • weakness, vertigo, blurred vision, confusion
20
Q

Health effects of heavy -OH use

A

Thiamin deficiency
Vit B6 and folate deficiency
increased disease risk
malnutrition

21
Q

How does excess alcohol cause liver injury

A

Chronic alcohol - increases gut permeability which increase endotoxin from gram -ive bacteria entering this activates kupffer cells in liver which then released cytokines (like TNFa) and ROS which lead to inflammatory response, oxidative stress and activation of hepatic stellate cell

22
Q

Role of hepatic stellate cell in liver dibrosis

A

in normal cells , HSC = store Vit A and maintain ECM like collagen and regulate BF
activated in liver injury by Kupffer cells –> increase cell proliferation and migration and increase collagen type 1 synthesis which leads to liver scarring and fibrosis

23
Q

3 pathways leading to detrimental effects of alcohol oxidation

A
  1. acetaldehyde adduct formation
  2. Increase ROS formation
  3. Increase NADH:NAd ratio
24
Q

Acetaldehyde adducts

A

Excess acetaldehyde combined with DNA, lipid or protein can induce immune response that leads to liver damage

25
Q

Sources of oxidative stress

A
  1. Due to increase MEOS CYP2E1 - which leads to production of ROS
  2. due to excess NADH, which is oxidised to NAD and causes O2 to go to O2 -ive
26
Q

Excess NADH formation

A

Alters NADH and NAD ration - changes carb and lipid metabolism - redox state, –> hypoxia –> liver damage

27
Q

why can’t be metabolise glucose in excess NADH formation

A

inhibition of TCA cycle

28
Q

Result of NADH excess and altered glucose metabolism

A
  • no gluconeogenesis, –> depletion of glycogen stores –> hypoglycemia
  • increase lactate –> lactic acidosis
29
Q

Lipid metabolism nd NADH excess

A

can’t enter citric cycle as Acetyl CoA

reduced FA metabolism and increase FA synthesis

30
Q

Result of NADH excess and altered lipid metabolism

A

excess FA and acetyl CoA accumulates in liver –> alcohol induced ketosis –> fatty liver and alcoholic steatosis

31
Q

Effect of acute alcohol ingestion on NT

A 
- inhibit excitatory glu NT
agonist for GABA a thus -
- increase GABA release 
also 
- increase 5-HT
- activate opioids and -
- cannabinoid R
increase DA release
32
Q

Dry beri beri

A

peripheral neuropathy

33
Q

Wet beri beri

A

congestive heart fail

34
Q

Effects of Thaimine deficiency

A

Beriberi = lesion in PNS

Wenicke-Korsakoff syndrome - lesions in CNS

35
Q

Some features of Wernicke’s encephalopathy

A
  • gait ataxia (lack of coordination)
  • ophthalmoplegia (eye nerve paralysis)
  • mental confusion/memory loss
36
Q

Treatment of wernicke’s encephalopathy

A

IV B-vitamin complex

37
Q

Korsakoff

A

chronic debilitating amnesia

38
Q

Role of Thaimine

A
  1. important in cellular reactions - pentose phosphate pathway, glycolysis, citric acid cycle
  2. imp in carb –> energy
  3. critical in CNS function - synthesis of Ach and GABA
39
Q

pathway for brain damage in alcoholics

A
  1. altered cerebral energy metabolism
  2. oxidative stress and inflammation
  3. impaired NT function
40
Q

Which alcohol metabolism pathway happens in the mitocondria

A

Acetaladehyde –> acetate via ALDH2

41
Q

Which alcohol metabolism pathway happens in the cytosol

A

Ethanol –> acetaladehyde via ADH

42
Q

Which alcohol metabolism pathway happens in the Perisomes

A

Ethanol –> acetaladehyde via Catalases

43
Q

Which alcohol metabolism pathway happens in the Microsomes

A

Ethanol –> acetaladehyde via CYP2E1 MEOS pathway

3.1 cards (13 decks)

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