620 Alcohol Lecture
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1. How many calories in 12 oz beer or 7.5 oz wine?
2. Where does absorption occur? Does it require transporters, regulation etc?
3. How does gender make a difference? Why?
4. What is avg clearance g/hr? How long does it take the process one beer?
5. What are the 3 main mechs of ethanol metabolism? where do they occur?
- 1. 150 calories
- 2. Stomach (no, quickly absorbed)
- 3. Females experience higher ethanol absorption and slower clearance b/c men have ADH in the stomach (it's metabolized before it enters bloodstream, so less absorbed & less to process)
4. 10g/hr. 8 hrs to clear to driving limit
5. ADH, MEOS (microsomal ethanol oxidizing system) and catalase. Liver
Alcohol Dehydrogenase Pathway
1. Requires what? (3) What implication does this have?
2. How much of alcohol is processed this way?
3. Where does this occur?
4. What is int?
- 1. Alcohol dehydrogenase, acetalydehyde dehydrogenase, 2NAD+ as electron acceptor (using NAD+ disrupts metabolism)
- 2. >90% of EtOH
- 3. Liver
- 4. Int = acetaldehyde
1. Where does it occur?
2. What enzyme is used?
3. What cofactor is required?
4. How is it regulated?
5. Is this pathway preferred? Why or why not?
- 1. Present in smooth ER
- 2. Carried out by cytochrome p450
- 3. NADPH (not NAD+!)
- 4. Upregulated in the liver by alcohol presence
- 5. No, b/c it requires p450 and produces oxidants.
Describe catalase & ethanol metabolism
1. What can it do?
2. What does it require? Not?
3. Where does this mainly occur?
4. Does it contribute a lot to metabolism?
5. Why is this preferred or not preferred?
- 1. Converts ethanol to acetaldehyde
- 2. NOT NAD+, but uses hydrogen peroxide which is nice.
- 3. Liver
- 4. No.
- 5. NOT preferred b/c it takes up valuable catalase activity which could be used to preventing other oxidant activity.
1. Where is ALDH present in cell?
2. What is it necessary for?
3. What can limit or inhibit its activity & mit localization?
4. What inhibits this?
5. What is required for its use? (2)
- 1.Cytosol and mitochondria (liver)
- 2. All 3 metabolizing pathways (all of them require acetaldehyde --> acetate)
- 3. polymorphisms
- 4. Antibuse
- 5. NAD+ and glutathione (when large quantities are consumed, this is a problem)
1. Describe mech behind ALDH polymorphism
2. Who is most susceptible to symptoms?
3. What are the symptoms? (2)
3. What race is esp susceptible?
1. Glu487Lysine of ALDH2 gene (referred to as ALDH2^2)
- 2. Heterozygotes
- 3. Facial flushing and intolerance to alcohol
- 4. Asians - 40% ahve this gene
1. Define alcoholism
2. Why did diagnosis increase in the mid 1980s?
3. What metabolites/etc do we have to worry about? (3)
- 1. Disorder characterized by excessive consumption of & dependence on alcohol disrupting psych, social and vocational function.
- 2. B/c of better diagnosis
- 3. Ethanol itself, NAD+ consumption, and acetaldehyde production
What are the direct effects of ethanol? (14)
- 1. Induces microsomal cytochrome p450
- 2. Alters cell membranes
- 3. Alters blood pressure
- 4. Suppresses immune cell function/increased infection
- 5. Destroys intestinal barrier
- 6. Inhibits ADH/Dehydration
- 7. Depresses sensory and emotional sensors/Depression
- 8. Replaces food intake
- 9. Heart attack/stroke
- 10. Empty calories
1. How does EtOH affect BP acutely?Chronically? How?
2. Which negative effects of ethanol do we go into detail about? (4)
3. Functional unit of the liver?
4. What is found in the liver cells?
- 1. Decreases (Increases NO productoin & vascular smooth muscle production)/increases (increase of vascular responseiveness to B-adrenergic receptor agonists - NE.
- 2. Hypertension, immune cell function, pancreatitis and diabetes, alcoholic liver disease
- 3. Liver acinus
- 4. Lots of hepatocytes - specifically in the liver sinusoid
How does EtOH affect:
1. Immune cell function? (4)
- Response to acute & chronic alcohol
-How it alters food composition/intake (3)
3. What heart problem is it associated w/?
1. Chronic alcoholics shows increased susceptibility to infection. Mech: suppression of peripheral T cell response --> decreased endothelial cell adhesion expression --> increases macrophages responsiveness in liver.
2. Acute ethanol --> NO release --> vasodilation. Chronic heavy EtOH --> increases vascular responsiveness to B-adrenergic receptor agonists (NE). Et OH meatbolism decreases monoamine clearance.
Also contributes to central obesity, which is associated w/ hypertension development (alters food intake, increases caloric intake, promotes lipid accumulation).
3. Left ventricular dilatation (cardiomyopathy)
1. How can EtOH lead to diabetes?
2. What is the amount in g needed per day for how many years?
3. What cells are specifically affected?
4. What is the result? (3)
- 1. By atrophying the pancreas
- 2. 150 g/day for 10 years
- 3. Acinar cells
- 4. (1) Decreased enzyme/protein secretion (2) Activation of pancreatic stellate cells --> FIBROSIS and (3) inhibition of glucose production by liver (stops pyruvate decarboxylase activity)
1. What is the consequence of NAD+ consumption? (6)
- 1. Decreased pyruvate
- 2. Increased lactate
- 3. Gout
- 4. Decreased glycolysis & GNG
- 5. Decreased lipid metabolism --> less acetate
1. What is the impact of acetaldehyde production? (5)
- 1. Cross-links cellular proteins
- 2. Peroxidation of lipids
- 3. Inhibits DNA repair by adducting to DNA
- 4. Acute peripheral vasodilation (flushing)
- 5. Sedative effects
1. What effects of ethanol are the ones that contribute to alcoholic liver disease? (3) 1-1, 2-2, 3-2)
2. What does this lead to? (4)
1. Disrupted intestinal barrier function (increased gut permeability), increased oxidant stress in liver (less available antioxidants and lipid accumulation), activation of immune cells in liver (Kupffer cells, lymphocytes)
2. Steatosis, inflammation, fibrosis, cirrhosis.
1. What can prevent EtOH induced liver injury?
2. What is increased in blood of chronic alcoholics?
3. How does the above affect the gut?
4. How is the above handled by liver?
- 1. Gut sterilization (no bacteria)
- 2. Endotoxin (LPS)
- 3. Increases permeability
- 4. (1) LPS is sensed by Kuppfer cell
- (2) TLR4 and CD14 dimerize and bind LPS to clear infection
- (3) These immune cells activate transcription of 1- pro-inflammatory cytoines and -2- oxidants (superoxide) to kill bacteria.
1. What is responsible for EtOH induced liver injury? How was this proven?
2. What drives fatty liver? (Steatosis)
1. Endotoxin (LPS). CD-14 knockout alcoholic mice did not develop EtOH induced injury. They had low ALT (liver enzyme) AND TNF-a
2. Inflammatory component drives lipid accumulation
1. Role of TNFa in EtOH induced liver injury? (3)
2. Why do females have increased blood ethanol levels?
3. What do they also have that causes more hepatocellular damage? (2)
1. Inhibits mit function, increases oxidant production, activates macrophages & other immune cell populations that propagate inflammation.
MEDIATES hepatocyte damage.
2. No ADH in stomach
3. Estrogen --> upregulates CD14 on kupffer cells --> worse ethanol induced liver pathology.
1. What % of chronic alcoholics become cirrotic?
2. Can liver fibrosis be reversed? At what cost?
3. What is irreversible?
4. What is the toxic metabolite?
5. What happens to liver? (2)
6. What cytokines contribute to this?
7. What does this eventually lead to?
- 1. 20
- 2. Yes, but scar tissue will remain
- 3. Cirrhosis
- 4. Acetaldehyde
- 5. Chronic liver injury --> apoptotic hepatocytes
- 6. TnFa and B from Kuppfer cells
- 7. Activation of stellate cells.
How does alcohol affect nutrition?
- Calorie % in heavy drinkers?
- What types of deficiency?
- Intestinal function
-Urine output (2)
- 1. 60%
- 2. Protein/vitamin deficiency due to decreased food intake
- 3. Reduced intestinal function --> disrupted absorption
- 4. Fluid loss, dehydration
1. How does alcohol relate to breast cancer?
2. How do probiotics help liver damage?
1. Increased alcohol --> increases risk of developing breast cancer
2. Probiotics suppress specific pathogneic bacteria preventing T cell activation & function --> less inflammatory response.
1. How can low to moderate consumption help health? (5) 1 is bad
2. How does heavy consumption NOT help health? (7)
- 1. Reduces BP
- 2. REduces risk of other diseases (stroke, diabetes, arthiritis, dementia, cancer)
- 3. Inhibits atherosclerotic plque formation
- 4. Suppresses sensory/emotional centres of brian
- 5. Decreases insulin sensitivity & glucose tolerance (NOT GOOD)
- HEAVY CONSUMPTION:
- 1. Increases BP
- 2. Promotes cardiomyopathy
- 3. Disrupts glucose homeostasis
- 4. Impairs normal drug metabolism
- 5. Induces oxidant productoin
- 6. Increases carcinogenesis in the liver
- 7. Promotes liver injury and scarring.
How does alcohol affect CVD? (5)
- 1.. Decreases risk of MI & stroke
- 2. Decreaed thrombin and coagulation factors
- 3. Incrases HDL
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