Week 4 - CASE 4 - ALCOHOL - Skildum Flashcards Preview

Uncategorized > Week 4 - CASE 4 - ALCOHOL - Skildum > Flashcards

Flashcards in Week 4 - CASE 4 - ALCOHOL - Skildum Deck (8):

After consumption, in what tissues does ethanol partition? What tissues exclude ethanol?

Alcohol preferentially goes to muscle and brain
Doesn't like adipose and bone


Pathway alcohol is metabolized:

Ethanol to acetaldehyde by ADH. Acetaldehyde to Acetate by aldehyde dehydrogenase.
Microsomal Ethanol Oxidizing System (MEOS)
Cyp2 converts alcohol to acetaldehyde. More active in chronic alcoholics. Also linked to ethanol aversion to those with overactive Cyp2


Question #3: How do inherited mutations in ethanol metabolizing enzymes alter carriers’ susceptibility to alcoholism?

ALDH mutation to decrease function can give you TERRIBLE hangovers
ADH*3, ADH*2, ADH*2 – increase Vmax of enzyme, these mutations make you less susceptible to alcoholism.
Ethanol makes you euphoric, converted quickly to acetaldehyde – makes you sick


What does disulfiram target and what kind of inhibition is it?

IT targets ALDH. It inhibits it competitively. This means that the Vmax stays the same and the Km is going to increase.


While you were considering options to resolve your patient's hypotension, you briefly considered administering intravaneous dopamine, but you ultimately decided to give him norepinephrine instead. Would dopamine have been effective in restoring normal blood pressure in a patient taking disulfuram?

NO! Super low blood pressure you could give dopamine, but in this case you don’t want to do it because disulfiram actually inhibits dopamine hydroxylase. That’s the reaction that would eventually turn it into nroeprinephrine. So it's not going to help with hypotension at all.


What receptor(s) does norepinephrine activate? What type(s) of cells express this receptor?

Norepinephrine acts predominantly on alpha-adrenergic receptors to produce constriction of resistance and capacitance vessels, thereby increasing systemic blood pressure and coronary artery blood flow.


Can products of ethanol metabolism contribute to triglyceride production?

Acetyl Coa – the product of ethanol breakdown cab be used to synthesize fatty acids and TAGs


During episodes of hypertrigeleridemia, a patient's serum cholesterol only rose modestly. Is this observation significant in suggesting an underlying cause of the hypertriglyceridemia?

NADH and acetyl Coa will inhibit oxidation of FAs. Fats can’t be oxidized so they are just floating around in the blood. They also can’t be stored. This is because serum cholesterol would be coming from dietary fats, ethanol is going straight into triacylglycerides, causing elevated amounts in the blood.