doc_clotaire
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A 24 yo chinese woman is brough to the ER in the morning 3 hours after she took 20 acetaminophen 500 mg tablet . She never had alcohol until last night when she drank alcohol for the first time . She had seafood and grapefruit juice for dinner last evening . She is otherwise healthly . She has 5 pack history of smoking . She is alert and oriented . Her Temp is 37.2 BP: 110 / 60 Pulse : 90/min RR : 20 /min Lab :
Hct ------------40 %
WBC ------------6000mm3
Platelet----------390000mm3
AST--------------30
ALT --------------20
Alkaline Ph -----60
Which of the following factor decrease her risk for hepatic injury ?
a ) smoking
b ) alcholol
c ) seafood
d ) grapefruit juice
e ) race
f ) gender
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| star1
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b ) alcholol
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| Justice
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b ) alcholol
but not a chronic use of it...
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| SILVER
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Justice wrote:
b ) alcholol
but not a chronic use of it...
could you plz explain ur reason
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| sprint123
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Acute alcoholism will not increase the toxicity -only chronic increases the risk of renal failure...
But,does alcohol,in this case,does it decrease the risk?????
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| me007
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it is grapefruit juice
blocks intestinal P-glycoprotein, which is modulator of intestinal drug transport
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| me007
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actually, might be not bcs
important drugs that are normally expelled by P-gp include digoxin, cyclosporine, saquinavir.
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| Justice
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silver wrote:
could you plz explain ur reason
Yes, please:
Patients with malnutrition, AIDS, chronic ethanol abuse, or anorexia nervosa may be at increased risk for morbidity because of deficient glutathione stores and inadequate detoxification of NAPQI. Patients with enhanced ability to make NAPQI due to induction of the P450 system, specifically cyp2E1, may be at increased risk of morbidity due rapid metabolism of a/ph into toxic substances.
In non-abusers, this cyp2E1 is not activated. Moreover, acute and simultaneous alcohol uptake suppresses it and compete with a/ph at a bnding site...
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| SILVER
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thanks justice
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| new_n_lost
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b ) alcholol
the reason being one the drug Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. When all the conjugation pathways r saturated then the excess APAP ( paracetamol or N-acetyl-p-aminophenol) gets picked up by the liver P450 Enzyme 2E1 ( CYP2E1) which coverts it into N-acetyl-p-benzoquinone-imine (NAPQI)which is highly toxic to the hepatocytes. Alcohol competes for this enzyme in the liver. In Acute Cases or First Time Over Ingestion of Alcohol leads to the complete saturation of this enzyme therefore the toxic metabolite of Acetaminophen is not formed.
While in Chronic Ingestion of Alcohol the Enzyme activity is increased n therefore there is increased production of NAPQI due up regulation/induction of the enzyme thus leading to the Alcohol - Acetaminophen syndrome.
Edited by new_n_lost on 05/01/07 - 05:17 PM
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| doc_clotaire
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 BIG TIME B
Same explanation given by Justice and New and Lost
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| doyoudig
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BBBBBB, competes for the same enzyme as acetaminophen, n as mentioned only in people that are social drinkers, not chronic alcoholics
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