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11 Cards in this Set
- Front
- Back
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Explain under normal conditions how tylenol is excreted at an normal dose
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-acetaminophen is broken down through phase 1 and pase 2 metabolism
-it goes through phase two metabolism through glurcoronidation and sulfiation -CYP2E1 will attempt hydroxylation |
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explain under normal conditions how tylenol is excreted at a high dose
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-CYP2E1 will deal with the larger dose, some will still go through phase one and phase 2 metabolism as normal,
-the large amount of aceptaminophine will be transformed into NAPQI (a quinone) -NAPQI will either bind to liver Thiols and and cause cell death or NAPQI will congugate to GSH to be excreted with the help of GST |
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what would change about the large dose acetamiophen excretion is there was a SAA dietary protein deficiency
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- if there was a SAA deficiency there would be a decrease in PAPS which are crucial in sulfation conjucation and excretion in phase II metabolism
-this would result in a decrease in urinary surfur output -there would be a decrease in hepatic GSH and GTS and the glucoronidation pathway of phase two metabolism -an increase of urunary glucuronides and MA conjgates -there woul be an increase in liver damage |
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REgarding the clearnece of xenobiotics in the blood: the clearnece rate is ___________ to the current concentration
it follows ___ kinetics |
proportienet , first
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true or false the Kel is the elimination rate constant it predicts the proportion of does excreted per hour. It is reletivle constant and percice.
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false. the kel is the eliminaton of hte rate contant and it does predict the proportion of does excreted per hour, however the actual clearnece is always lower than the kel
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why is the clearnece of kel actually less than the number itself?
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this is because there are many pools of the xenobiotic around the body ( GI, liver, kidney, lung) and they will equilibriate at different rates
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increased liver necrosis over time will lead to a tollerence and there for overall decrease in liver ciroisis
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false, increase liver necrosis over a long time will lead to increase cirosiss
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in what case would mercapuric acid formation occur and how
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in a SAA deficinecy, ,most of the acetaminophen will go through CYP450 to produce a NAPQI quinone, of the NAPQI that will conjucate to GSH, the mecuapturic acid will actylate and conjugate from GST.
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explain acetaminophen excretion under fasting conditions
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-becasue glucouse is low, glucuronidation will be lower to conjugate
-fasting low carb diet will produce ketones that will incuce CYP2E1 -fasting will decrease GSH -this will mean that that there is an increase in NAPQI which can increase bingding of NAPQI to thiols and increase liver damage |
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explain how consuming acetominophen at the same time as ethanol can alter excretion
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an increase of ethanol will increase CYP2E1, CYP2E1 will convert ethanol to aldehyde, this will competitively inhibit the spot on the CYP2E1 so that acetaminophen will not be able to bind and it will be metabolized more slowly, this will decrease necrosis
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explain how taking a large dose of acetaminophen after a night of drinking alcohol can alter excretion , including vomiting and dihereas
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-ethanol the night before will mean an increase in CYP2E1 in liver already
-vomiting and diharea will mean a decrease in both SAA and glucouse, meaning a decrease in sulfation and glucuronidation -the CYP2E1 will convert ethanol to acetaldehyde and casue oxygen radical leakage as well as H2O2, -H2O2 will use GSH to convert into H2O to be excreted -There will be a decrease in the GSH -overall there will be a large amount of the acetaminophen converted to NAPQI and the lack of GSH will mean the majority of the NAPQI will bind to protein thiols and cause liver cell necrosis |
