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20 Cards in this Set
- Front
- Back
Recommended max daily dose of acetaminophen?
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4g for adults
75mg kids |
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How does hepatic necrosis occur in acetaminophen tox
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Hepatic metabolism through glucuronidation and sulfation gets saturated
so the acetaminophen is metabolized by the P450 system breaks down to N acetyl-p-benzoquinoneimine (NAPQI) which depletes intracellular glutathione. When less than 30% of normal, NAPQI binds to other hepatic macromolecules and hepatic necrosis begins |
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When hepatic stores of glutathione are < ___% hepatic injury beings
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30%
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Which stage of acetaminophen tox does the following describe, and at what time frame does this occur:
Anorexia, nausea, vomiting, malaise lab: hypokalemia |
Stage 1
first 24 hours |
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Which stage of acetaminophen tox does the following describe, and at what time frame does this occur:
Improvement in anorexia, nausea, and vomiting. Abdominal pain, hepatic tenderness Labs: elevated serum transaminases; elevated bili and prolonged PT time if severe |
Stage 2
2-3 days |
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Which stage of acetaminophen tox does the following describe, and at what time frame does this occur:
Recurrence of anorexia, nausea, and vomiting; encephalopathy; anuria; jaundice Labs: hepatic failure, metabolic acidosis; coagulopathy; renal failure; pancreatitis |
Stage 3
3-4 days |
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Which stage of acetaminophen tox does the following describe, and at what time frame does this occur:
Clinical improvement and recovery or deterioration and death/multi organ failure |
Stage 4
after day 5 |
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what populations are at greater risk for developing acetaminophen induced hepatotox following OD?
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Alcoholics and pts on anticonvulsants
both of these have reduced glutathione reserves because of increased P450 activity |
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give the toxic acetaminophen exposure for a single ingestion
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>10 grams or 200 mg/kg
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give the toxic acetaminophen exposure for a 24 hour period
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>10 grams or 200 mg/kg over a 24 hour period
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give the toxic acetaminophen exposure for a 2 consecutive days
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>6 grams or 150 mg/kg per 24 hour period
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In what time frame is the Rumack-Matthew nomogram for acetaminophen applicable?
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single exposure
between 4 hours and 24 hours post ingestion treatment should be given if above the line |
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patients above the line in the APAP nomogram have what kind of risk?
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60% hepatotox
1% renal failure 5% mortality |
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T/F
aggressive forms of decontamination such as gastric lavage or whole bowel irrigation should be used in APAP OD |
FALSE
acetaminophen is rapidly absorbed so these often do not help. Plus NAC works well |
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GI decontamination that should be used in APAP tox
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Activated charcol
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Tx for APAP OD?
how does it work |
acetylcysteine
in early poisoning (<8 hrs): prevents NAPQI binding to hepatic macromolecules by possibly reducing it (acts as glutathione precursor or substitute) >24 hours: acts as an antioxidant decreasing neutrophil infiltration improving microcirculatory blood flow and preventing necrosis |
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If treatment of APAP OD is initiated within WHAT TIME FRAME you will see a nearly 100% effective prevention of hepatotox
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8 hours
|
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T/F
NAC should not be given after 24 following APAP ingestion |
FALSE
still effective |
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loading dose for NAC?
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150 mg/kg
remember the tox dose is 150, the tx is 150 |
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T/F
Activated charcoal inhibits the clinical effectiveness of acetylcysteine |
FALSE
it does absorb it but there is no evidence that it inhibits its effectiveness |