Intern Year: Tintinalli- Section 15-Ch 184-Acetaminophen Tox

Front 1

Recommended max daily dose of acetaminophen?

Back 1

4g for adults

75mg kids

Front 2

How does hepatic necrosis occur in acetaminophen tox

Back 2

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

Front 3

When hepatic stores of glutathione are < ___% hepatic injury beings

Back 3

30%

Front 4

Which stage of acetaminophen tox does the following describe, and at what time frame does this occur:

Anorexia, nausea, vomiting, malaise

lab: hypokalemia

Back 4

Stage 1

first 24 hours

Front 5

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

Back 5

Stage 2

2-3 days

Front 6

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

Back 6

Stage 3

3-4 days

Front 7

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

Back 7

Stage 4

after day 5

Front 8

what populations are at greater risk for developing acetaminophen induced hepatotox following OD?

Back 8

Alcoholics and pts on anticonvulsants

both of these have reduced glutathione reserves because of increased P450 activity

Front 9

give the toxic acetaminophen exposure for a single ingestion

Back 9

>10 grams or 200 mg/kg

Front 10

give the toxic acetaminophen exposure for a 24 hour period

Back 10

>10 grams or 200 mg/kg over a 24 hour period

Front 11

give the toxic acetaminophen exposure for a 2 consecutive days

Back 11

>6 grams or 150 mg/kg per 24 hour period

Front 12

In what time frame is the Rumack-Matthew nomogram for acetaminophen applicable?

Back 12

single exposure

between 4 hours and 24 hours post ingestion

treatment should be given if above the line

Front 13

patients above the line in the APAP nomogram have what kind of risk?

Back 13

60% hepatotox
1% renal failure
5% mortality

Front 14

T/F

aggressive forms of decontamination such as gastric lavage or whole bowel irrigation should be used in APAP OD

Back 14

FALSE

acetaminophen is rapidly absorbed so these often do not help. Plus NAC works well

Front 15

GI decontamination that should be used in APAP tox

Back 15

Activated charcol

Front 16

Tx for APAP OD?

how does it work

Back 16

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

Front 17

If treatment of APAP OD is initiated within WHAT TIME FRAME you will see a nearly 100% effective prevention of hepatotox

Back 17

8 hours

Front 18

T/F

NAC should not be given after 24 following APAP ingestion

Back 18

FALSE

still effective

Front 19

loading dose for NAC?

Back 19

150 mg/kg

remember the tox dose is 150, the tx is 150

Front 20

T/F

Activated charcoal inhibits the clinical effectiveness of acetylcysteine

Back 20

FALSE

it does absorb it but there is no evidence that it inhibits its effectiveness