I found this, Kittie, quite informative: http://www.snowtigermed.com/cgi-local/viewarticle.pl?doc=20000919200157

It states the stages of apap toxicity as these:

"Clinical Stages of Hepatic Toxicity in APAP Poisoning

Phase I (occurs between 1/2 and 24 hours post-ingestion): Initially, the patient experiences nausea and vomiting with anorexia. The patient may display pallor and sweating with a complaint of malaise, or they may appear entirely normal. Extreme, repetitive vomiting may be the only clue to severe phase I poisoning. This can be mistaken for a viral or other illness including other toxic ingestion.

Phase II (occurs between 24 and 72 hours post-ingestion): There is a decrease in phase I symptoms. Hepatic involvement clinically begins to declare itself clinically with RUQ discomfort. Elevations of both the liver enzymes (aminotransferases: AST and ALT) and the bilirubin begin to appear. Absolute elevation of the liver function tests (LFTs) does not predict degree of hepatic damage. Prolongation of the PT occurs. Diminished hepatic urea production may lead to a diminished BUN; however, despite the low BUN, renal function may also be at risk secondary to APAP - induced effects on the kidneys. Oliguria is a clinical marker and may appear in phase II.

Phase III (occurs between 72 and 96 hours post-ingestion): GI symptoms reoccur with nausea and vomiting as the most prominent. Hepatic necrosis with a centrilobular pattern leads to jaundice, and possibly, hepatic encephalopathy or even coma. Coagulopathy may produce bleeding and renal dysfunction may develop with a decreased urine output and possibly, anuria. Myocardial dysfunction with microscopic changes is reported. Death may occur in phase III secondary to liver failure.

Phase IV (occurs between 4 days and 2 weeks hours post-ingestion): Resolution may begin as early as the 4th day post-ingestion if hepatic injury is not too severe. Complete recovery of hepatic structure and function will occur if there is resolution of the hepatotoxicity and the patient had no hepatic parenchymal abnormality prior to the ingestion. If the patient had prior hepatic structural injury and recovers from an APAP overdose the only residual structural changes are those that were present prior to the overdose. Progressive hepatic dysfunction and need for liver transplantation occurs if the damage is irreversible."

And I feel kind of stupid right now, because I just realized I totally miscalculated how much APAP I took today. It is more like 5000 mgs, which is not so serious considering the top dosage is 4000 mgs. Not that it is good for my liver anyway. I am going to be MUCH more aware of how much APAP I am taking each day from now on and I am grateful to have had an eye opener like this.