NAPLEX Exam Dumps : North American Pharmacist Licensure Examination

Acetaminophen is metabolized by choices A through D. The major route is glucuronidation catalyzed by UDP- glucuronyl transferase in the liver. Sulfation is the next most common route and is the target mechanism for NAC therapy. Oxidation by cytochrome P-450 results in the formation of N-acetyl-p-benzoquinone imine, which is responsible for the hepatic necrosis caused by acetaminophen overdose. Direct renal excretion represents approximately 5% of the metabolism of acetaminophen. Plasma metabolism of acetaminophen does not generally occur.

Metformin should be stopped when eGFR falls below 30. This is the only cutoff that is recommended for absolute discontinuing. If the eGFR falls between 30-44 while ontherapy, benefits and risks of discontinuing should be evaluated. New initiation is only recommended when eGFR >45.

It is reasonable to add triglyceride-lowering medications such as fibrates or niacin to prevent pancreatitis in those with triglyceride levels >500 mg/dL, which applies to this patient as his TG level is 640 mg/dL . C. is wrong because gemfibrozil should not be initiated in patients on statin therapy because of an increased risk for muscle symptoms and rhabdomyolysis. Fenofibrate may be considered concomitantly with a low- or moderate- intensity statin when triglycerides are above 500 mg/dL,2, however he is on a high intensity statin therapy. For niacin, the IR dose should start at 100 mg TID2 and niacin does not lower triglyceride levels as much as fibrate do.4 Fenofibrates are dose adjusted for renal function lower than 60 mL/min to 54 mg/mL, so this dose is appropriate for this patient because of his renal function being above 60 mL/min. The best option is fenofibrate 162 mg daily, but this needs to be monitored for any symptoms of muscle pain exhibited by the patient, especially as the patient is at a higher risk due to being a diabetic. Fish oil is not a first line agent to treat hypertriglyceridemia.