NAPLEX Exam Dumps : North American Pharmacist Licensure Examination

Thiazolidinediones may cause fluid retention through proposed mechanism of increasing reabsorption in the collecting duct of the kidney and increasing vascular permeability in adipose tissue. Bile acid sequestrants work in the intestine to bind bile acids which doesn’t affect fluid retention. GLP-1 receptor agonists work to activate these receptors to secrete insulin from beta pancreatic cells/decrease glucagon secretion/ increase satiety and doesn’t affect fluid retention. SGLT2 inhibitors actually cause increase of fluid elimination through the kidneys. Alpha-glucosidase inhibitors work in the gut to decrease carb absorption/digestion and have no affect on fluid retention.

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.

The following NSAIDs belong to the propionic acid derivatives group - Ibuprofen - Ketoprofen - Naproxen - Fenoprofen - Flurbiprofen - Oxaprozin whereas piroxicam belongs to the class of Enolic acid derivative which also includes other agents like meloxicam and Nabumetone. They are non-selective COX inhibitors and act by preventing the production of certain prostaglandins.