Flashcards in MSK drugs Deck (13):
allopurinol: mechanism, uses, side effects, interactions
inhibits xantine oxidase and decreases the conversion of xanthine to uric acid. also used in lymphoma and leukemia to prevent tumor lysis-associated urae nephropathy.
side effects and interactions:
1. increases the concentrations and toxicities of azathioprine and 6-MP.
What are the preventive drugs for gout?
allopurinol, febuxostat (also inhibits xanthine oxidase), probenecid, colchicine
probenecid: mechanism and interactions
inhibits reabsorption of uric acid in the PCT (also inhibits secretion of penicillin)
What drugs can be given for acute gout attacks?
NSAIDs (naproxen, indomethacin), glucocorticoids, colchicine
How does colchicine work?
binds to and stabilizes tubulin to inhibit microtubule polymerization, impairing leukocyte chemotaxis and degranulation. it has value as both an acute or a prophylactic agent
TNF-alpha inhibitors: side effects, names
names: etanercept, infliximab, adalimumab
all TNF-alpha inhibitors predispose to infection, including reactivation of latent TB, since TNF blockade prevents activation of macrophages and destruction of phagocytosed micorbes
etanercept: mechanism, use
fusion protein made by recombinant DNA that works as a TNF decoy receptor to inhibit TNF-alpha. used for RA, psoriasis, ankylosing spondilitis.
infliximab, adalimumab: mechanism, use
anti-TNF alpha monoclonal antibodies used for IBD, RA, ankylosing spondylitis, and psoriasis.
bisphosphonates: names, mechanism of action
aldronate, other -dronates.
these ar epyrophosphate analogs that bind hydroxyapatite in bone and inhibit osteoclast activity.
bisphosphonates: uses and toxicities
used for osteoporosis, hypercalcemia, and paget disease of bone.
may cause corrosive esophagitis (pts need to take it with water and remain upright for 30 minutes afterward) and osteonecrosis of the jaw. you must exercise caution in patients with renal failure.
acetaminophen: mechanism, overdose, antidote
reversibly inhibits cyclooxygenase, mostly in the CNS. inactivated peripherally.
overdose produces hepatic necrosis. NAPQI depletes glutathione and forms toxic tissue adducts in the liver. N-acetylcysteine is the antidote- it regenerates glutathione.
What are the COX-2 inhibitors? advantages and disadvantages?
reversibly inhibit specifically the COX-2 enzyme, which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain. spares COX-1, which helps maintain the gastric mucosa. Also spares platelet function as TXA2 production is dependent on COX1. therefore, there is an increased risk of thrombosis. sulfa allergy.
used for RA, osteoarthritis, gastritis, ulcers.