Pharmacology Flashcards
Acetaminophen
Reversible COX inhibitor, mostly in CNS
Non-inflammatory
N-acetylcystein is antidote to regenerate glutathione
Aspirin mechanism
Irreversibly inhibits COX 1/2 via acetylation–>decrease in TXA2 and protaglandins
Aspirin clinical use
low dose (less than 300mg)-decreases platelet aggregation med dose (300-2400)-antipyretic and analgesic high dose (2400-4000)-anti-inflammatory
Aspirin toxicity
Gastric ulceration, tinnitus, chronically can lead to renal failure, Risk of Reye syndrome in children with viral infections.
Causes resp. alkalosis early but transitions to mixed met. acid.-resp. alk.
Celecoxib mechanism
Reversibly inhibits COX2 only-found in inflammatory cells and vascular endothelium and mediates inflammation and pain (spares COX1 so helps with gastric mucosa)
Spares platelet function as TXA depends on COX 1
Celecoxib clinical use
RA, Osteoarthritis
Celecoxib toxicity
Increased risk of thrombosis. Sulfa allergy
Indomethacin
Closes PDA
Bisphosphonates mechanism
-dronates
Pyrophosphate analygs; bind hydroxyapatite in bone. Inhibits osteoclast activity
Bisphosphonates clinical use
Osteoporosis, hypercalcemia, Paget’s disease
Bisphosphonates toxicity
Corrosive esophagitis, osteonecrosis of jaw
Teriparatide mechanisms
Recombinant PTH analog given subcutaneously daily
^ osteoblastic activity
Teri has osteoporosis
Teriparatide clinical use
Osteoporosis, causes increased bone growth (vs. -dronates that are anti-osteoclast)
Teriparatide toxicity
Transient hypercalcemia
Allopurinol
Chronic gout-Xanthine oxidase inhibitor (decreases production of uric acid)
Also use with lymphoma and leukemia to prevent tumor lysis associated urate nephropathy
Increases azathioprine/6-MP