Gout drugs Flashcards
Blocks formation of uric acid
allopurinol
Breaks down uric acid
Pegloticase
Increases excreation of uric acid in urine
Probenecid
reduces degree of inflammation in pts from gout crystal depois
steroids, indomethacin, Colchicine
Goals of gout tx
• Increase excretion of uric acid • Inhibit inflammatory cells • Inhibit uric acid biosynthesis • Provide symptomatic relief – Typically with NSAIDS or steroids (short-term)
Why is aspirin contraindicated in tx of gout
dose depended effect: low dose see decreased uric acid excreation large dose: see increase uric acid excreation via blocking reabsorpiton by interaction with OAT transporter
A patient that cannot take a NSAID for relief to acute gout symptoms has the following options
• Wait until symptoms subside (usually within a few days, in some cases longer) • Take low dose colchicine (within 48 hrs of attack) • Intraarticular glucocorticoid injections • Take celecoxib Low dose oral steroids
What do the following have in common: • Methotrexate • Sulfasalazine • Hydroxychloroquine • Azathioprine • N-penicillamine • Mycophenolate mofetil • Leflunomide
NON-Biological DMARDs
What do the following have in common: • Etanercept • Infliximab • Adalimumab • Rituximab • Anakinra • Abatacept • Tocilizumab • Belimumab • Apremilast • Tofacitinib • Secukinamab • Ustekinumab
Biological DMARDS
are a class of drugs which includes monoclonal antibodies, receptor analogues, and chimeric small molecules designed to bind to or mimic their molecular targets
biologics
Advantages of biological DMARDS
advantages over conventional therapy in terms of potency, specificity, and theoretically decreased side effects, since the product is engineered to bind to or interfere with a distinct molecular target
blocks the co-stimulation of T cells.
Abatacept
____and____ inhibit the proliferation and activity of T cells and B cells.
Methotrexate leflunomide
Etanercept, infliximab, adalimumab, golimumab, and certolizumab work by:
inactivate TNF - α.
____blocks the action of IL-1, and_____ inactivates IL-6.
Anakinra tocilizumab
that inhibit T-cell activation and IL-2 production by regulation of gene transcription.
glucocorticoids
– irreversibly binds to and inhibits dihydrofolate reductase, resulting in inhibition of purine and thymidylic acid synthesis, thus interfering with DNA synthesis, repair, and cellular replication.
Methotrexate
– metabolized to sulfapyridine and 5-aminosalicylic acid; Mechanism not known but IgA and IgM rheumatoid factor production are decreased. In vitro suppression of T-cell activation and inhibition of B-cell proliferation; inhibit the release of inflammatory cytokines
Sulfasalazine
– Mechanism unclear. suppression of T-lymphocyte responses to mitogens, decreased leukocyte chemotaxis, stabilization of lysosomal enzymes, inhibition of DNA and RNA synthesis, and the trapping of free radicals.
Hydroxychloroquine
– cleaved to 6-mercaptopurine, which in turn is converted to additional metabolites that inhibit de novo purine synthesis; Cell proliferation thereby is inhibited, impairing a variety of lymphocyte functions
Azathioprine
– Chelates with lead, copper, mercury and other heavy metals to form stable, soluble complexes that are excreted in urine; depresses circulating IgM rheumatoid factor, depresses T-cell but not B-cell activity;
N-penicillamine
– converted to active metabolite that inhibits inosine monophosphate dehydrogenase, leading to suppression of T- and B-lymphocyte proliferation
Mycophenolate mofetil
– undergoes rapid conversion to its active metabolite, A77-1726. This metabolite inhibits dihydroorotate dehydrogenase, leading to a decrease in ribonucleotide synthesis and the arrest of stimulated cells in the G1 phase of cell growth. inhibits T-cell proliferation and production of autoantibodies by B cells.
Leflunomide
MOA of Sirolimus
inhibition of IL-2 REceptor signaling
