rheumatoid arthritis Flashcards
what type of disorder is rheumatoid arthritis
it is a Chronic systemic inflammatory auto-immune disorder
what are some symptoms of rheumatoid arthritis
Joint inflammation, synovial proliferation, destruction of articular cartilage
what is the pathogenesis of rheumatoid arthritis
immune complexes activate complement which in turn releases cytokines. the cytokines release one of the two
- TNF-a, IL-1
- prostaglandins
what would DMARDs (disease modifying anti-rheumatic drugs) do to a patient suffering with rheumatoid arthritis
To inhibit / halt the underlying immune process /prevent the long-term damage (articular cartilage damage, bone erosions)
what are some side effects of taking methrotrexate
Oral ulcerations, Nodulosis, nausea, GI upset, cytopenias, liver damage, chest infection
how does cyclosporine treat RA
inhibits IL-1 and IL-2 receptor production. Its major adverse effect is nephrotoxicity, which gets attenuated with NSAIDs, enzyme inhibitors.
NOTE ( NOT IN USE CURRENTLY)
why is azathioprine not used frequently in the medical field
Use in RA is declined due to toxicity (BM depression, leukopenia, thrombocytopenia, alopecia, increased risk of infections etc)
what is the advantage of using hydroxychloroquine instead of other DMARDS
has less effects on the liver and immune system than other DMARDs
what are some mechanisms of action of leflunomide
It reduces DNA / RNA synthesis, hence lymphocyte proliferation
Antibody production by B-cells may be depressed.
what are some side effects of leflunomide
diarrhoea, headache, rashes, loss of hair, thrombocytopenia, liver damage, increased chances of chest infections
what is the mechanism of action of sulfasalazine
Sulfapyridine- active moiety, suppress the generation of superoxide free radicals and cytokine release by inflammatory cells
Also used for early, mild R.A in combination with methotrexate and / or hydroxychloroquine.
what do TNF-a inhibitors do to reduce effects of RA
Shown to decrease signs and symptoms of R.A, reduce progression of structural damage, and improve physical function.
by inhibiting the TNF-a
what are the risks of using TNF-a inhibitors
increased risk for infections (tuberculosis, sepsis), fungal opportunistic infections, and pancytopenia.
what is the mechanism of action of adalimumab
antibody that binds to TNF-α, thereby interfering with endogenous TNF-α activity by blocking its interaction with cell surface receptors
what is the mechanism of action of etanercept
Genetically engineered, soluble, recombinant, fully human receptor fusion protein that binds to TNF-α, thereby blocking its interaction with cell surface TNF-α receptors.
what is the mechanism of action of golimumab
neutralizes the biological activity of TNF-α by binding to it and blocking its interaction with cell surface receptors.
what is the mechanism of action of infliximab
binds specifically to human TNF-α and inhibits binding with its receptors. Approved for use in combination with methotrexate in patients with RA who have had inadequate response to methotrexate monotherapy.
what is the mechanism of action of Anakinra which is a IL-1 receptor antagonist
Anakinra treatment leads to a modest reduction in the signs and symptoms of moderate to severe R.A in patients, Used in DMARDs failure cases, Less clinically effective than TNFα inhibitor
why are corticosteroids used to treat RA
Can be inducted at any stage in R.A along with first / second line drugs
Commonly used in patients with R.A to provide symptomatic relief and bridge the time until DMARDs are effective
how are corticosteroids administered
In case of single/few joint involvement with severe symptoms, intra-articular injection of glucocorticoid afford relief for several weeks, joint damage may be slowed
how do we choose which drug to use dependant of how far the patient is
In low disease activity: Monotherapy may be initiated with any of the DMARDs
In moderate to high disease: activity or inadequate response to monotherapy: combination DMARD therapy or use of anti-TNF drugs
For patients with more established disease, use of other biologic therapies (Non-TNF like abatacept, rituximab) can be considered.
