| Term 
 
        | What are some causes of gout? |  | Definition 
 
        | genetics, gender, overweight, too much alcohol, foods (liver, dried beans, peas, anchovies, gravies), enzyme defect, Pb expsoure, drugs (diuretics, aspirin, niacin, cyclosporin, L-dopa) |  | 
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        | Term 
 
        | What is the most common treatment for an acute attack of gout? |  | Definition 
 
        | NSAIDS (indomethacin, naproxen) |  | 
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        | Term 
 
        | What can one due to prevent an accute attack? |  | Definition 
 
        | take small daily doses of colchicine/NSAIDs, maintain healthy weight, eat properly, drink fluids |  | 
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        | Term 
 
        | How does colchicine work? |  | Definition 
 
        | binds to tubulin>prevents polymerization/microtubule formation>inhibits leukocyte migration/phagocytosis>inhibts leukotriene B4 formation |  | 
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        | Term 
 
        | When and how is colchicine administered? |  | Definition 
 
        | When NSAIDs/corticosteroids don't work, administer orally every hour until symptoms improve |  | 
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        | Term 
 
        | What are the ways to treat hyperuricemia? |  | Definition 
 
        | reduce UA production: allopurinol increase UA excretion: probenicid, high doses of aspirin
 |  | 
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        | Term 
 
        | What you should be careful of when using probenicid? |  | Definition 
 
        | can't use in patients w/renal dysfxn, or patients already secreting large amounts of uric acid GI irritation (take w/food), rash, may intiially aggravate gout (treat w/colchicines first)
 |  | 
        |  | 
        
        | Term 
 
        | Why should you not use aspirin as an analgesic for patients w/gout? |  | Definition 
 
        | at low doses, aspirin will inhibit secretory transporters and cause uric acid retention |  | 
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        | Term 
 
        | What are the adverse effects of long term glucocorticoid use? |  | Definition 
 
        | weight gain, diabetes, cataracts, osteoporosis |  | 
        |  | 
        
        | Term 
 
        | What drugs can you use to slow the progression of RA? |  | Definition 
 
        | mehtotrexate (most common): increases release of adenosine/anti-inflam mediator hydroxycholoquine: inhibits TNF signal
 sulfasalazine: may prevent absorption of antigens from GI tract
 |  | 
        |  | 
        
        | Term 
 
        | What are the risks of TNF alpha inhibitors? |  | Definition 
 
        | can cause serious infections, possibility of demyelinating diseases, may reactive latent TB |  | 
        |  | 
        
        | Term 
 
        | When do you use etanercept, and how does it work? |  | Definition 
 
        | use etanercept as subcut injection 2x/week, for RA, psoriatic arthritis, ankylosing arthritis it binds/inhibits TNF molecules
 |  | 
        |  | 
        
        | Term 
 
        | When should you not use etanercept? |  | Definition 
 | 
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        | Term 
 
        | What is the use of infliximab, and what is it's MOA? |  | Definition 
 
        | used for Chron's, alone or w/MTX a monoclonal antibody that inhibits TNF-A
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | fully human antibody against TNF-A (blocks it from interacting w/p55 and p75 surface receptors) subcutaneous injection every other week, alone or with methotrexate
 used for RA
 AE: injection site reactions, opportunistic infections
 |  | 
        |  | 
        
        | Term 
 
        | What is the MOA of anakinra? |  | Definition 
 
        | IL1R antagonist: blocks IL1 from cartilage degradation by induction of loss of proteoglycans and bone resorption |  | 
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        | Term 
 
        | When do you use anakinra? |  | Definition 
 
        | in patients >18yo who failed 1 or more DMARD, do NOT use w/anti-TNF drugs AE: injection site rxn, serious infections, lymphoma
 |  | 
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        | Term 
 
        | Name the lymphocyte antagonists. |  | Definition 
 
        | leflunomide, abatacept, rituximab |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | inhibits dihidroorotate dehydrog>decreased UMP: cells arrest in G phase, mostly reduces B cells, some T cells converted to active drug in intestines and liver
 similar efficacy to MTX
 AE: diarrhea, reversible alopecia, elevated liver enzymes, C/I in pregnancy, may increase ibuprofen/other NSAIDs
 |  | 
        |  | 
        
        | Term 
 
        | What is the MOA of abatacept? |  | Definition 
 
        | prevents binding w/ CD28 on T cells (inhibits T-cell activation) used IV every 2 weeks
 used for mod/severe RA w/inadequate response to other DMARDs, do NOT use w/TNF antagonists or anakinra
 |  | 
        |  | 
        
        | Term 
 
        | What are the AEs of abatacept? |  | Definition 
 
        | increase in infections, headache, nasopharyngitis, nausea, may exacerbate COPD |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | monocolonal antibody, binds CD20 on B cells and causes lysis used IV @ day 1 and 15; used w/MTX when unresponsive to anti-TNF
 AE: chills, fever, headache, nausea, myelosuppression (long term use)
 |  | 
        |  | 
        
        | Term 
 
        | What do you use to treat psoriatic or ankylosing arthritis? |  | Definition 
 | 
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        | Term 
 
        | What do you use to treat Chron's disease? |  | Definition 
 | 
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        | Term 
 
        | Which drug can increase your risk of opportunistic infections? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Which drug do you need to do a CBC for because of the risk of neutropenia? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | cholestyramine can increase the elimination of what drug? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | How is rituximab administered? |  | Definition 
 | 
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