| Term 
 
        | Describe the inherent contradiction involved in initiating DMARD treatment early |  | Definition 
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        | Term 
 
        | Describe why the term DMARD is a misnomer |  | Definition 
 
        | It wont reverse the damage done to bone and cartilage. It will only prevent future damage. |  | 
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        | Term 
 
        | Explain how its MOA makes methotrexate a DMAARD and an anti-cancer agent |  | Definition 
 
        | Slows down immune system and inflammation response. Stops DNA replication so fast replicating cells like cancer cells, immune cells, and GI cells cant replicate as fast. |  | 
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        | Term 
 
        | Apply the dosing of leflunomide to a clinically-relevant case study |  | Definition 
 
        | Need a loading dose bc it has a long half life |  | 
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        | Drug that has best benefit-to-risk ratio, I.e. fewer pts. drop out for toxicity or failure |  | Definition 
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        | DMARDs work better when given early but the problem is that they are |  | Definition 
 
        | usu given after other txs |  | 
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        | Term 
 | Definition 
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        | Term 
 | Definition 
 
        | slow acting anti rheumatic drug |  | 
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        | Term 
 | Definition 
 
        | disease modifying anti rheumatic drug |  | 
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        | Term 
 
        | At low dose inhibits aminoimidazolecarboxamide ribonucleotide (AICAR) transformylase and thymidylate synthetase. Thus it inhibits immune cell proliferation and stimulates apoptosis in them.
 Also inhibition of pro-inflammatory cytokines.
 |  | Definition 
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        | Term 
 
        | Active metabolite, A77-1726, inhibits dihydroorotate dehydrogenase, leading to arrest of stimulated cells in the G1 phase; inhibits T-cell proliferation and B-cell antibodies. A.E. include diarrhea (25%), elevation of liver enzymes, weight gain and increased blood pressure.
 |  | Definition 
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        | Term 
 
        | what two drugs can be combined for a greater effect |  | Definition 
 
        | methotrexate and leflunomide |  | 
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        | Term 
 
        | Apply the length of time that DMARDs and Mabs need to show effects of reducing new lesions to a clinically-relevant case scenario. |  | Definition 
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        | Term 
 
        | Describe the role of the major histocompatibility complex and T-cell surface antigens in T-cell activation. |  | Definition 
 
        | Presents the antigen to the TCR. Know the 3things that have to happen |  | 
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        | Term 
 
        | Apply one advantage and one disadvantage of treating RA with glucocorticoids to a clinically-relevant case scenario |  | Definition 
 
        | You suppress the inflammatory response and they work fast but you get withdrawal when you stop and can get asthma for instance and hyperglycemia. |  | 
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        | Term 
 | Definition 
 
        | adalimumab etanercept
 infliximab
 golimumab
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        | Term 
 | Definition 
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        | Term 
 | Definition 
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        | Term 
 | Definition 
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        | Term 
 | Definition 
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        | Term 
 | Definition 
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        | Term 
 
        | three things needed for T cell activation |  | Definition 
 
        | APC CD80/86 - T cell CD28 APC MHC - T cell TCR
 APC LFA - T cell CD2
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        | Term 
 
        | Mab that targets CD20 B lymphocytes. Used for RA that is refractory to anti-TNF agents.
 Used with methotrexate.
 Given in two IV infusions 2 weeks apart.
 |  | Definition 
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        | Term 
 
        | Abatacept binds to CD80 and 86 on the antigen-presenting cell, which normally would bind to CD28 on a T cell. Both MHC and this linkage need to occur for T cell to be activated to eventually stimulate macrophages. Abatacept blocks this. |  | Definition 
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        | Term 
 
        | Attach piece of leukocyte-function-associated antigen-3 (LFA-3) to Ab so that it binds to CD2 on T cell stops T-cell activation. Approved for plaque psoriasis. Reduces T cells in plaques, so must monitor T cell levels (stop if CD24 lymphocytes fall below 250 cells/μl).
 |  | Definition 
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        | Term 
 
        | Antibody complexes with soluble TNF-α itself. This prevents activation of macrophages and interrupts T-cell function.
 Indicated for RA, ankylosing spondylitis, and psoriatic arthritis.
 It decreases the rate of formation of NEW lesions.
 Ankylosing spondylitis is inflammation of vertebrae resulting in a fibrous or bony union.
 Psoriatic arthritis is arthritis with silvery-scaled maculopapules, predominantly at the elbows, knees, scalp and trunk.
 |  | Definition 
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        | Term 
 
        | Another TNF-α Ab that may also bind to bound TNF. Indicated as adalimumab but also for Crohn’s disease.
 This and methotrexate was better than methotrexate alone in reducing new erosions over 52-104 weeks.
 |  | Definition 
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        | Term 
 
        | Antibody generated from moieties of the TNF receptor. It binds to TNF-α. Approved for juvenile chronic arthritis and psoriasis as well.
 Monotherapy or with methotrexate.
 |  | Definition 
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        | Term 
 
        | Inhibit phospholipase A2, which liberates arachidonic acid. Inhibit COX II.
 When prednisone is used, do not exceed 7.5 mg/day. Gradual reduction should be encouraged.
 Insomnia, hypomania, acute peptic ulcers are occasionally seen after only a few days. Treating for more than 2 weeks can result in adrenal suppression.
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 | Definition 
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