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Describe the inherent contradiction involved in initiating DMARD treatment early |
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Describe why the term DMARD is a misnomer |
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It wont reverse the damage done to bone and cartilage. It will only prevent future damage. |
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Explain how its MOA makes methotrexate a DMAARD and an anti-cancer agent |
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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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Apply the dosing of leflunomide to a clinically-relevant case study |
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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 |
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DMARDs work better when given early but the problem is that they are |
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usu given after other txs |
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slow acting anti rheumatic drug |
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disease modifying anti rheumatic drug |
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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. |
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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. |
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what two drugs can be combined for a greater effect |
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methotrexate and leflunomide |
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Apply the length of time that DMARDs and Mabs need to show effects of reducing new lesions to a clinically-relevant case scenario. |
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Describe the role of the major histocompatibility complex and T-cell surface antigens in T-cell activation. |
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Definition
Presents the antigen to the TCR. Know the 3things that have to happen |
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Apply one advantage and one disadvantage of treating RA with glucocorticoids to a clinically-relevant case scenario |
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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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adalimumab etanercept infliximab golimumab |
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three things needed for T cell activation |
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APC CD80/86 - T cell CD28 APC MHC - T cell TCR APC LFA - T cell CD2 |
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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. |
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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. |
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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). |
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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. |
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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. |
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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. |
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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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