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-immunosuppression -anti-inflammatory -Chronic use: increased infections, ulcers, hypergylcemia, osteoporosis -treats: autoimmmune diseases, transplant rejection, hypersensitivity |
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-inhibits calcineurin phosphatase -impairs t-cell response to antigen -GVHD (bone marrow trnspt), aplastic anemia (ineligible), autoimmune diseases |
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-inhibits calcineurin phosphatase -impairs t-cell response to antigen -100x more ptoent then cyclosporine --GVHD (bone marrow trnspt), aplastic anemia (ineligible), autoimmune diseases |
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-inhibit t-cell activation and proliferation -tolerance -decrease t-cell response -transplant rejection, GVHD, autoimmune diseases |
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-immunosupression -converted to thioinosinate- stops purine synthesis -transplant rejection, RA -coadm w/allopurinol toxic -increased risk of skin caner |
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-inhibition of inosine monophosphate dehydrogenase, therefore blocks purine synthesis -transplant rejection -DO NOT admin. with antacids! -co.adm with antacids containing magnesium and aluminum hydroxides decreases absorption |
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-sphingospine 1-P receptor agonist -sequesters lymphocytes in the lymph nodes and Peyer’s patches of the small intestines -transplant rejection -decreased HR in 30% - |
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-MOA; Induces a T-cell response cytolytic for tumor cells -Therapeutic use: Advanced malignant melanoma and renal cell cancer. Toxicity: Hypotension, arrhythmias, peripheral edema, elevated liver function, anemia, thrombocytopenia, nausea, diarrhea, fever. |
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-mAb- Anti-IL2 Receptor -given with Basiliximab (mAb) -MOA: block interleukin-2 receptor on T-lymphocytes Use:transplant rejection (kidney) Toxicity: none, well tolerated |
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-Ig against CD3 on T-cells -blocks antigen recognition site -Tox: ctokine release syndrome -transplant rejection |
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-Ig against TNFa -Uses: both w/ Methotrexate for RA patients who do not respond to methotrexate alone -Crohn’s disease inflammatory bowel disease Toxicity: increased infections |
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-Ig against TNFa -Uses: both w/ Methotrexate for RA patients who do not respond to methotrexate alone Toxicity: increased infections |
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-anti-D antibodies -blocks anti-Rh antibodies -MOA: Block antibody response of Rh-mother an to Rh+ baby. - Use:Prevention of hemolytic disease of Rh+ newborns |
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Bacillus Calmette-Guerin (BCG) |
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-viable attenuated strain of Myobacterium bovis -MOA: T cells and natural killer cells stimulation -Uses:bladder cancers -Toxicity: severe hypersensitivity and shock |
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-MOA: promote T lymphocyte and early stem cells differentiation -SCID |
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Filgrastim (Granulocyte colony stimulating factor) |
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-MOA: Expands the population of neutrophil granulocyte precursors and augments granulocyte function. -Therapeutic use: Prophylaxis of chemotherapy-induced neutropenia. -Toxicity: Bone pain in lower back, sternum and pelvis |
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Sargramostim (Granulocyte-macrophage colony stimulating factor) |
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-MOA: effective on bone marrow progenitors -Uses: anemia resulting from AIDS, renal failure, cancer chemotherapy, prematurity and some chronic inflammatory conditions. -Toxicity: During hemodialysis patients may need more anticoagulants. A readjustment of hypertensive drug dose may be required for hypertensive patients to avoid encephalopathies and seizures. |
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Thalidomide + Lanalidomide |
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NEVER GIVE TO PREGNANT WOMEN -MOA: dont know yet -Uses: Treat multiple myeloma patients, both newly diagnosed and those who previously received chemotherapy and have relapsed or now have refractory cancer. -Lenalidomide is also used to treat myelodysplastic syndrome in which the blood stem cells do not mature or function normally and either die in the bone marrow or soon after they enter the blood -Toxicity: Thalidomide: sedation and constipation and peripheral neuropathy Lenalidomide: toxicity is less severe but may cause leucopenia, hepatotoxicity and renal dysfunction. |
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