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FAimmunosuppressants
immunosupression drugs (Immuno Chap of First Aid 2010)
| Question | Answer |
|---|---|
| antibody mediated rejection | hyperacute. type II hypersensitivity. presence of preformed donor ab's in transplant recipient. MINUTES. |
| transplant rejection that happens minutes after transplantation | hyperacute |
| cell-mediated rejection due to cytotoxic t cells | Acute. Due to cytotoxic t cells reacting against FOREIGN MHC. occurs weeks after transplantation. Reversible with cyclosporine and OKT3 |
| rejection: weeks after transplant | acute. Reversible with cyclosporine and OKT3. CTL's react against foreign MHC. |
| cause of acute rejection | cytotoxic t-cells react against foreign MHC's. Reversible with cyclosporine and OKT3 |
| T-cell and antibody mediated organ rejection. | chronic. type IV hypersensitivity. causes vascular damage (obliterative vasc damage); occurs months to years after transplant. IRREVERSIBLE. MHC I (non-self) is perceived by cytotoxic t-cells as MHC-I (SELF) presenting NON-SELF ANTIGEN. |
| occurs months to years after transplant | chronic. type IV hypersensitivity. causes vascular damage (obliterative vasc damage); occurs months to years after transplant. IRREVERSIBLE. MHC I (non-self) is perceived by cytotoxic t-cells as MHC-I (SELF) presenting NON-SELF ANTIGEN. |
| acute transplant - reversible? | yes with cyclosporine and OKT3 |
| chronic rejection - reversible? | no. |
| cause of chronic rejection | chronic. type IV hypersensitivity. causes vascular damage (obliterative vasc damage); occurs months to years after transplant. IRREVERSIBLE. MHC I (non-self) is perceived by cytotoxic t-cells as MHC-I (SELF) presenting NON-SELF ANTIGEN. |
| cause of hyperacute rejection | antibodies against donor tissue (preformed). minutes after transplant. type II hypersensitivity. |
| damage that occurs with chronic rejection | vascular fibrosis (obliterative). |
| graft-versus-host disease cause | GRAFTED IMMUNOCOMPETENT T CELLS proliferate in the irradiated immunocompromised host and reject cells wtih "foreign" proteins (considered non-self bc these are found in recipient). result: severe organ dysfunction. |
| GVH Dz symptoms | maculopapular rash, jaundice, hepatosplenomegaly, diarrhea |
| Grafted immunocompetent t cells attack foreign proteins in immunocompromised host | Graft vs host disease. result: severe organ dysfunction. symptoms: maculopapular rash, jaundice, hepatosplenomegaly, diarrhea |
| types of cells in gvhd | t-cells from immunocompetent donor. results in severe organ dysfxn as these t-cells attack "foreign" proteins of host. |
| Cyclosporine - MOA | binds to cyclophylins. complex blocks differentiation and activation of t-cells by INHIBITING CALCINEURIN, preventing IL-2 and receptor production. |
| inhibit calcineurin | cyclosporine. blocks il-2 production and its receptor as well. |
| toxicity of cyclosporin. preventable? | predisposed to viral infections and lymphoma. nephrotoxic (preventable with mannitol diuresis) |
| predisposed to viral infections and lymphoma. nephrotoxic (preventable with mannitol diuresis) | toxicity of cyclosporin. |
| how to prevent cyclosporin toxicity | mannitol diuresis |
| uses of cyclosporin | organ transplant - prevent rejection. autoimmune disorders. |
| Use of immunosuppressant: organ transplant - prevent rejection. autoimmune disorders. | uses of cyclosporin |
| Tacrolimus - MOA | similar to cyclosporin (inhib calcineurin). binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines. |
| tacrolimus - toxicity | significant - nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion, hyperglycemia |
| tacrolimus - use | potent immunosuppressive in organ transplant rejections |
| similar to cyclosporin (inhib calcineurin). binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines. | Tacrolimus - MOA |
| significant - nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion, hyperglycemia | tacrolimus |
| potent immunosuppressive in organ transplant rejections | tacrolimus (FK506) |
| azathioprine - MOA | antimetabolite precursor of 6-MP. interferes w/metabolism and production of nucleic acids. toxic to proliferating lymphocytes. |
| azathioprine - clinical use | kidney transplant, autoimmune (glomerulonephritis, hemolytic anemia) |
| azathioprine - toxicity | bone marrow suppression. mercaptopurine (active metabolite) is metabolized by xanthine oxidase. thus toxic effects may be increased by allopurinol. |
| antimetabolite precursor of 6-MP. interferes w/metabolism and production of nucleic acids. toxic to proliferating lymphocytes. | azathioprine |
| clinical uses: kidney transplant, autoimmune (glomerulonephritis, hemolytic anemia) | azathioprine |
| toxicity: bone marrow suppression. mercaptopurine (active metabolite) is metabolized by xanthine oxidase. thus toxic effects may be increased by allopurinol. | azathioprine |
| muromonab-CD3 (OKT3) - MOA | monoclonal ab that binds to CD3 (epsilon chain) on the surface of t-cells. blocks cellular interaction with CD protein responsibl for t-cell signal transduction = decreased cell activation |
| muromonab-CD3 (OKT3) - clinical use | kidney transplant |
| muromonab-CD3 (OKT3) - toxicity | cytokine release syndrome. hypersensitivity. |
| tox: cytokine release syndrome. hypersensitivity. | muromonab-CD3 (OKT3) |
| clinical use: kidney transplant | muromonab-CD3 (OKT3) |
| MOA: monoclonal ab that binds to CD3 (epsilon chain) on the surface of t-cells. blocks cellular interaction with CD protein responsibl for t-cell signal transduction = decreased cell activation | muromonab-CD3 (OKT3) |
| MOA: binds to mTOR and inhibits t-cell proliferation in response to IL-2. | sirolimus (rapamycin) |
| sirolimus (rapamycin) MOA | MOA: binds to mTOR and inhibits t-cell proliferation in response to IL-2. |
| use: kidney transplant (with cyclosporine and corticosteroids) | sirolimus (rapamycin) |
| sirolimus (rapamycin) - cinical use | use: kidney transplant (with cyclosporine and corticosteroids) |
| sirolimus - toxicity | hyperlipidemia, thrombocytopenia, leukopenia |
| tox: hyperlipidemia, thrombocytopenia, leukopenia | sirolimus - toxicity |
| mycophenolate mofetil - MOA | inhibits de novo guanine synthesis and blocks lymphocyte production, bc lymphocytes do not have a purine salvage pathway and rely on de novo synth of purines. |
| MOA: inhibits de novo guanine synthesis and blocks lymphocyte production, bc lymphocytes do not have a purine salvage pathway and rely on de novo synth of purines. | mycophenolate mofetil - MOA |
| MOA: monoclonal ab with high affinity for the IL-2 receptor on activated t cells | daclizumab (basilimab is newer and more potent) |
| daclizumab (basilimab is newer and more potent) - MOA | MOA: monoclonal ab with high affinity for the IL-2 receptor on activated t cells |
| recombinant cytokines | aldesleukin (IL-2), epo, filgrastim (G-CSF), sargramostim (GM-CSF), a-interferon, b-interferon, g-interferon, oprelvekin (IL-11), thrombopoietin |
| aldesleukin | aldesleukin. IL-1. renal cell carcinoma and metastatic melanoma |
| IL-1. renal cell carcinoma and metastatic melanoma | aldesleukin. |
| anemias (esp in renal failure) | Erythropoietin. anemias (esp in renal failure). |
| Erythropoietin. | Erythropoietin. anemias (esp in renal failure). |
| filgrastim | G-CSF. recovery of bone marrow. filgrastim |
| G-CSF. recovery of bone marrow. | filgrastim |
| sargramostim | sargramostim. GM-CSF. recovery of bone marrow. sargramostim |
| GM-CSF. recovery of bone marrow. | sargramostim |
| alpha-interferon - use and MOA | Hep B, C, kaposi's sarcoma, malignant melanoma, leukemia. MOA: inhibit viral DNA synthesis by inducing ribonuclease (which degrades viral mRNA not host) |
| Hep B, C, kaposi's sarcoma, malignant melanoma, leukemia. MOA: inhibit viral DNA synthesis by inducing ribonuclease (which degrades viral mRNA not host) | alpha-interferon |
| beta-interferon - use and MOA | multiple sclerosis. MOA: inhibit viral DNA synthesis by inducing ribonuclease (which degrades viral mRNA not host) |
| multiple sclerosis. MOA: inhibit viral DNA synthesis by inducing ribonuclease (which degrades viral mRNA not host) | beta-interferon |
| gamma-interferon - use and MOA | chronic granulomatous disease. MOA: increase MHC1 and 2 expression and antigen presentation in all cells. Activates NK cells to kill virus-infected cells. |
| chronic granulomatous disease. MOA: increase MHC1 and 2 expression and antigen presentation in all cells. Activates NK cells to kill virus-infected cells. | gamma-interferon |
| oprelvekin | IL-11. use for: thrombocytopenia |
| IL-11. use for: thrombocytopenia | oprelvekin |
| thrombopoietin | use for thrombocytopenia |
| use for thrombocytopenia | thrombopoietin. |
Created by:
pecanpie792
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