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FAimmunosuppressants

immunosupression drugs (Immuno Chap of First Aid 2010)

QuestionAnswer
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