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112 Cards in this Set
- Front
- Back
Glucocorticoids mechanism: 2 points
|
1. interfere with cell cycle of activated lymphoid cells. 2. inhibited production of inflammatory mediators
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|
Glucocorticoids 4 clinical use:
|
1. first line immunosuppressive therapy. 2. organ rejection or graft v host disease. 3. rhematoid arthritis, 4. inflammatory bowel disease
|
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Glucocorticoids 4 side effects:
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1. protein break down. 2. hyperglycemia 3. avascular / aseptic necrosis of bone. 4. iatrogenic Cushing's syndrome
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Glucocotricoids precautions and contraindications:
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precautions: hyperglycemia and osteoporosis; contraindications: diabetes and osteoporosis
|
|
Cyclosporine Mechanism including thing that metabolized it:
|
forms complex with cyclophilin and inhibits calcineurin; inhibits IL-1 and IL-2 productions; net results is inhibition of T cell activation; metabolized by liver P450 enzymes
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Cycloporine: clinical use
|
organ transplantation, graft v host disease, autoimmune disorders
|
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Cyclosporine: side effects
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nephrotoxicity (renal dysfunction) and hypertension; note dose dependent.
|
|
Cyclosporine Drugs that inhibit CYP3A:
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glucocorticoids (methyprednisolone) - results in elevated cycloporine blood concentrations
|
|
Cyclosporine: drug interactions
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Syngerstic nephrotoxictiy if coadministered with Tacrolimus
|
|
Tacrolimus: Mechanism:
|
inhbitis calcinerurin; metabolized by liver P450.
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tacrolimus Clinical use:
|
organ transplantation and graft v host disease
|
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tacrolimus: 3 side effects:
|
nephrontoxicity; hyperglycemia and diabetes and neurotoxicity.
|
|
Sirolimus: mechanism
|
inhibits activity of a protein kinase (mTor) involved in CELL CYCLE PROGRESSION thus blocking G1-S transition . not T CELL specific
|
|
Sirolimus: clinical use:
|
prevention of organ transplant rejections in combinatiion thearpy with a calcineirun
|
|
Sirolimus: side effects:
|
hyperlipemia and bone marrow suppression
|
|
Mycophenolate Mofetil mechanism:
|
inhbits activity of inosine monophosphate dehydrogenase ( INHBITS guanine nucleotide synthesis). B and T cells highly dependent on this pathway for cell proliferation thus the net result is inhibition of lymphocyte proliferation
|
|
Mycophenolate: Clinical Use:
|
prevention of transplant rejection in combination with glucocorticoids and calcineurin inhibitor
|
|
Mycophenolate Mofetil: side effect
|
hematologic (bone marrow suppression - leukopenai); gastrointestinal (diarrhea and vomiting)
|
|
Azathioprine mechanism:
|
production of a fradulent nucleotide (6-thio-IMP) that when incorporated into DNA prevents translation and cell proliferations
|
|
Azathioprine: 3 clinical use:
|
prevention of organ transplant rejection; rhematoid arthritis; induction and maintenance of remission of ulcerative colitis and crohn's disease
|
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Azathioprine: side effects:
|
bone marrow suppression (leukopenia, thrombocytonpenia and or anemia); hepatic toxicity
|
|
Methotrexate: mechanism:
|
inhbitis dihyrdrofolate reductase ( this interferes with synthesis of thymidylate purine nucleotides and amino acids serine and methionine)
|
|
Methotrexate: Clinical Use:
|
induce and maintain remission inflmmatoryy bowel disease (Crohn's); rheumatoid arthritis and graft vs host disease
|
|
Methotrexate: side effects
|
1. bone marrow depression, and hepatic damage
|
|
Cyclophosphamide: mechanism:
|
transfer alkyl group to cellular constituents (proteinsm DNA, RNA); DNA becomes crosslinked leading to cytoxicity loss of proliferating lymphoid cells supresses T and B cell function by 30-40%)
|
|
Cyclophosphamide: Clincal use:
|
MAJOR stoppage of T and B cells. Organ rejection after transplantation. high does over several days
|
|
Cyclophosphamide: Side effects
|
dose related toxicities in rapidly growing tissues (bone marrow, reproductive organs); nausea and vomiting
|
|
Antihymocyte Globin (ATG) mechanism:
|
a polyclonal antibody that upon binding activates cytotoxicity (complement and cell mediated); block lymphocyte function.
|
|
Antithymocyte Clinical use:
|
induction of immunosuppression and to treat acute renal transplant rejection.
|
|
Antithymocyte: Side effectss:
|
fever and chills (potential for hypotension); patient will develop antibodies. HAMA reaction.
|
|
Rho D immune Globuin: Mechanism
|
binds Rho antigens prevents sensitization of Rh negative women to Rh-positive fetus .
|
|
Muromonab-CD3: mechanism
|
blocks antigen recognition - naive T cells and CTLs. Binds to CD3.
|
|
Muromonab-CD3: Side effects:
|
- cytokine release syndrome and HAMA reactions.
|
|
Basilizimab and Daclizumab Mechanism:
|
IL-2 antagonist; blocks IL-2 binding
|
|
Basilizimab and Dacilizumab Clinical use and Side effects:
|
used to prevent acute organ rejections; Side effects Gastronintestinal disorders
|
|
Alefacept everything
|
Mechanisms: inhibits T cell activation by binding to CD; Clinical use plaque psoriasis; Side effects: dose dependent reduction of circulating T cells - monitor carefully.
|
|
Etanercept: everyhing mechanism and clinical use:
|
binds to TNF alpha and TNF beta. blocks TNF alpha from binding receptor leads to suppression of inflammatory cytokines and adhesion molecules. ; Clinical use: rheumatoid arthritis and crohn's disease
|
|
Adalimumab and Golimumab: mechanismm and rhematoid arthritis
|
recognizes TNFalpha NOTE: does not recognized TNFbeta. ; clinical use rhematoid arthritis.
|
|
Infliximab and Certolizumab: Mmechanism and Clinical Use
|
recognized TNF alpha not TNF beta. . Clinical use: rheumatoid arthritis Crohn's diesease.
|
|
TNF alpha and blockers Side effects:
|
infusion reaction (reaction, uticaria, hypotension and dyspnea) plus others including serious infection that result in death due to suppression of inflammatory response.
|
|
Glucocorticoids mechanism: 2 points
|
1. interfere with cell cycle of activated lymphoid cells. 2. inhibited production of inflammatory mediators
|
|
Glucocorticoids 4 clinical use:
|
1. first line immunosuppressive therapy. 2. organ rejection or graft v host disease. 3. rhematoid arthritis, 4. inflammatory bowel disease
|
|
Glucocorticoids 4 side effects:
|
1. protein break down. 2. hyperglycemia 3. avascular / aseptic necrosis of bone. 4. iatrogenic Cushing's syndrome
|
|
Glucocotricoids precautions and contraindications:
|
precautions: hyperglycemia and osteoporosis; contraindications: diabetes and osteoporosis
|
|
Cyclosporine Mechanism including thing that metabolized it:
|
forms complex with cyclophilin and inhibits calcineurin; inhibits IL-1 and IL-2 productions; net results is inhibition of T cell activation; metabolized by liver P450 enzymes
|
|
Cycloporine: clinical use
|
organ transplantation, graft v host disease, autoimmune disorders
|
|
Cyclosporine: side effects
|
nephrotoxicity (renal dysfunction) and hypertension; note dose dependent.
|
|
Cyclosporine Drugs that inhibit CYP3A:
|
glucocorticoids (methyprednisolone) - results in elevated cycloporine blood concentrations
|
|
Cyclosporine: drug interactions
|
Syngerstic nephrotoxictiy if coadministered with Tacrolimus
|
|
Tacrolimus: Mechanism:
|
inhbitis calcinerurin; metabolized by liver P450.
|
|
tacrolimus Clinical use:
|
organ transplantation and graft v host disease
|
|
tacrolimus: 3 side effects:
|
nephrontoxicity; hyperglycemia and diabetes and neurotoxicity.
|
|
Sirolimus: mechanism
|
inhibits activity of a protein kinase (mTor) involved in CELL CYCLE PROGRESSION thus blocking G1-S transition . not T CELL specific
|
|
Sirolimus: clinical use:
|
prevention of organ transplant rejections in combinatiion thearpy with a calcineirun
|
|
Sirolimus: side effects:
|
hyperlipemia and bone marrow suppression
|
|
Mycophenolate Mofetil mechanism:
|
inhbits activity of inosine monophosphate dehydrogenase ( INHBITS guanine nucleotide synthesis). B and T cells highly dependent on this pathway for cell proliferation thus the net result is inhibition of lymphocyte proliferation
|
|
Mycophenolate: Clinical Use:
|
prevention of transplant rejection in combination with glucocorticoids and calcineurin inhibitor
|
|
Mycophenolate Mofetil: side effect
|
hematologic (bone marrow suppression - leukopenai); gastrointestinal (diarrhea and vomiting)
|
|
Azathioprine mechanism:
|
production of a fradulent nucleotide (6-thio-IMP) that when incorporated into DNA prevents translation and cell proliferations
|
|
Azathioprine: 3 clinical use:
|
prevention of organ transplant rejection; rhematoid arthritis; induction and maintenance of remission of ulcerative colitis and crohn's disease
|
|
Azathioprine: side effects:
|
bone marrow suppression (leukopenia, thrombocytonpenia and or anemia); hepatic toxicity
|
|
Methotrexate: mechanism:
|
inhbitis dihyrdrofolate reductase ( this interferes with synthesis of thymidylate purine nucleotides and amino acids serine and methionine)
|
|
Glucocorticoids 4 clinical use: 1. first line immunosuppressive therapy. 2. organ rejection or graft v host disease. 3. rhematoid arthritis
|
4. inflammatory bowel disease
|
|
Cycloporine: clinical use organ transplantation
|
graft v host disease
|
|
Azathioprine: side effects: bone marrow suppression (leukopenia
|
thrombocytonpenia and or anemia); hepatic toxicity
|
|
Methotrexate: side effects 1. bone marrow depression
|
and hepatic damage
|
|
Cyclophosphamide: mechanism: transfer alkyl group to cellular constituents (proteinsm DNA
|
RNA); DNA becomes crosslinked leading to cytoxicity loss of proliferating lymphoid cells supresses T and B cell function by 30-40%)
|
|
Cyclophosphamide: Side effects dose related toxicities in rapidly growing tissues (bone marrow
|
reproductive organs); nausea and vomiting
|
|
TNF alpha and blockers Side effects: infusion reaction (reaction
|
uticaria
|
|
Rituximab. recognizes CD20. mechanism: complement mediated lysis
|
antibody depedent cellular toxicity. pan B cell protein)
|
|
Glucocorticoids mechanism: 2 points
|
1. interfere with cell cycle of activated lymphoid cells. 2. inhibited production of inflammatory mediators
|
|
Glucocorticoids 4 clinical use:
|
1. first line immunosuppressive therapy. 2. organ rejection or graft v host disease. 3. rhematoid arthritis, 4. inflammatory bowel disease
|
|
Glucocorticoids 4 side effects:
|
1. protein break down. 2. hyperglycemia 3. avascular / aseptic necrosis of bone. 4. iatrogenic Cushing's syndrome
|
|
Glucocotricoids precautions and contraindications:
|
precautions: hyperglycemia and osteoporosis; contraindications: diabetes and osteoporosis
|
|
Cyclosporine Mechanism including thing that metabolized it:
|
forms complex with cyclophilin and inhibits calcineurin; inhibits IL-1 and IL-2 productions; net results is inhibition of T cell activation; metabolized by liver P450 enzymes
|
|
Cycloporine: clinical use
|
organ transplantation, graft v host disease, autoimmune disorders
|
|
Cyclosporine: side effects
|
nephrotoxicity (renal dysfunction) and hypertension; note dose dependent.
|
|
Cyclosporine Drugs that inhibit CYP3A:
|
glucocorticoids (methyprednisolone) - results in elevated cycloporine blood concentrations
|
|
Cyclosporine: drug interactions
|
Syngerstic nephrotoxictiy if coadministered with Tacrolimus
|
|
Tacrolimus: Mechanism:
|
inhbitis calcinerurin; metabolized by liver P450.
|
|
tacrolimus Clinical use:
|
organ transplantation and graft v host disease
|
|
tacrolimus: 3 side effects:
|
nephrontoxicity; hyperglycemia and diabetes and neurotoxicity.
|
|
Sirolimus: mechanism
|
inhibits activity of a protein kinase (mTor) involved in CELL CYCLE PROGRESSION thus blocking G1-S transition . not T CELL specific
|
|
Sirolimus: clinical use:
|
prevention of organ transplant rejections in combinatiion thearpy with a calcineirun
|
|
Sirolimus: side effects:
|
hyperlipemia and bone marrow suppression
|
|
Mycophenolate Mofetil mechanism:
|
inhbits activity of inosine monophosphate dehydrogenase ( INHBITS guanine nucleotide synthesis). B and T cells highly dependent on this pathway for cell proliferation thus the net result is inhibition of lymphocyte proliferation
|
|
Mycophenolate: Clinical Use:
|
prevention of transplant rejection in combination with glucocorticoids and calcineurin inhibitor
|
|
Mycophenolate Mofetil: side effect
|
hematologic (bone marrow suppression - leukopenai); gastrointestinal (diarrhea and vomiting)
|
|
Azathioprine mechanism:
|
production of a fradulent nucleotide (6-thio-IMP) that when incorporated into DNA prevents translation and cell proliferations
|
|
Azathioprine: 3 clinical use:
|
prevention of organ transplant rejection; rhematoid arthritis; induction and maintenance of remission of ulcerative colitis and crohn's disease
|
|
Azathioprine: side effects:
|
bone marrow suppression (leukopenia, thrombocytonpenia and or anemia); hepatic toxicity
|
|
Methotrexate: mechanism:
|
inhbitis dihyrdrofolate reductase ( this interferes with synthesis of thymidylate purine nucleotides and amino acids serine and methionine)
|
|
Methotrexate: Clinical Use:
|
induce and maintain remission inflmmatoryy bowel disease (Crohn's); rheumatoid arthritis and graft vs host disease
|
|
Methotrexate: side effects
|
1. bone marrow depression, and hepatic damage
|
|
Cyclophosphamide: mechanism:
|
transfer alkyl group to cellular constituents (proteinsm DNA, RNA); DNA becomes crosslinked leading to cytoxicity loss of proliferating lymphoid cells supresses T and B cell function by 30-40%)
|
|
Cyclophosphamide: Clincal use:
|
MAJOR stoppage of T and B cells. Organ rejection after transplantation. high does over several days
|
|
Cyclophosphamide: Side effects
|
dose related toxicities in rapidly growing tissues (bone marrow, reproductive organs); nausea and vomiting
|
|
Antihymocyte Globin (ATG) mechanism:
|
a polyclonal antibody that upon binding activates cytotoxicity (complement and cell mediated); block lymphocyte function.
|
|
Antithymocyte Clinical use:
|
induction of immunosuppression and to treat acute renal transplant rejection.
|
|
Antithymocyte: Side effectss:
|
fever and chills (potential for hypotension); patient will develop antibodies. HAMA reaction.
|
|
Rho D immune Globuin: Mechanism
|
binds Rho antigens prevents sensitization of Rh negative women to Rh-positive fetus .
|
|
Muromonab-CD3: mechanism
|
blocks antigen recognition - naive T cells and CTLs. Binds to CD3.
|
|
Muromonab-CD3: Side effects:
|
- cytokine release syndrome and HAMA reactions.
|
|
Basilizimab and Daclizumab Mechanism:
|
IL-2 antagonist; blocks IL-2 binding
|
|
Basilizimab and Dacilizumab Clinical use and Side effects:
|
used to prevent acute organ rejections; Side effects Gastronintestinal disorders
|
|
Alefacept everything
|
Mechanisms: inhibits T cell activation by binding to CD; Clinical use plaque psoriasis; Side effects: dose dependent reduction of circulating T cells - monitor carefully.
|
|
Etanercept: everyhing mechanism and clinical use:
|
binds to TNF alpha and TNF beta. blocks TNF alpha from binding receptor leads to suppression of inflammatory cytokines and adhesion molecules. ; Clinical use: rheumatoid arthritis and crohn's disease
|
|
Adalimumab and Golimumab: mechanismm and rhematoid arthritis
|
recognizes TNFalpha NOTE: does not recognized TNFbeta. ; clinical use rhematoid arthritis.
|
|
Infliximab and Certolizumab: Mmechanism and Clinical Use
|
recognized TNF alpha not TNF beta. . Clinical use: rheumatoid arthritis Crohn's diesease.
|
|
TNF alpha and blockers Side effects:
|
infusion reaction (reaction, uticaria, hypotension and dyspnea) plus others including serious infection that result in death due to suppression of inflammatory response.
|
|
Alemtuzumab
|
recognized CD52. used to treat B cell chronic lymphocytic leukemia.
|
|
Rituximab.
|
recognizes CD20. mechanism: complement mediated lysis, antibody depedent cellular toxicity. pan B cell protein)
|