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65 Cards in this Set
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- Back
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prednisone MOA
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Suppress macrophage fxn
Prevent T cell proliferations Inhibit cytokine production decreases adhesion molecule expression Induce apoptosis Alter lymphocyte trafficking, inhibit lymphocyte transmigration Reduce MHC expression |
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Prednisone therapeutic use
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Solid organ transplant
Bone marrow transplant Immune-mediated kidney response |
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Prednisone side effects
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Hypertension
Hyperglycemia Liver dysfunction Hirsutism Nephrotoxicity |
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Cyclosporine MOA
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Calcineurin inhibitors: alter
IL-2 transcription |
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Cyclosporine therapeutic use
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Solid organ transplant
Bone marrow transplant Immune mediated kidney disease |
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Cyclosporine side effects
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Hypertension
Hyperglycemia Liver dysfunction Hirsutism Nephrotoxicity |
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Tacrolimus MOA
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Calcineurin inhibitors: alter
IL-2 transcription |
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Tacrolimus use
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Solid organ transplant
Bone marrow transplant Immune mediated kidney diseas |
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Tacrolimus side effects
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Hypertension
Hyperglycemia Liver dysfunction Hirsutism Nephrotoxicity |
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sirolimus MOA
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Inhibits TOR → prevents T cells from moving into S phase of cell cycle, so move into apoptosis instead
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Sirolimus Uses
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solid organ transplant
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sirolimus side effects
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Wound healing
Bone marrow suppression Hyperlipidemia Renal dysfunction Lymphoma |
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azathioprine MOA
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Purine analog → inhibits DNA synthesis → decreases proliferation of T & B cells (non-specific)
Also decreases the # of circulating monocytes b/c arrests cell cycle in bone marrow |
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azathioprine uses
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Solid organ transplant
Autoimmune diseases: lupus, RA, Crohns, MS Used w/ steroids to “spare” steroid dose |
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azathioprine side effects
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Bone marrow suppression w/ cytopenias
Rash Fever N/V/D Secondary malignancies |
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mycophenolate mofetil MOA
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Decreased guanine, increased adenine → suppresses rate limiting enzymes in de novo purine synthesis → selectively inhibits lymphocyte proliferation (b/c lymphocytes ~dependent on de novo purine synthesis) → Decreased antibody formation,Decreased cytotoxic T cell activity, Decreased adhesion molecule expression
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mycophenolate mofetil uses
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Solid organ transplant
Bone marrow transplant Lupus nephritis RA |
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mycophenolate mofetil side effects
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GI toxicity
Bone marrow suppression |
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cyclophosphamide MOA
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DNA cross-linking agent:
Blocks lymphocyte proliferation Alkylates resting cells Can induce tolerance to new antigens if given w/ Ag |
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cyclophosphamide uses
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Autoimmune diseases: lupus, MS, autoimmune hemolytic anemia, membranous glomerulonephritis
Bone marrow transplant conditioning regimen Cancer |
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cyclophosphamide Side effects
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Cytopenias
Hemorrhagic cystitis Secondary leukemias |
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How is methotrexate excreted?
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renally
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methotrexate MOA
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Antimetabolite: interferes w/ uracil to thymidine conversion
Blocks lymphocyte proliferation |
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Methotrexate uses?
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RA
Graft vs. host disease (tx & prevention) Cancer |
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Methotrexate side effects
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Stomatitis (Mouth sores), diarrhea, myelosuppression
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antithymocyte globulin (ATG) MOA?
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Antithymocyte antibodies trigger complement-mediated lysis of circulating T cells & trapping of T cells in reticuloendothelial system, also block T cell fxn via interaction w/ cell surface molecules
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antithymocyte globulin (ATG) uses?
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Prevent solid organ graft rejection
Acute graft vs. host disease |
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antithymocyte globulin (ATG) side effects?
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Effectiveness limited by development of immune response to foreign antibodies
Serum sickness Anaphylaxis Infections Secondary lymphomas |
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intravenous immune globulin (IVIG) MOA?
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Pooled human IgG:
Inhibits complement mediated injury & circulating immune complex injury Binds to regulatory Fc receptors on B cells Blocks Fc receptors on macrophages Neutralizes antibodies & cytokines Other effects poorly understood |
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IVIG uses?
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Agamma-globulinemia
Autoimmunity: ITP Systemic inflammation: Kawasaki's disease (Experimental use: stop antibody mediated transplant rejection) |
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Rhogam MoA
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Concentrated human IgG containing high titer antibodies against RBC RH(D) antigen
Prevents formation of memory B cell response to infant cells that enter maternal circulation |
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Rhogam uses?
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Give to Rh(-) mother at time of delivery of Rh(+) infant
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Rituximab MOA
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Chimeric anti-CD20 antibody that depletes normal & malignant B cells (but not plasma cells) via complement lysis, antibody-dependent cytotoxicity, & apoptosis induction
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Rituximab uses
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B cell lymphomas
Antibody-mediated rejection (only agent specifically targeted to B cells!) |
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thalidomide moa
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Anti-inflammatory & immuno-modulatory, inhibits angiogenesis
Enhances cell-mediated immunity via interactions w/ T cells Inhibits TNF-alpha, reduces phagocytosis by neutrophils, increases production of IL-10, enhances cell mediated immunity via interactions with T cells. |
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Thalidomide uses
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Multiple myeloma
Leprosy E nodosum |
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thalidomide side effects
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Teratogenic!! (used to be used as sedative in pregnancy → short limb syndrome)
Sedation Constipation Rash Neuropathy DVT |
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what is Chronic Granulomatous Disease ?
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Phagocytes cannot make oxidative burst and cannot kill bacteria
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What is DiGeorge Syndrome?
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No thymus; no t cells
And w/out t cells B cells cannot make antibodies (need help) |
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What is X linked agammaglobulinemia?
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No immunoglobin
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What is Hyper IgM syndrome ?
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Cannot switch from IgM to IgG
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What type of sensitivity is:
crosslinking of IgE on mast cells by antigen Release of histamines, leukotrienes, eosinophil chemotactic factor |
Type I hypersensitivity
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What is Hay fever an example of?
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Type I hypersensitivity
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What is Rx for type I hypersensitivity
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Rx: Decrease IgE production: steroids
Antihistamines block effects of degranulated mast cells |
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What type of hypersensitivity is formation of antibody-antigen complexes
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Type II
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What is transfusion rxn an example of?
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Type II hypersensitivity
Transfusion reaction: antibody binds to rbc antigens and then activates complement cascade causing RBC lysis |
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What is good pasteur's an example of?
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Hypersensitivity Type II
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What type of hypersensitivity is:
Antibody-antigen complexes that cause tissue damage via complement activation, FcR signaling, ADCC, etc |
Type III
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What are glomerulonephritis and arthritis examples of?
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Type III hypersensitivity
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Is type IV hypersensitivity cell or humoral mediated?
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Cell mediated
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Which hypersensitivity rxn:
Causes local inflammation and tissue damage and involves non antigen specific inflammatory cells: macrophages and neutrophils And starts 2-3 days after exposure |
Delayed Type Hypersensitivity (IV
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Is immunosuppression antigen specific?
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No!!!
Immunosuppression is not antigen specific, but instead is an induced state of immune non-responsiveness to all antigenic stimuli. |
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Do corticosteroids act on T or B cells
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T cells!!!
No real immunosuppression therapies that act on B cells yet... |
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What do corticosteroids inhibit?
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INHIBTIS IL-2 PRODUCTION!!!!!
Corticosteroids bind to steroid receptor w/in cell that binds to DNA that activatesI KAPPA B MOTOR --> Helps to activate NF kappa B which binds to IL promotoer --> INHIBTIS IL-2 PRODUCTION!!!!! |
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What does cyclosporin & tacrolimus inhibit?
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Calcineurin inhibitors
POTENT T CELL INHIBITORS --> makes Kidney transplant possible |
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What is an ironic side effect of cyclosporine & tacrolimus
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Cause nephrotoxicity despite being used for kidney transplants
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What drugs bind to FK binding proteins
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Siorlimus & tacrolimus (but different parts)
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Does Sirolimus effect IL2?
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No!
It prevents T cells from moving from G1 into S phase of the cell cycle. Does not inhibit the apoptotic effect of IL-2. |
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What is Azathioprine metabolized to?
What is its MOA? |
The liver metabolizes it to to 6-mercaptopurine (6MP)
It basically inhibits DNA synthesis and thus proliferation of T and B cells--a nonspecific inhibitory event. It also decreases the number of circulating monocytes by cell cycle arrest in the bone marrow. |
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When combined w/ steroids, what is the advantage of azathioprine?
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ALLOWS YOU TO DROP THE LEVEL OF CORTICOSTEROIDS!
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Does Sirolimus effect IL2?
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No!
It prevents T cells from moving from G1 into S phase of the cell cycle. Does not inhibit the apoptotic effect of IL-2. |
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What is Azathioprine metabolized to?
What is its MOA? |
The liver metabolizes it to to 6-mercaptopurine (6MP)
It basically inhibits DNA synthesis and thus proliferation of T and B cells--a nonspecific inhibitory event. It also decreases the number of circulating monocytes by cell cycle arrest in the bone marrow. |
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When combined w/ steroids, what is the advantage of azathioprine?
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ALLOWS YOU TO DROP THE LEVEL OF CORTICOSTEROIDS!
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What is Mycophenolate Mofetil MOA?
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Is a reversible uncompetitive inhibitor of inosine monophosphate dehydrogenase Causes a deficiency of guanine and deoxyguanine nucleotides and an excess of adenine nucleotides, which in turn suppress rate-limiting enzymes in de novo purine synthesis
“Selectively” inhibits lymphocyte proliferation. Relatively selective for lymphocytes because lymphocytes are relatively dependent on de novo purine synthesis |
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How is guanine & adenine nucleotides effected by Mycophenolate Mofetil?
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Excess adenine which suppress rate limiting enzymes
deficiency of guanine |
