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Indications of corticosteroids and immunosuppressants
Indications of corticosteroids and immunosuppressants ( 4 Questions)
A nurse is caring for a client who has rheumatoid arthritis and is prescribed prednisone, a glucocorticoid. What is the primary mechanism of action of prednisone in this condition?
It inhibits the synthesis of inflammatory mediators and suppresses the activation and proliferation of immune cells: Prednisone acts by suppressing the synthesis of various inflammatory mediators, including prostaglandins, leukotrienes, and cytokines. It also inhibits the activation and proliferation of immune cells such as lymphocytes and macrophages. By reducing inflammation and immune response, it helps manage the symptoms of rheumatoid arthritis.
It blocks the activation of T cells by inhibiting the enzyme calcineurin, which is required for the transcription of interleukin-2: This mechanism of action is associated with a different class of immunosuppressive medications called calcineurin inhibitors, such as cyclosporine. Prednisone does not directly block T-cell activation by inhibiting calcineurin.
It interferes with the synthesis of nucleic acids, which are essential for the replication and function of immune cells: While prednisone may have some impact on nucleic acid synthesis, it is not the primary mechanism of action for its therapeutic effects in rheumatoid arthritis. The anti-inflammatory and immunosuppressive effects of prednisone primarily result from the inhibition of inflammatory mediators and immune cell activity.
It binds to specific antigens or receptors on the surface of immune cells and either neutralizes them or induces their destruction: This mechanism of action is associated with targeted therapies such as monoclonal antibodies. Prednisone, as a glucocorticoid, exerts its effects through genomic mechanisms by binding to cytoplasmic receptors and modulating gene expression, rather than direct binding to specific antigens or receptors on immune cells.
Prednisone, a glucocorticoid, is commonly used in the treatment of rheumatoid arthritis. Its primary mechanism of action in this condition is related to its anti-inflammatory and immunosuppressive effects.
A. It inhibits the synthesis of inflammatory mediators and suppresses the activation and proliferation of immune cells: Prednisone acts by suppressing the synthesis of various inflammatory mediators, including prostaglandins, leukotrienes, and cytokines. It also inhibits the activation and proliferation of immune cells such as lymphocytes and macrophages. By reducing inflammation and immune response, it helps manage the symptoms of rheumatoid arthritis.
B. It blocks the activation of T cells by inhibiting the enzyme calcineurin, which is required for the transcription of interleukin-2: This mechanism of action is associated with a different class of immunosuppressive medications called calcineurin inhibitors, such as cyclosporine. Prednisone does not directly block T-cell activation by inhibiting calcineurin.
C. It interferes with the synthesis of nucleic acids, which are essential for the replication and function of immune cells: While prednisone may have some impact on nucleic acid synthesis, it is not the primary mechanism of action for its therapeutic effects in rheumatoid arthritis. The anti-inflammatory and immunosuppressive effects of prednisone primarily result from the inhibition of inflammatory mediators and immune cell activity.
D. It binds to specific antigens or receptors on the surface of immune cells and either neutralizes them or induces their destruction: This mechanism of action is associated with targeted therapies such as monoclonal antibodies. Prednisone, as a glucocorticoid, exerts its effects through genomic mechanisms by binding to cytoplasmic receptors and modulating gene expression, rather than direct binding to specific antigens or receptors on immune cells.