Rosenberg on Immunosuppression
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Alex Rosenberg is an Intensivist who was working in a transplant centre last year. He gave this talk on immunosupression at last year's Bedside Critical Care Conference and managed to make a fairly dry subject seem understandable and relevant. Go to www.intensivecarenetwork.com for the podcast.
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Cyclosporine
Cyclosporine is an immunosuppressant used to prevent transplant rejection and treat arthritis and psoriasis. It works by inhibiting interleukin-2, which is necessary for T-cell activity and distinguishing self from foreign cells. Common side effects include hypertension, nephrotoxicity, nausea, vomiting, and tremors. When taking cyclosporine, patients should take it at the same time each day, avoid grapefruit, and report symptoms of organ rejection or adverse reactions like seizures immediately to their physician. Nurses should monitor for infection risk, pain, fatigue, and skin and tissue integrity issues in patients receiving cyclosporine therapy.
Immunosuppression
This document discusses short and long term immunosuppression. Short term immunosuppression uses steroids which act by lysing and redistributing lymphocytes, dampening antigen presentation, blocking T cell activation, and enhancing apoptosis of activated T cells. Long term immunosuppression uses antiproliferative drugs like azathioprine and mycophenolate mofetil which inhibit purine biosynthesis and cell proliferation, as well as calcineurin inhibitors like cyclosporine and tacrolimus which bind to immunophilins to inhibit T cell signaling pathways. Sirolimus also prevents T cell proliferation by inhibiting phosphorylation of p70 kinase.
Introduction immunosuppression akl_isneap2017
The document provides an introduction and outline for a presentation on immunosuppression for transplantation. It discusses the history of immunosuppression, mechanisms of transplant rejection, categories of immunosuppressant agents including induction agents, calcineurin inhibitors like cyclosporine and tacrolimus, antiproliferative agents, side effects and drug interactions of immunosuppressants, and monitoring of drug levels. The presentation aims to provide an overview of current immunosuppression protocols and management of side effects.
Cyclosporine by Aseem
Cyclosporine-A is a cyclic non-ribosomal peptide composed of 11 amino acids that was discovered in 1970 from the fungus Tolypocladium inflatum. It is an immunosuppressant drug used to prevent rejection in organ transplant recipients and for certain autoimmune and inflammatory diseases. It works by inhibiting T-cell activation. Cyclosporine-A is metabolized by the CYP3A4 enzyme system and primarily excreted in the bile. It has a half-life of 5-18 hours and peak levels occur 2-4 hours after administration. Common side effects include renal dysfunction, hypertension, hyperlipidemia and hirsutism. It requires careful monitoring due to its
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Plasmapheresis is a medical procedure that separates blood components to remove plasma. There are three main types: autologous, therapeutic exchange, and donation. Autologous plasmapheresis removes a patient's own plasma, treats it, and returns it to remove antibodies, immune complexes, or toxins. It is used to treat various neurological, hematological, metabolic, dermatological, and renal diseases. Complications can include hypotension, allergic reactions, hemorrhage, hypocalcemia, and infections from replacement fluids. Plasmapheresis removes drugs and proteins from plasma like IVIG and monoclonal antibodies but not drugs like steroids that are widely distributed in tissues. It is used pre- and
Immunosuppressants
The document discusses various immunosuppressive drugs used for organ transplantation under the following categories: selective inhibitors of cytokine production and function, immunosuppressive antimetabolites, antibodies, and corticosteroids. It then provides more detailed information on specific drugs like cyclosporine, tacrolimus, sirolimus, azathioprine, mycophenolate, muromonab-cd3, basiliximab/daclizumab, alemtuzumab, and corticosteroids including their mechanisms of action, uses, and common adverse drug reactions.
Immunosuppressant drugs by Pankaj Maurya
This document discusses immunosuppressant drugs used to inhibit immune response in organ transplantation and autoimmune diseases. It begins by introducing immunosuppressants and their uses. It then provides an overview of the cascade of immune responses. The main body of the document classifies and describes various immunosuppressant agents including calcineurin inhibitors, mTOR inhibitors, antiproliferative drugs, glucocorticoids, and biological agents. For each drug class and individual drugs, it discusses mechanisms of action, pharmacokinetics, and adverse effects. References are provided at the end.
Immunosuppressive Antibodies
This document discusses the history and development of monoclonal antibodies and their uses in medicine. It describes how hybridoma technology allows for the mass production of antibodies and mentions some early monoclonal antibodies produced against lymphocyte antigens that were used to prevent transplant rejection and treat autoimmune diseases. The document then summarizes the development of monoclonal antibody classes from murine to humanized to fully human and some of their clinical applications in diseases like cancer, transplant rejection, and autoimmune/inflammatory conditions.
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Cyclosporine
Cyclosporine is an immunosuppressant used to prevent transplant rejection and treat arthritis and psoriasis. It works by inhibiting interleukin-2, which is necessary for T-cell activity and distinguishing self from foreign cells. Common side effects include hypertension, nephrotoxicity, nausea, vomiting, and tremors. When taking cyclosporine, patients should take it at the same time each day, avoid grapefruit, and report symptoms of organ rejection or adverse reactions like seizures immediately to their physician. Nurses should monitor for infection risk, pain, fatigue, and skin and tissue integrity issues in patients receiving cyclosporine therapy.
Immunosuppression
This document discusses short and long term immunosuppression. Short term immunosuppression uses steroids which act by lysing and redistributing lymphocytes, dampening antigen presentation, blocking T cell activation, and enhancing apoptosis of activated T cells. Long term immunosuppression uses antiproliferative drugs like azathioprine and mycophenolate mofetil which inhibit purine biosynthesis and cell proliferation, as well as calcineurin inhibitors like cyclosporine and tacrolimus which bind to immunophilins to inhibit T cell signaling pathways. Sirolimus also prevents T cell proliferation by inhibiting phosphorylation of p70 kinase.
Introduction immunosuppression akl_isneap2017
The document provides an introduction and outline for a presentation on immunosuppression for transplantation. It discusses the history of immunosuppression, mechanisms of transplant rejection, categories of immunosuppressant agents including induction agents, calcineurin inhibitors like cyclosporine and tacrolimus, antiproliferative agents, side effects and drug interactions of immunosuppressants, and monitoring of drug levels. The presentation aims to provide an overview of current immunosuppression protocols and management of side effects.
Cyclosporine by Aseem
Cyclosporine-A is a cyclic non-ribosomal peptide composed of 11 amino acids that was discovered in 1970 from the fungus Tolypocladium inflatum. It is an immunosuppressant drug used to prevent rejection in organ transplant recipients and for certain autoimmune and inflammatory diseases. It works by inhibiting T-cell activation. Cyclosporine-A is metabolized by the CYP3A4 enzyme system and primarily excreted in the bile. It has a half-life of 5-18 hours and peak levels occur 2-4 hours after administration. Common side effects include renal dysfunction, hypertension, hyperlipidemia and hirsutism. It requires careful monitoring due to its
Irm 3
Plasmapheresis is a medical procedure that separates blood components to remove plasma. There are three main types: autologous, therapeutic exchange, and donation. Autologous plasmapheresis removes a patient's own plasma, treats it, and returns it to remove antibodies, immune complexes, or toxins. It is used to treat various neurological, hematological, metabolic, dermatological, and renal diseases. Complications can include hypotension, allergic reactions, hemorrhage, hypocalcemia, and infections from replacement fluids. Plasmapheresis removes drugs and proteins from plasma like IVIG and monoclonal antibodies but not drugs like steroids that are widely distributed in tissues. It is used pre- and
Immunosuppressants
The document discusses various immunosuppressive drugs used for organ transplantation under the following categories: selective inhibitors of cytokine production and function, immunosuppressive antimetabolites, antibodies, and corticosteroids. It then provides more detailed information on specific drugs like cyclosporine, tacrolimus, sirolimus, azathioprine, mycophenolate, muromonab-cd3, basiliximab/daclizumab, alemtuzumab, and corticosteroids including their mechanisms of action, uses, and common adverse drug reactions.
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This document discusses immunosuppressant drugs used to inhibit immune response in organ transplantation and autoimmune diseases. It begins by introducing immunosuppressants and their uses. It then provides an overview of the cascade of immune responses. The main body of the document classifies and describes various immunosuppressant agents including calcineurin inhibitors, mTOR inhibitors, antiproliferative drugs, glucocorticoids, and biological agents. For each drug class and individual drugs, it discusses mechanisms of action, pharmacokinetics, and adverse effects. References are provided at the end.
Immunosuppressive Antibodies
This document discusses the history and development of monoclonal antibodies and their uses in medicine. It describes how hybridoma technology allows for the mass production of antibodies and mentions some early monoclonal antibodies produced against lymphocyte antigens that were used to prevent transplant rejection and treat autoimmune diseases. The document then summarizes the development of monoclonal antibody classes from murine to humanized to fully human and some of their clinical applications in diseases like cancer, transplant rejection, and autoimmune/inflammatory conditions.
Immunopharmacology
The document discusses various topics in immunopharmacology including:
1. The two major components of the immune system - innate and adaptive immunity.
2. Mechanisms of action and indications for commonly used immunosuppressant drugs like corticosteroids, cyclosporine, and tacrolimus.
3. Immunomodulators and cytokines used to treat various cancers and infectious diseases.
Cyclosporine
This document summarizes information about cyclosporine, an immunosuppressant drug used to prevent organ transplant rejection. It was first isolated from the fungus Tolypocladium inflatum in 1970. Cyclosporine is a cyclic polypeptide composed of 11 amino acids that suppresses T cell activity. It is used to prevent rejection of kidney, heart, and liver transplants and is also approved to treat severe psoriasis and rheumatoid arthritis. While an effective immunosuppressant, cyclosporine can increase risks of high blood pressure, kidney problems, and cancer growth due to its suppression of the immune system.
Immunosuppression immunomodulation
This document provides information about Dr. Ahmed Akl, an expert in nephrology and transplantation from Egypt. It then discusses the history of immunosuppression including early transplant attempts and the development of drugs like azathioprine. The remainder of the document summarizes various immunosuppressive agents including calcineurin inhibitors like cyclosporine and tacrolimus, antiproliferative drugs, mTOR inhibitors like sirolimus, as well as their dosing, monitoring, side effects and drug interactions.
Immunosuppressant drugs
This document discusses various types of immunosuppressant drugs used to inhibit immune responses in organ transplantation and autoimmune diseases. It describes the main categories as calcineurin inhibitors like cyclosporine and tacrolimus, antiproliferative drugs including azathioprine and methotrexate, glucocorticoids, and immunosuppressant antibodies such as muromonab CD3 and antithymocyte globulin. Cyclosporine is highlighted as the most effective prevention of graft rejection by selectively suppressing T-cell mediated immunity while leaving other immune functions intact.
Beauty of cyclosporine
Cyclosporine is an immunosuppressant derived from the fungus Tolypocladium inflatum. It was discovered in 1970 and found to be an immunosuppressant in 1976. Cyclosporine works by suppressing T-cell function to prevent transplant rejection. It was approved for use in organ transplants in 1983 and for severe psoriasis in 1997. Cyclosporine comes with risks of increased infection and kidney toxicity due to its immunosuppressive effects.
immunosupresant agent
This document discusses various immunosuppressant drugs used to prevent rejection after organ transplantation. It describes six classes of immunosuppressants: inhibitors of cytokine production/action like calcineurin inhibitors cyclosporine and tacrolimus; inhibitors of cytokine gene expression like corticosteroids; cytotoxic drugs like antimetabolites azathioprine and mycophenolate mofetil; alkylating agents like cyclophosphamide; immunosuppressive antibodies; interferon; and thalidomide. It provides details on mechanisms of action, pharmacokinetics, uses, and side effects of specific drugs like cyclosporine, tacrolimus, sirolimus, corticosteroids, and azath
Immunosuppressive Drugs
Immunosuppressive drugs used to treat transplant rejection include calcineurin inhibitors like cyclosporine and tacrolimus, mTOR inhibitors like sirolimus and everolimus, anti-proliferatives like azathioprine and mycophenolic acid, corticosteroids like prednisolone and hydrocortisone, and antibodies like the monoclonal anti-IL-2Rα receptor antibodies basiliximab and daclizumab or polyclonal anti-T-cell antibodies like anti-thymocyte globulin. The IL-2 receptor antagonist daclizumab is approved for use in renal, cardiac transplant, and multiple sclerosis.
Cyclosporine in dermatology
Cyclosporine is an immunosuppressive drug that was originally isolated from fungi in 1970 and approved by the FDA for transplant rejection in 1983. It is a cyclic polypeptide consisting of 11 amino acids that acts by inhibiting T cell activation through the calcineurin/NFAT pathway. It has since been approved for treating various dermatological conditions like psoriasis, atopic dermatitis, and pyoderma gangrenosum. While effective, cyclosporine use can cause nephrotoxicity, hypertension, and increased risk of infection and skin cancer with long term use. It can also interact with various other drugs that are metabolized through the CYP3A4 pathway.
Azathioprine.ppt
Azathioprine is an immunosuppressive drug used as an adjunct to prevent rejection in renal transplants and to treat severe rheumatoid arthritis. It works by suppressing cell-mediated immune responses and altering antibody production. Common side effects include nausea, vomiting, rash, and hematologic issues like leukopenia. Nurses monitor patients for signs of infection or toxicity and educate them about proper administration and reporting any adverse reactions. Precautions are needed due to teratogenicity and increased risk of infections and cancers with long term use.
immunosuppressive drugs in dermatology
The drugs included in the presentation are Methotrexate, Cyclosporine, Azathioprine, Cyclophosphamide, Mycophenolate mofetil and Intravenous Immunoglobulin.
It is useful mainly for dermatologists.
Immunosuppressive drugs
This document provides an overview of immunosuppressive drugs. It begins with an introduction to immunosuppression and the roles of immunosuppressive drugs in treating autoimmune diseases and preventing organ transplant rejection. The document then classifies immunosuppressive drugs and discusses several classes in more detail, including glucocorticoids, calcineurin inhibitors like cyclosporine and tacrolimus, sirolimus, cytostatics like cyclophosphamide, and mycophenolate mofetil. For each drug, the document provides information on mechanisms of action, indications, dosages, and side effects. The document aims to provide clinicians an overview of commonly used immunosuppressive drugs.
Introduction of immunity and immunosuppressed drugs
introduction of immunity and immunosuppressive Drugs
Hargeisa somalia, specially university of hargeisa
immunosuppression drugs
This document summarizes several types of immunosuppressant drugs used to inhibit immune responses for organ transplantation and autoimmune diseases. It describes calcineurin inhibitors like cyclosporine and tacrolimus, mTOR inhibitors like sirolimus, antiproliferative drugs like azathioprine and mycophenolate mofetil, glucocorticoids like prednisone, and biological agents like TNFα inhibitors and IL-2 receptor antagonists. It provides details on the mechanisms of action, pharmacokinetics, adverse effects and uses of these major immunosuppressive drug classes and examples like cyclosporine, tacrolimus and sirolimus.
Mtor inhibitors in renal transplant
mTOR inhibitors like sirolimus and everolimus are immunosuppressants that provide an alternative to calcineurin inhibitors for renal transplant patients. They have antiproliferative properties, cause less nephrotoxicity than CNIs, and are associated with lower rates of malignancy, viral infections, and improved renal function when used to convert patients from a CNI-based regimen. However, mTOR inhibitors are less effective at preventing acute rejection when used without a CNI in de novo transplants.
Immunosuppressive drugs
This document summarizes immunosuppressive drugs. It discusses how they work to suppress the immune system and are used to prevent organ rejection after transplantation and treat autoimmune diseases. The main classes of immunosuppressive drugs covered are glucocorticoids, calcineurin inhibitors like cyclosporine and tacrolimus, antiproliferative drugs including mycophenolate mofetil and mTOR inhibitors, immunosuppressive antibodies, and others. Specific drugs within each class are described in terms of their mechanisms of action, pharmacokinetics, uses, and side effects.
Glucocorticoids
The document discusses adrenocortical steroids, which are synthesized in the adrenal cortex and have glucocorticoid and mineralocorticoid activities. Glucocorticoids penetrate cells, bind to receptors, and regulate protein synthesis. Examples include hydrocortisone, prednisolone, and dexamethasone. Corticosteroids are powerful drugs that can cause both improvements in disease and adverse effects, so proper use and monitoring is important. They have a variety of ophthalmic and non-ophthalmic uses and indications.
Complications of immunosuppression
This document discusses immunosuppressant drugs, their mechanisms of action, uses, and complications. It describes how immunosuppressants work by inhibiting cytokines, cytokine production, or cytotoxic immune cells. Major drugs covered include calcineurin inhibitors cyclosporine and tacrolimus, mTOR inhibitor sirolimus, corticosteroids, antimetabolites azathioprine and mycophenolate, cytotoxic drugs, and immunosuppressive antibodies. Complications of immunosuppression can include infection, nephrotoxicity, bone marrow toxicity, and increased cancer risk. Each drug profile provides therapeutic uses and adverse effects.
Azathioprine
Azathioprine is an immunosuppressive drug used to treat rheumatoid arthritis and prevent rejection in organ transplant recipients. It works by suppressing the immune system and altering antibody production. The presentation discusses the mechanism of action, indications, contraindications, dosages, adverse reactions, and drug interactions of azathioprine. Azathioprine is used as an adjunct treatment for severe, active rheumatoid arthritis not responsive to other therapies. It can cause side effects like rash, nausea, vomiting, bleeding, infections, and increased risk of cancer. Patients should be monitored for blood abnormalities and use caution with other drugs that may increase myelosuppression.
Class immunosuppressants 2
This document discusses various classes of immunosuppressant drugs used to prevent rejection of transplanted organs or treat autoimmune diseases. It describes glucocorticoids, calcineurin inhibitors like cyclosporine and tacrolimus, mTOR inhibitors like sirolimus and everolimus, antiproliferative agents, biological agents targeting cytokines like TNF inhibitors, monoclonal antibodies, adhesion molecule inhibitors, and tolerogens. Specific drugs are discussed within each class along with their mechanisms of action, pharmacokinetics, and adverse effects.
Immunosuppressant drugs
This presentation is about immunosuppressant drugs which are used to suppress cell mediated/humoral or both types of immunity.
Methods of immunosuppression
Immunosuppression involves reducing the activation of the immune system through medications, surgery, radiation or other means. The document discusses the history of immunosuppression and developments in transplantation including the identification of cortisone and research on the immune system. It outlines current methods of immunosuppression including calcineurin inhibitors, mTOR inhibitors, antimetabolites, corticosteroids, depleting antibodies and fusion proteins. The mechanisms, types and treatment of allograft rejection such as hyperacute, acute and chronic rejection are also summarized.
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1) Hospital acquired acute kidney injury (AKI) is a problem for clinicians due to the complex renal physiology, limited clinically useful biomarkers for renal injury, difficulties with fluid management in sepsis, and limited therapies for early AKI.
2) The kidney is at risk of both hyperoxia and hypoxia due to its oxygen regulation and blood flow, making renal function difficult to assess. Global renal blood flow may not correlate with glomerular filtration rate, medullary flow, or oxygenation.
3) While a positive fluid balance and elevated central venous pressure are associated with worse outcomes in septic shock, fluid management remains challenging without reliable ways to directly measure renal blood flow or the integrity of the endothelial glyc
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Was ist angesagt?
Immunopharmacology
The document discusses various topics in immunopharmacology including:
1. The two major components of the immune system - innate and adaptive immunity.
2. Mechanisms of action and indications for commonly used immunosuppressant drugs like corticosteroids, cyclosporine, and tacrolimus.
3. Immunomodulators and cytokines used to treat various cancers and infectious diseases.
Cyclosporine
This document summarizes information about cyclosporine, an immunosuppressant drug used to prevent organ transplant rejection. It was first isolated from the fungus Tolypocladium inflatum in 1970. Cyclosporine is a cyclic polypeptide composed of 11 amino acids that suppresses T cell activity. It is used to prevent rejection of kidney, heart, and liver transplants and is also approved to treat severe psoriasis and rheumatoid arthritis. While an effective immunosuppressant, cyclosporine can increase risks of high blood pressure, kidney problems, and cancer growth due to its suppression of the immune system.
Immunosuppression immunomodulation
This document provides information about Dr. Ahmed Akl, an expert in nephrology and transplantation from Egypt. It then discusses the history of immunosuppression including early transplant attempts and the development of drugs like azathioprine. The remainder of the document summarizes various immunosuppressive agents including calcineurin inhibitors like cyclosporine and tacrolimus, antiproliferative drugs, mTOR inhibitors like sirolimus, as well as their dosing, monitoring, side effects and drug interactions.
Immunosuppressant drugs
This document discusses various types of immunosuppressant drugs used to inhibit immune responses in organ transplantation and autoimmune diseases. It describes the main categories as calcineurin inhibitors like cyclosporine and tacrolimus, antiproliferative drugs including azathioprine and methotrexate, glucocorticoids, and immunosuppressant antibodies such as muromonab CD3 and antithymocyte globulin. Cyclosporine is highlighted as the most effective prevention of graft rejection by selectively suppressing T-cell mediated immunity while leaving other immune functions intact.
Beauty of cyclosporine
Cyclosporine is an immunosuppressant derived from the fungus Tolypocladium inflatum. It was discovered in 1970 and found to be an immunosuppressant in 1976. Cyclosporine works by suppressing T-cell function to prevent transplant rejection. It was approved for use in organ transplants in 1983 and for severe psoriasis in 1997. Cyclosporine comes with risks of increased infection and kidney toxicity due to its immunosuppressive effects.
immunosupresant agent
This document discusses various immunosuppressant drugs used to prevent rejection after organ transplantation. It describes six classes of immunosuppressants: inhibitors of cytokine production/action like calcineurin inhibitors cyclosporine and tacrolimus; inhibitors of cytokine gene expression like corticosteroids; cytotoxic drugs like antimetabolites azathioprine and mycophenolate mofetil; alkylating agents like cyclophosphamide; immunosuppressive antibodies; interferon; and thalidomide. It provides details on mechanisms of action, pharmacokinetics, uses, and side effects of specific drugs like cyclosporine, tacrolimus, sirolimus, corticosteroids, and azath
Immunosuppressive Drugs
Immunosuppressive drugs used to treat transplant rejection include calcineurin inhibitors like cyclosporine and tacrolimus, mTOR inhibitors like sirolimus and everolimus, anti-proliferatives like azathioprine and mycophenolic acid, corticosteroids like prednisolone and hydrocortisone, and antibodies like the monoclonal anti-IL-2Rα receptor antibodies basiliximab and daclizumab or polyclonal anti-T-cell antibodies like anti-thymocyte globulin. The IL-2 receptor antagonist daclizumab is approved for use in renal, cardiac transplant, and multiple sclerosis.
Cyclosporine in dermatology
Cyclosporine is an immunosuppressive drug that was originally isolated from fungi in 1970 and approved by the FDA for transplant rejection in 1983. It is a cyclic polypeptide consisting of 11 amino acids that acts by inhibiting T cell activation through the calcineurin/NFAT pathway. It has since been approved for treating various dermatological conditions like psoriasis, atopic dermatitis, and pyoderma gangrenosum. While effective, cyclosporine use can cause nephrotoxicity, hypertension, and increased risk of infection and skin cancer with long term use. It can also interact with various other drugs that are metabolized through the CYP3A4 pathway.
Azathioprine.ppt
Azathioprine is an immunosuppressive drug used as an adjunct to prevent rejection in renal transplants and to treat severe rheumatoid arthritis. It works by suppressing cell-mediated immune responses and altering antibody production. Common side effects include nausea, vomiting, rash, and hematologic issues like leukopenia. Nurses monitor patients for signs of infection or toxicity and educate them about proper administration and reporting any adverse reactions. Precautions are needed due to teratogenicity and increased risk of infections and cancers with long term use.
immunosuppressive drugs in dermatology
The drugs included in the presentation are Methotrexate, Cyclosporine, Azathioprine, Cyclophosphamide, Mycophenolate mofetil and Intravenous Immunoglobulin.
It is useful mainly for dermatologists.
Immunosuppressive drugs
This document provides an overview of immunosuppressive drugs. It begins with an introduction to immunosuppression and the roles of immunosuppressive drugs in treating autoimmune diseases and preventing organ transplant rejection. The document then classifies immunosuppressive drugs and discusses several classes in more detail, including glucocorticoids, calcineurin inhibitors like cyclosporine and tacrolimus, sirolimus, cytostatics like cyclophosphamide, and mycophenolate mofetil. For each drug, the document provides information on mechanisms of action, indications, dosages, and side effects. The document aims to provide clinicians an overview of commonly used immunosuppressive drugs.
Introduction of immunity and immunosuppressed drugs
introduction of immunity and immunosuppressive Drugs
Hargeisa somalia, specially university of hargeisa
immunosuppression drugs
This document summarizes several types of immunosuppressant drugs used to inhibit immune responses for organ transplantation and autoimmune diseases. It describes calcineurin inhibitors like cyclosporine and tacrolimus, mTOR inhibitors like sirolimus, antiproliferative drugs like azathioprine and mycophenolate mofetil, glucocorticoids like prednisone, and biological agents like TNFα inhibitors and IL-2 receptor antagonists. It provides details on the mechanisms of action, pharmacokinetics, adverse effects and uses of these major immunosuppressive drug classes and examples like cyclosporine, tacrolimus and sirolimus.
Mtor inhibitors in renal transplant
mTOR inhibitors like sirolimus and everolimus are immunosuppressants that provide an alternative to calcineurin inhibitors for renal transplant patients. They have antiproliferative properties, cause less nephrotoxicity than CNIs, and are associated with lower rates of malignancy, viral infections, and improved renal function when used to convert patients from a CNI-based regimen. However, mTOR inhibitors are less effective at preventing acute rejection when used without a CNI in de novo transplants.
Immunosuppressive drugs
This document summarizes immunosuppressive drugs. It discusses how they work to suppress the immune system and are used to prevent organ rejection after transplantation and treat autoimmune diseases. The main classes of immunosuppressive drugs covered are glucocorticoids, calcineurin inhibitors like cyclosporine and tacrolimus, antiproliferative drugs including mycophenolate mofetil and mTOR inhibitors, immunosuppressive antibodies, and others. Specific drugs within each class are described in terms of their mechanisms of action, pharmacokinetics, uses, and side effects.
Glucocorticoids
The document discusses adrenocortical steroids, which are synthesized in the adrenal cortex and have glucocorticoid and mineralocorticoid activities. Glucocorticoids penetrate cells, bind to receptors, and regulate protein synthesis. Examples include hydrocortisone, prednisolone, and dexamethasone. Corticosteroids are powerful drugs that can cause both improvements in disease and adverse effects, so proper use and monitoring is important. They have a variety of ophthalmic and non-ophthalmic uses and indications.
Complications of immunosuppression
This document discusses immunosuppressant drugs, their mechanisms of action, uses, and complications. It describes how immunosuppressants work by inhibiting cytokines, cytokine production, or cytotoxic immune cells. Major drugs covered include calcineurin inhibitors cyclosporine and tacrolimus, mTOR inhibitor sirolimus, corticosteroids, antimetabolites azathioprine and mycophenolate, cytotoxic drugs, and immunosuppressive antibodies. Complications of immunosuppression can include infection, nephrotoxicity, bone marrow toxicity, and increased cancer risk. Each drug profile provides therapeutic uses and adverse effects.
Azathioprine
Azathioprine is an immunosuppressive drug used to treat rheumatoid arthritis and prevent rejection in organ transplant recipients. It works by suppressing the immune system and altering antibody production. The presentation discusses the mechanism of action, indications, contraindications, dosages, adverse reactions, and drug interactions of azathioprine. Azathioprine is used as an adjunct treatment for severe, active rheumatoid arthritis not responsive to other therapies. It can cause side effects like rash, nausea, vomiting, bleeding, infections, and increased risk of cancer. Patients should be monitored for blood abnormalities and use caution with other drugs that may increase myelosuppression.
Class immunosuppressants 2
This document discusses various classes of immunosuppressant drugs used to prevent rejection of transplanted organs or treat autoimmune diseases. It describes glucocorticoids, calcineurin inhibitors like cyclosporine and tacrolimus, mTOR inhibitors like sirolimus and everolimus, antiproliferative agents, biological agents targeting cytokines like TNF inhibitors, monoclonal antibodies, adhesion molecule inhibitors, and tolerogens. Specific drugs are discussed within each class along with their mechanisms of action, pharmacokinetics, and adverse effects.
Immunosuppressant drugs
This presentation is about immunosuppressant drugs which are used to suppress cell mediated/humoral or both types of immunity.
Was ist angesagt? (20)
Introduction of immunity and immunosuppressed drugs
Introduction of immunity and immunosuppressed drugs
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Methods of immunosuppression
Immunosuppression involves reducing the activation of the immune system through medications, surgery, radiation or other means. The document discusses the history of immunosuppression and developments in transplantation including the identification of cortisone and research on the immune system. It outlines current methods of immunosuppression including calcineurin inhibitors, mTOR inhibitors, antimetabolites, corticosteroids, depleting antibodies and fusion proteins. The mechanisms, types and treatment of allograft rejection such as hyperacute, acute and chronic rejection are also summarized.
ICN Victoria: Botha on Acute Renal Failure
1) Hospital acquired acute kidney injury (AKI) is a problem for clinicians due to the complex renal physiology, limited clinically useful biomarkers for renal injury, difficulties with fluid management in sepsis, and limited therapies for early AKI.
2) The kidney is at risk of both hyperoxia and hypoxia due to its oxygen regulation and blood flow, making renal function difficult to assess. Global renal blood flow may not correlate with glomerular filtration rate, medullary flow, or oxygenation.
3) While a positive fluid balance and elevated central venous pressure are associated with worse outcomes in septic shock, fluid management remains challenging without reliable ways to directly measure renal blood flow or the integrity of the endothelial glyc
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Regulation of pten activity by its carboxyl terminal autoinhibitory
Regulation of PTEN Activity by Its Carboxyl-terminal Autoinhibitory Domain.
Leticia Odriozola, Gobind Singh, Thuong Hoang, and Andrew M. Chan
From the Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York, 10029
THE JOURNAL OF BIOLOGICAL CHEMISTRY, VOL. 282, NO. 32, pp. 23306–23315, August 10, 2007
目前已知PTEN(Phosphatase and tensin homolog)是腫瘤抑制蛋白，其由403個氨基酸組成，主要分PTPase及C2 domain，C2 domain使PTEN可與細胞膜作用連結。
PTEN之C-tail(aa 350~403)被發現具有調控PTEN自身活性之功能。前人研究指出C-tail有6個可磷酸化之位置(Thr-366、Ser-370、Ser-380、Thr-382、Thr-383及Ser-385)，這些位置可調控PTEN之腫瘤抑制能力、胞內之分佈及穩定性。前人產生以上位置突變之PTEN變異株，發現這些變異株具有更強的腫瘤抑制能力，但穩定性將降低，這可能是因這些變異株具有更開放結構所致。
本報告針對研究PTEN C-tail在連結細胞膜和在其本身催化活性中扮演的功能。作者先產生一系列之PTEN磷酸化位置變異株，發現S385A會促使PTEN之membrane localization in vivo及加強phosphatase活性in vitro，而且此突變會使Ser-380/Thr-382/Thr-383 cluster的磷酸化程度降低，因此知Ser-385可透過被去磷酸化以調控PTEN。而以phosphomimic residues取代Ser-380/Thr-382/Thr-383會使上述S385A所產生之PTEN催化活性反轉。之後利用免疫沉澱方法，發現C-tail之71-amino acid region會與C2 domain上之CBR3 motif作用，暗示C-tail參與連結細胞膜之調控。最後利用合成之PTEN C-tail peptide，發現其可抑制PTEN之催化活性in vitro，而在細胞表現此peptide則會抑制PTEN之membrane localization，磷酸化之Akt量亦上升。以上實驗顯示C-tail在PTEN之membrane recruitment及PTPase活性調控中扮演Autoinhibitory domain角色。
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The document discusses two scientific articles about factors that can lead to skin cancer and Ewing's sarcoma. The first article discusses how targeting the PTEN protein, which regulates cell growth, may help prevent skin cancer. The second article discusses how ultraviolet light can affect the function of the EWS protein involved in Ewing's sarcoma by changing the expression of genes it regulates and preventing an appropriate DNA damage response. The document emphasizes the importance of DNA repair mechanisms in protecting against UV radiation and preventing disease.
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Clive Woolfe, Irishman and RPA Intensivist, speaks at Bedside Critical Care Conference. In this podcast, he gives an overview of the prognostication and management of chronic liver disease. See www.intensivecarenetwork.com for the podcast.
C.diff
C. difficile is a spore-forming, toxin-producing bacterium that can cause severe diarrhea and life-threatening complications. While historically most cases were mild, beginning in 2000 morbidity and mortality increased, potentially due to the emergence of a hypervirulent strain. Laboratory diagnosis has been challenging due to limitations of enzyme immunoassays and the need for multi-step testing algorithms. Newer molecular tests like PCR provide improved accuracy and allow for timely treatment decisions.
Cell cycle dysregulation in cancer
Cell cycle dysregulation is a hallmark of cancer cells. Cancer cells progress relentlessly through rounds of cell division even when it would be more appropriate to pause, exit the cycle, or undergo apoptosis. Progression through the cell cycle is controlled by cyclins and cyclin-dependent kinases and regulated at checkpoints. Three key tumor suppressor genes - RB1, TP53, and CDKN2A - control events in G1 phase and are commonly mutated in cancers. Mutations in these genes allow inappropriate cell cycle progression.
Lecture 5 immunology
Humoral immunity refers to antibody production and related processes like B cell activation, cytokine production, affinity maturation, and memory cell generation. Antibodies secreted by plasma cells constitute the humoral immune response, which follows distinct phases after antigen exposure. B cell activation requires two signals: antigen binding and T cell help. T cells provide the second signal through cell surface molecules and cytokines, triggering B cell proliferation and differentiation into plasma cells that secrete antibodies. Isotype switching increases antibody diversity but maintains antigen specificity. It occurs through DNA recombination mediated by cytokines from T helper cells. Affinity maturation enhances antibody affinity through somatic hypermutation and selection of higher affinity B cell clones.
The role of the endothelium as a mediator of critical illness
Endothelium was once thought to be an inert organ. However, it plays an important role in multiple functions. These include coagulation, inflammation and determination of vascular permeability.
He then gives a brief overview of the endothelial arrangement, function of the glycocalyx layer and how an injury causing a loss of the protective layer results in holes in the endothelium. The inflammatory cells enter via these holes and causes oedema in the affected organs leading to multiple pathologies.
Danny then explains the role of endothelium in controlling cell barrier function.
Activation of cortactin protein and the myosin light-chain kinase (MLCK) enzymes activate stress fibres resulting in pulling of endothelial cells thereby increasing its permeability.
Danny discusses the role of endothelial dysfunction in acute respiratory distress syndrome (ARDS) at macrovascular, microvascular and molecular levels. Macrovascular thrombosis is related to an increase in severity of ARDS, pulmonary hypertension, and mortality.
At a microvascular level there is a loss of vascularity and increased blood vessel thickness. At a microscopic level, endothelial cells appear swollen and damaged in ARDS. Endothelial dysfunction drives organ dysfunction and mortality. Changes in various endothelial markers like increased von Willebrand factor (vWF), decreased protein C and increased pulmonary dead space correlate with increased mortality.
Studies show that endothelial dysfunction is a more specific and sensitive method to predict mortality of critically ill patients when compared to SOFA score, SAPS 2 score and WCC. Danny discusses ventilator strategies for endothelial cells in ARDS patients. Lowering the tidal volume of ventilators and employing recruitment manoeuvres are such strategies.
Both of these cause a decrease in oedema by reducing endothelial permeability. He then shares the various potential pharmacological treatments for treating endothelial damage. These include statins and spingosine-1-phosphate (S1P). Different studies on the effect of statins in ARDS show contradicting result.
However, targeted therapies can be designed by studying the phenotypes and molecular basis of ARDS in each patient.
The role of the endothelium as a mediator of critical illness by Danny McAuley
Finally, for more like this, head to our podcast page. #CodaPodcast
subdural haematoma
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help boost feelings of calmness, happiness and focus.
Pseudogene Journal Club Presentation
A journal club style presentation on a publication about the effect of microRNAs and pseudogenes on tumor gene regulation.
(Note: The animations in the slides do not work on SlideShare, please download the PowerPoint file to view.)
adoptive T cell therapy
This document discusses adoptive T cell therapy and strategies to harness the adaptive immune system to fight cancer and other diseases. It provides an overview of T cell activation pathways and the role of accessory proteins like CD28 and CD3. It also summarizes methods to engineer T cells, including using tumor-infiltrating lymphocytes and genetically modifying T cells to express chimeric antigen receptors targeting cancers like CD19-positive leukemia. The document discusses approaches like lympho-depletion prior to therapy and highlights some toxicities seen with CAR-T therapy.
Holley on Coagulation Management
Anthony Holley, a world famous transfusion and coagulation guru, draws on his military, ED and ICU experience and talks about the most recent blood transfusion guidelines. They are a great resource and can be downloaded here. This talk is different to the last one he gave at Bedside Critical Care 2012!
TLCDBU-2016: Road to the artificial pancreas 2016
Researchers are making progress toward the artificial pancreas (AP) with 2016 focusing on real-world testing of algorithms. Key areas of interest for 2017 include transparency of researcher methods and data, effort required by patients, and reimbursement discussions. Continuous glucose monitoring accuracy and wear time remain barriers, as do pump reliability and immune responses. Both algorithmic and heuristic approaches are being studied, with personalization seen as important. Success has also come from grassroots integration and sharing of existing technologies.
Fractura Epicondilo Medial en Niños
La fractura del epicóndilo medial es una lesión frecuente en pediatría que ocurre más comúnmente en adolescentes varones. Existen controversias sobre el tratamiento, pero generalmente se recomienda el manejo quirúrgico para fracturas expuestas, luxaciones irreductibles, fragmentos intraarticulares o inestabilidad en valgo. Los estudios a largo plazo muestran buenos resultados funcionales independientemente del tratamiento, con desviaciones axiales menores a 9 grados y déficit de movimiento menor a 19 grados, además de fuerza muscular
BCC4: Lockie on Resuscitating the Lungs
Fran Lockie, provides a useful update on paediatric drowning sequalae and outcomes. This talk was recorded at Bedside Critical Care Conference.
For audio for this and similar talks, please visit www.intensivecarenetwork.com
The next BCC will be held in Cairns, 29th September - 3rd of October: http://bedsidecriticalcare.com/
How to survive a gas attack
Slides for a short talk on some tips and tricks for trainees when interpreting ABGs (arterial blood gases). Talk given at the free registrar's day at Bedside Critical Care 2013 in the Whitsunday Islands.
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Regulation of pten activity by its carboxyl terminal autoinhibitory
Regulation of pten activity by its carboxyl terminal autoinhibitory
The role of the endothelium as a mediator of critical illness
The role of the endothelium as a mediator of critical illness
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Immunosuppressive Drugs.ppt
This document provides information on the immune system, cytokines, cell-mediated immunity, humoral immunity, immunosuppressant drugs, and cyclosporine. It discusses the components and functions of the immune system, the roles of cytokines and different types of immunity. It also describes several commonly used immunosuppressant drugs, including their mechanisms of action, pharmacokinetics, therapeutic uses, and adverse effects. Specifically, it provides detailed information about cyclosporine, including its chemistry, mechanism of action, pharmacokinetics, uses, toxicity, and drug interactions.
calcineurin inhibitors, friend or foe
a journey through immunosuppressive effect of CNI, How they work, pharmacokinetic polymorphism side effect, avoidance and minimization
Spindle Poisons
This document summarizes several classes of spindle poisons (microtubule-targeting agents), including vinca alkaloids, taxanes, estramustine, epothilones, colchicine, benzimidazoles, and griseofulvin. For each class or drug, it describes the source, mechanism of action, drug resistance, pharmacokinetics, clinical applications, and toxicity profile. The vinca alkaloids discussed are vinblastine, vincristine, vinorelbine, and vindesine. For taxanes, it covers paclitaxel and docetaxel.
IMMUNIZING AGENTS ppx.pptx
This document discusses various immunizing agents, immunosuppressants, and hematopoietic drugs. It provides an overview of immunization including active and passive immunization. It also lists several common vaccines such as BCG, cholera, diphtheria, and pertussis vaccines. The document then discusses immunosuppressants including cytokine IL-2 inhibitors like cyclosporine and tacrolimus, inhibitors of cytokine gene expression like corticosteroids, and cytotoxic drugs. Finally, it covers several classes of hematopoietic drugs including platelet aggregation inhibitors like aspirin, thrombolytic drugs, and anticoagulants.
Basic considerations of chemotherapy
This document provides information about basic chemotherapy considerations and describes several common chemotherapeutic agents. It discusses why multiple cycles of chemotherapy are needed and the typical 21-day treatment cycle. It also outlines which patients are suitable for chemotherapy based on performance status. Several classes of chemotherapeutic drugs are then described in detail, including their mechanisms, formulations, dosing considerations, toxicities and administration guidelines. These include alkylating agents, platinum compounds, topoisomerase inhibitors, antibiotics and others.
Toxicity of aminoglycoside antibiotics
This document discusses the toxicity of aminoglycoside antibiotics. It notes they are bactericidal, inhibiting protein synthesis through binding to bacterial ribosomes. Their toxicity includes nephrotoxicity due to accumulation in kidney tubules, ototoxicity due to accumulation in the inner ear, and potential neuromuscular blockade when used with other drugs. Toxicity is related to the number of amino groups in each drug, with neomycin typically being the most toxic. Proper dosing and avoiding interactions are important to prevent adverse effects.
Microsomal enzyme induction
Microsomal enzymes like cytochrome P450 and UDP glucoronosyl transferases are important for drug metabolism in the liver and other tissues. Cytochrome P450 enzymes catalyze oxidation, reduction, and other phase I reactions. UDP glucoronosyl transferases catalyze phase II conjugation reactions like glucoronidation. Drug metabolism can be induced or inhibited by other drugs and environmental factors, leading to potential drug-drug interactions. A better understanding of an individual's genetic polymorphisms and environmental factors can help optimize drug therapy and avoid adverse reactions.
immunosuppressants.pptx
The document summarizes various immunosuppressant drugs used to prevent rejection of organ transplants. It discusses calcineurin inhibitors like cyclosporine and tacrolimus, mTOR inhibitors sirolimus and everolimus, antiproliferative drugs, glucocorticoids, and biological agents. Cyclosporine inhibits T-cell activation by blocking calcineurin. Tacrolimus is more potent than cyclosporine. Sirolimus inhibits T-cell proliferation by blocking mTOR. Other drugs discussed include azathioprine, mycophenolate mofetil, methotrexate, cyclophosphamide, chlorambucil, prednisone, infliximab,
Immunomodulators
This document provides an overview of immunomodulators. It begins with definitions of immunity and antigens. It describes the types of immunity and components of the immune system. It then discusses mechanisms of immunomodulation and how drugs can suppress or stimulate the immune response. The document focuses on clinically used immunomodulators, dividing them into immunosuppressants and immunostimulants. Several commonly used immunosuppressants are described in detail, including their mechanisms of action, uses, and toxicities.
ENDOCRINE PANCREAS, INSULIN, GLUCAGON
A TRIANGULAR GLAND, WHICH HAS BOTH EXOCRINE AND ENDOCRINE CELLS, LOCATED BEHIND THE STOMACHACINAR CELLS PRODUCE AN ENZYME-RICH JUICE USED FOR DIGESTION (EXOCRINE PRODUCT)PANCREATIC ISLETS (ISLETS OF LANGERHANS) PRODUCE HORMONES INVOLVED IN REGULATING FUEL STORAGE AND USE.
Treament of malaria
This document discusses various antimalarial drugs, their mechanisms of action, pharmacokinetics, and uses. It begins by outlining the objectives of antimalarial treatment, including preventing and treating malaria attacks, eradicating parasites, and reducing transmission. It then classifies and describes over a dozen classes of antimalarial drugs. A large portion of the document focuses on chloroquine, discussing its mechanism of action, resistance, pharmacokinetics, side effects, and cautions. It also provides details on other commonly used antimalarial drugs and their properties. The document concludes by comparing the characteristics of different antimalarial drugs and outlining their roles in causal prophylaxis, suppressive prophylaxis,
antimicrobial.pptx
In 3 sentences:
Penicillin was the first antibiotic discovered from the fungus Penicillium. It works by interfering with bacterial cell wall synthesis. There are several classes of penicillin including natural penicillin, semisynthetic penicillins, and extended spectrum penicillins.
Anti Tubercular Drugs - Mechanism of Action and Adverse effects
A brief outline of the mechanism of action and adverse effects of anti tubercular drugs
Only First line and second line drugs are dealt with.First line drugs may be useful for MBBS students and the rest is directed for postgraduate students.
Hope you find it useful.
Drugs for Malaria
Malaria is caused by four protozoan parasites and is treated with several classes of antimalarial drugs. Chloroquine was formerly widely used but resistance emerged. Artemisinin derivatives like artesunate are now usually given in combination therapies due to their rapid action against the parasite and ability to prevent resistance when paired with other drugs. Tu Youyou received a Nobel Prize for discovering artemisinin from traditional Chinese medicine.
Malaria presentation
This document discusses drug therapy for malaria. It defines malaria and describes the life cycle and species of Plasmodium that cause malaria in humans. It then discusses the clinical presentation of malaria and diagnosis. The bulk of the document categorizes and describes various classes of antimalarial drugs, including quinine, chloroquine, primaquine, atovaquone, lumefantrine, and artemisinin derivatives. It provides details on the mechanisms of action, pharmacokinetics, uses, and adverse effects of many common antimalarial medications.
Immunosuppresant mbbs
This document discusses various immunosuppressant drugs and their mechanisms of action. It begins by describing the immune system and cytokines. It then discusses several classes of immunosuppressant drugs including inhibitors of cytokine production/action like cyclosporine and tacrolimus, inhibitors of cytokine gene expression like corticosteroids, cytotoxic drugs like azathioprine and mycophenolate mofetil, antibodies that block T cell surface molecules, and others like sirolimus. It provides details on the mechanisms, pharmacokinetics, uses, and adverse effects of these immunosuppressant drugs.
Immunosuppressants Pharmacology
Immunosuppressants are drugs which inhibit cellular/humoral or both types of immune responses and have their major use in organ transplantation and autoimmune diseases.
Pathophysiology Chemotherapy of Cancer
The document discusses various aspects of cancer chemotherapy including:
1. Guiding principles of cancer chemotherapy aim for total cell kill through early diagnosis, combination chemotherapy, and intermittent regimens.
2. Chemotherapeutic agents are classified based on their mechanism of action and cell cycle specificity, and include alkylating agents, antimetabolites, natural products, and hormones/antagonists.
3. Common chemotherapeutic drugs are discussed including their mechanisms of action, uses, and adverse effects. Chemotherapy aims to destroy cancer cells while limiting toxicity to normal cells.
Capsules
This document summarizes several topics in nephrology:
1) A case of a hemodialysis patient presenting with vomiting is discussed. Possible causes of vomiting in hemodialysis patients include inefficient dialysis, fluid retention, high BUN, acidosis, and medications.
2) Guidelines for infection control in hemodialysis are mentioned.
3) Diet recommendations for patients with calcium-containing kidney stones are provided, including reducing sodium, animal proteins, and foods high in oxalate while ensuring sufficient calcium intake.
4) Causes and management of hypoglycemic coma are reviewed, including drug durations of action and non-antihyperglycemic agents that can
Obstetric management of SLE and APLS
This document discusses the obstetric management of systemic lupus erythematosus (SLE) and antiphospholipid antibody syndrome (APLS). It provides information on:
1) The increased risks of adverse pregnancy outcomes for patients with SLE/APLS including preeclampsia, intrauterine growth restriction, and preterm birth.
2) Medication management during pregnancy focusing on continuing hydroxychloroquine and tapering corticosteroids due to their safety profiles. Other immunosuppressants are generally avoided due to risks.
3) Increased monitoring is recommended during pregnancy for SLE/APLS patients including frequent visits and testing to monitor for disease flares and complications. Delivery planning focuses
Ähnlich wie Rosenberg on Immunosuppression (20)
Anti Tubercular Drugs - Mechanism of Action and Adverse effects
Anti Tubercular Drugs - Mechanism of Action and Adverse effects
Mehr von SMACC Conference
Precision Medicine in Acute Brain Injury
Systematic review of 26 studies with 55,792 patients found that dedicated neurocritical care (NCC) was associated with decreased risk of mortality (17% relative risk reduction) and decreased risk of poor functional outcomes (17% relative risk reduction) in critically ill brain-injured adults. A survey of Australian ICUs found limited availability of NCC, with only 4 centers specializing in it and 9 employing an intensivist subspecializing in NCC. Continuous EEG monitoring was found to have higher sensitivity for detecting nonconvulsive seizures than routine EEG monitoring, and was associated with reduced in-hospital mortality, though barriers to its universal use include infrastructure and personnel requirements.
CSD by Jeffcote Coda 22.pdf
CORTICAL SPREADING DEPOLARISATION IN NEUROLOGICAL DISEASE – AN INTRODUCTION
By Toby Jeffcote
Cortical spreading depolarization (CSD) is a spreading loss of ion homeostasis, altered vascular response, change in synaptic architecture, and subsequent depression in electrical activity following an inciting neurological injury.
It was first described by Leão in 1944, a disturbance in neuronal electrophysiology has since been demonstrated in a number of animal studies, and recently a few human studies that examine the occurrence of this depolarizing phenomenon in the setting of a variety of pathological states, including migraines, cerebrovascular accidents, epilepsy, intracranial hemorrhages, and traumatic brain injuries. The onset of CSD has been demonstrated experimentally following a disruption in the neuronal environment leading to glutamate-induced toxicity. This initial event leads to pathological changes in the activity of ion channels that maintain membrane potential. Recovery mechanisms such as sodium-potassium pumps that aim to restore homeostasis fail, leading to osmolar shifts of fluid, swelling of the neuron, and ultimately a measurable depression in cortical activity that spreads in the order of millimeters per minute. Equally important is the resulting change in vascular response. In healthy tissue, increased electrical activity is coupled with release of vasodilatory factors such as nitric oxide and arachidonic acid metabolites that increase local blood flow to meet increased energy expenditure. In damaged tissue, not only is the restorative vascular response lacking but a vasoconstrictive response is promoted and the ischemia that follows adds to the severity of the initial injury. Tissue threatened by this ischemic response is then at elevated risk for CSD propagation and falls into a vicious cycle of electrical and hemodynamic disturbance. Efforts have been made to halt this spreading cortical depression using N-methyl-D-aspartate receptor antagonists and other ion channel blockers to minimize the damaging effects of CSD that can persist long after the triggering insult.
Subdural Haemorrhage and MMA embolisation
Celia Bradford takes us through the latest on the management of subdural haemorrhage (SDH). She covers acute SDH, chronic SDH and middle meningeal artery embolisation, a novel treatment for chronic SDH management in certain circumstances.
Andy Neill - More neuroanatomy pearls for neurocritical care
Andy Neill shares some more neuroanatomy wisdom that's highly practical for anyone working with neuro emergencies. This time he covers brain herniation syndromes, hydrocephalus, extradural vs subdural haematomas, cervical spinal imaging, vertebral artery dissection and "things you read on CT reports but don't know what they mean"!
The BONANZA Trial and PbTO2 Monitoring
Andrew Udy talks about Brain Tissue Oxygen Monitoring:
It’s Not What You’ve Got It’s What You Do With It
The BONANZA Trial
Andrew Udy talks about the ongoing BONANZA Trial which is assessing whether an algorithm that incorporates both ICP and brain tissue oxygen (PbTO2) can improve outcomes after traumatic brain injury (TBI). Like with all monitoring, how the PbTO2 is interpreted and managed is critical and the devil is in the detail!
More on BONANZA here
More on BOOST3 here
Dilating the Dogma of Vasospasm
R. Loch Macdonald, M.D., Ph.D.
Community Neurosciences Institute
Fresno, California, USA
Angiographic vasospasm and more accurately, delayed cerebral ischemia, continue to contribute to morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). It is known that angiographic vasospasm is common after SAH, occurring in two-thirds of patients. Cerebral infarctions that developed days after the SAH have been attributed to angiographic vasospasm, occuring in about a third of patients, although this has always been controversial. Angiographic vasospasm theoretically can only damage the brain by restricting blood flow but there is no easy, accurate, widely available method to measure cerebral blood flow and this is not the measurement we need. Blood flow depends on metabolic demand so what we need to know to determine if angiographic vasospasm is causing ischemia is oxygen extraction fraction in the brain tissue supplied the the spastic artery. Without this measurement, the attribution of ischemia to vasospasm is subjective. Since angiographic vasospasm is essentially the only detectable delayed phenomenon after SAH, we focus on it and apply tremendous resources to preventing or reversing the vasospasm. Undoubtedly angiographic vasospasm can cause cerebral infarctions, but it has to be severe and flow limiting. But SAH is a complex disease. There are many other causes for cerebral infarctions after SAH, the most common being due to the aneurysm repair procedure. And a given degree of vasospasm may cause infarction in a volume-depleted patient with poor collateral blood supply but not in a patient without these things. There also are hypodense brain lesions after SAH that are due to intracerebral hemorrhages. There can be hypodensities in the brain directly under usually thick SAH where the brain dies. This observation in particular supports a role for cortical spreading depolarizations/ischemia as a cause of infarction after SAH. Other macromolecular processes that are hypothesized to cause brain damage after SAH include microthromboembolism, changes in the microcirculation, delayed brain cell apoptosis and capillary transit time heterogeneity. Determining the importance of these things is hindered by the lack of an easy way to detect them in patients. It is also known that poor grade patients, who presumably have more early brain injury and ischemia than good grade patients, are more prone to delayed cerebral ischemia, suggesting increased sensitivity to secondary insults of the already injured brain. We also assume delayed neurological deterioration when attributed to vasospasm or delayed cerebral ischemia, is purely due to ischemia. While knowledge about what happens pathophysiologically after SAH is increasing, management of delayed cerebral ischemia still focuses on detecting angiographic vasospasm and then augmenting the blood pressure to improve cerebral blood flow or dilating the spastic arteries with balloons or drugs.
EVD Tips and Tricks
By Catherine Bell and Andrew Udy
Catherine Bell takes us through how to troubleshoot problems commonly encountered when looking after patients who have an external ventricular drain (EVD) in situ. Issues with using brain tissue oxygen monitors are also discussed. A highly practical session aimed at bedside clinicians.
There is no such thing as mild, moderate and severe TBI - by Andrew Udy
Part 2 of a debate over the classification of TBI. Andrew Udy then argues that this classification is fundamentally flawed. He discusses the issues with the Glasgow Coma Scale, and therefore the follow-on issues in TBI classification, including all the confounders to the GCS, the issues with timing of the score as well as GCS not taking baseline function or specifics subtypes of TBI into account. He makes teh argument that biomarkers may better categorise the diffuse entity we call TBI.
TBI Debate - Mild, moderate and severe categories work
Andrew Chow, Intensivist with a neurosurgical background, argues that the current categorisation system for traumatic brain injury (TBI) works, and makes sense! He tackles us through the history of this system, and why it’s important to differentiate different types of TBI. The arguments in favour of this categorisation include the consistency and benefits of a universal language, the implications for triage and management, and the fact that this system has been endorsed by all major organisations
TBI: when to stop and when to give time
Dr Nick Little is an experienced Neurosurgeon who's looked after patients with traumatic brain injury for his whole career. Here he discusses the difficulties of prognostication following traumatic brain injury (TBI). He talks about the statistics of outcomes following mild, moderate and severe TBI and then goes on to tackle the harder topic of how we try to work out what an individual would want if they knew the spectrum of outcomes that they may face. The issues with the clinical examination findings we use to prognosticate are covered, as well as which imaging findings he finds most helpful. He also mentions the difficulties with current prognostic calculators.
Ketamine in Brain Injury by Toby Jeffcote
Historically, when it came to brain injury, ketamine had a bad rap. Much of that dogma was dispelled in the last decade, and ketamine is now frequently used as an induction agent in acute brain injury, especially traumatic brain injury, due to it’s favorable effects on haemodynamics.
However a new application of ketamine is now being explored - whether ketamine may be able to reduce secondary brain injury.
Managing Complications of Chronic SCI by Bonne Lee
20 million people around the world are living with a spinal cord injury (SCI). The medical issues they develop over the years differ to any other patient cohort.
These complications include autonomic dysreflexia, management of pressure areas, specific infections, nuanced peri-operative care and highly specific issues such as baclofen pump management and syringomyelia
Do look at the NeuroResus section on this and listen to Spinal Rehab Specialist Bonne Lee talk about this side of SCI care.
Keywords
SCI, spinal, spinal cord injury, autonomic dysreflexia, pressure areas, infection, peri-operative care, baclofen pump, syringomyelia, chronic SCI, spinal trauma, spinal rehab, incomplete SCI
EEG and Status Eplilepticus by Tania Farrar
Tania is a neurologist and epileptologist with expertise in continuous EEG (cEEG) and status epilepticus (SE). This talk covers what a seizure is, what status is, including focal and generalised status epilepticus.
So why do we do cEEGs for patients with suspected SE?
To confirm the diagnosis
To see if patient just post ictal or still seizing
To establish that the clinical and electric seizures have stopped
To see if burst suppression is achieved
To exclude other differential diagnoses
She makes a good argument for why cEEG is such an important tool in managing SE.
In the questions after the talk, the issue of availability of cEEG in the Australian setting was discussed. Limited montage EEGs are discussed including their pros and cons.
Browne Neuro symposium.pptx
Stuart Browne is a Neuro Rehab specialist from Sydney. These slides accompany a talk he gave at the Brian Symposium in 2023. He discusses what "severe disability" really means.
Severe disability is more common than many realise - about 6% of the Australian population.
Stuart discusses how health is more than simply physical recovery and how it is a multidimensional construct. He covers how permanent disability doesn't necessarily equate to a poor quality of life. He also discusses the long timespan of recovery, which is often much longer than appreciated.
He specifically discusses "Locked-in Syndrome" and how the survivors have surprisingly positive self-reported health-related quality of life and well-being.
Stuart also covers how severely disabled people face various forms of discrimination.
Paediatric Stroke by Shree Basu
Shree Basu is a Paediatirc Intensivist in Sydney. These slides from the Brain Symposium 2023 accompany the talk she gave. She discusses how Paediatric stroke presents, what neuroimaging is required and what interventions are available, including thrombolysis and the role of endovascular thrombectomy.
Hypertensing Spinal Cord Injury - gold standard or wacky?
This document discusses the concept of maintaining higher blood pressure levels, known as hypertension, after a spinal cord injury to improve spinal cord perfusion pressure and reduce secondary injury. It notes that while animal studies and some human trials have shown improved neurological outcomes, the evidence is still limited. It calls for larger randomized controlled trials in humans that also incorporate multi-modal monitoring and standardized outcome measures to further evaluate if inducing hypertension after spinal cord injury should be considered the gold standard of care.
Optimal Cerebral Perfusion Pressure
Mark Weedon takes us through the increasingly utilised concept of an optimal cerebral perfusion pressure (CPPopt) for each unique patient. He discusses the background to CPPopt, including intrcranial pressure (ICP), the Monroe Kelly hypothesis, neurovascular coupling, and cerebral autoregulation in health and following brain injury. He shows how intracranial pressure is affected by intracranial compliance and how this affects ICP waveforms. Cerebral perfusion pressure in relation to the Brain Trauma Foundation guidelines is covered including management of elevated ICP (EICP). The currently recommended tiered approach to managing cerebral perfusion pressure and EICP is mentioned citing recent guidelines. He uses a clinical case of a TBI to illustrate how the CPPopt can be ascertained and used to guide therapy, including the easy to perform “MAP Challenge”. Mark also describes the Pressure Reactivity Index (PRx) and how it can be used as a target for therapy. Finally, he covers the exciting results of the preliminary COGiTATE pilot study.
The Power of Words - Death and Language.ppt
Social Worker Victoria Whitfield and Bereavement councilor Louise Sayers discuss the power of words when health professionals are communicating topics around of death and serious injury with relatives and patients in critical care. They use role plays to bring theories to life.
Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin
Undertreatment of sepsis can lead to mortality, while overdiagnosis and overtreatment can increase future risk of antimicrobial resistance. Antimicrobial stewardship aims to balance these risks by prioritizing patient safety and appropriate antimicrobial use. Data shows variability in appropriateness of antimicrobial prescribing between different types of hospitals. Embedding antimicrobial stewardship principles throughout sepsis diagnosis and treatment, from initial microbiology testing to post-treatment review, can help standardize care and optimize outcomes.
Brain injury outcomes and predictors
Being able to prognosticate in the aftermath of a traumatic brain injury (TBI) is important as it assists with counselling patients and families. Moreover, it helps rationally allocate healthcare resources.
However, due to the heterogenous nature of TBI and variable pre brain injury patient factors and post brain injury course, this has proven to be a difficult task.
Large cohort studies have enabled improved accuracy in the prediction of 6 month mortality and unfavourable outcome.
Furthermore, many of the factors that contribute to long-term outcome have also emerged. However, it is not yet possible to use them in prediction algorithms or mathematical models.
There is emerging evidence that pre injury psychosocial and demographic factors may be of more relevance than injury severity. Moreover, that 'outcome' becomes increasingly subjective and complex as the post injury duration increases.
We end with three brief vignettes which highlight the fraught nature of long term outcome prediction.
Mehr von SMACC Conference (20)
Andy Neill - More neuroanatomy pearls for neurocritical care
Andy Neill - More neuroanatomy pearls for neurocritical care
There is no such thing as mild, moderate and severe TBI - by Andrew Udy
There is no such thing as mild, moderate and severe TBI - by Andrew Udy
TBI Debate - Mild, moderate and severe categories work
TBI Debate - Mild, moderate and severe categories work
Managing Complications of Chronic SCI by Bonne Lee
Managing Complications of Chronic SCI by Bonne Lee
Hypertensing Spinal Cord Injury - gold standard or wacky?
Hypertensing Spinal Cord Injury - gold standard or wacky?
Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin
Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin
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NARCOTICS- POLICY AND PROCEDURES FOR ITS USE
This document outlines policies and procedures for handling narcotic and controlled drugs in NABH accredited hospitals.
Histololgy of Female Reproductive System.pptx
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Identifying Major Symptoms of Slip Disc.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Post-Menstrual Smell- When to Suspect Vaginitis.pptx
Do you have abnormal smell after periods? It may be vaginitis. Do not worry, herbal medicine Fuyan Pill can help you get a cure.
The Electrocardiogram - Physiologic Principles
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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pathology MCQS introduction to pathology general pathology
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There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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Rosenberg on Immunosuppression
- 1. Immunosuppression Alex Rosenberg Clinical Fellow In Transplantation St Vincent’s Hospital, Sydney
- 2. Rejection • Acute Rejection • T cell mediated • Humoral. •Chronic Rejection Bronchiolitis obliterans syndrome
- 5. Calcineurin Inhibition • Cyclosporin A – Isolated 1979 from Tricoderma polysprum Rifai – Binds to Cyclophilin – inhibits Calcineurin. – Highly Lipid Soluble. – Monitoring best with Peak Levels.
- 6. • Tacrolimus. – Macrolide Antibiotic. – Isolated 1984 from Streptomyces tskubaensis. – Binds to FK-Binding protein. – Tacrolimus-FKBP complex inhibits calcineurin. – Empty stomach – Monitoring
- 7. Drug Interactions • Metabolized via cytochrome P-450 system.
- 8. Toxicities • Nephrotoxicity. • Hypertension • Hyperkalaemia • Hyperglycaemia • Hyperlipidaemia • Neurological side effects • Hirsuitism • Gingival hypertrophy.
- 10. Antimetabolites • Azathioprine – Pro drug: metabolized to 6-MP – Inactivated by TPMT. – Interferes with purine synthesis and so inhibits DNA replication. – Adverse effects: myelosupression, GI symptoms – Interacts with allopurinol.
- 11. • Mycophenolate – Pro drug of mycophenolic acid. – Blocks inosine monophosphate dehydrogenase. – Selectively inhibits T & B lymphocyte clonal expansion. – Side effects: Diarrhoea, marrow suppression.
- 13. Corticosteroids • Immunosuppressive and anti-inflammatory. • Inhibit transcription factors (IL2 / NFkB) • Down regulate expression of graft self molecules. • Usually lifelong. • First line treatment of acute rejection
- 15. Proliferation Signal Inhibitors • Sirolimus – Streptomyces hygroscopicus – 1975 in Easter Island. – Binds to FK binding protein. – Inhibits activation of mTOR. – Prevents T and B cell proliferation – Synergistic with CNIs – Toxicities: Poor wound healing
- 17. To name a few…. • Basiliximab – anti CD25. • Antithymocyte Globulin – CD 45 and multiple others • Muromonab – anti CD3 • Alemtuzumab – anti CD52 • Rituximab – anti CD20 • Bortezomib – proteasome inhibitor
- 18. 10 years post lung transplant
- 19. 13 years post lung transplant
- 20. 9 years post lung transplant
- 21. Thanks
Hinweis der Redaktion
- three forms of renal injury including: 1) an acute renal dysfunction due to vasoconstriction of the afferent arteriole, 2) an thrombotic microangiopathy that leads to thrombotic thrombocytopenic purpura and hemolytic uremic syndrome 3) chronic interstitial fibrosis and arteriolar sclerosis associated with persistent deterioration of renal function
- 2 case series of anastomoticdehisence