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29 Cards in this Set
- Front
- Back
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what lymphs area assoc with graft rejection
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CD8+ cells cause tissue destruction and CD4+ cells cause a delayed hypersensitivity reaction
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what does the recipients IS recognize and react to in the graft
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donor MHC molecules on the surface of APCs in the graft
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what type of effector cells do the CD4+ cells in a graft rejection become
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Th1
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what are the 2 pathways of graft rejection
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direct and indirect pathways
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what is the indirect pathway of graft rejection
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T lymphs in the recipient recognize MHC Ags of the graft donor after they are presented by the recipients own APCs
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what is the main cause of rejection due to the indirect pathway
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delayed-hypersensitivity
the CTLs can only recognize the Ag that is displayed to them and do not directly recognize or kill the graft tissue |
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what is the direct pathway of graft rejection
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Cd8+ T cells recognize the MHCs of the donor tissues and attacks them
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what causes a hyperacute graft rejection
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preformed antidonor Abs are present in the circulation of the recipient
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what is the initial target in a hyperacute graft rejection
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the graft vasculature(rejection vasculitis)
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what are the morphologic features of the kidney in hyperacute rejection
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1) Ig and complement deposition in the BV walls, causing endothelial injury and fibrin-platelet thrombi
2) the glomeruli undergoe thrombotic occlusion 3) fibrinoid necrosis occurs in the arterial walls |
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what are the differences in humoral and cellular acute rejection
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humoral--> vasculitis
cellular--> interstitial mononuclear cell infiltrate |
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what is the marker of an activated T cell in acute cellular rejection
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alpha chain of the IL2 receptor
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what types of damage occur in cellular acute rejection
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tubular necrosis
endothelitis |
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what damage occurs in acute humoral rejection
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necrotizing vasculitis
endothelial necrosis neutrophilic infiltration deposition of Igs, complement, and fibrin thrombosis necrosis of the renal parenchyma |
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what are the characteristics of vasculitis in acute humoral rejection
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thickening of the intima with proliferating fibroblasts, myocytes, and foamy macrophages
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what is a strong indicator of humoral rejection and why
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C4d because if it induced during the activation of the complement system in the classic pathway
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what are the main features of chronic rejection
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vascular changes(dense obliterative intimal fibrosis in the cortical arts)
interstitial fibrosis tubular atrophy with loss of renal parenchyma |
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chronic transplant glomerulopathy
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scarring of the glomeruli with duplication of basement membranes
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what are matched in organ matching
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HLA types
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what is the DOC for immunosuppression
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cyclosporine
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MOA of cyclosporine
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blocks activation of a transcription factor called nuclear factor of activated T cells
this is req for the transcription of cytokine genes such as IL2 |
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second line drugs that are used in immunosupression
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azathioprine, steroids, rapamycin and mycophenolate mofetil, monoclonal anti-T cell Abs
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MOA of azathioprine
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inhib leukocyte development from bone marrow precursors
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MOA of rapamycin and moycophenolate mofetil
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inhib lymph prolif
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what monoclonal Abs are used in immunosupression
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anti-CD3 and Abs to IL2 receptor alpha chain
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what dzs are pts on immunosupression at an inc risk of
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EBV-induced lymphomas, HPV-induced squamous cell carcinomas, and kaposi sarcoma
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what is graft versus host disease
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when immunologically competent cells or their precursors are transplanted into immunologically crippled recipients and the transferred cells recognize alloantigens in the host
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what are the major organs effected in GVH disease
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epithelia of the skin, liver, and intestines
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what infection is important in pts receiving bone marrow transplants
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CMV
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