Transplant Flashcards
What interleukin fascilitates acute rejection?
Clinical importance: Activation of a particular T cell by a foreign HLA peptide results in clonal proliferation of that type of T lymphocyte, a process that is mediated by IL-2 and leads to acute rejection
What are absolute contraindications for transplant?
Absolute contraindications for organ donation include incurable or metastatic malignancy, sepsis, transmissible spongiform encephalopathies (e.g., Creutzfeldt-Jakob disease), and cardiac arrest that occurred before brain death, none of which apply to this patient.
Preformed antibodies against class I HLA of the graft are responsible for ____________rejection
Preformed antibodies against class I HLA of the graft are responsible for hyperacute rejection
Abdominal pain, hypertension, generalized fatigue, and an increase in creatinine within 6 months of renal transplantation are concerning for __________ rejection of the renal allograft.
acute
What staining results would we expect for an acute cellular rejection
The biopsy confirms an acute cellular rejection (the absence of C4d staining indicates no antibody deposition).
C4d stainng looks for antibody deposition which we would see in hymoral rejection
Acute liver transplant rejection can occur within 6 months after transplantation and may manifest with vomiting, jaundice, rising bilirubin, and pain in the graft region. What imaging modality would you start with?
US!
Since clinical findings for acute liver transplant rejection are nonspecific, duplex ultrasound of the liver should be performed to rule out possible vascular complications (e.g. portal vein thrombosis, bleeding), biliary complications (e.g., leak, stricture), and liver infection (e.g. perihepatic abscess).
What group of immunosuppressant drugs act by inhibiting IL-2 to precent rejection?
Calcineurin inhibitors
A group of immunosuppressant drugs that act by inhibiting interleukin-2 production and IL-2 receptor expression, reducing T-cell activation. Examples include tacrolimus and cyclosporine.
Prophylaxis against the most common opportunistic pathogens, such as Pneumocystis jirovecii and human cytomegalovirus (CMV), should be administered in posttransplant patients on immunosuppressive therapy.
What can we give?
Trimethoprim-sulfamethoxazole
What prophylaxis must we think about for post-transplant patients?
CMV and ipprotunitsitc pathogens Pneumocystis jirovecii
< 48 hours after transplantation, usually within minutes to hours
Hyperacute rejection
< 6 months after transplantation, usually within weeks to months
Acute rejection
> 6 months after transplantation, usually after a few years
Chronic rejection
What rejection: on biopsy Dense interstitial lymphocytic infiltrate with vasculitis
acute
What rejection: on biopsy Small vessel thrombosis → ischemia → graft necrosis
hyperacute
What kind of rejection does not require removal of the graft?
Acute rejection
What is this describing: recipient’s preformed cytotoxic antibodies against donor’s class I HLA molecules or blood group antigens → activation of the complement system and adhesion to cells → thrombosis of vessels → graft ischemia and necrosis
Humoral rejection (type II hypersensitivity reaction)
THIS IS HYPERACUTE
What is the pathophysiology behing acute rejection?
Acute cellular rejection (type IV hypersensitivity reaction)
Donor MHC class II antigens react with recipient CD4+ T cells, which then differentiate into Th1 helper T cells → cytokine (INF-γ) release → macrophage recruitment → parenchymal and endothelial inflammation
Donor MHC class I antigens react with recipient CD8+ T cells → direct cytotoxic cell damage
Acute humoral rejection (type II hypersensitivity reaction): recipient antibodies, formed before or after transplantation, react against donor HLA antigens
What types of hypersensitivities are seen in acute rejection?
type IV and II
Acute cellular rejection (type IV hypersensitivity reaction)
Donor MHC class II antigens react with recipient CD4+ T cells, which then differentiate into Th1 helper T cells → cytokine (INF-γ) release → macrophage recruitment → parenchymal and endothelial inflammation
Donor MHC class I antigens react with recipient CD8+ T cells → direct cytotoxic cell damage
Acute humoral rejection (type II hypersensitivity reaction): recipient antibodies, formed before or after transplantation, react against donor HLA antigens
What type of pathophysiology do we see in chronic rejection?
A mix of type II and IV hypersensitivity
Combination of humoral rejection (type II hypersensitivity reaction) and cellular rejection (type IV hypersensitivity reaction)
Donor MHC class II antigens react with recipient CD4+ T cells → differentiation into Th1 helper T cells → cytokine (INF-γ) release → macrophage recruitment → parenchymal and endothelial inflammation
an immunological response that occurs when donor T lymphocytes in the graft recognize the recipient as foreign, resulting in a systemic inflammatory reaction
Graft versus host disease
