Transplant rejection and Immunosupression Flashcards
What is hyperacute rejection?
Recipient already has pre-existing donor specific antibodies (humoral response). Should NEVER happen.
What happens in a hyperacute rejection?
Antibodies activate he complement pathway and blood clotting cascade is initiated.
When does a hyperacute rejection become noticed?
Within minutes of transplantation
What is an acute rejection?
When HLA is mismatched and endothelial cells are attacked by cytotoxic T cells.
What is activated in an acute rejection?
T lymphocytes.
How long until an acute rejection is noticed?
Several days.
How can an acute rejection be prevented?
HLA matching and immunosupressants.
What are de novo DSAs in an acute rejection?
Donor specific Antibodies detected after transplantation. Cause antibody-dependent and cell-mediated cytotoxicity.
What is an acute rejection ALWAYS due to?
Vascular endothelial damage!
What is a chronic rejection?
Always happens to some degree. Multiple immune mechanisms, cell mediated and humoral.
What does a chronic rejection eventually lead to?
Vascular disease.
Which immune components can be involved in chronic rejection?
Lymphocytes, Phagocytes, Antibodies, Complement
Stages of chronic rejection?
Allo-antibodies bind to endothelial cells and recruit Fc-receptors.
What do Fc-receptors have?
Monocytes.
Where are inflammatory components located in chronic rejection?
Vessel wall
What do inflammatory components cause in chronic rejection?
Damage of wall, thickening of blood vessel and narrow lumen. Inadequate blood supply.
How long does chronic rejection happen for?
10 years post-transplant.
What is the need for immunosuppressive drugs?
Required for allogenic transplant to survive.
ha caused patient infection deaths in he 1950’s? (immunosuppressive drugs)
Sub-lethal doses of total body irradiation (TBI) and cortisone. (Destroys the immune system)
