Just wanted to clarify if this mechanism is correct for ABO incompatibility:
Theoretical situation - Person with type A blood gets transfusion of type B blood (stupidity as goljan would say)..
Pathophysiology =
Recipient's anti-B-IgM will recognize RBCs as foreign, bind to foreign RBCs and stimulate classical complement cascade --> cascade forms membrane attack complex (C5b-C9), thus forming a pore and lysing the donor RBC within the blood. This causes increased level of indirect bilirubin and decreased level of haptoglobin (haptoglobin binds free heme in serum)?????
I think i saw this mechanism questioned on NBME 5
Theoretical situation - Person with type A blood gets transfusion of type B blood (stupidity as goljan would say)..
Pathophysiology =
Recipient's anti-B-IgM will recognize RBCs as foreign, bind to foreign RBCs and stimulate classical complement cascade --> cascade forms membrane attack complex (C5b-C9), thus forming a pore and lysing the donor RBC within the blood. This causes increased level of indirect bilirubin and decreased level of haptoglobin (haptoglobin binds free heme in serum)?????
I think i saw this mechanism questioned on NBME 5