Question

When temperatures drop below 30*C, IgM AIHA antibodies may bind RBCs and activate complement. This occurs particularly in the extremities, as the RBC IgM complexes return back to the core the temperature increases - causing IgM to dissociate and leave C3 behind (which gets inactivated by DAF / MIRL); opsonized cells are cleared by the spleen. However, extreme activation of complement can lead to intravascular hemolysis. What is the consequence of extreme activation of complement?

1) Intravascular hemolysis
2) Extravascular hemolysis
3) Decreased RBC production
4) Increased RBC production

Answer 1

The consequence of extreme activation of complement due to antigen-antibody reactions in type II hypersensitivity, such as during a mismatched blood transfusion, is intravascular hemolysis. This can lead to severe complications including organ blockage, fever, and potentially fatal conditions like shock and organ failure.

Step-by-step explanation:

The consequence of extreme activation of complement in the context of immune reactions against red blood cells (RBCs) is intravascular hemolysis. When an individual with type B blood receives a transfusion of type A blood, for instance, the recipient's anti-A antibodies bind to the transfused RBCs. This binding triggers the classical complement cascade, leading to a strong inflammatory response that includes the formation of the complement membrane attack complex (MAC), which in turn mediates the destruction of the transfused RBCs, an event known as intravascular hemolysis. The by-products of this hemolysis, such as free hemoglobin, can cause further complications by blocking blood vessels in vital organs like the lungs and kidneys. Such type II hypersensitivity reactions can lead to severe symptoms, including fever, itching, hives, dyspnea, hemoglobinuria, and hypotension, which can lead to shock, organ failure, and potentially death.