Answer to Question 1
Answer: In drug adsorption, a drug binds to the erythrocyte and then antidrug antibodies attach to the drug. There is extravascular lysis from the interaction between the Fc fragment of the antibody and the Fc receptors of macrophages and resulting phagocytosis of the coated cell. In immune complex, the drug and antibody to it form a complex that adsorbs to the cell membrane and activates complement. This results in intravascular lysis.
In the autoantibody induction type, the drug alters the RBC membrane, causing formation of a neoantigen. The immune system reacts by forming an antibody that reacts with all RBCs.
Answer to Question 2
Answer: In intravascular hemolysis the antibody (usually an IgM) is able to fix complement and cause activation through the MAC. Once C9 has been fixed, the lysis of the cell begins, resulting in intravascular hemolysis. IgG antibodies are not efficient complement fixers, and complement often is fixed only through the C3 component. C3a is released into the plasma and C3b remains on the cell. There are receptors for C3b on splenic and liver macrophages so that cells are removed extravascularly.
Immunization and Immune Testing1
Compare the Final Code with the Documentation
Feedback mechanisms of the thyroid gland.
Drug Label for Cefdinir
Nucleotide excision repair (NER) of a UV-induced thymine dimer
Mechanisms of Dosage Compensation in Animals