Transfusion Reactions and Complement Mechanisms

A process of tracing blood products from donor to recipient to ensure the safety and efficacy of transfusion.

Mandatory criteria refer to essential blood group matching requirements for a safe transfusion, like ABO and RhD blood group, while discretionary criteria include additional matching based on specific patient needs, like antibody screening to avoid transfusion reactions.

Unique identification wristbands or similar devices with necessary patient information for accurate blood product administration.

An audit trail digitally records the entire journey of a blood unit. This includes details of its collection, processing, storage, and delivery to the recipient, ensuring a complete and traceable history.

Carefully checking the information on blood bags labels helps prevent inadvertent mistakes. These labels provide crucial details connecting donors, donations, recipients, and even potential adverse reactions.

Unexpected reactions to a blood transfusion can occur due to various factors like incorrect blood typing, pre-existing antibodies, or contaminated blood products.

Antibodies that are naturally present in the blood and can cause immediate hemolytic transfusion reactions.

A type of transfusion reaction characterized by the destruction of red blood cells due to incompatibility between donor and recipient blood groups.

A diagnostic test used to detect the presence of antibodies and complement proteins attached to red blood cells.

A complex set of proteins that mediate the immune response and can contribute to the destruction of red blood cells.

An antibody that recognizes and binds to specific antigens on red blood cells, leading to hemolytic transfusion reactions.

A type of hemolytic transfusion reaction that occurs immediately after transfusion, usually due to incompatibility in the ABO blood group system.

A type of hemolytic transfusion reaction that develops over time due to the presence of antibodies against non-ABO blood group antigens.

Identifying the specific antigens present on an individual's red blood cells.

The complement cascade is a complex system of proteins that work together to destroy pathogens and clear immune complexes. It consists of a series of reactions activated by specific triggers, where each step involves the activation of a specific complement protein.

The first stage of the classical complement pathway involves the binding of the C1 complex, composed of C1q, C1r, and C1s, to the antibody-antigen complex. This binding initiates the cascade by activating C1r, which then activates C1s.

The C4b2a complex is formed in the activation stage of the classical pathway and acts as the C3 convertase. It cleaves C3 into C3a and C3b, amplifying the pathway. C3b binds covalently to the cell surface, while C3a acts as an anaphylatoxin.

The membrane attack complex (MAC) is formed at the end of the classical complement pathway. It comprises C5b, C6, C7, C8, and multiple C9 molecules. The MAC inserts into the cell membrane, creating a pore that allows the influx of water and solutes, leading to cell lysis.

The regulation of the classical pathway is essential to prevent uncontrolled activation of complement and ensure that the cascade is targeted and specific. It involves inhibitors acting directly on activated complement components, rapid dissociation of newly formed complexes, and transient binding sites on activated components.

Different isotypes of immunoglobulins (Ig) have varying efficiencies in activating complement. IgM is the most efficient, followed by IgG3, IgG1, and IgG2. Importantly, IgG4 does not activate complement.

The classical complement pathway is activated by antibodies binding to antigens on a cell surface. This triggers a cascade of enzyme reactions, ultimately leading to the destruction of the antibody-coated cell.

The alternate complement pathway can be activated independently of antibodies. It acts as a positive feedback loop, amplifying the immune response by generating large amounts of C3b.

Immune Hemolysis is the destruction of red blood cells by the immune system. It can be mediated by antibodies, complement, or both.

Macrophages and other phagocytic cells express FcyR receptors that bind to IgG antibodies coating target cells, leading to their destruction through extravascular hemolysis.

Complement activation leads to the formation of the membrane attack complex (MAC), which creates pores in the cell membrane, causing cell lysis and intravascular hemolysis.

Complement plays a critical role in the immune response by eliminating pathogens and generating inflammatory mediators.

Agglutination: IgM antibodies can bind to multiple epitopes on red blood cells, causing them to clump together.

Opsonization is a process where complement components, such as C3b, coat a target cell, making it more attractive to phagocytic cells.

Complement activation is regulated by a complex system of proteins that prevent excessive activation and tissue damage.

Complement pathway activation can result in the generation of anaphylatoxins, such as C3a and C5a, which trigger mast cell degranulation and inflammation.