In CPB circuit, which complement component gets activated leading to inflammatory response?

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Multiple Choice

In CPB circuit, which complement component gets activated leading to inflammatory response?

Explanation:
During CPB, blood contact with non-endothelial surfaces activates the complement system, and the inflammatory response is driven by anaphylatoxins released during the cascade. The molecule that directly promotes this inflammatory process is C3a, an anaphylatoxin released when C3 is cleaved. C3a travels through the blood to cause vasodilation and increased vascular permeability and to recruit and activate mast cells and neutrophils, fueling systemic inflammation seen with CPB. C1q starts the classical pathway but isn’t itself the inflammatory mediator; the C3 convertase (C4b2a) cleaves C3 but is an enzyme, not the inflammatory molecule; the membrane attack complex (C5b-9) causes cell lysis rather than driving inflammation. While C5a is also a potent inflammatory mediator, the option pointing to the inflammatory mediator most directly associated with initiating this response is C3a.

During CPB, blood contact with non-endothelial surfaces activates the complement system, and the inflammatory response is driven by anaphylatoxins released during the cascade. The molecule that directly promotes this inflammatory process is C3a, an anaphylatoxin released when C3 is cleaved. C3a travels through the blood to cause vasodilation and increased vascular permeability and to recruit and activate mast cells and neutrophils, fueling systemic inflammation seen with CPB.

C1q starts the classical pathway but isn’t itself the inflammatory mediator; the C3 convertase (C4b2a) cleaves C3 but is an enzyme, not the inflammatory molecule; the membrane attack complex (C5b-9) causes cell lysis rather than driving inflammation. While C5a is also a potent inflammatory mediator, the option pointing to the inflammatory mediator most directly associated with initiating this response is C3a.

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