Tissue Damage

Activation of Factor XII of the ntrinsic Coagulation Pathway

Factor XII (a) Converts Pre-kallikrein to Kallikrein

Fig. 5.11. Tissue damage leads to increases in vascular permeability. Kallikrein is a protease acting on kininogen and C5 of the complement system. Hydrolysis of kininogen produces brady-kinin, while one of the products of C5 proteolysis is C5a, an anaphylatoxin. C5a binds to receptors on basophils and mast cells inducing degranulation and histamine release. Histamine alters vascular permeability, while bradykinin mediates vasodilatation and increased vascular permeability.

Fig. 5.11. Tissue damage leads to increases in vascular permeability. Kallikrein is a protease acting on kininogen and C5 of the complement system. Hydrolysis of kininogen produces brady-kinin, while one of the products of C5 proteolysis is C5a, an anaphylatoxin. C5a binds to receptors on basophils and mast cells inducing degranulation and histamine release. Histamine alters vascular permeability, while bradykinin mediates vasodilatation and increased vascular permeability.

C1 esterase inhibitor deficiency: Disrupted regulation

C1 esterase inhibitor (C1 INH) deficiency is an inherited autosomal and recessive complement disorder associated with the disease hereditary angioedema (HAE). HAE may result from the synthesis of a mutated C1 INH protein or insufficient production of a normal protein. Clinical manifestations are recurrent episodes of facial/tongue and laryngeal edema that may cause obstruction of the upper airways. C1 INH deficiency may lead to edema of the gastrointestinal tract which presents as colic or diarrhea. These clinical manifestations occur following

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