Anaphylaxis is classified as an Immediate Hypersensitivity Reaction (Class 1).
The exact reason why someone becomes hypersensitive to a particular antigen is currently unknown, but research has shown that hypersensitivity occurs after an initial exposure to the antigen.
When antigens are present in a person with hypersensitivity the B Cells (immune cells) produce IgE which then activates the mast cells. The mast cells cause Calcium (Ca++) to exit causing an inflammatory response. The mast cells also release ‘mediators‘. An allergy goes from local to systemic when mediators enter the bloodstream and effect multiple systems.
There are 2 stages to anaphylaxis. The first is the release of preformed mediators which cause vasodilation, vascular leakage and smooth muscle contraction, which leads to a large decrease in blood pressure and bronchoconstriction (if anaphylactic). The second is the creation of mediators from the breakdown of the mast cell walls which cause tissue destruction, inflammation, and eosinophil infiltration.
The main difference between anaphylaxis and a local allergic reaction is that anaphylaxis is system wide and may become a type of distributive shock (aka circulatory failure) and/or result in respiratory failure.
Histamine: bronchoconstriction, mucous secretion, vasodilation, vascular permeability.
Kininogenase: kinins and vasodilation, vascular permeability, edema.
ECF-A (tetrapeptides): attract eosinophil and neutrophils.
Newly Formed Mediators:
Leukotriene B4: basophil attractant.
Leukotriene C4, D4: same as histamine but 1000x more potent.
Prostaglandins D2: edema and pain.
PAF (platelet activation factor): platelet aggregation and heparin release: microthrombi.”
Porth, Carol, Glenn Matfin, and Carol Porth. Pathophysiology: Concepts of Altered Health States. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2009. Print.