IgE is formed will be bound by the existing mast cells and basophils in the existing network role in the circulation. When this process occurs in a person, then that person has been sensitized or have become vulnerable. When people who are vulnerable or exposed two times more with the same allergen, the allergen will be bound by the existing IgE in mastoit surface and basophils. This bond will cause influk Ca + + into the cells and changes in cell cAMP levels.
Decrease in cAMP levels cause cell degranulation. Degranulation of these cells will lead to the release of chemical mediators include histamine, slow releasing suptance of anaphylaksis (SRS-A), eosinophilic chomotetik factor of anaphylaxis (ECF-A) and others. This will lead to the emergence of three main reactions: smooth muscle contraction both large airways or small that will cause bronchospasm, increased capillary permeability play a role in the occurrence of mucosal edema that adds to the narrowing of the airways, increased secretion of mucous glands and an increase in mucus production. Three such reactions cause interference ventilation, uneven ventilation distribution by blood circulation and impaired pulmonary alveoli level of gas diffusion, the result would be hypoxemia, and acidosis hypercapnea at a very advanced stage, (Barbara CL, 1996, Karnen B., 1994, William RS 1995)
Based on the etiology, asthma can be classified into two types: intrinsic asthma and extrinsic asthma. Extrinsic asthma (atopy) is characterized by allergic reaction to the originator-specific triggers that can be identified as: mold pollen, dust, animal dander, milk fish eggs drugs and substances other allergens. Whereas intrinsic asthma (non-atopic) is characterized by non-allergic mechanisms that react to specific triggers that do not like: cold air, chemical substances, which acts as an irritant such as ozone, ether, nitrogen, changing seasons and weather, excessive physical activity, stress mental as well as other intrinsic factors. (Antoni C, 1997 and Tjen Daniel, 1991).
Clinically sudden asthma attack can be divided into three stages. The first stage is characterized by periodic coughing and dry. This cough occurs because a thick mucosal irritation and clump together. At this stage in edema and swelling of the bronchi. The second stadium is marked by cough with mucus is clear and foamy. Clients feel shortness of breath, trying to breathe deeply, stretching followed expiratory wheezing. Clients prefer to sit with your hands resting on the edge of the bed, the patient was pale, agitated, and began to turn blue color around. While the third stadium characterized hardly breath because of the sound of a small air flow, no coughing, breathing becomes shallow and irregular, high respiratory rhythm due to asphyxia, (Tjen daniel, 1991).
