Patofisiologi
Asthma in children occur in the way of refinement of the breath and hyperactive with response to stimulus material and other irritation.
With the allergen irritation or muscle-muscle bronkus be spasm antibody substances and the body appears (immunoglobulin E or IgE) with the allergy. IgE in caused on receptor mast cells and IgE due to bond and cause the expenditure histamine antigen and other mediator substances. Mediator will give symptoms of asthma.
Response asthma happened in three stages: the first phase is marked with the immediate bronkokontriksi (1-2 hours); delayed phase where brokokontriksi can repeat in 4-6 hours and constantly 2-5 minutes longer; late stages with marked inflammation hiperresponsif breath and the way a few weeks or months.
Asthma can also occur because of factors cause exercise, fear, and cold air.
During the attack asthmatic, bronkiulus become excited and increase sekresi mucus. This way the lumen of breath becomes swollen, and then increase the path resistance of breath and can cause respiratory distres
Children who experience easy for astma inhalation and difficult because of edema in ekshalasi on the road breathing.Dan this hiperinflasi cause changes in the alveoli and the exchange gas. Breathing way, which then become obstructs not adequate ventilation and saturation 02, so a decline P02 (hypoxia). During the attack asthmatics, CO2 increased resistance with bated breath for ekspirasi road, and cause respiratory acidosis and hypercapnea. And respiratory system will make compensation by increasing the respiratory (tachypnea), compensation is hyperventilate and can cause a decrease in blood CO2 content (hypocapnea).
1. Allergen, Health, Exercise (Stimulus Immunologic and Non Immunologic) 2. Stimulate B cells to form IgE with the assistance of T helper cells 3. IgE bound by the cells mastosit through receptor FC is in the way of the breath 4. When the body exposed back with the same antigen, the antigen will be bound by the IgE on the surface of the existing mastosit 5. Ties due to antigen-IgE, mastosit experience degranulasi and inflammation mediator release (histamin) 6. Increased capillary permeability (edema bronkus) Increased production mucus ( sekret) Smooth muscle contraction directly or through saraf simpatis (NX) 7. Hiperresponsif the way the breath 8. Asthma
Disturbance gas exchange, ineffective way clean breath, and do not effectively deal with the pattern of breath bronkospasme, edema and increased mucosa production secret.
Fatigue related to the Hypoxia increased breath effort.
worries associated with respiratory distress and hospitalises
Risks related to lack of fluid volume with increased respiration and decreased fluid intake
Changes in the process of family-related conditions chronicles
Lack of knowledge related to the disease process and treatment.
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