Bronchial asthma:
Bronchial asthma is characterised by bouts of dyspnoea as a result of temporary narrowing of bronchi due to bronchial spasm, mucosal edema and thick secretions. It is caused due to hyper-reactivity by bronchial tree to a variety of stimuli. Asthma may be extrinsic or allergic is. when symptoms are induced by hyperimmune response to the inhalation of a specific allergen. It may be intrinsic asthma or non-allergic type in which symptoms are produced in response to non-specific factors in the environment.
Etiology:
The exact etiopathogenesis is not known but there are some excitatory factors and predisposing factors which are as follows:
Excitatory Factors
i) Allergic factors/Allergy to certain foreign substances:
a) Inhalants like pollen, smoke, dust and powder
b) Foods like egg, meat, wheat and chocolate
c) Drugs like aspirin and morphine
ii) Respiratory infections
iii) Emotional disturbances like "row" with the siblings or the parents and fear of punishment
iv) Exhaustion
v) Change of climate
Predesposing Factors
i) Heredity: A family histroy of asthma or some other allergic disorder is usually present
ii) Childhood infections like measles and pertussis (i) Constitution: Asthmatics are high stung, emotional and intelligent Pathology The major pathologic mechanism responsible for airways obstruction, associated with asthma are caused by (i) Spasm of smooth muscles of the bronchi, (ii) Edema of the bronchial mucosa, (iii) Increased secretion and accumulation of the tenacious mucus within the lumen of the bronchi and bronchioles. As a result of this the resistance to outflow increase, manifesting as reduction in forced expiratory volume and flow rate. The airway closes prematurely during expiration which results in hyperinflation of lungs and increase in functional residual capacity, the patient has to breath in while the lungs are already hyperinflated. Therefore there is a marked distress in breathing and compliance of lung is decreased. Initially the patient tries to hyperventilate and therefore arterial PC02 rises. As the compensation by buffering mechanism fails, PH of blood falls causing respiratory acidosis, All the obstructive processes interfere with ventilation and result in the characteristic symptoms of coughing, shortness of breath, and wheezing.