Young and co-workers described Asthma and Emphysema as respiratory ailments and in many respects the symptoms overlapped. Asthma is recognized as restricted airflow through air pipes or bronchial. The restricted airway and airway edema could be due to muscular constriction of air pipes and/ or layering of sticky mucus towards inner wall. Typical asthmatic symptoms are breathlessness, wheezing, occasional exacerbations and other airway hyper-responsiveness. Allergens are the principal cause for Allergic asthma. Intrinsic asthma is independent of allergens, due to cold or exercise. Hay fever asthma can be triggered by mast cell degeneration. The early response of asthmatic attack is release of histamine, leukotrienes and prostaglandin, leading to airway constriction, blood vessel dilation and mucus buildup. Late responses involve release of interleukins, tumor necrosis factor, and platelet activating factor, resulting in adhesion of inflammatory cells – eosinophils and neutrophils towards inner bronchial tissue. Series of oxidative and toxic manifestations lead to upper respiratory tract edema, muscular hypertrophy and mucus plugging (24-30).
Emphysema affects the distal parts of air pipes, i.e. the alveolar sacs, which get clogged up due to mucus or phlegm. It is hard to clinically distinguish Asthma and Emphysema as the symptoms are largely similar, although as O2 supply to the brain reduces and CO2 concentration goes up, impaired mental ability and blue nail, skin, lips associate with emphysema (Fletcher & Pride 81-85). According to Kinsella and others, etiology of emphysema is often associated with smocking, and this led to the hypothesis that emphysema develops with age whereas asthma is mostly prevalent in children. Much of the diagnostic pulmonary functions like FEV1, FVC, TLC, and DLco etc. also can not differentiate asthma from emphysema. In computer tomography that distinguishes the images of aerated lungs from malfunctioned alveoli; quantitative difference between the two disorders can be obtained. Bronchial wall thickening and fibrosis at different peripheral pulmonary regions is associated with emphysema and not asthma. Increased level of IgE is associated with smocking and is more prevalent in emphysema patients. Another important biomarker associated with emphysema is α-1 antitrypsin deficiency, which is poor prognosis marker for asthma (286-289).