Get pathogenesis of asthma management guidelines
The airways of asthmatics show characteristic changes such as:
Accumulation of inflammatory cells (eosinophils and lymphocytes—T cells).
Damage to the lining cells (epithelial cells).
Thickening of the muscles of air-tube.
Increase in size of mucus-secreting glands and cells.
Plugging of air-tubes (bronchioles) with thick mucus in severe asthma (see Figs. 1, 2, 3).
MECHANISMS OF ASTHMA
Chronic inflammation of the airways is the main factor in the causation of asthma. This inflammation involves interaction between inflammatory cells (macrophages, mast cells, T lymphocytes, eosinophils, etc.) and cells and tissues in the. airways (Fig. 4)these cells secrete various inflammatory mediators such as histamine, leukotrienes, prostaglandins and bradykinin.
Intracellular messengers called cytokines (Interleukin-1,Interleukin-5) co-ordinate and perpetuate inflammation. Mediators of inflammation produce constriction of air-ways, mucus secretion and increased responsiveness of airways to various stimuli such as viral infection,
allergens, air pollutants, chemical fumes, etc. Psychogenic and neurogenic factors may amplify asthmatic inflammation. Relationship between airway inflammation, hyper responsiveness and asthma is depicted in Fig. 5.
The causes of the tendency to develop initial inflammatory response in those who are prone to develop asthma are not yet certain. The strongest risk factor is an inherited familial tendency to have allergic reactions (atopy). Genetic factors may be involved. Risk factors known as ‘triggers’ provoke attacks in asthmatic patients but they leave the non-asthmatic untouched. The common triggers are house dust mites (Fig 6), pollen (Fig. 7), pet animals, sulfur dioxide of air pollution, smoke, viral infection and cold dry air. Some drugs such as Aspirin and Ibuprofen, beta blockers such as Atenolol.
MECHANISM OF ASTHMA
Fig. 4: Allergens, viruses, etc. are taken up by macrophages which process and present them to T lymphocytes, which produce cytokines and stimulate B lymphocytes to produce IgE antibody. When IgE on the mast cell comes in contact with antigen, it induces the mast cell to secrete mediators of asthma (atopic asthma). Cytokines recruit neutrophils and eosinophils. Eosinophils are the crucial cells. They release toxic proteins (MBP) which damage airway epithelium and expose sensory nerve endings to irritants (triggers) which in turn cause , muscle spasm, vasodilation, mucus secretion and thickening of submucosa. Inflammation comes first.