2. DEFINITION
• Asthma is a chronic lung disease that leads to burning and
narrowing of the respiratory airways often in response to a
“trigger” to an allergen, cold air exercise, or an emotional
stress.
• Asthma cause chronic period of puff ( a whistle noise when you
breathe), chest rigidity , shortness of breath and coughing.
5. PATHOGENESIS
ASTHMA PRECIPITATED BY ALLEGENS
• Allergens enter the inner airways passage and cause immune reaction in the
respiratory passages which lead to Bronchial constriction and Bronchial
inflammation
• There they are ingested by Antigen Presenting cells where inside them they are
cut into shorter peptide and combined with MHC.
• This antigen-MHC Complex is represented at the surface of these cells where
Helper T cells (TH0)
combine with them and get activated .
• After activation the TH0 Cells differenciate into TH1 and TH2 Cells
• The TH1 cells leads to costimulation of Cytotoxic Tcells leading to cell
mediated immunity and TH2 cells leads to costimulation of B cells leading to
humoral immunity
6. IN CASE OF HUMORAL IMMUNITY RESPONSE
• The cytokines secreted by TH2 cells in combination with other cytokines stimulate the B
cells to secrete antibodies (IgE) against the allergen.
• These antibodies go and bind to receptors on the mast cells, basophils and eosinophils in
the airway epithelium.
• Subsequent exposure of the same antigen to these cells in the airway epithelium initiates
acute phase reaction of asthma.
• The binding of the allergen to the mast cells make them release the granules present in
them.
• These granules rupture and release Histamine and TNFα Proteases.
• These are responsible for bronchoconstriction and vasodilation.
• The rupture of lipid membrane of the mast cells also cause release of mediators like
prostaglandins, leukotrienes and platelet activating factors which also cause
bronchoconstriction and vasodilation and increase in vascular permeability.
• The cytoplasm of the mast cells cause production of cytokines 1,2,3,4,5,6,8 which causes
stimulation of neutrophils, macrophages and adhesion of molecules.
7. • These mediators diffuse throughout the airways and cause
constriction of bronchial muscle, edema, cellular infiltration,
mucus hypersecreation
• Due to vasodilation, increased vasopermeability,
increasedendothelial adhesiveness to leukocytes there occurs
influx of inflammatory cells(lymphocytes, eosinophils,
macrophage) from circulation to the tissues..
• Once these inflammatory cells reach lungs they release their
own mediators which have further inflammatory effects.
• This results in late phase attack of asthma.
• It is also hypothesised that the imbalance in the cyclic AMP and
cyclic GMP also results in asthma.
8. • Asthma is also caused by reversible airway obstruction by stimuli
which are non- antigenic like emotional upset, stress, anxiety and
excercise.
• There is abnormality in the parasympathetic nervous system.
• Certain agents stimulate rapid adopting irritant receptors which are
present immediately beneath the epithelial region of trachea-
bronchial tree.
• The impulses from these receptors are carried by afferent vagal
fibres through the reflex arc to the efferent vagal fibres which
innervate bronchial smooth muscle which cause bronchoconstriction.
• Also disturbances in parasympathetic system leads to abnormalities
in mucus production and secretion.
• In case of heavy exercise heat and water loss trigger mediator release
from mast cells which cause bronchoconstriction and vasodilation.
13. PROGNOSIS
• The prognosis of asthamatics is good especially in children
with mild disease.
• Those who suffer from mild symptoms corticosteroids can help
to live a better life.
• The mortality rate of asthma is low with around 6000 deaths
per year in a population of some 10 million patients.
