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DAWN V TOMY M.Pharm., Asst.Professor, Dept. of Pharmacology, ST.JOSEPHS COLLEGE OF PHARMACY, CHERTHALA.

ASTHMA
It is a chronic inflammatory obstructive disorder of the respiratory airway tract.
Symptoms:
It causes recurrent episodes of wheezing, breathlessness, chest tightness and cough usually at
night or early in the morning.
Reasons for asthma:
Intermittent and reversible airway obstruction, chronic bronchial inflammation with
eosinophils, bronchial smooth muscle, mast cell hypertrophy and hyperactivity, and increased
mucus secretion.
Different cells involved in chronic inflammation are the eosinophil, mast cells, macrophages,
lymphocytes, neutrophils and epithelial cells.
Pathogenesis:
Major etiology is genetic type 1 hypersensitivity (atopy) which leads to acute and chronic
airway inflammation and bronchial hyper-responsive to stimuli. The type 2 helper T cells
(TH2) give excess reaction to environmental antigen resulting in atopic asthma. The cytokines
from the TH2 cells include interleukin 4 (IL4) which stimulates immunoglobulin E (IgE), IL 5
which activates eosinophil by secreting eotaxin and it also secrete IL 13 which stimulates
mucous production and release IgE from B cells.
IgE coats submucosal mast cells which on exposure to antigen releases different types of
chemical which results in 2 types of reactions.
a. An early phase (immediate phase)
b. Late phase.
In early phase there is domination of bronchoconstriction, increased mucous production and
variable vasodilation. Bronchoconstriction is due to stimulation of sub-epithelial vagus
receptors.
Late phase consist of inflammation by activation of eosinophils, neutrophils, and T-cells. In
addition epithelial cells are activated to produce chemokines which results in chemotaxis of
TH2 cells, eosinophils and leukocytes thereby amplifying the inflammation.
Airway Remodelling:
The repeated inflammation leads to structural changes in bronchial walls resulting in
hypertrophy of the bronchial smooth muscle and mucous gland. It also increase vascularity
and results in deposition of sub-epithelial collagen.
Types of asthma:
a. Atopic asthma

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DAWN V TOMY M.Pharm., Asst.Professor, Dept. of Pharmacology, ST.JOSEPHS COLLEGE OF PHARMACY, CHERTHALA.

b. Non-atopic asthma
c. Drug induced asthma
d. Occupational asthma

a. Atopic asthma: (+ve family history is common)


It is the common type developed in childhood e.g. IgE mediated hypersensitivity reaction.
The etiology is genetic type 1 hypersensitivity reaction. The asthma attack is usually followed
by allergic rhinitis, urticarial, eczema (dermatitis due to atopy).
Triggering factors include environmental antigen (dust, pollen, animal dander, mold and
food.)
Hypersensitivity to an allergen can be determined by doing skin test (flesh, flare and wheal).
Another method is by serum radioallegsorbent tests (RASTs).
b. Non-atopic asthma: In this type no evidence of the allergen sensitization, skin test is
negative, less common positive family history.
It is triggered by respiratory infections due to viruses (rhino, parainfluenza virus) and inhaled
air pollutants (SO2, O3, NO2). It results in ultimate humoral or cellular mediated airway
obstruction.
c. Drug induced asthma (drug sensitivity): E.g. aspirin induced rhinitis, nasal polyps,
urticaria and bronchospasm.
Etiology is drug hypersensitivity. Aspirin inhibits the enzyme cyclooxygenase and promote
leukotriene synthesis by lipooxygenase pathway resulting in the shifting of balance resulting
in bronchial spasm.
d. Occupational asthma: It is stimulated by fumes (epoxy resins, plastics), organic and
chemical dusts (wood, cotton, platinum) and gases (toluene). Triggering factor is the
repeated exposure to antigen.