Asthma is a Greek word which means Pan ng. It is characterised by paroxysmal and reversible
obstruc on of the airways.
Simply, asthma is best described as a chronic disease that involves inflamma on of the pulmonary
airways and bronchial hyperresponsiveness that results in the clinical expression of a lower airway
obstruc on that usually is reversible.
Asthma is caused by –
1. Bronchospasm (smooth muscle spasm narrowing the airways)
2. Excessive produc on of mucus secre ons (plugged airways)
Classifica on:
Atopic Asthma Non-Atopic
Extrinsic Asthma Intrinsic Asthma
Most common Not common
Trigger by environment Not caused by an
allergen
Layers of Lung (inner to outer):
Normal Lungs –
i) Mucus (pseudostra fied columnar epithelial cells & goblet cells which is responsible for
secre ng mucus to the lumen)
ii) Basement membrane
iii) Lamina propria (mast cells response for histamine) iv) Smooth muscle
Submucosa
layer – Smooth
muscle
Lamina Propria –
Epithelial cells
Mucus Layer
, vii. Mucus gland hypersecre on
Microscopically, asthma is characterized by the presence of
• Increased numbers of eosinophils, neutrophils, lymphocytes
• Increased plasma cells in the bronchial ssues
• Increased bronchial secre ons & mucus
Ini ally, there is recruitment of leukocytes from the bloodstream to the airway by ac vated CD4
Tlymphocytes. The ac vated T-lymphocytes also direct the release of inflammatory mediators from
eosinophils, mast cells, and lymphocytes. In addi on, the subclass 2 helper T-lymphocytes subset of
ac vated T-lymphocytes produces interleukin (IL)-4, IL-5, and IL-13. IL-4 in conjunc on with IL-13
signals the switch from IgM to IgE an bodies. The cross-linkage of two IgE molecules by allergen
causes mast cells to degranulate & releasing histamine, leukotrienes, and other mediators that
perpetuate the airway inflamma on.
IL-5 ac vates the recruitment and ac va on of eosinophils. The ac vated mast cells and eosinophils
also generate their cytokines that help to perpetuate the inflamma on. Regardless of the triggers of
asthma, the repeated cycles of inflamma on in the lungs with injury to the pulmonary ssues
followed by repair may produce long-term structural changes ("remodeling") of the airways.
Risk Factors of Asthma:
Gene c factors – certain genes have been iden fied that increase the risk of developing
asthma
Posi ve family history
Environmental factors - air pollu on like cigare e smoke and car exhaust, as well as allergens
like dust, pet dander, perfume, cold air, pollens, cockroaches, and mold.
Medicine – NSAIDS, Aspirin, Beta-blocker
obstruc on of the airways.
Simply, asthma is best described as a chronic disease that involves inflamma on of the pulmonary
airways and bronchial hyperresponsiveness that results in the clinical expression of a lower airway
obstruc on that usually is reversible.
Asthma is caused by –
1. Bronchospasm (smooth muscle spasm narrowing the airways)
2. Excessive produc on of mucus secre ons (plugged airways)
Classifica on:
Atopic Asthma Non-Atopic
Extrinsic Asthma Intrinsic Asthma
Most common Not common
Trigger by environment Not caused by an
allergen
Layers of Lung (inner to outer):
Normal Lungs –
i) Mucus (pseudostra fied columnar epithelial cells & goblet cells which is responsible for
secre ng mucus to the lumen)
ii) Basement membrane
iii) Lamina propria (mast cells response for histamine) iv) Smooth muscle
Submucosa
layer – Smooth
muscle
Lamina Propria –
Epithelial cells
Mucus Layer
, vii. Mucus gland hypersecre on
Microscopically, asthma is characterized by the presence of
• Increased numbers of eosinophils, neutrophils, lymphocytes
• Increased plasma cells in the bronchial ssues
• Increased bronchial secre ons & mucus
Ini ally, there is recruitment of leukocytes from the bloodstream to the airway by ac vated CD4
Tlymphocytes. The ac vated T-lymphocytes also direct the release of inflammatory mediators from
eosinophils, mast cells, and lymphocytes. In addi on, the subclass 2 helper T-lymphocytes subset of
ac vated T-lymphocytes produces interleukin (IL)-4, IL-5, and IL-13. IL-4 in conjunc on with IL-13
signals the switch from IgM to IgE an bodies. The cross-linkage of two IgE molecules by allergen
causes mast cells to degranulate & releasing histamine, leukotrienes, and other mediators that
perpetuate the airway inflamma on.
IL-5 ac vates the recruitment and ac va on of eosinophils. The ac vated mast cells and eosinophils
also generate their cytokines that help to perpetuate the inflamma on. Regardless of the triggers of
asthma, the repeated cycles of inflamma on in the lungs with injury to the pulmonary ssues
followed by repair may produce long-term structural changes ("remodeling") of the airways.
Risk Factors of Asthma:
Gene c factors – certain genes have been iden fied that increase the risk of developing
asthma
Posi ve family history
Environmental factors - air pollu on like cigare e smoke and car exhaust, as well as allergens
like dust, pet dander, perfume, cold air, pollens, cockroaches, and mold.
Medicine – NSAIDS, Aspirin, Beta-blocker
