Asthma
Inflammatory disease of the airways characterised by recurrent attacks of
breathlessness and wheezing varying in severity and frequency. Airway
obstruction is mostly reversible with treatment or spontaneously
Epidemiology
More common in children
Higher incidence in males
30-70% symptom free by adulthood
Bronchi
Bronchoconstriction – parasympathetic (vagus) M1 and M3
Bronchodilation – sympathetic beta 2, alpha 1 and 2
NANC – VIP, NO and NK can do either
Aetiology
Smoking, age, gender, pollutants, gender, diet and genetics
Atopic – extrinsic
Non-atopic – intrinsic
Histopathology
Goblet cell hyperplasia
Subepithelial fibrosis (collagen deposits)
Increased smooth muscle volume (hypertrophy and hyperplasia)
Angiogenesis
Pathophysiology
Early and late phase reactions
Spasm of airway smooth muscle
Oedema of airway mucosa
Cellular infiltration (lymphocytes and
eosinophils)
Hypersecretion of mucous
Loss of ciliary function
1. Early phase is rapid response to allergen
2. Mast cell degranulation releases histamine
3. Immune response and inflammation leads to late
phase
4. Accumulation of monocytes and lymphocytes
5. Prolonged airway dysfunction due to IgE damage
Bronchial Hyper-responsiveness:
Late phase
Cytotoxic mediators from eosinophils damage
epithelium exposing sensory neurones
Leads to bronchoconstriction, bleeding and
hypersecretion
Inflammatory disease of the airways characterised by recurrent attacks of
breathlessness and wheezing varying in severity and frequency. Airway
obstruction is mostly reversible with treatment or spontaneously
Epidemiology
More common in children
Higher incidence in males
30-70% symptom free by adulthood
Bronchi
Bronchoconstriction – parasympathetic (vagus) M1 and M3
Bronchodilation – sympathetic beta 2, alpha 1 and 2
NANC – VIP, NO and NK can do either
Aetiology
Smoking, age, gender, pollutants, gender, diet and genetics
Atopic – extrinsic
Non-atopic – intrinsic
Histopathology
Goblet cell hyperplasia
Subepithelial fibrosis (collagen deposits)
Increased smooth muscle volume (hypertrophy and hyperplasia)
Angiogenesis
Pathophysiology
Early and late phase reactions
Spasm of airway smooth muscle
Oedema of airway mucosa
Cellular infiltration (lymphocytes and
eosinophils)
Hypersecretion of mucous
Loss of ciliary function
1. Early phase is rapid response to allergen
2. Mast cell degranulation releases histamine
3. Immune response and inflammation leads to late
phase
4. Accumulation of monocytes and lymphocytes
5. Prolonged airway dysfunction due to IgE damage
Bronchial Hyper-responsiveness:
Late phase
Cytotoxic mediators from eosinophils damage
epithelium exposing sensory neurones
Leads to bronchoconstriction, bleeding and
hypersecretion
