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Bronchial asthma Asthma is defined as a chronic inflammatory disease of airwaysthat is characterized by increased responsiveness of the

tracheobronchial tree to a multiplicity of stimuli.It is manifested physiologically by a widespread narrowing of theair passages, which may be relieved spontaneously or as a result oftherapy,

And clinically by of dyspnoea, cough, chest tightness and

wheezing.

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Types A). Clinically

Episodic asthma- symptom free in between Episodes

Severe acute asthma- live threatening attacks of DyspnoeaChronic asthma- persistence of Symptoms without any symptomfree period

B). AetiologicallyExtrinsic Asthma (Early onset Asthma/Allergic/Atopic Asthma)-Specific immunoglobulin (IGE) are produced in response to allergensIntrinsic Asthma (Late onset Asthma/ idiosyncratic/Non Atopic

Asthma) There is no role of allergen in the production of disease.Mixed

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EXTRINSIC : - Atopic or allergic : -Most common formUsually begins in childhood and have personal & family history ofallergies to pollens, dusts, animal dander, moulds some chemicalfumes if working in a factory.They have high level of IgE and gives positive skin test with thespecific allergen representing Type I hypersensitivity mediated byIgE antibodies.

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This is type I reaction which may be immediate & late

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Immediate response : - Occurs within minutes Binding of antigen (allergen) with Ig E coated mast cells & releasingPrimary mediators Histamine, neutrophil chemotatic factor, eosinophil

chemotactic factor &Secondary mediators Cytokines IL-1, TNF & IL6, Leukotrienes-

B4,C4,D4, Prostaglandin D2, Platelet activating factor There is bronchospasm, eodema, mucus secretion , & infiltration of

leucocytes They release a second wave of mediators that cause late reaction

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Late phase response : -This follows the acute phase.This is due to excessive mobilization of neutrophils, eosinophils andbasophils.This results in a continuous & prolonged release of mediators,which accentuate the above mentioned effects.Thers is persistant bronchospasm, oedema, leucocyte infiltration &necrosis of epithelial cells

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Pathophysiological features of Asthma Airway hyper responsiveness- exaggerated Bronchial constriction

to a wide range of non-Specific stimuli e.g. exercise, cold air. Airway Inflammation- Muscle thickness, Oedema, increased

mucous secretion, mucous plugging, epithelial damage. Airflow limitation- usually reverses spontaneously or with

treatment

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Morphology

Grossly:

1. The lungs are remarkably distended with air.

2. The airways are filled with thick, tenacious, adherent mucous plugs.

3. Lungs are over inflated with occlusion of air passages by viscidmucus plugs.

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Microscopically cont..2. Bronchial submucosal mucous glands are hyperplastic. An increase in

goblet cells.

3. The epithelial BM appears thickened.4. The mucosa is edematous and contains a mixed inflammatory

infiltrate, including eosinophils.

5. Hyperplasia of bronchial smooth

muscle.

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