Bronchial asthma is a chronic respiratory condition characterized by inflammation of the airways and hyperresponsiveness to various triggers. Symptoms include shortness of breath, wheezing, coughing, and chest tightness. Triggers include allergens, infections, air pollution, weather changes, emotions, and certain drugs. There are two main types - extrinsic (allergic) asthma associated with family history of allergies and intrinsic asthma initiated by non-allergic factors. Pathogenesis involves airway inflammation from mast cells, eosinophils, and lymphocytes, bronchoconstriction, edema, remodeling, and obstruction leading to symptoms.

1. Patho-physiology of Asthma

2. Asthma
 Bronchial asthma is chronic respiratory condition
associated with inflammation of the airway wall.
• Associated with Hyper-responsiveness of tracheo-
bronchial smooth muscles to a variety of stimuli/
Triggering factors.
 Intermittent Symptomatic episodes of
 Dyspnoea (shortness of breath)
 Wheezing (additional sound)
 Cough (persistent)
 Chest tightness
 Additionally: limitation of activity

3. Etiology/ Triggering factors
 Tobacco smoke
 Infections such as colds, flu, or pneumonia
 Allergens such as food, pollen, mold, dust mites, and
pet dander
 Exercise
 Air pollution and toxins
 Weather, especially extreme changes in temperature
 Drugs (such as aspirin, NSAID, and beta-blockers)
 Food additives
 Emotional stress and anxiety
 Singing, laughing, or crying
 Smoking, perfumes, or sprays
 Acid reflux

4. Types of Asthma
Extrinsic (atopic, allergic)
• Allergens: food, pollen, dust, etc.
• History of `atopy` in childhood
• Family history of allergies
• Positive skin test
• Raised IgE level
• Below 30 years of age
• Less prone to status asthmaticus
Intrinsic (non-atopic)
• Initiated by infections, drugs, pollutants, chemical irritants
• No family history of allergy
• Negative skin test
• No rise in IgE level
• Middle age onset
• Prone to status asthmaticus

5. Pathogenesis
Airflow limitation in asthma is recurrent and caused by a
variety of changes in the airway:
 Airway inflammation (Mast cell degranulation,
eosinophill infiltration )
 Bronchoconstriction (tightening of muscles)
 Airway edema (Mucous hypersecretion; Mucus plug
formation)
 Bronchial hyperresponsiveness to various stimulii
 Airway remodelling (thickening of the sub-basement
membrane, subepithelial fibrosis, airway smooth muscle
hypertrophy and hyperplasia, angiogenesis and
vasodilation, and mucous gland hyperplasia and
hypersecretion)
 Airflow obstruction (narrowing of air passage)

6. Inflammatory cells
 Lymphocytes: T-helper 2 cells (Th2 cells), activates
eosinophillic inflammation by releasing cytokines(IL-4,
IL-5 and IL-3) leads to: Eosinophill infiltration, Ig E
overproduction, development of bronchial
hyperresponsiveness.
 Mast cells: releases bronchoconstrictor mediators
(histamine, cysteinyl-leukotrienes, prostaglandin D2 )
 Eosinophils: generates inflammatory enzymes and
leukotrienes, most cases of asthma linked with
increased number of eosinophills.
 Dendritic cells: These cells function as key antigen-
presenting cells that interact with allergens from the
airway surface and then stimulate Th2 cell production
from naïve T cells
 Macrophages: Macrophages are the most numerous
cells in the airways
 Neutrophils: Neutrophils are increased in the airways

7. Transverse section

8. Airway Narrowing
Symptoms:
Cough
Dyspnoea
(breathlessness)
Wheezing
Tightness of chest

9. Morphology
 Bronchial obstruction with overinflation
 Small areas of atelectasis (collapse) may be seen
 Inflammation & thickening of mucosa.
 Bronchial wall smooth muscle hypertrophy
 Thickening of bronchial basement membrane.
 Mucus plugging of bronchi
 Curschmann spirals: whorls of shed epithelium
within mucus plugs
 Charcot-Leyden crystals: Within aggregates of
eosinophils ;crystalloids of galectin-10
Lung Hyperinflation

10. Histological findings in Sputum

11. Summary

12. Thank You