1. By – Dr. SAMIA FATIMA

3.  1. Eosinophils
 2. Mast cells
 3. T-lymphocytes
 4. Neutrophils
 5. Basophils

4. Acute inflammation
Chronic inflammation
Remodeling of airways
Symptoms
of bronchoconstriction
Exacerbation
nonspecific
hyperreactivity
Ongoing
obstruction of
airways

5. Pathogenesis of asthma

7. 1.Early phase
 Inhaled Antigen
 Sensitised mast cells on the mucosal surface 
bronchoconstriction
 Histamine bronchoconstriction, increased vascular
permeability.
 prostaglandin D 2 
bronchoconstriction, vasodilatation.
 Leucotriene C4,D4, E4  Increased vascular
permeability, mucus secretion and
bronchoconstriction.
 Direct subepithelial parasympathetic stimulation 
bronchoconstriction.

8. 2.Late phase
 starts 4 to 8 hours later
 Mast cell release additional cytokine
 Influx of leukocytes(neutrophil,eosinophil)
 Eosinophils are particularly important- exert a
variety of effect

9. Bronchial inflammation
Environment factor Genetic prediposition
Bronchial hyperreactivity + trigger factors
Cough, Wheeze, Breathlessness, Chest tightness
Oedema
BronchoC
Mucus production
Airways narrowing

10. MAST CELLS
release histamine,cysteinyl-leukotrienes,cytokines,chemokines,
growth factors and neutrophins
causes bronchoconstriction
MACROPHAGES AND DENDRITIC CELLs
release cytokines,IL-10.
dendritic cells are the antigen presenting cells
EOSINOPHILS
release of basic proteins and oxygen derived free
radicals
causes airway hyperresponsiveness

11. NEUTROPHILS
increased numbers of activated neutrophils are found
in sputum and airways of patients with severe asthma.
T Lymphocytes
Th2 cells release IL-5 eosinophilic inflammation
IL-4,13 increased IgE formation

12. PRIMARY MEDIATORS
1.Th2 cells > IL 4,5 > IgE production & Mast cell
recruitment
2.Histamine - bronchconstriction by direct and
cholinergic reflex actions
3.ECF and NCF

13. Secondary mediators
LT C4, D4, and E4.
prolonged bronchospasm
increased vascular permeability
increased mucus secretion.
Prostaglandins (D2) Bronchospasm
Vasodilation
PAF platelet aggregation
granule secretion.

14. i. Inflammatory cell infiltration of the airways
ii. Increased thickness of the bronchial smooth
muscle
iii. Partial or full loss of the respiratory epithelium
iv. Subepithelial fibrosis
v. Hypertrophy and hyperplasia of the submucosal
glands and goblet cells
vi. Partial or full occlusion of the airway lumen by
mucous plugs
vii. Enlarged mucous glands and blood vessels

15.  Acute bronchoconstriction
 Swelling of bronchial wall
Chronic production of mucous
 Remodeling of airways walls