bronchial asthma and its pathogenesis very useful to students and also various source of drugs in asthma

1. Bronchiectasis and
asthma

2.  Definition : A disease characterized by
permanent dilatation of bronchi &
bronchioles caused by destruction of
muscle and elastic tissue resulting from or
associated with chronic necrotizing
infection
 Clinical presentation: Cough with
expectoration, fever
 Less common than previously
Bronchiectasis

3. Predisposing factors
 Bronchial obstruction
 Congenital/ hereditary conditions-cystic
fibrosis,primary ciliary dyskinesia –mucus
 Bronchial obstruction tumour ,foreign body
 Weakening of bronchial walls by
infections
 Post infectious conditions :Necrotizing
pneumonia (TB etc ),viral,fungal
 Idiopathic : SLE,RA, IBD

4. Etiology & Pathogenesis
 Obstruction
 Bronchial obstruction (mucus ,foreign
body)
 Impaired clearing
 Pooling of secretions distal to obstruction
 Inflammation of airway
 Infection
 inflammation,necrosis ,fibrosis

5. Primary ciliary dyskinesia
 Kartagener syndrome
 Defect in ciliary motility
↓
Lack of bacterial clearance
↓
Predisposes to sinusitis & bronchiectasis
Situs inversus
Immotile celia of spermatozoa→infertility

6. Morphology
Lower lobes, bilateral
localized when associated with
tumour,FB etc
Dilated airways –seen upto pleural
surface grossly.
Filled with pus

7. Bronchiectasis

8. Morphological types
 Cylindroid
 Fusiform
 Saccular

9. Microscopy
 Desquamation & ulceration of lining
epithelium,
 Acute and chronic inflammatory infiltrate in
bronchial and bronchiolar wall.
 Squamous metaplasia of remaining lining
epithelium
 Chronic cases-
 Fibrosis of bronchial wall.
 Peribronchiolar fibrosis → obliteration

10. Clinical feature & Complications
 Productive cough morning >,purulent ,
 Dypsneoa ,hemoptysis ,fever
 Obstructive ventilation
 Amyloidosis
 Cor pulmonale
 Brain abscess

11. Asthma
 Definition :chronic inflammatory disorder of
the airways that causes recurrent
episodes of wheezing ,breathlessness and
cough.
 Associated with reversible widespread
bronchoconstriction and airflow limitation
 Common -10% children, 5% adults
Increased incidence in the West

12. Classification
 Severity
 Response to CS
 Causative agent eg dust, cold,seasonal
 Pathophysiology :
 Extrinsic (initiated by type I
hypersensitivity)
 Intrinsic (non immune )
….but overlap common

13. Pathogenesis
 Predisposition to type I hypersensitivity
(Atopy)
 Acute and chronic airway inflammation
 Bronchial hyperesponsiveness

14. Pathogenesis
 Allergens
 Extrinsic ;pollen,allergens,dust mites
 Intrinsic : non immune mechanisms aspirin
pulm infection esp viral, stress, cold etc
 Cells involved
 Eosinophils, mast cells ,macrophages ,
T lymphocytes ,epithelial cells
 Mediators

15. Atopic asthma -Initial
sensitization
 Stimulate induction of T H2 type cells
 Release of IL 4→mast cells,
 B lymphocytes → Ig E
 Release of IL 5→Eosinophils

16. Sensitization to allergen

17. Acute/immediate response
 Antigens bind to presensitized IgE coated
mast cells → cross linking of mast cells →
 Degranulation of mast cells and release of
chemical mediators
 Direct stimulation of vagus receptors –
broncho constriction,mucus secretion,
oedema
 Chemotaxis of leukocytes following
cytokines released by mast cells, Eo,PMN

18. Immediate phase

19. Late phase reaction
 Mast cells, other leucocytes ,vascular
endothelium,epithelium release mediators
that affect bronchi
 Mediators implicated in asthma
 Leukotrines LT C4,LT D4
 (Prostaglandins PG D2 )
 PAF
 Others IL 1,IL 6,TNF ,etc

20. Late phase

21. Non atopic asthma
 No atopic predisposition
 Viral disease makes the subepithelial
vagal receptors more prone to irritants
 Drug induced asthma –aspirin
 Occupational

22. Gross Morphology
 Overdistention of lungs
 Small areas of atelectasis occlusion of
bronchi and bronchioles by thick tenacious
mucous plugs

23. Microscopy “airway remodelling”
 Hyperplastic smooth muscle cells
 Deposition of collagen beneath the
bronchial epithelium
 Focal necrosis of epithelium
 Infiltration of mucosa by eosinophils ,mast
cells ,lymphoid cells and macrophages
 Oedema.
 Increase in size of submucosal glands

24. Normal morphology

25. Airway remodelling

26. Sputum findings
 Charcot –Leyden crystals
 Curschmann spirals
 Eosinophils

27. Clinical features /diagnosis
 Episodic attacks of breathlessness
 Cough with mucous secretions --relief
 Status asthmaticus
 Cyanosis ,death
 Clinical diagnosis
 AEC
 Sputum

28. In conclusion
 Asthma
 Definition, atopic ,non atopic asthma
 Pathogenesis
 Gross and microscopy
 Bronchiectasis
 Definition ,pathogenesis
 Morphology
 Clinical features ,complications

29. References
 Robbins basic pathology
 Rubins clinical pathology
 Davidsons textbook of medicine