pathology of bronchial asthma

1. PATHOPHYSIOLOGY OF
BRONCHIAL ASTHMA
MODERATOR RESOURCE FACULTY PRESENTER
Prof. G.P. Rauniyar DR. Santosh Upadhyaya Bimal Khadka

2. OBJECTIVES
• PATHOPHYSIOLOGY OF BRONCHIAL ASTHMA
• MODEL FOR ALLERGIC ASTHMA
• MORPHOLOGY OF BRONCHIAL ASTHMA

3. DEFINITION
 ASTHMA is a chronic inflammatory disorder of the airways that causes:
– recurrent episodes of wheezing, breathlessness, chest tightness
– cough, particularly at night and/or in the early morning.
 Inflammation causes an increase in airway responsiveness to a variety of
stimuli
 Patients with asthma experience disabling attacks of severe dyspnea,
coughing, and wheezing triggered by sudden episodes of bronchospasm.
Rarely, a state of unremitting attacks, called status asthmaticus.
 Attacks triggered by
– Exercise
– Cold
– Exposure to an allergen

4.  intermittent,
 mild persistent,
Moderate persistent, and
severe persistent asthma.
Based on frequency and severity of
symptoms, categorized into:

5. Typically asthma is categorized
into
• 1. Extrinsic
• 2. Intrinsic
• Other categorisation according to agents or
events that trigger bronchoconstriction are:-
• a) seasonal
• b) exercise induced
• c) drug induced
• d) occupationl induced e) asthmatic bronchitis to
smokers

6. TYPES
• Atopic
• Non-atopic
• Drug-induced
• Occupational

7. ETIOLOGY
• Genetic Predisposition To Type I Hypersensitivity
Reaction
• Acute And Chronic Airway Inflammation
• Bronchial Hyperresponsiveness
• Childhood infections eg. Respiratory Syncytial Virus
• Allergen exposure eg. Pollens, Animal Dander
• Indoor Pollution

8. pappa

9. ATOPIC ASTHMA
• most common
• begins in childhood
• triggered by environmental antigens such as
dusts, pollens, animal dander, and foods
• positive family history of atopy
• asthmatic attacks are often preceded by
allergic rhinithypersensitivity

11. MEDIATORS RESPONSIBLE
 1ST GROUP: role in bronchospasm is clearly supported by
pharmacological interventions
• e.g. leukotrienes C4,D4,E4, acetylcholine
 2nd GROUP:- have potent asthma like effects but their actual
clinical
role appears to be minor on the basis of lack of efficacy of
potent antagonists or synthesis inhibitors
• e.g. histamine, prostaglandin D2, PAF
 3RD GROUP:- whose specific antagonists are not available and
even their role in asthma is not clear
• e.g. IL-1, TNF, IL-6, chemokines, nitric oxide,
bradykinin , endothelins ,neuropeptides..

12. NON ATOPIC ASTHMA
• Triggered by respiratory tract infections
• viruses:-rhinovirus, para influenza
• positive family history of atopy is uncommon
• no associated allergies
• serum ige level normal
• skin test negative

13. PATHOGENESIS
 Virus, SO2, O3, NO2

Infect respiratory mucosa

Inflammation

lowers the threshold of subepithelial vagal receptors to irritants

Hyperreactivity of epithelial layer

14. DRUG INDUCED ASTHMA
 Aspirin sensitive asthma :
 recurrent rhinitis and nasal polyps.
• aspirin triggers asthma by:
• inhibiting the cycloxygenase pathway of arachidonic
acid
metabolism without affecting the lipoxygenase
route,this tipping the balance towards elaboration of
the bronchoconstrictor leukotrienes

15. OCCUPATIONAL ASTHMA
• stimulated by fumes(plastics), organic and
chemical
dusts(wood,cotton, platinum), gases(toluene)
and
other chemicals(formaldehyde, penicillin
products).
underlying mechanism is type I hypersensitivity
reactions

16. MORPHOLOGY OF BRONCHITIAL ASTHMA
GROSS:-
• lungs are overdistended due to
overinflation
• small areas of atelectasis can be
seen
• occlusion of bronchi and
bronchioles by thick tenacious
mucous plug:- most striking
finding.

17. MORPHOLOGY:-HISTOLOGICAL
 mucous plugs contain whorls of shed epithelium
which give rise to well known CURSCHMANN’S
SPIRALS

18. numerous eosinophils and CHARCO
LEYDEN CRYSTALS are present

21. Muscle hypertrophy Sub basement
membrane fibrosis

22. SUMMARY:
Allergen Irritant
cell activation
cytokine
cellular infiltration
cytokine/ mediator
Airway inflammation & Obstruction
ASTHMA

23. THANK YOU...