Bronchial asthma

This PDF is prepared for undergraduate teaching in pathology.

1. Bronchial Asthma
Dr.CSBR.Prasad, M.D.

2. Bronchial asthma - gist

3. Bronchial asthma
Disease characterized by increased
responsiveness of the tracheobronchial
tree to various stimuli, potentiating
paroxysmal constriction of the bronchial
tree.

4. Bronchial asthma
Patients with asthma experience:
1.Attacks of severe dyspnea, coughing, and
wheezing.
2.Rarely, “status asthmaticus” - may prove fatal.
3.Patients may be asymptomatic between the
attacks.

In some cases, the attacks are triggered by exercise
and cold or by exposure to an allergen, but often
no trigger can be identified.
There has been a significant increase in the incidence of asthma in the
Western world in the past three decades.
In Bangalore 50% of children suffer from asthma. Air pollution is
thought to be the main culprit.

5. Definition
Chronic inflammatory disorder of airways
that causes recurrent episodes of:
–Wheezing
–Breathlessness
–Chest tightness &
–Cough particularly at night and /or early
morning

6. These symptoms are usually associated
with wide spread but variable
bronchoconstriction and air flow limitation
that is at least partially reversible, either
spontaneously or with treatment
It is thought that inflammation causes
increase in airway responsiveness
(bronchospasm) to a variety of stimuli

7. Frequency and severity of
symptoms
1.Mild, intermittent
2.Moderate
3.Severe, persistent

8. Clinical categories
1.Steroid dependent
2.Steroid resistant
3.Difficult
4.Brittle asthma

9. Informal categories
1.Seasonal
2.Exercise induced
3.Drug induced
4.Occupational asthma
5.Asthmatic bronchitis in smokers
6.Allergic bronchopulmonary aspergillosis

10. Typical categories
1.Extrinsic (allergic, reagin mediated, atopic)
2.Intrinsic (idiosyncratic)
3.Mixed (intrinsic and extrinsic factors
operative)

11. Figure 15-10 A simplified scheme of the system of type 1 helper T (TH1) and
type 2 helper (TH2) cells.

12. Structural alterations
“Airway remodelling”
•Smooth muscle proliferation
•Subepithelial collagen deposition

Mediated by:
1.Skewed TH2 differentiation
2.ADAM-33 gene abnormality
3.Mast cells

13. Figure 15-12
Comparison of a normal
bronchiole with that in a
patient with asthma.

14. Atopic / Allergic asthma
•Most common type
•Environmental agent: dust, pollen, food,
animal dander
•Family history - present
•Serum IgE levels - increased
•Skin test with offending agent –wheal flare

15. Two reactions
Classic Ig E mediated hypersensitivity
reaction has 2 responses
1. Acute immediate response
2. Late phase reaction

16. Figure 15-11 A model
for allergic asthma.

17. Pathogenesis
•Ag + presensitised IgE coated mast cells
to same or cross reacting antigen
•Chemical mediators
•Mucosal surface
•Submucosal mast cells
•Direct stimulation of subepithelial vagal
receptors
•Minutes – Bronchoconstriction.

18. Primary mediators
1.Th2 cells > IL 4,5 > IgE production+EØ &
Mast cell recruitment
2.Histamine - bronchconstriction by direct
and cholinergic reflex actions
3.ECF and NCF

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

20. Late phase reaction
starts 4-8hrs later and persits for 12-24hrs
Caused by recruitment of BØs, NØs, EØs

•HRF – Histamine releasing factor
•MBP – Major basic protein from EØs
Direct epithelial damage
•Neutrophils – inflammatory injury.

21. Non atopic asthma
•Triggered by respiratory tract infection
•Viruses - most common culprits
•Family history uncommon
•IgE level normal
•No associated allergy
•Skin tests NEGATIVE
•Cause- hyperirritability of bronchial tree.

22. Drug induced asthma
•Several pharmcologic agents
•Aspirin sensitive asthma
occurs in recurrent rhinitis
nasal polyposis.
•Increased bronchoconstrictor leukotrienes.
Exqusitively sensitive to small doses of
aspirin.
•Inhibits COX pathway, without affecting
LPO pathway

23. Allergic Bronchopulmonary
Aspergillosis
•Caused by spores of aspergillus fumigatus
•Antigen challenge
•Type I IgE induced reaction
•4 to 6 hr later Type III mediated response.

24. Occupational asthma
•Fumes (epoxy resins, plastics)
•Organic / chemical (dust, wood, cotton)
•Gases (toluene)
•Other chemicals (formaldehyde, penicillin)
•Mechanism of injury:
type I IgG mediated reactions
liberation of bronchoconstrictors directly
unknown hypersensitivity.

25. Morphology - gross
•Lungs, over distended due to over inflation
•Small areas of atelectasis
•Occlusion of bronchi and bronchioles by
thick tenacious mucous plugs.

26. These lungs appear essentially normal, but are the hyperinflated lungs of
a patient who died with status asthmaticus.

27. This cast of the bronchial tree is formed of inspissated mucus and was coughed up by a
patient during an asthmatic attack. The outpouring of mucus from hypertrophied
bronchial submucosal glands, the bronchoconstriction, and dehydration all contribute to
the formation of mucus plugs that can block airways in asthmatic patients.

28. Morphology - Micro
•Mucous plugs-whorls of shed epithelium
CURSHMANN’S SPIRALS
•Numerous Eøs and
CHARCOT-LEYDEN CRYSTALS
• Crystalloids made of MBP.

29. Microscopy
(Airway remodeling)
•Thickening of BM of bronchial epithelium
•Edema and infammatory infiltrate in
bronchial walls with EØ (5 to 50 % )
•Increased in size of submucosal mucous
glands
•Hypertrophy of bronchial wall muscle.

30. Walk thru wheeze ?


Walk thru angina ?

31. E N D

32. Contact:

Dr.CSBR.Prasad, M.D.,
Associate Professor,
Deptt. of Pathology,
Sri Devaraj Urs Medical College,
Kolar-563101,
Karnataka,
INDIA.

[email protected]