Bronchial Asthma

Dr.CSBR.Prasad, M.D.
Bronchial asthma - gist
Bronchial asthma
Disease characterized by increased
responsiveness of the tracheobronchial
tree to various stimuli, potentiating
paroxysmal constriction of the bronchial
tree.
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.
Definition
Chronic inflammatory disorder of airways
that causes recurrent episodes of:
Wheezing
Breathlessness
Chest tightness &
Cough particularly at night and /or early
morning
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
Frequency and severity of
symptoms
1. Mild, intermittent
2. Moderate
3. Severe, persistent
Clinical categories
1. Steroid dependent
2. Steroid resistant
3. Difficult
4. Brittle asthma
Informal categories
1. Seasonal
2. Exercise induced
3. Drug induced
4. Occupational asthma
5. Asthmatic bronchitis in smokers
6. Allergic bronchopulmonary aspergillosis

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

Figure 15-10 A simplified scheme of the system of type 1 helper T (TH1) and
type 2 helper (TH2) cells.
Structural alterations
Airway remodelling
Smooth muscle proliferation
Subepithelial collagen deposition

Mediated by:
1. Skewed TH2 differentiation
2. ADAM-33 gene abnormality
3. Mast cells
Figure 15-12
Comparison of a normal
bronchiole with that in a
patient with asthma.
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
Two reactions
Classic Ig E mediated hypersensitivity
reaction has 2 responses
1. Acute immediate response
2. Late phase reaction
Figure 15-11 A model
for allergic asthma.
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.
Primary mediators
1.Th2 cells > IL 4,5 > IgE production+E &
Mast cell recruitment
2.Histamine - bronchconstriction by direct
and cholinergic reflex actions
3.ECF and NCF
Secondary mediators
LT C4, D4, and E4.
prolonged bronchospasm
increased vascular permeability
increased mucus secretion.
Prostaglandins (D2) Bronchospasm
Vasodilation
PAF platelet aggregation
granule secretion.

Late phase reaction
starts 4-8hrs later and persits for 12-24hrs
Caused by recruitment of Bs, Ns, Es

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

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.
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.

Morphology - gross
Lungs, over distended due to over inflation
Small areas of atelectasis
Occlusion of bronchi and bronchioles by
thick tenacious mucous plugs.
These lungs appear essentially normal, but are the hyperinflated lungs of
a patient who died with status asthmaticus.
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.
Morphology - Micro
Mucous plugs-whorls of shed epithelium
CURSHMANNS SPIRALS
Numerous Es and
CHARCOT-LEYDEN CRYSTALS
Crystalloids made of MBP.
Microscopy
(Airway remodeling)
Thickening of BM of bronchial epithelium
Edema and infammatory infiltrate in
bronchial walls with E (5 to 50 % )
Increased in size of submucosal mucous
glands
Hypertrophy of bronchial wall muscle.
Walk thru wheeze ?


Walk thru angina ?
E N D
Contact:

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

CSBRPRASAD@REDIFFMAIL.COM