BRONCHIAL ASTHMA

DEFINITION:

It is a chronic inflammatory disorder of the

bronchial airways.

It is a characterized by airflow obstruction

and recurrent episodes of wheezing,
breathlessness and cough.
 Asthma Types:
Classified according to the type of antigen
(responsible for the disease) -
1. Atopic asthma – ALLERGIC
- It is common type of asthma which
usually begins in childhood.
- It is due to genetically determined
production of specific IgE antibody.
- It is mediated by type I IgE mediated
hypersensitivity reaction.
 - It is triggered by environmental allergens
such as dusts, pollens, cockroach or
animal dander and foods.

2. Non-atopic / Intrinsic asthma –

 It does not show allergen sensitization.
 Adult-onset asthma
 ETIOLOGY : ASTHMA
Due to interplay between –

 GENETIC (endogenous) and

 Environmental (exogenous) factors.
 RISK FACTORS
 ENDOGENOUS RISK FACTORS –

* Genetic predisposition
* Atopy – allergic reaction for which there
is genetic predisposition
* Airway hyperresponsiveness to inhaled

triggers.
 RISK FACTORS
 ENVIRONMENTAL RISK FACTORS –
* Inhaled allergens – include house dust,
mites & household pets.
* Upper respiratory tract viral infections:
e.g rhinovirus, coronavirus
* Air pollution e.g. sulfur dioxide, ozone &
diesel particulates. Indoor pollutants –
exposure to nitrogen oxides from cooking
stove
* Passive smoking ; Drugs – e.g Aspirin ,
Beta-adrenergic blockers
 Hygiene hypothesis?
Asthma Pathogenesis: INDUCERS
Allergens,Chemical sensitisers,
Air pollutants, Virus infections
Airway
Hyper-responsiveness
Genetic*

INFLAMMATION
Airflow Limitation

SYMPTOMS
TRIGGERS
Cough Wheeze
Allergens, Exercise,
Dyspnoea
Cold Air, SO2 Particulates
Asthma : Pathogenesis

Early phase (immediate) and late phase reactions

 Leukotrienes
Ach
Asthma Pathology:
Histamine
Prostaglandin D Allergen
Platelet Macrophage/
activating factor dendritic cell Mast cell
Interleukins Leukotrienes
Th2 cell Neutrophil
C4, D4 & E4
Eosinophil
Mucus plug
Epithelial shedding
Nerve activation

Subepithelial
fibrosis
Plasma leak
Sensory nerve
Oedema activation
Vasodilatation Cholinergic
Mucus New vessels reflex
hypersecretion
Hyperplasia Bronchoconstriction
Hypertrophy/hyperplasia

Barnes PJ
 Asthma Morphology:
 GROSS: It may show occlusion of bronchi and
bronchioles by thick, tenacious mucus plugs.

 MICROSCOPY:

 Characterized by edema of bronchi and

bronchioles. The mucosa is infiltrated by mast
cells, eosinophils and lymphocytes.
 The lining epithelium of airways may shed into
lumen of airways.
 Curschmann spirals: mucus plugs may
form spiral shaped cast of the airways.
 Charcot-Leyden crystals: are crystallized
eosinophil lysophospholipase may also be
seen in the lumen of airways.
 There is an increase in size and number
(hypertrophy/hyperplasia) of the sub-
mucosal glands & also hypertrophy &/
hyperplasia of the bronchial wall smooth
muscle.
 Asthma
Morphology:

Asthma Microscopy
1.Mucous Plugs +eosinophils
2.Goblet cell hyperplasia
3.Inflammation + Eosinophils
4.Smooth muscle hyperplasia
5.Mucous gl. Hyperplasia.
 Asthma – Lung Gross features:
 Inflamed thick bronchi obstructed by mucous plugs.
Asthma : Microscopy

 Inflammed
bronchi
 Obstruction by
mucous plug
 Alveoli (normal)
Asthma : Microscopy
Curschmann spirals:
Charcot-Leyden Crystals:
 CLINICAL FEATURES

Acute asthmatic attack usually lasts upto several

hours.

• Dyspnea

• Wheezing – whistling sounds during difficult

breathing

• Cough with or without sputum production

 STATUS ASTHAMATICUS
• Severe acute asthma unresponsive to therapy
in which the severe acute paroxysm persists for
days and even weeks is termed status
asthmaticus.

• It may lead to severe cyanosis (blue

discoloration of the skin or mucous membranes)
and even death.