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Bronchial asthma

Dr. amira kamal El-Hawary

Dr. AZZa Abdel-AZiZ A. Ali
 Humoral Immunity
 B lymphocytes - Antibody
 Cell mediated Immunity
 T lymphocytes – Macrophages
 Non-Specific immunity
 Neutrophils, Macrophages
 Immunity is not inherited.

 Primary response – slow, weak.

 Learning period, memory cells.
 Secondary response – rapid,
:Immune Disorders
 Immunodeficiency disorders
 AIDS, antibody deficiency
 Hypersensitivity Disorders (allergy) excessive
or altered reaction to an antigen producing adverse
effects on the body. it is classified into 4 types

 Type-I (IgE),
 Type II-IgG,
 Type III-Immune complex,
 Type IV-Cell mediated.
 Autoimmune disorders
 SLE, Rheumatoid, Rheumatic fever.
Type I hypersensitivity reaction
- First exposure to an antigen
stimulation of B-lymphocytes to
transform to IgE secreting plasma cells
( helped by CD4+ T-lymphocytes)
IgE binds to the surface of mast cells
and basophils
First exposure
Type I hypersensitivity reaction
Second exposure to the same antigen-
results in cross-linking of Ig E on the
surface of mast cells
Degranulation of the cells with release
of chemical mediators
Chronic obstructive pulmonary
(disease (COPD
 COPD is a disease state characterized
by airflow limitation that is not fully
reversible. The airflow limitation is
usually both progressive and associated
with an abnormal inflammatory response
of the lungs to particles or gases.
 Obstructive Pulmonary Diseases
 Classical COPDs
 Emphysema

 Chronic Bronchitis

 Bronchial Asthma
Bronchial asthma
 Increased responsiveness of the
bronchial tree to various stimuli that
results in paroxysms of Bronchospasm
 reversible bronchospasm  later
chronic bronchial inflammation develop
and airflow is limited by bronchoconstriction,
mucus plugs, and increased inflammation and
obstructive lung disease develop
 It is episodic, reversible bronchospasm
resulting from an exaggerated
bronchoconstricton response to various
Incidence of asthma
It is a common disease affecting 5% of
. adults and 7-10% of children
There has been a significant increase in
the incidence of asthma in the
Western world in the past three
-Clinically, it is manifested by
recurrent episodes of wheezing,
breathlessness, and cough. These
symptoms are usually associated with
bronchoconstriction and airflow
limitation that is at least partly
reversible, either spontaneously or
with treatment. Between the attacks,
patients may be virtually

- Rarely, a state of unremitting attacks,

called status asthmaticus, proves
fatal; usually, such patients have had
a long history of asthma.
- -
 Why does constriction occur
Constriction occurs because bronchi are
hyper reactive to a variety of stimuli to
which the patient is exposed
?What are the Triggering Factors
 Domestic dust mites
 Air pollution
 Tobacco smoke
 Occupational
 Cockroach
 Animal with fur
 Pollen
.(Triggering Factors ( cont
 Respiratory (viral)
 Chemical irritants
 Strong emotional
 Drugs ( aspirin, beta
Pathogenesis INDUCERS
Allergens, Air pollutants,
Airway hypersensitivity Virus infections

Airflow Limitation

Allergens, Exercise,
Cough Wheeze
Cold Air, SO2 Particulates
 What initiates the inflammatory process in
the first place and makes some persons
susceptible to its effects is an area of active
 There is not yet a definitive answer to this
question . The expression of asthma is a
complex, interactive process that depends on
the interplay between two major factors—
host factors (particularly genetics) and
environmental exposures that occur at a
crucial time in the development of the immune
system early in life
Pathogenetic Types
Extrinsic and Intrinsic asthma

The concept that there are two

types of asthma, extrinsic (due to
and intrinsic ( due to constitutional
factors) is not so sharp and there is
much overlap between asthma with
different triggers.
Bronchial Asthma
Extrinsic Intrinsic
Type-I (IgE-mediated)- Not allergic-
hyper-sensitivity or
allergic reaction
Triggered by-
Triggered by- respiratory tract
environmental antigens infections &drugs
, ..( (dust, pollens, food (.(aspirin
Family history of Atopy-
No family history-
. Begins in childhood-
Bronchial Asthma - Pathophysiology
Pathogenesis of extrinsic (atopic) asthma-

Meeting the specific allergen causes sensitization of- 1

CD4+ (T н2) cells resulting in release of cytokines
(IL-4,5, and 13).
2- IL-4,5 and 13 cause
a. Stimulation of IgE production
b. Growth of mast cells.
c. Growth and activation of eosinophils.
3- Meeting the specific allergen for the second time
results in an immune reaction which passes into two
i- An early phase starting 30-60 min.after inhalation
of the antigen then
.ii- A late phase develops after 4-8 hours
Pathogenesis of extrinsic (atopic) asthma
During the early phase, primary- 4
mediators are released. They
- Leucotriens which are
sythesized from phospholipid by
phospholipase enzyme
- Histamine
- Platelet –Activating Factor

These mediators produce …..-

vasodilatation, increased
vascular permeability and
.increased mucin secretion
Pathogenesis of extrinsic (atopic) asthma
During the late phase secondary- 5
mediators are released including
- Eosinophil and neutrophil
chemotactic factors
- IL-4 &5
- Platelet Activating factor
- These mediators
produce…..eosinophil and neutrophil
infiltration to the site of the lesion
these cells produce
a- More mediators that activate
mast cells and intensify the initial
. b. Epithelial cell damage
Pathogenesis of intrinsic
Not fully understood, but a considerable
overlap with extrinsic asthma is present and
eosinophils seem to play an important role in
: both types. It may be
 Virus-induced inflammation of respiratory mucosa
lowers threshold of vagal receptors to irritants
 Aspirin-sensitive asthma

 Occupational asthma
Bronchial Asthma
 Atopic Asthma  Nonatopic Asthma
 Exposure of  Virus-induced
presensitised IgE-coated inflammation of
mast cells to antigen respiratory mucosa
causes acute immediate lowers threshold of
response vagal receptors to
 Chemical mediators irritants
(histamine, PAF,  Aspirin-sensitive
leukotrienes) asthma
 Late-phase reaction  Occupational asthma
:Pathogenesis - Atopic Asthma
?What is the Pathophysiology
 Trigger Factor
 Mast cell
 Mediators: histamine,prostaglandin,leukotrienes,as
well as cytokines.
 Inflammatory cells
 Contraction of airway smooth muscles
 Airway wall swelling (mucosal edema)
 Chronic changes
 Hypertrophy of the smooth muscles, Airway
Lung Morphology in Asthma

 Mucous plugging
 Bronchospasm
 Over inflation
Lung Hyperinflation in Asthma
Thick bronchi with Mucous

Normal Asthma

Barnes PJ
Asthma - Microscopic Pathology
 Patchy necrosis of epithelium
 Sub-mucosal glandular hyperplasia
 Hypertrophy of bronchial smooth muscle
 Eosinophils, mast cells; lympho (TH2, CD4)
 Mucous plugs, Whorled mucous plugs
(Curschmann’s spirals)
 Debris of eosinophils (Charcot-Leyden
Microscopic Pathology
Asthma Microscopic Pathology

Asthma - Bronchial morphology
 inflammation
 Gland hyperplasia
 Mucous plug in
Asthma - Bronchial morphology
 Inflammation
 Mucous Plug
 Eosinophils
Inflammation epithelial
:Eosinophils in Asthma
:Curschmann's spirals
Bronchial Asthma
:Therapy - Pathology

Barnes PJ
?What is Asthma
 Hypersensitivity – Allergy , Type I
of airways of lungs - Bronchi
 Allergens – in the air, mast cell - IgE ab.

 Inflammation of airways -Bronchitis.

 Genetic, Environmental, Age.

 High in industrial cities 4-19%,

Increasing incidence …!