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Bronchial

Asthma

Dr. Xing Lihua


邓丽君
1953~1995
因哮喘急性发作
病逝泰国
Beethoven
1770-1827
由于哮喘和束手
无策的医生而死
于维也纳
Outline

➤ Defination
➤ Epidemiology
➤ Pathogenesis
➤ Pathology
➤ Clinical Manifestations
➤ Diagnosis
➤ Disease management

recommendations
Definitio
n
Asthma is now defined as a chronic
inflammatory disorder of the airways in
which many cells and cellular elements
play a role, in particular, mast cells,
eosinophils, T lymphocytes, neutrophils,
and epithelial cells.
Definitio
n
In susceptible individuals, this
inflammation causes recurrent episodes of

wheezing,
breathlessness,
chest tightness,
cough,
particularly at night and in the early
Definitio
n
These episodes are usually associated
with widespread but variable airflow
obstruction that is often reversible either
spontaneously or with treatment. The
inflammation also causes an associated
increase in the existing bronchial
hyperresponsiveness to a variety of stimuli.
Epidemiology

➤ morbidity
1%-13%, 1%-4% in China
➤most common chronic disease of childhood
About one-half of the case develop before age 10
and another third occur before age 40
➤higher in developed country
➤higher in urban than in suburb
➤40% with family history
Pathogenesis:
Causes
Host factor (hereditary susceptibility )
FH of asthma or atopy (familial tendency for
allergic reactions)

Environmental factor (triggers)


allergens, chemicals, smoke, cold,
exercise, food additives, aspirin, extreme
emotional expressions
Pathogene
sis
certain triggers
Pathogene
sis
1. Airway Inflammation
 A specific type of inflammatory condition,
involving, in particular, mast cells, eosinophils
and T lymphocytes, which release a wide range
of inflammatory mediators
 These mediators act on cells in the airway,
leading to contraction of smooth muscle, edema
due to plasma leakage and mucus plugging
Pathogene
sis
Pathogene
sis
2. Airway Hyperresponsiveness
an exaggerated bronchoconstrictor response to a
wide variety of stimuli
leads to clinical symptoms of wheezing and
dyspnea after exposure to allergens,
environmental irritants, viral infections, cold air,
or exercise.
can be measured by inhalation challenge testing
with methacholine or histamine.
Pathogene
sis
3. Airflow Obstruction

Acute bronchoconstriction
Airway edema
Chronic mucus plug formation
Airway remodeling
The
症状tip
- - -of iceberg
冰山的一角
Pathology

Normal Asthma
A
Panel A Specimen of Bronchial Mucosa
From a Subject without Asthma.
The epithelium is intact; there is no
thickening of the sub-basement membrane,
and there is no cellular infiltrate.

B
Panel B Specimen of Bronchial Mucosa from
a Subject with Asthma. There is evidence
of goblet-cell hyperplasia in the epithelial
-cell lining. The sub-basement membrane
is thickened, with collagen deposition
in the submucosal area, and there is a
cellular infiltrate.

N Engl M .2001 ;344 (5): 350


(A) (A) A normal subject without asthma,
showing an intact surface
pseudostratified ciliated columnar
epithelium. The underlying reticular
basement membrane is indistinct; there
are few inflammatory cells, and small

amounts of bronchial smooth muscle.

(B) A subject with fatal asthma, showing


sloughing of the surface epithelium, a
(B) prominent homogeneous thickened
reticular basement membrane of hyaline
appearance, an intense infiltration of the
mucosa by inflammatory cells,
enlargement of bronchial
smooth muscle.

Am. J. Respir. Crit. Care Med., 2000; 161(5) :1720-1745


Airway Remodeling (structural changes)

Airway wall thickening of sufficient


magnitude to increase airflow resistance
and enhance airway responsiveness
The episodic airway narrowing caused
by three possible factors

➤ Constriction of airway smooth muscle

➤ Airway edema

➤ Thepresence of liquids within the


confines of the airway lumen
Clinical Manifestations
History
➤ Shortness of breath accompanied by chest tightness,
cough, wheezing and anxiety
recurrent episodes
may be obvious at night or in the early morning
reversible either spontaneously or with treatment
➤ Variants of asthma:

no wheezing, only cough or chest tightness


➤ Cold dry air may induce airway narrowing
Clinical Manifestations

➤episodes recur following one or


more triggers
➤wheezing rale as episodes
➤relief of symptoms occurs with a
bronchodilator or spontaneously
Clinical Manifestations

Physical Examination
Vital signs:
➤ A rapid respiratory rate

---often 25- -40 bpm


➤ Tachycardia
➤ Pulsus paradoxus ( systolic blood pressure
decrease >10mmHg during inspiratory period
than during expiratory period)
Clinical Manifestations

➤ Using accessory muscles of ventilation


➤ Hyperinflated thorax
➤ Prolonged expiratory phase
➤ Hyperresonance

➤ Wheezing
Clinical Manifestations

Laboratory Findings

1.Sputum examination
Eosinophils are often seen microscopically,
and eosinophilic granules from disrupted
cells may be seen throughout the sputum
smear.
Clinical Manifestations
2.Chest x-ray
Vary from normal to hyperinflation.
Lung markings are commonly increased,
particularly in chronic asthma.
3.Eosinophil count
Eosinophilia (> 250 to 400 cells/µL) is
common. In many asthmatics, the degree of
eosinophilia correlates with severity of
asthma.
Clinical Manifestations

Laboratory Findings
4.Allergen identification
measuring total serum IgE or specific IgE
antibodies
skin testing
Use appropriately selected allergens
A positive response indicates only potential
allergic reactivity to the tested allergens.
Clinical Manifestations

Laboratory Findings
5.Pulmonary function test
bronchial provocation test (BPT)
bronchial dilation test (BDT)
 peak expiratory flow (PEF) variability
Bronchial Provocation Test (BPT)

after inhale bronchial stimulor such as


metacholine or histamine, the decrease
of FEV1 > 20%. (BPT +)
Bronchial Dilation Test (BDT)

after inhale bronchodilator such as


salbutamol, the increase of FEV1>15%; or
the increase volume > 200ml .(BDT +)
Peak Expiratory Flow (PEF) Variability

PEF in am (usually lowest ) and 12 hours


later (usually highest), PEF variability ≥ 20%
. (reversible airflow obstruction )
Diagnosis:
Criteria
1. recurrent episodes of wheezing,breathlessness,or cough
following one or more triggers
2. wheezing rale as episodes
3. relief of symptoms occurs with a bronchodilator or
spontaneously
4. exclude other diseases
5. Pulmonary function test
bronchial provocation test (+)
or bronchial dilation test (+)
or PEF variability ≥ 20%
1-4 or 4-5
Classification of asthma
severity
Differential Diagnosis

 Cardiac asthma
 Chronic asthmatic bronchitis
 Lung cancer
 Allergic lung diseases :

eosinophilic lung disease


Cardiac asthma Bronchial asthma
history heart disease allergic atopy
symptoms mixed dyspnea expiratory dyspnea
Pink frothy sputum White mucous sputum
signs moist rales in base of pulmonary fullness of
lung wheezing rale
Small amounts of
wheezing rale
X ray cardiac enlargement emphysema
pulmonary congestion
treatment Theophylline Theophylline
morphine adrenalin
Complications
Goals of management

➤ minimal or no symptoms
➤ minimal asthma episodes / attacks
➤ no emergency visits to hospital

➤ minimal need for as needed β 2 agonist

➤ no limitations on physical activities


➤ nearly normal lung function
➤ minimal or no side effects from medication
Directed at airway obstruction and
inflammation
use of bronchodilators (rescue ) for acute asthma
airway obstruction
use of controllers for modifying the airway
inflammatory environment
Treatment options
Relievers: Controllers:
➤short-acting β 2 ➤inhaled steroids(ICS)
agonist ➤long-acting β 2 agonist
➤Anticholinergics ➤Leukotriene regulator
➤methylxanthine (LTRA)
➤systemic steroids ➤methylxanthine
➤mast cell stabilizers
➤systemic steroids
Relievers:
short-acting β 2 agonist
➤ MDI with a spacer or nebulizer
➤onset in 5 minutes, lasts 3-8 hours
➤equally effective
➤ tablets / syrup available for pediatrics
➤onset in 30 minutes, lasts 4-8 hrs
➤ side effects are bothersome, but transient
Relievers:
anticholinergic

➤ ipratropium bromide
➤may provide added benefit to β 2
agonist
➤ few side effects
Relievers:
methylxanthine

Theophylline :
Bronchodilator
cardiant
diuresis
central stimulant

<1~1.2g/d
Relievers:
systemic steroids
➤ prednisone or prednisolone:
➤2 mg/kg/d
➤IV or PO
➤ generally continue for 5 days
➤simultaneously initiate inhaled steroid
➤Usually <10-14d
➤no need to taper systemic steroids
Controllers:
inhaled steroids

➤ must be scheduled
➤ takes 4 to 5 days to see benefit
➤ minimal systemic adverse effects
Controllers:
long-acting β 2 agonist

➤ salmeterol or albuterol
➤ must be scheduled
➤ Incombination with inhaled steroid
for moderate or severe persistent
asthma
LABA bronchodilation antiinflammation ICS
ICS LABA
Controllers:

leukotriene regulator
 zafirlukast
montelukast
methylxanthines
➤sustained release theophylline
Controllers:

mast cell stabilizer


➤ cromolyn or nedocromil
➤ must be scheduled
➤ most useful in patients with:
➤exercise induced
➤associated allergies
➤ few side effects (cough)
Controllers:

systemic steroids
➤2 mg/kg/d (max 60 mg/d)
➤ numerous adverse effects
➤including growth retardation
Management plan for
asthma
➤ classifythe severity of the illness
➤ identify the appropriate regimen that will
maintain control of the illness
➤ review classification and management
plan every 1 to 6 months
➤ gain control as quickly as possible, then
adjust
Mild intermittent
disease
➤ symptoms < 1 / week
➤ nocturnal symptoms < 2 / month
➤ PEF > 80% predicted
➤ PEF variability < 20%

➨reliever: short-acting β 2 agonist PRN


➨controller: none
Mild persistent disease

➤ symptoms > 1 / week (but not daily)


➤ symptoms may affect activity
➤ nocturnal symptoms > 2 / month
➤ PEF > 80% predicted
➤ PEF variability = 20% - 30%

➨reliever: short-acting β 2 agonist PRN


➨controller: LD inhaled steroid or mast
cell stabilizer
Moderate persistent
disease
➤ symptoms daily
➤ symptoms affect activity
➤ nocturnal symptoms > 1 / week
➤ require short-acting β 2 agonist daily
➤ PEF 60% - 80% predicted
➤ PEF variability > 30%
➨reliever: short-acting β 2 agonist PRN
➨controller: MD inhaled steroid plus long-
acting bronchodilator
Severe persistent
disease
➤ continuous symptoms
➤ frequent exacerbations
➤ frequent nocturnal symptoms
➤ physical activities limited by asthma
➤ PEF < 60% predicted
➤ PEF variability > 30%
➨reliever: short-acting β 2 agonist PRN
➨controller: HD inhaled steroid plus long-
acting bronchodilator plus systemic
steroids
Thanks