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Epidemiology
It affects approximately 10-15% of children
and 5-10% of adults
Prevalence is greater in industrialized
countries
Prevalence is increasing world-wide
Pathology of asthma
Infiltration with inflammatory cells (esp.
eosinophils and T-lymphocytes)
Patchy epithelial shedding
Airway smooth muscle thickening
Subepithelial fibrosis
Mucus gland and goblet cell hyperplasia
widespread mucus plugging in fatal asthma
Mechanisms of asthma
Inflammation underlies airway
hyperresponsiveness
The inflammation is of characteristic pattern and it
involves interaction between many inflammatory
cells
This results in the release of multiple
inflammatory mediators
Inflammatory mediators result in
bronchoconstriction, mucus secrition, exudation of
plasma and airway hyperresponsiveness
Types of asthma
Allergic asthma
Intrinsic asthma
Onset in adults
No external inciter is recognized
Often associated with perennial non-allergic
rhinitis
Accounts for approx. 10% of adult asthma
Occupational asthma
Due to exposure to chemical sensitizers at
work
Unrelated to atopic status
Some occur in atopics due to allergen
exposure at work
Asthma of infancy
Recurrent bouts of significant airflow
limitation in small airways from viral
infections
Often remits as child gets older
not associated with atopy
Sometimes called wheezy bronchitis
Clinical features
Symptoms
Triggers
Physical signs
Symptoms
Wheeze-- intermittent, worse on expiration,
chracteristically relieved by an inhaled 2agonist
Cough-- usually unproductive
Chest tightness
SOB
Prodromal symptoms may precede an attack
Triggers
Physical signs
DD in adults
Principles of treatment
Educate patients to develop a partnership in
asthma management
Assess and monitor severity with objective
measurement of lung function
Avoid or control asthma triggers
Establish medication plans for chronic
management
Establish plans for managing exacerbations
Provide regular follow-up care
MEDICATIONS
Steroids
Beta-agonists
Cromolyn
Methylxanthines
Leukotriene modifiers
Anticholinergics
CORTICOSTEROIDS
Proven most effective benefit for chronic
control
Inhaled form preferred
Inhibit inflammatory cell migration and
activation
Decrease airway responsiveness
Reverse beta-receptor down regulation
Improve spirometry
CORTICOSTEROIDS
Side effects include thrush, cough,
dysphonia
Dexamethasone not included
Risks for children and growth suppression
not an issue
Used for any classification
Systemic steroids reserved for severe
CROMYLYN/NEDOCROMIL
Anti-inflammatory effect from blockage of
chloride channels for mast cells
Help inhibit allergy response and exercise
response
Proven to improve improve peak flow and reduce
beta-agonist use
Dosage usually 4 times per day
Safety well known
Less predictable response than corticosteroids
METHYLXANTHINES
? Mechanism but does provide mild
bronchodilation
Not the preferred chronic therapy
Numerous adverse effects, risk of toxicity,
drug interactions, and lab monitoring
LEUKOTRIENE MODIFIERS
Use in children not widely approved
Few side effects-reported liver effects
Drug interactions with theophylline, warfarin,
terfenadine
Oral formulations once daily
Work to decrease leukotrienes and decrease
inflammation
Studies mostly on mild asthma-improves sx and
increase peak flow
STEPWISE APPROACH
Severe Persistent
Moderate Persistent
Anti-inflammatory
Long acting bronchodil.
Mild Persistent
Anti-inflammatory or
Leukotriene mod
Mid Intermittent
No daily medications
Ask patients :
Dose the patients have ;
Reccurent attacks of wheezing
Cough or wheeze at night?
Cough or wheeze after exercise
Cough, wheeze of chest tightness of exposure to
allergens or pollutants
Classive severity of asthma :
Step I : INTERMITTEN
Step II: MILD PERSISTENT
Step III : MODERATE PERSISTENT
Step IV : SEVERE PERSISTENT
SABA
1. QUICK RELIEF
ANTI CHOLENERCKS
SHORTACTING THEOPHYLLIN
ADRENALIN INJECTION
2. LONGTERM PREVENTIVE
- Corticosteroid
- Soding cromoglycate
- Nedocromil
- LABA
- Sustained released theophylline
- Ketotifen