2. Definition
chronic inflammatory disease of
airways that is characterized
airflow obstruction,
Bronchial hyperresponsiveness,
and an underlying inflammation process.
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3. Interaction
between these
features determine
the response and
severity of asthma.
Treatment of
asthma targets
these same fetures
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4. Pathophysiology and
Pathogenesis of Asthma
Airflow limitation is recurrent and
caused by a variety of changes in the
airway.
These include:
Bronchoconstriction
Airway oedema
Airway hyperresoponsibility
Airway remodelling
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5. Bronchoconstriction may result from
IgE-dependent release of mediators from mast cells
ie.
histamine,
tryptase,
leukotrienes, and
prostaglandins that directly contract airway smooth
muscle
non-IgE-dependent response also involves mediator
release from airway cells eg. As induced by aspirin
other stimuli
exercise,
cold air,
irritants
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6. As disease becomes more persistent
and progressive other factors limit
outflow
oedema
Inflammation
Mucus hypersecretion
Formation of inspissated mucus plugs
Hypertrophy and hyperplasia of the
airway smooth muscle
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7. Airway hyperresponsiveness
An exaggerated bronchoconstrictor response to
a wide variety of stimuli.
Airway Remodeling
Permanent structural changes may occur in
airways. include
Inflammation
Mucus hypersecretion
Subepithelial fibrosis
Airway smooth muscle hypertrophy
Angiogenesis
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10. Pathogenesis
is a complex, interactive process that
depends on the interplay between
two major factors—
Host factors
Environmental exposures
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12. Host factors
Innate immune system
Genetics
Asthma has an inheritable component
Sex
In early life prevalence of asthma is higher in
boys
At puberty it is higher in girls
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14. Clinical Features
History of any of the following:
Cough, worse particularly at night
Recurrent wheeze
high-pitched whistling sounds when
breathing out—especially in children.
Lack of wheezing and a normal chest
examination do not exclude asthma
Recurrent difficulty in breathing
Recurrent chest tightness
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15. Clinical features continued
Symptoms occur or worsen in the
presence of
Exercise
Viral infection
Animals with fur or hair
House-dust mites (in mattresses, pillows,
upholstered furniture, carpets)
Mold
Smoke (tobacco, wood)
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16. Clinical features continued
Pollen
Changes in weather
Strong emotional expression (laughing or
crying hard)
Airborne chemicals or dusts
Menstrual cycles
Symptoms occur or worsen at night,
awakening the patient.
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17. Physical examination
Hyperexpansion of the thorax,
wheezing during normal breathing,
Chest may be silent in severe cases
Paradoxical pulse
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20. Treatment of acute asthma
OXYGEN
Give high flow oxygen to all patients with
acute severe asthma.
b2 AGONIST BRONCHODILATORS
Inhaler salbutamol
Nebulisation
STEROID THERAPY
Give steroid tablets in adequate doses in all
cases of acute asthma.
parenteral hydrocortisone 400 mg
Continue prednisolone 30 mg daily for ten days
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21. IPRATROPIUM BROMIDE
Nebulised ipratropium bromide (0.5
mg 4-6 hourly) should be added to b2
agonist treatment for patients with
acute severe or life threatening
asthma
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22. INTRAVENOUS MAGNESIUM
SULPHATE
A single dose of IV magnesium sulphate
has been shown to be safe and effective
in acute severe asthma who have not
had a good initial response to treatment
Consider magnesium sulphate in
Acute severe asthma
Life threatening or near fatal asthma
Dose 1.2-2g iv infusion over 20minutes
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23. INTRAVENOUS AMINOPHYLLINE
IV aminophylline (5 mg/kg loading dose over 20
minutes
then infusion of 0.5-0.7 mg/kg/hr).
LEUKOTRIENE RECEPTOR ANTAGONISTS
May be used but no studies have confirmed their
effecacy
ANTIBIOTICS
Routine prescription of antibiotics is not
indicated for acute asthma.
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