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2018-2019
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Pathophysiology
• Airway hyper-reactivity (AHR) – the tendency for
airways to narrow excessively in response to triggers
that have little or no effect in normal individuals – is
integral to the diagnosis of asthma and appears to be
related, although not exclusively, to airway
inflammation
6
• The relationship between atopy (the propensity to
produce IgE) and asthma is well established.
Common examples of allergens include house dust
mites, pets such as cats and dogs, pests such as
cockroaches, and fungi. Inhalation of an allergen
into the airway is followed by an early and late-
phase bronchoconstrictor response
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• In cases of aspirin-sensitive asthma, the ingestion
of salicylates results in inhibition of the
cyclooxygenase enzymes, preferentially shunting
the metabolism of arachidonic acid through the
lipoxygenase pathway with resultant production
of the asthmogenic leukotrienes.
10
Clinical Presentation
• Asthma may manifest with different syndromes,
often overlapping
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In the presence of hyperinflated lungs, high pitched
wheezes may be heard more easily over the trachea
than over the lung.
Tracheal auscultation has therefore been advocated
as part of the routine clinical assessment in asthma.
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• CXR Only necessary in severe asthma to
exclude other conditions (e.g., pneumonia,
Pneumothorax , pneumomediastinum, foreign
body).
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Allergic bronchopulmonary
aspergillosis
Allergic bronchopulmonary aspergillosis (ABPA)
occurs as a result of a hypersensitivity reaction to
germinating fungal spores in the airway wall.
The condition may complicate the course of
asthma(1–2%) and cystic fibrosis(5–10%), and is
a recognized cause of pulmonary eosinophilia.
Genetic susceptibility is important.
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• Management
ABPA is generally considered an indication for regular
therapy with low-dose oral corticosteroids
(prednisolone 7.5–10 mg daily), with the aim of
suppressing the immunopathological responses and
preventing progressive tissue damage.
In some patients, itraconazole (400 mg/day) facilitates a
reduction in oral steroids, and a 4-month trial is usually
recommended to assess its efficacy.
Exacerbations, particularly when associated with new
chest X-ray changes, should be treated promptly with
prednisolone 40–60 mg daily and physiotherapy.
If persistent lobar collapse occurs, bronchoscopy (usually
under general anesthetic) should be performed to
remove impacted mucus and ensure prompt re-
inflation.
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68

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L2 3-bronchial asthma

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  • 6. Pathophysiology • Airway hyper-reactivity (AHR) – the tendency for airways to narrow excessively in response to triggers that have little or no effect in normal individuals – is integral to the diagnosis of asthma and appears to be related, although not exclusively, to airway inflammation 6
  • 7. • The relationship between atopy (the propensity to produce IgE) and asthma is well established. Common examples of allergens include house dust mites, pets such as cats and dogs, pests such as cockroaches, and fungi. Inhalation of an allergen into the airway is followed by an early and late- phase bronchoconstrictor response 7
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  • 10. • In cases of aspirin-sensitive asthma, the ingestion of salicylates results in inhibition of the cyclooxygenase enzymes, preferentially shunting the metabolism of arachidonic acid through the lipoxygenase pathway with resultant production of the asthmogenic leukotrienes. 10
  • 11. Clinical Presentation • Asthma may manifest with different syndromes, often overlapping 11
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  • 23. In the presence of hyperinflated lungs, high pitched wheezes may be heard more easily over the trachea than over the lung. Tracheal auscultation has therefore been advocated as part of the routine clinical assessment in asthma. 23
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  • 60. • CXR Only necessary in severe asthma to exclude other conditions (e.g., pneumonia, Pneumothorax , pneumomediastinum, foreign body). 60
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  • 64. Allergic bronchopulmonary aspergillosis Allergic bronchopulmonary aspergillosis (ABPA) occurs as a result of a hypersensitivity reaction to germinating fungal spores in the airway wall. The condition may complicate the course of asthma(1–2%) and cystic fibrosis(5–10%), and is a recognized cause of pulmonary eosinophilia. Genetic susceptibility is important. 64
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  • 67. • Management ABPA is generally considered an indication for regular therapy with low-dose oral corticosteroids (prednisolone 7.5–10 mg daily), with the aim of suppressing the immunopathological responses and preventing progressive tissue damage. In some patients, itraconazole (400 mg/day) facilitates a reduction in oral steroids, and a 4-month trial is usually recommended to assess its efficacy. Exacerbations, particularly when associated with new chest X-ray changes, should be treated promptly with prednisolone 40–60 mg daily and physiotherapy. If persistent lobar collapse occurs, bronchoscopy (usually under general anesthetic) should be performed to remove impacted mucus and ensure prompt re- inflation. 67
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