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Patho BAIAE

The document describes the pathophysiology of bronchial asthma in acute exacerbation. It involves exposure to allergens triggering the release of immunoglobulin E and mast cell degranulation. This leads to the release of inflammatory chemical mediators like leukotrienes, prostaglandins, and histamine. These mediators cause bronchial constriction, mucus production, edema, and further inflammation resulting in common asthma symptoms like wheezing and shortness of breath.

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Catherine Ann Ea
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0% found this document useful (0 votes)
117 views2 pages

Patho BAIAE

The document describes the pathophysiology of bronchial asthma in acute exacerbation. It involves exposure to allergens triggering the release of immunoglobulin E and mast cell degranulation. This leads to the release of inflammatory chemical mediators like leukotrienes, prostaglandins, and histamine. These mediators cause bronchial constriction, mucus production, edema, and further inflammation resulting in common asthma symptoms like wheezing and shortness of breath.

Uploaded by

Catherine Ann Ea
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
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BRONCHIAL ASTHMA IN ACUTE EXACERBATION PATHOPHYSIOLOGY

Predisposing Factors Gender, Age, Family History, Race Precipitating Factors Viral Respiratory Infections, Allergen Exposure (animal dander, dust, pollen, etc.) Change in Weather, Smoking, Exercise

Exposure to different pathogens

Entry of the allergen

Release of immunoglobulin E (IgE)

Release of different chemical mediators

Mast cell degranulation

Release of the different inflammatory chemical mediators

Leukotrienes

Prostaglandins

Histamine, bradykinin, & other inflammatory mediators

Release of eosinophils (to combat allergen)

Opening of the mucosal inrtracellular junction

Inflammatory process

Mucus production

Increase vascular permeability

Direct stimulation of the vagal efferents

Mucosal edema

Bronchoconstriction

More release of other inflammatory mediators

Decrease ciliary function

Epithelial damage

Further edema

Mucus hypersecretion

Increased airway responsiveness

Wheezing, continuous coughing, feelings of chest tightness

dypnea, moist skin, tachypnea

fatigue, anxiety

View more pathophysiology and schematic diagrams at Nurseslabs.com

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