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Asthma Presentation by Ekene

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BRONCHIAL ASTHMA

By
Nwokoye Hilary Ekene
U2017/4710064
083

And
MIEBAKA GOLDEN
PATHOPHYSIOLOGY

The pathophysiology of bronchial


asthma involves complex
interactions between genetic
predisposition, environmental
triggers, airway inflammation,
and bronchial
hyperresponsiveness.
Airway Inflammation:
•Asthma is characterized by chronic inflammation of
the airways, involving infiltration of various
inflammatory cells, including eosinophils, mast cells,
T lymphocytes, and macrophages.
•Exposure to allergens, respiratory viruses,
pollutants, or other triggers leads to the release of
pro-inflammatory mediators, such as histamine,
leukotrienes, prostaglandins, and cytokines.
•These mediators promote inflammation,
vasodilation, mucous secretion, and recruitment of
inflammatory cells to the airway epithelium and
submucosa.
Bronchial Hyper responsiveness (BHR):
•Individuals with asthma exhibit increased sensitivity
of the airways to various stimuli, leading to
exaggerated bronchoconstriction and airflow
obstruction.
•BHR results from multiple factors, including airway
inflammation, smooth muscle hyper reactivity, altered
neurohumoral regulation, and structural changes in the
airway wall.
•Exposure to triggers such as allergens, cold air,
exercise, or respiratory infections can precipitate
bronchoconstriction and asthma symptoms in
susceptible individuals.
Smooth Muscle Contraction:
•Contraction of bronchial smooth muscle is
a central feature of asthma
pathophysiology, leading to airway
narrowing and obstruction.
•Mediators such as acetylcholine,
histamine, and leukotrienes promote
smooth muscle contraction, while
bronchodilators such as β2-adrenergic
agonists act to counteract this effect.
Airway Remodeling:
•Chronic inflammation and repeated episodes of
bronchoconstriction can lead to structural changes in
the airway wall, collectively termed airway
remodeling.
•Remodeling features include epithelial injury,
subepithelial fibrosis, increased airway smooth muscle
mass, mucous gland hyperplasia, and angiogenesis.
•These changes contribute to fixed airflow
obstruction, reduced responsiveness to
bronchodilators, and progressive decline in lung
function over time.
Immunological Dysregulation:
•Asthma is considered a heterogeneous disorder with
various phenotypes and endotypes, reflecting diverse
underlying immunological mechanisms.
•Type 2 inflammation, characterized by increased
levels of interleukin (IL)-4, IL-5, and IL-13, plays a
central role in allergic asthma driven by allergen
exposure.
•Non-allergic asthma may involve different pathways,
such as innate immune responses, Th1/Th17-mediated
inflammation, or viral-induced exacerbations.
COMPLICATIONS
• Severe asthma attacks that require emergency
treatment or hospital care.
• Permanent decline in lung function.
• Missed school days or falling behind in
schoolwork.
• Poor sleep and fatigue.
• Symptoms that interfere with play, sports or
other activities.

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