Lecture notes
asthma
- Module
- Core Body systems
- Institution
- University Of Leeds (UoL)
Lecture notes of 6 pages for the course Core Body systems at UoL
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Acute AsthmaStatus Asthmaticus
What is it?
evere asthma that does not respond well
An acute, severe asthma attack that doesn't to immediate care and is a life-threatening
respond to usual use of inhaled bronchodilators medical emergency. Ensuing respiratory
and is associated with symptoms of potential failure results in hypoxia, carbon dioxide
respiratory failure is called status asthmaticus retention and acidosis. The exact
mechanism underlying the development
How common is it? of an acute severe asthma attack remains
elusive but there appear to be two
There were over 79,800 emergency hospital phenotypes:
admissions for asthma in the UK in 2008-2009.
Of these, 30,740 were children aged 14 years or Gradual onset- in about 80%
under. severe attacks develop more
than 48 hours
There were 1,131 deaths from asthma in the UK Sudden onset- often in
in 2009 (12 were children aged 14 years or association with significant
under). allergen exposure
An estimated 75% of admissions for asthma are avoidable and as many as 90%
of the deaths from asthma are thought to be preventable.
Pathopysiology behind the process
The pathophysiology of asthma is complex and involves the following
components:
• Airway inflammation
• Intermittent airflow obstruction
• Bronchial hyperresponsiveness
Airway inflammation
The mechanism of inflammation in asthma may be acute, subacute, or
chronic, and the presence of airway edema and mucus secretion also
contributes to airflow obstruction and bronchial reactivity. Varying degrees of
mononuclear cell and eosinophil infiltration, mucus hypersecretion,
desquamation of the epithelium, smooth muscle hyperplasia, and airway
remodeling are present.[3] See the image below.
,Asthma treatment. Asthma causes and symptoms. Antigen presentation by the dendritic cell
with the lymphocyte and cytokine response leading to airway inflammation and asthma
symptoms.
Some of the principal cells identified in airway inflammation include mast cells,
eosinophils, epithelial cells, macrophages, and activated T lymphocytes. T
lymphocytes play an important role in the regulation of airway inflammation
through the release of numerous cytokines. Other constituent airway cells,
such as fibroblasts, endothelial cells, and epithelial cells, contribute to the
chronicity of the disease. Other factors, such as adhesion molecules (eg,
selectins, integrins), are critical in directing the inflammatory changes in the
airway. Finally, cell-derived mediators influence smooth muscle tone and
produce structural changes and remodeling of the airway.
The presence of airway hyperresponsiveness or bronchial hyperreactivity in
asthma is an exaggerated response to numerous exogenous and endogenous
stimuli. The mechanisms involved include direct stimulation of airway smooth
muscle and indirect stimulation by pharmacologically active substances from
mediator-secreting cells such as mast cells or nonmyelinated sensory
neurons. The degree of airway hyperresponsiveness generally correlates with
the clinical severity of asthma.
A study by Balzar et al reported changes in airway resident mast cell
populations from a large group of subjects with asthma and normal control
subjects.[7] A greater proportion of chymase-positive mast cells in the airways
and increased prostaglandin D2 levels were identified as important predictors
of severe asthma as compared with other steroid-treated subjects with
asthma.
, Chronic inflammation of the airways is associated with increased bronchial
hyperresponsiveness, which leads to bronchospasm and typical symptoms of
wheezing, shortness of breath, and coughing after exposure to allergens,
environmental irritants, viruses, cold air, or exercise. In some patients with
chronic asthma, airflow limitation may be only partially reversible because of
airway remodeling (hypertrophy and hyperplasia of smooth muscle,
angiogenesis, and subepithelial fibrosis) that occurs with chronic untreated
disease.
Airway inflammation in asthma may represent a loss of normal balance
between two "opposing" populations of Th lymphocytes. Two types of Th
lymphocytes have been characterized: Th1 and Th2. Th1 cells produce
interleukin (IL)-2 and IFN-α, which are critical in cellular defense mechanisms
in response to infection. Th2, in contrast, generates a family of cytokines (IL-4,
IL-5, IL-6, IL-9, and IL-13) that can mediate allergic inflammation. A study by
Gauvreau et al found that IL-13 has a role in allergen-induced airway
responses.[8]
The current "hygiene hypothesis" of asthma illustrates how this cytokine
imbalance may explain some of the dramatic increases in asthma prevalence
in westernized countries.[9] This hypothesis is based on the concept that the
immune system of the newborn is skewed toward Th2 cytokine generation
(mediators of allergic inflammation). Following birth, environmental stimuli
such as infections activate Th1 responses and bring the Th1/Th2 relationship
to an appropriate balance.
Airflow obstruction
Airflow obstruction can be caused by a variety of changes, including acute
bronchoconstriction, airway edema, chronic mucous plug formation, and
airway remodeling. Acute bronchoconstriction is the consequence of
immunoglobulin E-dependent mediator release upon exposure to
aeroallergens and is the primary component of the early asthmatic response.
Airway edema occurs 6-24 hours following an allergen challenge and is
referred to as the late asthmatic response. Chronic mucous plug formation
consists of an exudate of serum proteins and cell debris that may take weeks
to resolve. Airway remodeling is associated with structural changes due to
long-standing inflammation and may profoundly affect the extent of
reversibility of airway obstruction.[10]
Airway obstruction causes increased resistance to airflow and decreased
expiratory flow rates. These changes lead to a decreased ability to expel air
and may result in hyperinflation. The resulting overdistention helps maintain
airway patency, thereby improving expiratory flow; however, it also alters
pulmonary mechanics and increases the work of breathing.
Bronchial hyperresponsiveness
Hyperinflation compensates for the airflow obstruction, but this compensation
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