Asthma: Pathophysiology, Treatment and Education

RUNNING HEAD: ASTHMA 1
ASTHMA
Students name
Institutional affiliation

ASTHMA 2
Introduction
The current paper is a case study analysis of a patient, Tegan Smith, a 6-year-old girl with
asthma. The case study will be analyzed in order to better understand the asthma disease process
and management. The pathophysiology of asthma and treatment in the Australian context will be
discussed. Lastly, the standard asthma education offered to parents and children will be analyzed
in the Australian context.
Type of asthma.
The asthma subtypes are due to the different presentations in different people and depend
on the pathogenesis, age, and occupation and include allergic asthma, non-allergic asthma, cough
variant asthma, occupational asthma, exercise-induced asthma, and nocturnal asthma (Mukherjee
& Zhang, 2011). Tegan Smith has presentation suggestive of allergic asthma. Her symptoms
suggest atopy, a range of conditions including eczema, allergic conjunctivitis, allergic
rhinosinusitis, and asthma (O'Connell, 2014). A symptom suggestive of allergic conjunctivitis is
watery eyes while nasal discharge is highly suggestive of allergic rhinosinusitis (Van Aalderen,
2012). There is a familial history of atopy. Atopy is defined as a genetic predisposition to allergy
and is hereditary (O'Connell, 2014). Tegan’s mother had a history of atopy including symptoms
of nasal polyposis that follows chronic rhinosinusitis, and allergy. Since atopy is hereditary,
Tegan could have inherited her allergic predisposition from her mother. Tegan and her family
moved to the highlands recently and this corresponded to the onset of symptoms. This could be
due to exposure to new allergens for example pollen supporting the idea that it is allergic asthma.
Allergic asthma has environmental triggers including animal dander, pollen and foods (Vernon,
Wiklund, Bell, Dale, & Chapman, 2012).

ASTHMA 3
Pathophysiology of allergic asthma
Asthma is a chronic airway disease characterized by hyperresponsiveness to various
stimuli leading to bronchoconstriction, airway remodeling and symptoms of wheezing and cough
that are related to various environmental triggers (Kumar, Abbas & Aster, 2015). After exposure
to an allergen, the body mounts a Th2 mediated immune response with production of IgE
antibodies (Just et al, 2014). On re-exposure to the same allergens, there is crosslinking of the
antibodies that bind to the surface of mast cells leading to mast cell degranulation with release of
inflammatory mediators and histamine (Kim, Kim, Jeon, & Kim, 2011). This is a common
pathway in most type 1 hypersensitivity reactions of which asthma is one. (Kumar, Abbas &
Aster, 2015). There are two phases of reaction, an early phase, and a late phase. Mast cell
degranulation and release of cytokine drive the early phase with mucosal hyperstimulation
leading to excess mucus production, vessel dilatation and the direct effect of mediators on vagal
receptors causes bronchoconstriction (Kim, Kim, Jeon, & Kim, 2013). The late phase occurs due
to the recruitment of T lymphocytes, neutrophils and eosinophils that will mediate acute and
chronic inflammation (Bogaert et al, 2011). Inflammation in the wall of the respiratory tree leads
to smooth muscle hypertrophy and deposition of collagen with gland hypertrophy. This is termed
airway remodeling (Kumar, Abbas & Aster, 2015). This underlying pathology will present
clinically as wheezing due to blockage of the airflow and cough due to the hyperresponsiveness
of the airway with excess mucus production (Van Aalderen, 2012).
Treatment
The treatment of asthma involves the use of medications in a systematic stepwise manner
with clear regard for the severity of Asthma and symptomatology (Queensland Health, 2015).
The category of asthma according to the symptoms is assessed so medication can be given in a