RESPIRATORY SYSTEM CASE STUDY 2022

Running head: CLINICAL SCENARIO
Clinical scenario
Name of the Student
Name of the University
Author Note

CLINICAL SCENARIO1
Pathophysiology and pharmacology:
Benji is a 11 year old child who has asthma which is demonstrated by chronic
inflammation of the respiratory tract. Benji on admisiion to the hospital showed exacerbation
which describes the continuous wheezing, tightness in the chest, cough and shortness of
breath. These recurrent symptoms ocuur due to reversible blocking of the airway. Asthma can
be triggered by various environmental factors or can be caused by genetic predisposition
(Guarnieri & Balmes, 2014). This allergic response to environmental allergens is mediated by
an immunoglobulin in the body known as IgE. Asthma can further affect the trachea, bronchi
and bronchioles as a result of inflammation of the bronchioles along with constriction in the
airway. Bronchospasm occurs due to bronchoconstriction leading to a number of symptoms.
The respiratory tract of an asthmatic patient is narrower compared to a normal patient due to
thickening and inflammation of the mucosal lining. During the asthmatic attack the smooth
mucles of the on the outside of the respiratory tract contact and the inside airway is shortened
causing breathlessness. Asthma may also increase the secretion of mucus from the mucosal
galnds and cells. This excessive mucus secretion can form mucus plugs which blocks the
upper respiratory tract. Hyperresponsive state in asthma is occurred when the airway is
impaired allowing allergens to enter (Caggiano et al., 2017).
Asthma that occurs is children like in case of Benji is an atopic asthma where
recurrent wheezing occurs due to exposure to specific allergens that include pollens, smoke,
dust, food or certain medications (Bush et al., 2017). When exposure to this triggering agent
occurred, IgE antibodies where secreted in large amounts in the body that further activated
the B-lymphocytes by binding to them causing inflammation. As a response of inflammation,
release of inflammatory mediators occur which include interlukins, chemokines, cytokines
and histamine (Sullivan et al., 2016). Early onset atopic asthma is driven with the help of T-

CLINICAL SCENARIO2
helper 2 cells that produces the interlukin 4, 5 and 1. IL-4 is associated with production of
chemokines from the epithelium of the airways and promotes class switching in B-cell that
further helps in development of the T-helper 2 cell. IL-5 is plays a significant role in
development and survival of eosinophils, another type of leukocyte. Whereas IL-13
contributes in inflammation of the airway and its’ hyperesponsiveness leading to mucus
secretion (Lynn & Kushto-Reese, 2015). Upper respiratory tract infection by bacteria can
also cause exacerbation during asthma as seen in case of Benji who is suffering from cold due
to bacterial infection. His exacerbation has increased after bacterial infection. Infections
caused by atypical bacteria such as Mycoplasma and Chlamydia species can can also act as
allergen in triggering asthma attack and increasing wheezing frequency. Bacteria such as
Haemophilus influenza, Moraxella catarrhalis and Streptococcus pneumonia can enter and
colonize the upper respitatory tract of children and increase the risk of wheezing and
development of childhood asthma. This happens because presence of these pathogenic
organisms reflects the change in the immune system that is followed by altered responses
from the host airways against these pathogens. Similar responses were given by Benji’s
immune system where he showed symptoms of cold that was cough and fever signifying
inflammatory response against bacterial infection of the upper respiratory tract (Darveaux &
Lemanske 2014).
The most important anatomical change that occurs in Benji’s respiratory system due
to asthma is breathlessness. This feeling is termed as dyspnea which is a common symptom
in asthmatic patients. Normal patients take adequate number breaths per minute but in case of
Benji, oxygen saturation was low that is below 92% for which he took more number of
breaths and it states that he has severe asthma (Ww2.health.wa.gov.au, 2020). This happened
because of the blockage in his airways and high lung volume. The shortening of the
respiratory tract and bronchospasm did not allow much of oxygen to enter the lungs through