Case Study Analysis: Asthma Pathophysiology in a 7-Year-Old

This case study focuses on the pathophysiology of asthma, using the subjective observational study of a 7-year-old child, Benji, as an example. It details the chronic lung disorder characterized by airway constriction and inflammation, classifying asthma into atopic and non-atopic types. The paper describes the anatomical structure of the lungs, the role of WBCs (Eosinophils), and the release of chemical mediators that trigger inflammation, leading to bronchospasm and mucus production. It analyzes Benji's symptoms, including coughing, wheezing, and shortness of breath, and explains the physiological mechanisms behind these symptoms. Furthermore, it outlines intervention strategies, including the administration of medications such as Salbutamol, Corticosteroids (Prednisolone), and Ipratropium, detailing their mechanisms of action and effects on the respiratory system. The paper also references relevant literature on asthma and its management.

This paper focusses on the different aspects related to the Pathophysiology of Asthma
concerning the subjective observational study of a 7-year-old child named Benji, who was
diagnosed with this respiratory ailment. Asthma refers to the chronic or persistent lung
degenerative disorder that is characterized by constriction or stenosis and resultant inflammation
of the pathways to the lungs The pathways, that is the Airways generally means the smaller
airways (bronchi and bronchioles).
The problem arises when these airways are subjected to narrowing and consequent
inflammation (Forno, E., & Saglani, Sejal (2019)). Generally, asthma is devoid of any
confirmatory healing or cure, but surely it can be treated by medicines (the relevant medications
are mentioned below). Usually, the thin layer enveloping the respiratory muscles, residing in the
airways, contracts and relaxes to permit the airflow within the lungs (Mondrinos, Lelkes,
Samadikuchaksaraei, Mantalaris, & Polak, Mark, Peter, Ali, Athanasios, Julia J. I. M. 2017).
However, in patients with asthma, these airway muscles get constricted, due to inflammation,
which occurs as a result of the accumulation of unwanted substances. Moreover, this leads to an
obstructed airflow, accompanied by repeated and variant episodes of breathing, coughing, chest
pain, and respiratory distress (Mcfarlane-Parrott, & Atkins, Sally, William C. A. 2016).
From the pathophysiological context, asthma is classified into two types - Atopic
(allergic) and non-atopic (non-allergic). While the former is generally the most common type of
asthma caused due to external reasons (Environmental causes). This type of asthma is caused due
to allergic reactions mediated by IgE Lymphocytes. On the contrary, Non-atopic Asthma is not
so common, and it occurs due to stenosis of respiratory muscles and associated airways resulting
from the stimulation of local IgE, culminating from stress or accumulation of irritant substances
(smoke, dust).

The anatomical structure of the lungs comprises the upper and lower respiratory tract.
The passage of airflow starts from the trachea, which divides into right and left bronchi, and
subsequently, each bronchiole branches into several bronchioles. Each bronchiole then opens
into the air sacs known as Alveoli. Alveoli are the site of the primary gaseous exchange. In
normal conditions, the lumen, the mucous and the sub-mucosal membranes, lamina propria, and
the associated smooth respiratory muscles also play a role in the exchange of respiratory gases.
However, due to the onset of an abnormal condition like asthma, the WBCs (Eosinophils)present
in the epithelial layer underlying the Lamina propria reacts to the entry of any foreign substances
or irritant materials(such as cigarette smoke, dust, allergens). As a result, these leucocytes release
granules full of lyophilic chemical mediators like histamines, leukotriene, prostaglandin, and
platelet-activating factor. This chemically receptive materials, as a sort of defense mechanism,
spill out and degrading lipids, protein, nucleic acid, destroying the primary cell constituents. This
triggers the strong inflammatory reaction in bronchioles walls, resulting in two pathological
scenarios – Firstly, a condition that arises from the difficulty in breathing due to the narrowing of
the airways and relative smooth muscles around the bronchioles. That is why asthma is termed as
chronic obstructive pulmonary disease.
The entire mechanism of the onset of the defense mechanism initiated by the IgE
lymphocytes is carried on by the dendritic cells. These cells present and transport the foreign
bodies (Antigens) to the receptor site of T-lymphocytes. These T-cells then recognizes the
antigens and sends a signal to the B-cells. The B-lymphocytes are antibody-producing cells and
generates IgE. Following this, the IgE-Mast cell complex is formed, which gets attached to the
allergen or antigen. The consequent Antigen-Antibody complex mediates the release of anti-

allergic substance- Hsistamine that ultimately cascades a series of reactions, starting from the
stimulation of the A.N.S. pathway and followed by an increased contractibility of Smooth
respiratory muscles (in Bronchioles). This is again followed by a narrowing of the airways,
which is also known as bronchospasm. This abnormal pathological syndrome is further triggered
by Leukotrienes C4, D4, E4. These pro-inflammatory agents enhance the vascular permeability
and cause mucus production within the airways.
Moreover, increased vascular exchange and dilation of Blood vessels lead to an excessive
influx of E.C.F fluids into the bronchiolar space that causes Edema, ultimately leading to
swelling of the bronchioles. Also, the mucous secreting Goblet cells, present in bronchioles and
epithelial tissue lining the bronchi, causing overproduction of Mucous, which further triggers the
stenosis of the bronchioles and simultaneous reduced and impaired gaseous exchange. The
pathophysiology mentioned above is the reason behind most of the asthma patients suffers from
a chronic cough. Also, it is because of the obstructive airflow through the accumulative mucous
filled airways, which leads to a wheezing sound during an asthma attack.
Another mechanism involves the stimulation of Eosinophil, by the mast cells and
Interleukin-5(a pro-inflammatory agent) that further accelerates the inflammation and damage
caused to the lung tissue. However, the damage becomes irreversible in the case of fibrosis of the
scarred inflamed lung tissues resulting in an impaired process of inhalation and exhalation.
According to the given case study, Benji – the seven-year-old child was symptomized
with coughing, wheezing followed by incoherent speech and shortness of breath(dyspnea). The
repeated and prolonged shortness of breath or Dyspnoea is a pathological condition which arises
from improper inspiration or expiration of respiratory gases into the lungs. This shortness of

breath might be due to the defective functioning of the heart or lungs in conducting the
circulation of oxygenated and deoxygenated blood associated with the gaseous exchange.
Moreover, symptoms like coughing and wheezing were observed in the subject. Wheezing,
which is the primary symptom of asthma, mostly happens due to difficulty in inhalation and
exhalation, resulting from the muscular spasms and the alveolar cells constructed by the over-
accumulation of mucous. The entire process of gaseous exchange gets stalled in asthma patients.
As the oxygen passes through the alveoli or Carbon Di-oxide exits it, the latter gets trapped in
the mucous accumulated alveoli sacs making the blood less oxygenated, This consequently,
reduces the oxygen content in the blood resulting in an immediate reduction in blood P.H. value,
as well as the cumulative onset of respiratory acidosis. Also, as an innate defense mechanism, the
lungs try to exhale the excess carbon-di-oxide and inhale in more oxygen, which ultimately
results in coughing, wheezing, and respiratory distress. And this is the reason why Asthma
people have a higher respiratory rate than normal ones.
As a part of the intervention strategy, it is only feasible through the administration of
medications. The first and foremost drug, which is used for the treatment of asthma, is
Salbutamol. It is a bronchodilator that primarily dilates the contracted bronchioles and reduces
the bronchial muscular spasms. This drug directly affects the sympathetic pathway of the
Autonomic Nervous system (A.N.S.) and thereby the Berta-2 adreno-receptors, which relaxes the
bronchioles. The route of administration of this drug is a mostly intravenous infusion or through
metered-dose inhaler and nebulizer. It takes four to six hours and is absorbed in the lungs and
gastrointestinal tract, followed by metabolism in the liver and excretion through kidneys.
However, improper or inefficient use of this drug dosage can impart adverse effects on health.
Regarding the use of this drug for treating Benji, it can be used as Salbutamol helps to relax the

blocked airways by reducing the mucous overload in alveolar spaces. The butyl group (present in
the tertiary position of the salbutamol structure) also makes it more specific towards Beta-2
receptors, which again, relaxes the stringent bronchial muscles.
Next comes the use of Corticosteroids. These are natural hormones secreted from the
adrenal cortex of the adrenal glands in the kidneys. This hormone is necessary for the normal
functioning of the body. Prednisolone is human-made or synthetic corticosteroids(or Steroids).
The synthetic or human-made forms of this drug are used for the treatment of inflammation-
based ailments, such as rheumatoid arthritis (R.A.), systemic lupus erythematosus, and other
inflammatory conditions. These drugs act as an effective anti-inflammatory agent that curbs the
swelling and pain in joints and other organs. Therefore this drug can antagonize the effect of pro-
inflammatory agents(such as IL-5, Leucotrienes) though they don’t cure the disease but can bring
down the inflammations, which is a primary cause behind the ailment. It is administered via
tablets or liquids. Unlike Salbutanol, this drug is absorbed rapidly after oral administration
within 1 to 3 hours. It is metabolized in the liver, resulting in the formation of primary and active
metabolites which gets converted to inactive glucuronide and sulfate metabolites. These inactive
or secondary metabolites, along with the unmetabolized and unabsorbed drug, are eliminated
through renal excretion. A considerable amount of these drugs are also excreted through feces.
The half-life of this drug is three to four hours.
Ipratropium is another drug in use that directly affects the contractibility and relaxation of
the smooth muscles of the bronchioles. This type of drug antagonizes the action of muscarinic
receptors that triggers excitatory or inhibitory responses of the post-synaptic neurons or muscle
cells through G-proteins(the membrane proteins). Thus, this drug, when administered, inhibits
the formation of G-protein coupled complexes and the resultant hydrolytic action of the enzyme -

phospholipase C, on the cell membrane. This also reduces the production of IP3(Inositol
Phpspate) and D.A.G. that ultimately controls the closure of calcium channels. These closed
ionic channels diminish the calcium-load within the smooth muscle cells. Consequently, this also
brings down the rate of formation of the calcium calmodulin complex. Summatively, greater is
the reduction of the calcium load, the lesser will be the activity of the actin-myosin complex.
This is again cascaded by a light chain kinase enzyme, followed by the activation of the
phosphatase enzyme, myosin phosphate, that converts myosin phosphate enzyme into myosin.
This myosin ultimately complexes with actin, but the drug effectively reduces the rate of this
complex formation. As a result, smooth. Its muscles of the bronchioles undergo relaxation that
reduces the spasms ad distress as well. This drug is comparatively more active but poorly
absorbed agent, unlike the other two kinds.
Absorption
Distribution
Metabolism
Excretion

References:
Forno, E., & Saglani, Sejal. (2019). Severe asthma in children and adolescents : Mechanisms and
management (1st ed. 2019. ed.).
Mondrinos, Lelkes, Samadikuchaksaraei, Mantalaris, & Polak, Mark, Peter, Ali, Athanasios,
Julia J. I. M. (2017). Lungs. 1561-1577
Mcfarlane-Parrott, & Atkins, Sally, William C. A. (2016). Lungs. 2009-2016

.