Pathophysiology Health care

Running head: HEALTHCARE
Pathophysiology
Name of the Student
Name of the University
Author Note

HEALTHCARE1
Pathophysiology- The case study involves a five year old girl Jessica, who had been
admitted to the Emergency Department of a hospital, following a sudden asthma attack at
night. She reported shortness of breath and cough initially, and was administered salbutamol
puffer. Nonetheless, after two hours, her situation worsened and she became increasingly
short of breath, with no signs of improvement after salbutamol administration. Therefore, the
major illness in this case that resulted in her hospitalisation is asthma attack. Asthma is
generally defined as a prevalent pulmonary condition that is characterised by inflammation in
the respiratory tract, which in turn results in bronchoconstriction and tightening of the
muscles in the airways. In other words, this variable and heterogeneous inflammatory disease
affects the airways and leads to relapse of symptoms.
The anatomy of human lungs comprises of membranous bronchi, cartilaginous
bronchi, bronchioles and alveolar ducts, which play an important role in exchange of
respiratory gases. The airways of the lungs include basement membrane, mucosa made up of
epithelial cells, and fibrocartilaginous tissues. Cellular elements like mast cells are
responsible for histamine release and the neutrophils, eosinophil, basophils, and macrophages
govern mediator release (Tortora & Derrickson, 2018). The pathophysiology of asthma attack
as involves three components that are inflammation of the airways, hyperresponsiveness of
the bronchioles and intermitted obstruction to airflow. There is mounting evidence for the
fact that inflammation of airway can be subacute, chronic or acute and presence of mucus
secretion and oedema in the airways significantly contribute to bronchial reactivity and
airflow blockade. According to Li et al. (2018) inflammation is generally associated with
neural abnormalities in the noncholinergic and cholinergic bronchopastic tone. Researchers
have identified asthma to be a “T-helper 2 (Th2)-linked disease,” and this is explained by the
generation of immunoglobulin E-mediated activation of mast cells, Th2-type cytokines such
as, interleukin [IL]-4, -13, and release of mediators. Furthermore, an increase in levels of

HEALTHCARE2
prostaglandin D2 and higher proportion of mast cells that are chymase positive have also
been correlated asthma (Sverrild et al., 2016). Airway inflammation can also be explained by
the hygiene hypothesis that highlights the fact that there occurs an imbalance in control of Th
cells, thus casing prolonged domination of cells that bring about allergic response. The
immune system present in an infant remains aligned towards the production of Th2 cytokine,
which mediates allergic inflammation. After birth of an infant, infections result in activation
of the Th1 responses, thereby striking a balance between the Th1/Th2 associations (Zhu et
al., 2016).
Bronchoconstriction in asthma can be explained by the fact that the normal
functioning of bronchus is controlled by a balanced operation of the autonomic nervous
system. There are several afferent nerve endings present in the parasympathetic reflex look
that develop near the bronchus linings (Larson & Jaffe, 2017). Upon stimulation of the
aforementioned nerve endings due to cold air, dust or fumes, there occurs transmission of
nerve impulse to the vagal centre at the brain stem, following which the impulse reaches the
small airways of the bronchus, while passing through the vagal efferent pathway (Khosravi,
Lin & Lee, 2018). This leads to the release of the neurotransmitter acetylcholine from the
efferent nerve endings, which in turn stimulates the production of inositol 1,4,5-trisphosphate
(IP3) in the smooth muscle cells of the bronchus, thereby causing shortening of the muscles
and subsequent bronchoconstriction (André-Grégoire et al., 2018).
It has often been found that hyperinflation acts as a compensation mechanism of
obstruction of airflow. However, this compensation is typically restricted when the tidal
volume becomes near or almost equal to the pulmonary dead space, thereby causing alveolar
hypoventilation (Ostrovskyy et al., 2020). During the early phases, when there occurs a
mismatch in ventilation-perfusion patients generally suffer from hypoxia, thus preventing
hypercarbia by the immediate diffusion of carbon dioxide gas across the capillary membranes

HEALTHCARE3
of the alveoli. In addition, hyperventilation during asthma attack might also get stimulated by
the hypoxic drive that brings about a reduction in the amount of PaCO2. With worsening of
obstruction in the airways and an augmentation in the ventilation-perfusion mismatch, asthma
attack is characterised by retention of carbon dioxide. During the initial phases of an acute
asthma episode, hyperventilation leads to the onset of respiratory alkalosis (Reddi, 2020).
This is soon followed by greater oxygen consumption, high work of breathing, and an
increase cardiac output that eventually causes metabolic acidosis. Asthma attack is also
characterised by sudden respiratory failure that gradually leads to the onset and progress of
respiratory acidosis owing to carbon dioxide retention, with a decrease in alveolar ventilation.
Research evidences have also established a correlation between preterm birth and
asthma in children. A probable mechanism for explaining this correlation is that preterm birth
amid babies is characterised by a deficit in the functioning and structure of the lungs, the
principle respiratory organs, which in turn augments the risk of gradual asthma development
(Zhang et al., 2018). Furthermore, scientists are of the opinion that risk factors that trigger the
onset of eczema in children often progress and lead to development of asthma. Symptoms of
asthma typically get triggered by the production and circulation of thymic stromal
lymphopoietin (TSLP) that is formed from damaged skin (Tidwell & Fowler Jr, 2018). This
compound has the capability of eliciting significant immune response and owing to the
efficacy of the skin in secreting this protein in circulating bloodstream, it travels throughout
the human body. On reaching the lungs, it triggers hypersensitive reactions and causes
asthma. Furthermore, proteins present in pet dander, saliva, urine and skin flakes stimulate
allergic reactions and aggravate symptoms of asthma in several people. This can be further
accredited to the fact that pet hair often collects mold spores, pollen and outdoor allergens, all
of which lead to hypersensitivity (SIJU, 2016). Hence, preterm birth of Jessica, eczema
symptoms and presence of two dogs and a cat triggered her asthma attack.