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Pathophysiology And Pharmacology - Case Study

   

Added on  2022-08-20

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Running head: PATHOPHYSIOLOGY AND PHARMACOLOGY – CASE STUDY
PATHOPHYSIOLOGY AND PHARMACOLOGY – CASE STUDY
Name of the Student:
Name of the University:
Author note:

PATHOPHYSIOLOGY AND PHARMACOLOGY – CASE STUDY1
Part 1: Pathophysiology
Upper Respiratory Tract Infection
From the given case study, one of the first observations which pave the way for
expounding upon the disease pathophysiology, is Benji’s recent preoccupation with an upper
respiratory tract infection. Upper respiratory tract infections (URTIs) are an acute form of
respiratory disorder which are characterized by both viral or bacterial infiltration and resultant
pathological transmission across the regions of the upper respiratory tract, mainly: the sinus, the
nose, the larynx or the pharynx (Aglipay et al., 2017). In the case of Benji, it is observed that he
has been diagnosed with URTI associated with bacterial etiology. Common bacterial strains
responsible for URTI pathophysiology, include: Streptococcus pyogenes, Staphylococcus aureus,
Haemophilus and Mycoplasma pneumoniae. Such bacterial strains generate URTI disease
pathophysiology via either the inhalation of droplets or via contact if droplets accumulate upon
the hands and the concerned individual uses the same to touch the nose or mouth (Gaarslev, Yee,
Chan, Fletcher-Lartey & Khan, 2016). Streptococcal sp. strains associated of the group A type
have been demonstrated to be transmitted via droplets in the surrounding coupled with prolonged
survival in environments which are dusty and dry (Lewnard et al., 2016). Considering that
Benji’s diagnosis and exacerbation of symptoms have been associated since the time he caught a
cold and specifically after playing soccer, thus demonstrating that the current URTI pathogenesis
is closely related to dust and infected droplet inhalation.
Childhood Asthma
Upon close examination of Benji’s current case presentation, it has been reported by his
mother that he received an asthma diagnosis during the 7 years of age. Childhood asthma is the

PATHOPHYSIOLOGY AND PHARMACOLOGY – CASE STUDY2
name given to a chronic respiratory disorder associated with inflammatory mechanisms
contributing to an obstruction in the respiratory tract (King, James, Harkness & Wark, 2018).
Childhood asthmatic symptoms associated with the allergic type are largely contributed by
inhalation of common, potential allergens like pollen and dust – of which the latter seem to the
most relevant to Benji considering his symptom exacerbation in response to a cold, specifically
after playing soccer (McGeachie et al., 2016). The pathophysiology of atopic or allergic asthma
is facilitated by the inhalation of the above potential allergens which in turn, triggers the
asthmatic processes of pulmonary airway oedema, bronchoconstriction, airway remodelling and
airway hyper responsiveness across organs like the trachea, nasal passage, bronchial tree, lungs
and alveoli (Carpaij, Burgess, Kerstjens, Nawijn & van den Berge, 2019). Due to the inhalation
of allergens like dust by asthmatic children like Benji for a period of 2 hours or more, these
allergens are trapped by dendritic cells which in turn, facilitate antigen digestion in minute
particles followed by their transfer to the lamina propia. This facilitates the production of
immunoglobulin E (IgE) by plasma cells which in turn, causes bronchoconstriction, airway
narrowing and reduced air inhalation. This is due to the binding of IgE with smooth muscle cells
of the airways resulting in development of IgE muscle complex (King, Farrow & Chapman,
2019). Production of IgE characteristic of allergic asthma facilitates the production antigen
across the dendritic cells lining the upper respiratory tract which in turn paves the way for the
production of pro-inflammatory immunological cells like mast cell, eosinophil and lymphocyte
(Craft, Gordon, Huether, McCance & Brashers, 2015) – a key mechanism demonstrating
similarity to the URTI pathophysiology Benji’s current symptomatic presentation and
associated fever. These cells, as a part of immunological defense response stimulate the
production of pro-inflammatory substances like interleukins and cytokines. Eosinophils

PATHOPHYSIOLOGY AND PHARMACOLOGY – CASE STUDY3
specifically attack various sections of the lung to contribute to the secretion of leukotrienes and
resultant airway obstruction. This in turn contribute to secretion of pro-inflammatory bradykinin,
prostaglandins and histamines resulting in smooth muscle constriction and airway obstruction.
Asthma persisting for 12 to 24 hours facilitates interleukin-5 and eosinophil generation which
causes hyperplasia, thickness and vasodilation of airways resulting in mucous accumulation. The
accumulated mucous contributes to airway obstruction and airway epithelial damage (Pelaia et
al., 2019). Thus, the production of these substances, in turn contributes to respiratory tract
inflammation, excretion of mucosal exudate and possible edema and thus, progression of URTI
symptoms of bronchiole clogging, tightening and narrowing of the upper respiratory tract, and
resultant symptoms of wheezing coughing, fever and shortness of breath as observed in Benji
(Yamauchi & Ogasawara, 2019).
Part 2: Signs and Symptoms associated with Disease Pathophysiology
Fever
Upon entry, as evidenced by Regli, Becke and von Ungern-Sternberg (2017), the bacteria
strain undergoes invasion across the nasal mucosal lining and paves the way for destruction of
the lining of epithelial cells and resultant impairment of the ciliary functioning characteristic of
the sinuses present in the upper respiratory tract. The associated destruction facilitates the
immunological response comprising of pro-inflammatory cell funcionng such as lymphocytes,
macrophages and eosinophils which in turn, causes inflammation and redness of the upper
respiratory tract, increased internal temperatures as a consequence of the inflammatory response
and resultant fever – the first notable symptom which has been prevalently observed in Benji.

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