Pathophysiology of Asthma and Pneumonia in Pediatric Patients: A Comparative Analysis
Post
Brian seems to have an acute exacerbation of asthma. Asthma is most common in boys prior to adolescence. Also asthma exacerbation triggers are common after bacterial or viral cold infections. Asthma occurs in two phases, an early and late phase. The early phase of asthma occurs upon initial exposure to an irritant or antigen. Antigen exposure to bronchial mucosa attracts T-helper cells to release interleukins.
Interleukins are a protein made by white blood cells. The release of interleukins activates an immune response causing B-lymphocytes to flood the area and create antibodies. Antibodies bind to pathogens in the form of IgE on mast cells. Mast cells release chemical mediators which create cell and tissue injury in an attempt to destroy the pathogen, this process is called degranulation.
Some chemical mediators released are histamine, which causes smooth muscle constriction, and bradykinin which causes vasodilation and bronchoconstriction. At the end of the early phase there is a narrowing of the airway, bronchospasm, mucosal edema, and increased amounts of mucosal secretions along with airway obstruction with extreme cases (Brashers & Heuter, 2020).
The late phase of asthma occurs at least 4-8 hours after initial exposure. In this phase leukotrienes are released, causing prolonged smooth muscle contraction. Eosinophils destroy fibroblasts, which are the cells that create fibrosis tissue. This leads to airway scarring and damage to cilia which eventually causes airway remodeling.
This airway remodeling causes airway obstruction due to the decreased ability of cilia to remove forgien matter and decreased airway compliance. The result is impaired expiration, increased airflow resistance, and uneven distribution of air. These factors are contributing to the patient having tachypnea of 32 breaths a minute, tachycardia, the use of accessory muscles and expiratory wheezes. (Brashers & Heuter, 2020).
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Pneumonia would be ruled out in this scenario because this patient is young and he is at decreased risk of pneumonia compared to older adults. Pneumonia occurs when a bacteria or virus enters the respiratory tract and is unable to be removed by coughing, cilla clearance or alveolar macrophages. Most commonly the signs and symptoms of pneumonia include crackles, productive cough, malaise and dyspnea.
COVID-19 would also be ruled out in this patient because children usually manifested symptoms such as rhinorrhea, headache, and fatigue when diagnosed with COVID-19 (Molteni et al., 2022). No matter the potential diagnosis a chest x ray and labs will need to be obtained. To rule out COVID-19 a respiratory nasal swab is warranted and to actually diagnose asthma a pulmonary function test will be performed with attention on peak flow meter readingsa before and after treatment.
References
Brashers,V.L., & Heuter, S.E. (2020). Alterations of pulmonary function. In S.E. Huether, K.L. McCance, V.L. Brashers & N.S. Rote (Eds.), Understanding pathophysiology (7th ed., pp. 670-696). Elsevier.
Molteni, E., Sudre, C. H., Canas, L. D. S., Bhopal, S. S., Hughes, R. C., Chen, L., Deng, J., Murray, B., Kerfoot, E., Antonelli, M., Graham, M., Kläser, K., May, A., Hu, C., Pujol, J. C., Wolf, J., Hammers, A., Spector, T. D., Ourselin, S., & Modat, M. (2022). Illness Characteristics of COVID-19 in Children Infected with the SARS-CoV-2 Delta Variant. Children, 9(5), 652–N.PAG. https://doi-org.wilkes.idm.oclc.org/10.3390/children9050652
Response
The initial discussion was looking into the pathophysiology of pneumonia and asthma. The student provided good points about the topic of discussion. This reply is just to support the initial discussion and add some new knowledge. As stated by the student, it is indeed true that the early phase of asthma happens upon the initial exposure by the individual to an antigen.
It is also true that the exposure of the antigen to the bronchial mucosa depicts the beginning of asthma complications. According to King et al. (2018), severe asthma remains a global problem and its pathophysiology is not yet fully understood. Asthma involves a complex interplay that occurs between airway remodeling and airway inflammation which leads to airway hyper-responsiveness.
According to King et al. (2018), severe asthma is also associated with a certain extent of fixed airflow limitation. The widespread inflammatory infiltrate and thickening of the airway walls causes a small-sized airway. Consequently, these changes lead to reduced functioning of the lung and excessive, severe airway narrowing due to contraction of smooth muscles, compared to a normal airway or mild asthma (King et al., 2018).
Briefly, the airway can be perceived as a simple elastic tube contained within the elastic lung parenchyma. Airway walls become thick in asthma. Continued thickening of airway walls leads to airway narrowing due to airway smooth muscle (ASM) contraction. Fixed reduction in lung function is significantly variable among asthma individuals.
Reduction in lung functioning due to asthma severity is often tracked from infancy, childhood, and into adulthood (King et al., 2018). Airflow obstruction originates from the utero since reticular basement membrane (RBM) thickening and inflammation are noticeable in wheezy infants. In addition, ASM remodeling has been noticed in preschool children who later develop asthma.
Regarding pneumonia, it is true, as indicated by the student in the initial discussion, that the disease occurs when a virus or bacteria enters the respiratory tract. The most common signs and symptoms of pneumonia include malaise, cough, and others. According to Jain et al. (2022), pneumonia is an umbrella term for syndromes caused by different pathogenic agents that result lead to infections of the lung parenchyma.
Experts have tried to classify pneumonia into different categories based on etiology. These categories include community-acquired pneumonia, hospital-acquired pneumonia, and ventilator-acquired pneumonia (Jain et al., 2022). Pneumonia can affect individuals from all populations.
There is always an intricate balance between organisms living inside the lower respiratory tract and the local and systemic defense mechanisms. When this balance is disturbed, inflammation of the lung parenchyma may occur (Jain et al., 2022). Pathogenesis of pneumonia compromises the defense mechanisms, such as humoral and complement-mediated immunity that is affected in diseases such as common variable immunodeficiency (CVID), functional asplenia (acquired), and X-linked agammaglobulinemia (inherited).
Impaired cell-mediated immunity increases one’s chance of infection by intracellular organisms such as viruses, Pneumocystis pneumonia (PJP), fungal causes, and others (Jain et al., 2022). Other affected defense mechanisms include mucociliary clearance, impaired cough reflex, and accumulation of secretions.
References
Jain, V., Vashisht, R., Gizem Yilmaz, & Bhardwaj, A. (2022). Pneumonia Pathology. https://www.ncbi.nlm.nih.gov/books/NBK526116/
King, G. G., James, A., Harkness, L., & Wark, P. A. (2018). Pathophysiology of severe asthma: We’ve only just started. Respirology, 23(3), 262-271. https://doi.org/10.1111/resp.13251