Pulmonary Embolism Case
The lodging of the thrombus in the pulmonary circulation results in the activation of the sympathetic nervous system. This results in several changes hemodynamically. Foremost, vasodilatation of the pulmonary vessels occurs. Resultantly, the pulmonary artery pressure is decreased (Sarkar, Niranjan, & Banyal, 2017) . Since the patient has suffered an infarction of his lung tissue, there is evidence that blood flow to a segment of his lungs is impeded. The long-term effects of this injury would include surfactant impairment. As a result, the alveoli may collapse (Huether & McCance, 2017). Absorption atelectasis could also ensue. Failure to manage the patient promptly and appropriately could also result in the collateral ventilation of the alveoli (Sarkar, Niranjan, & Banyal, 2017) . Additionally, bronchiectasis could develop.
Asthma Case
In the early asthmatic response, the pulmonary dendritic cells are activated upon the exposure of antigens to the bronchial mucosa. The dendritic cells present the antigens to T-helper (Th) cells, which then differentiate into Th type 2 cells. The release of pro-inflammatory interleukins and cytokines cause the activation of eosinophils and B cells (Huether & McCance, 2017). The B-cells produce antigen-specific immunoglobulin E (IgE) that binds to the surfaces of mast cells. When the IgE antibodies and the antigen cross-link, mast cells are degranulated and pro-inflammatory mediators are released. (Gauvreau, El-Gammal, & O’Byrne, 2015) Resultantly, bronchial capillaries become more permeable following vasodilation. Mucosal edema, bronchospasm, and the hyper-secretion of mucus ensue reducing airway patency. Eosinophils exert direct injury to the tissues and produce noxious neuropeptides than enhance bronchial hyper-responsiveness.
Delegate your assignment to our experts and they will do the rest.
The late asthmatic response occurs 4 to 8 hours after the early response. During the early phase, neutrophils, lymphocytes, and eosinophils are recruited chemotactically. Resultantly, there is pro-inflammatory mediators are produced latently. Therefore, mucus hyper-secretion, bronchospasms, and airway edema are aggravated (Gauvreau, El-Gammal, & O’Byrne, 2015) . The direct injury by eosinophils contributes to the scarring of the airway. Gradually, there is damage to the ciliated epithelial cells with resultant impairment of mucociliary function. Accordingly, mucus and cellular debris plug the airway. In the absence of treatment, the airway is remodeled due to subepithelial fibrosis and smooth muscle hypertrophy (Huether & McCance, 2017).
References
Gauvreau, G. M., El-Gammal, A. I., & O’Byrne, P. M. (2015). Allergen-induced airway responses. European Respiratory Journal , 46 (3), 819–831. https://doi.org/10.1183/13993003.00536-2015
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Elsevier.
Sarkar, M., Niranjan, N., & Banyal, P. (2017). Mechanisms of Hypoxemia. Lung India , 34 (1), 47. https://doi.org/10.4103/0970-2113.197116
