NUR3101 Primary Health Care

Make a case study that includes the disease and its pathophysiology and that has to be written on a form that is enclosed and all the fields are mandatory to fill in the form. The topic can choose from the Modules 1,2,3,4,5 or 6 and the topics which are covered in modules are as follows:-

1: Cell injury, inflammation, and immunity.

2: Fluids and electrolytes, acids base imbalances and urinary disorders.

3: Cardiovascular and respiratory disorders.

4: Disorders of endocrine function.

5: Gastrointestinal and hepatobiliary alterations.

6: Neoplasia and alterations in nervous function

Answer:

Pathophysiology

Brian Smith is a 7-year-old boy from Queenstown who presented with a seven-day history of wheezing, cough, fatigue, runny nose and watery eyes. The symptoms began shortly after relocation to Queenstown from Christchurch.  He has no history of similar complaints although he has a family history of allergy as his mother had atopic dermatitis, rhinosinusitis, and nasal polyposis. On presentation, he was increasingly dyspnoeic and agitated. His respiratory rate was raised at 35 breathes per minute and the heart rate was increased at 125 beats per minute. His other vitals were however within normal. He was assessed with the impression of an acute asthmatic attack. He was admitted for management and observation immediately after. He was put on oxygen by mask and nebulized salbutamol on admission and put on 1mg/kg prednisolone for three days. He was discharged later that day with discharge medication including salbutamol reliever via a nebulized inhaler and an inhaled corticosteroid.

Asthma is a chronic disease of airways with the following as the main pathologic mechanisms: hyperresponsiveness to various stimuli in the environment leading to bronchoconstriction, manifestations of wheezing and cough that are related to various environmental triggers and airway remodeling (Kumar, Abbas & Aster, 2015). The main characterizing pathology is chronic inflammation that is present even in the absence of symptoms.

On exposure to an environmental allergen, for example, animal dander, food, pollen or chemicals, the body mounts an immune response to the allergens (Vernon et al., 2012) This is mediated by Th2 with the production of IgE antibodies (Just et al, 2014). Brian has an inherited genetic predisposition to allergy as shown by his mother’s past medical history of atopic dermatitis and rhinosinusitis (Mukherjee & Zhang, 2011). This is defined as atopy and is a genetic predisposition to allergy (O’Connell, 2014). It encompasses a range of conditions including atopic dermatitis, allergic conjunctivitis, allergic rhinosinusitis, and asthma (O’Connell, 2014).  His symptom of watery eyes suggests conjunctivitis while a runny nose is highly suggestive of allergic rhinitis (Van Aalderen, 2012). When re-exposed to the triggering allergens, there is crosslinking of the IgE antibodies on the surface of mast cells leading to degranulation with release of inflammatory mediators and histamine (Kim, Kim, Jeon, & Kim, 2011). This is a common pathway in most type 1 hypersensitivity reactions of which asthma is one (Kumar, Abbas & Aster, 2015). The exposure to new allergens could have occurred due to the family relocating to a new area.

The reaction includes an early and late phase. During the early phase, there is mast cell degranulation that produces mediators leading to vasodilation and mucosal hyperstimulation with excess mucus production. The direct effect of mediators on vagal receptors causes bronchoconstriction (Kim, Kim, Jeon, & Kim, 2013). The bronchoconstriction gives the characteristic wheeze and forced expiration seen in most asthma presentations (National Asthma Control Council of Australia, 2018).

The late phase is due to the recruitment of T lymphocytes, neutrophils, macrophages and eosinophils that will mediate acute and chronic inflammation (Bogaert et al, 2011). This inflammation is driven by a myriad of released chemokines such as eotaxin, Thymus and Activation Regulated Chemokines (TARC), Macrophage-derived chemokines (MDC), Cysteinyl leukotrienes, nitric oxide, prostaglandin D2, histamine, and cytokines such as interleukin 1, 4, 5, 13 and TNF (Kumar, Abbas & Aster, 2015). Inflammation in the wall of the respiratory tree leads to smooth muscle hypertrophy and deposition of collagen with gland hypertrophy. The cells involved include fibroblasts, myofibroblasts, epithelial cells, endothelial cell and smooth muscle cells. This is termed airway remodeling (Kumar, Abbas & Aster, 2015). This adds to the airway narrowing through airway thickening, airway edema, and excessive mucus production. This underlying pathology will present clinically as wheezing due to blockage of the airflow and cough due to the hyperresponsiveness of the airway (Van Aalderen, 2012). The presentation of fatigue is due to increased work of breathing as the child attempts to force air through a constricted airway.

The deranged blood gases are due to the pathologic changes during an asthma attack. The airway obstruction due to the bronchoconstriction leads to a relative hypoxic state that stimulates the respiratory centers leading to hyperventilation. This is the reason for a high respiratory rate seen in the patient. Hyperventilation, consequently, leads to loss of acid in the form of carbon dioxide. This is evidenced by the reduction in partial pressures of carbon dioxide. This then raises the PH leading to a respiratory alkalosis (Johansen et al., 2013).

References

Bogaert, P., Naessens, T., Koker, S. D., Hennuy, B., Hacha, J., Smet, M., . . . Grooten, J. (2011). Inflammatory signatures for eosinophilic vs. neutrophilic allergic pulmonary inflammation reveal critical regulatory checkpoints. American Journal of Physiology-Lung Cellular and Molecular Physiology, 300(5), L679-L690.

Johansen, T., Ejskjær, N., Johansen, P., Kidmose, P., & Dahl, R. (2013). Arterial blood gas levels in asthma: A systematic literature review.

Just, J., Saint-Pierre, P., Gouvis-Echraghi, R., Laoudi, Y., Roufai, L., Momas, I., & Annesi Maesano, I. (2014). Childhood Allergic Asthma Is Not a Single Phenotype. The Journal of Pediatrics, 164(4), 815-820.

Kim, Y. M., Kim, Y. S., Jeon, S. G., & Kim, Y. K. (2013). Immunopathogenesis of Allergic Asthma: More Than the Th2 Hypothesis. Allergy Asthma Immunol Res, 5(4), 189-196.

Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease. (Ninth edition.). Philadelphia, PA: Elsevier/Saunders

Mukherjee, A. B., & Zhang, Z. (2011). Allergic Asthma: Influence of Genetic and Environmental Factors. Journal of Biological Chemistry, 286(38), 32883-32889.

National Asthma Control Council of Australia. (2018). Australian asthma handbook. Melbourne, Australia: National Asthma Council Australia

O’Connell, E. J. (2014). The burden of atopy and asthma in children. Allergy, 59(s78), 7-11.

Royal College of Pathologists Australia (RCPA). (2018). Pathology tests. [online]. Retrieved on 1 may, 2018 from

https://www.rcpa.edu.au/Library/Practising-Pathology/RCPA-Manual/Items/Pathology-Tests

Van Aalderen, W. M. (2012). Childhood Asthma: Diagnosis and Treatment. Scientifica, 2012, 18

Vernon, M. K., Wiklund, I., Bell, J. A., Dale, P., & Chapman, K. R. (2012). What Do We Know about Asthma Triggers? A Review of the Literature. Journal of Asthma, 49(10), 991-998.