Asthma and Pathophisiological Template Case Study - Essay Example

Case Study Regarding Asthma and a Pathophysiological Template The essay aims address the following objectives: (1) toexplain the process that leads to the structural and functional changes resulting from Jason’s asthma; (2) to explain how four of Jason’s clinical manifestations are related to the structural and functional changes; and (3) to select and discuss two drugs that have been used in the treatment of Jason’s asthma. Case Study Regarding Asthma and a Pathophysiological Template Structural and Functional Changes in Asthma Asthma is a heterogeneous disease process referring to a symptom, an exacerbation or attack, or underlying diseases of the airway characterize by episodic airways inflammation, airways hyperresponsiveness, and mucous hypersecretion (Harver& Kotses, 2010, 19).

Asthma affects 300 million people worldwide with increasing prevalence among children. According to World Health Organization (WHO), approximately 15 million disability-adjusted life-years are lost and 250,000 asthma deaths are reported worldwide with 500, 000 annual hospitalizations in individuals 18 years old and younger (Harver& Kotses, 2010, 19). In order to understand the pathophysiology of asthma, one must first understand the normal physiological process of a normal airway, particularly air exchange in the lungs.

Lungs primary function is to deliver oxygen into the bloodstream and remove carbon dioxide from the blood. In the lungs are small air sacs called alveoli where exchange of gases occur (Harver& Kotses, 2010, 19). The bronchioles, which are classified as smaller tubes are very fragile compared to the larger tubes of the respiratory system such as the trachea as these smaller tubes lacks cartilaginous rings and only have a layer of smooth muscle. As the muscle contracts, airways are extremely narrowed due to the lack of cartilaginous support.

Thus, contraction of the smooth muscles in the lungs may increase airway resistance and diminish airflow (Harver& Kotses, 2010, 19). In addition, there are cells that line the respiratory tract called the respiratory epithelium which vary from hair-like structure cilia and mucus-producing cells, and small blood vessels lying beneath the airway that supplies nutrients to the respiratory epithelium and smooth muscle cells. Asthma is generally categorize as an inflammatory disease in response to triggering stimuli such as allergens, irritants, colds, exercise, and respiratory infections (Harver&Kotses, 2010, 20).

Based on Jason’s history, possible triggering stimuli of asthma exacerbation are history of recurrent cough when he was 6 months old, family history of hay fever and eczema, and history of respiratory infections.Jason’s exposure to triggering stimuli will cause the initial release of inflammatory mediators from bronchial mast cells, epithelial cells, and macrophages and will lead to the activation of other inflammatory cells. This will cause inflammation of the bronchioles and increased secretion of mucus-producing cells which explains Jason’s condition of having cough and runny nose two days prior to admission.

Leak of inflammatory cells will cause edema and the autonomic neural control of airway tone and epithelial integrity will be altered leading to hyperresponsiveness of airways smooth muscles and airway obstruction. Hyperresponsiveness of Jason’s airways smooth muscles has led to clinical manifestations of audible wheezing sound, severe dyspnea, and supraventricular, intercostal, and subcostal retractions. Continuous narrowed airways brought by asthma exacerbation eventually affect oxygen supply to the vital organs of the body especially the brain.

Affectations of Jason’s nervous system includes mental state of being anxious and the ability to respond only in single words. As Jason suffers from asthma, various structural and functional changes may occur such as airway disturbance, filling of mucous plugs in the airways, larger and numerous mucus-producing cells, edematous bronchioles, increasing number of inflammatory cells infiltrating airways, thickened connective tissue, denuded respiratory epithelium, and increased amount of smooth muscles surrounding the airway.

In addition, Jason might be suffering from airway remodelling in which persistent airway inflammation will cause thickened airway walls and larger muscle mass making medication ineffective and the subsequent attacks more severe (Harver& Kotses, 2010, 20). Four Clinical Manifestations and Structural and Functional Changes Jason was admitted to the hospital with clinical manifestation of cough for two days, loud inspiratory and expiratory wheeze, supraventricular, intercostal and subcostal retractions, and severe dyspnea.

Cough is usually the result of the inflammatory response of a patient suffering from asthma. Mononuclear cell and eosinophil infiltrates the bronchioles when surrounding blood vessels leakleading to hypersecretion of mucus-producing cells (Morris, 2011, n.p.). Mucus plug consisting of exudate of cell proteins and debris formed at the respiratory epithelium and obstruct the air flow which explains the manifestation of cough in asthmatic patients. Loud inspiratory and expiratory wheeze heard upon auscultation are brought by chronic inflammation.

In Jason’s medical history, the mother stated that Jayson was admitted twice in the hospital due to respiratory infections. We all know that respiratory infections could cause inflammation and seeing the situation, this has brought the exacerbation of asthma. Chronic inflammation of airways is associated with increased bronchial hyperresponsiveness or bronchospasm and results to the clinical manifestation of wheezing(Morris, 2011, n.p.). Supraventricular, intercostal, and subcostal retraction is linked with airway obstruction.

Due to edema, mucus plug formation, bronchoconstriction, and remodeling, the amount of oxygen entering the lungs diminish and carbon dioxide retention(Morris, 2011, n.p.). Jayson’s costal retractions signal difficulty of breathing as airway obstruction causes increased resistance to airflow and decreased expiratory flow rates. Worsening of airway obstruction will increased oxygen consumption and work of breathing seen as costal retractions. Severe dyspnea results from airway inflammation and obstruction.

As stated earlier, inflammation in asthma causes the release of inflammatory cells such as mucus-producing cells. These immune responses narrow the air passages and diminish the exchange rate of oxygen and carbon dioxide.The same reason applies toairway obstruction which has caused Jayson to be dyspneic because ofnarrowed air passages limited amount of oxygen entering the lungs (Morris, 2011, n.p.) Drug Study Patients with asthma are usually given anti-inflammatory and bronchodilator medications, examples of which are Fluticasone Propionate and Ipratropium Bromide - two of the drugs that were used in treating asthma exacerbation of Jason.

Fluticasone Propionate is classified as an anti-inflammatory steroid with extremely potent vasoconstrictive and anti-inflammatory activity.Fluticasone Propionate is used as a maintenance treatment for asthma in children aged 4-11 and the recommended dose is 50-100 mcg inhaled PO BID (Spratto, 2009, 67). Fluticasone Propionate is the preferred treatment for asthma patient like Jayson to combat inflammation of the bronchioles by inhibiting the accumulation of inflammatory cells such as macrophage and leukocytes to the inflammation site thus, relaxing the bronchioles and reduced airway obstruction of Jayson.

On the other hand, Ipratropium Bromide is a cholinergic blocking drug that antagonizes the action of acetylcholine and leads to bronchodilation by preventing the increase of intracellular levels of cyclic guanosine monophosphate brought by the interaction of acetylcholine and the muscarinic receptors in bronchial smooth muscle. The usual dose for children aged 6 years and older is 168-252 mcg/day(Spratto, 2009, 85). Ipratropium Bromide was used in the case of Jayson to dilate the inflamed and obstructed bronchioles and promote effective gas exchange.

References Harver, A. & Kotses, H. (2010). Asthma: Pathophysiology and Diagnosis. Asthma, Health and Society: A Public Perspective (p. 19-42). New York: Springer Science+Business Media, LLC. Morris, M.J. (2011). In Medscape Reference. Pathophysiology. Retrieved on August 17, 2011, from http://emedicine.medscape.com/article/296301-overview#a0104 Spratto, G.R. (2009). Fluticasone Propionate and Ipratropium Bromide. Nurse’s MiniGuide to Pediatric Drugs (p. 67-85). Florence: Cengage Learning, Inc.