Paper Example on Pathophysiology of Asthma

Paper Type:  Essay
Pages:  6
Wordcount:  1646 Words
Date:  2022-08-18


Asthma is a chronic lung illness in which the bronchioles constrict as a result of oversensitivity. Difficulty in breathing is one of the primary functions of this disease since the bronchioles and bronchi become compressed and inflamed. This paper studies the pathophysiology of asthma by looking at its background and statistics, the anatomy and physiology of the lungs, mechanisms of asthma on the respiratory system, as well as the prevention and treatment measures.

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Background and Statistics

The notion of asthma has changed over the years. Initially, asthma was thought to be an ailment of airway reactivity but is now perceived to be a condition of chronic inflammation of the bronchial walls (Bousquet et al., 2010). For several asthmatic individuals, the illness has its background in early childhood and infancy. Pathological respiratory infections produce episodes of wheezing in the first three years in about fifty percent of the children (Lemanske & Busse, 2010). While some will stop gasping for air, others continue to show persistent signs which can either disintegrate before adolescence or progress into puberty. When it declines, the condition can remain inactive, or the patient might relapse in the future. Symptoms of asthma include tight chests, wheezing and persistent coughs (lasts for more than ten days) (Bousquet et al., 2010). In diagnosis, the physician carries out breathing tests referred to as spirometry, to know if the lungs are in good condition.

Globally, estimations show that around 334 million individuals are currently asthmatic and the mortality rate associated with this disease is at 250, 000 annually. The disease prevalence is still on the rise and is generally estimated to progress by 100 million by 2025 (Bousquet et al., 2010). Individuals from all life spans may have asthma, although the symptoms of the disease are most common in children. In children, asthma is the top cause of chronic illness and accounts for around 10% of the Emergency Room visits for children under fifteen years. It affects as many as ten to twelve percents of US children, and the statistics continue to rise (Bousquet et al., 2010). Asthma can start at any age of an individual's lifespan, although most asthmatic children experience their first symptoms by age five.

Normal Anatomy of the Lungs

The lungs are air-filled organs with a spongy feeling located on the left and right side of the thorax area, with the left side being smaller since it accommodates the heart (Zeeb et al., 2014). In the lungs, the trachea (airway) divides into smaller bronchioles and bronchi that end up in alveoli, where gaseous exchange occurs. The pleurae enclose the lungs and connect it to the mediastinum. It then breaks down into lobes (two on the left and three on the right) supplied by lobar bronchi. The lymphatics, bronchial and pulmonary veins and arteries, and the bronchi all enter and exit the lung through its hilum or root. Each lobe of the lung breaks into a pyramidal bronchopulmonary segment. This segment has the pyramid apex in the hilum where they get a tertiary bronchus, and appropriate blood vessels and gaseous exchange whereby the surrounding membranes provide the lungs with enough space to expand when filled up with air (Zeeb et al., 2014).

Normal Physiology of the Lungs

The physiology of the lungs is the homeostatic regulation of breathing (eupnea) (Zeeb et al., 2014). When the body demands an increase in carbon dioxide and oxygen levels, chemoreceptors will respond these demands and triggers the brain which in turn signals the lungs to adjust to the breathing rate thus increasing the pulmonary ventilation. Pulmonary ventilation is a process whereby there is the gaseous exchange in the lungs. This process is accomplished by muscle contractions and a pressure system which is attained through the protection of the lungs by the pleural membrane (Zeeb et al., 2014). When this membrane entirely seals the lungs, they sustain a slightly lower pressure than that of the lungs at rest. Due to this, air automatically gets into the lungs until the pressure difference is no longer there. When breathing out, the muscles relax, reversing the pressure dynamic, raising the outside lung pressure, and exhales the air until there is equalization of the pressure. The lungs elastic nature helps in reverting the organs to their relaxed position, and the whole process automatically repeats.

Mechanisms of Asthma Pathophysiology

The bronchioles and bronchi have smooth muscles with linings of ciliated cells that push the muscles towards the throat and goblet cells which secrete mucus. Next, to the airways blood supply, there are several mast cells. Once there is stimulation, the mast cells produce several chemical messengers referred to as cytokines, that lead to physiological changes to the bronchioles and bronchi's lining (Lugogo & MacIntyre, 2008). These protein cytokines contribute to capillary permeability, a rise in mucus production, and smooth muscle contraction (Barnes & Drazen, 2002). The airway gets obstructed leading to a wheeze. From this scarce flow of air, the patient becomes fatigued, and their breathing effort becomes weak leading to hypercapnia and hypoxemia. When there is constriction of the bronchial airway by anatomical variations with inflammatory cells and mucus inside the airway lumen, any trigger which raises smooth muscle constriction results in obstruction of the airways.

In asthma, there is infiltration of the trachea with mononuclear cells that are mostly eosinophils and CD4 T cells. Neutrophils, plasma cells, macrophages, and mast cells practically increase in the airways of asthma patients. Activated macrophages, sloughed epithelial cells, eosinophils, lymphocytes, are mixed with mucus in the airway leading to inflammation (Lugogo & MacIntyre, 2008). Smooth muscle mass raises occupying around three times the average area, predominantly due to cell hyperplasia (Barnes & Drazen, 2002). Inflammation of the airway leads to airway obstruction and hyperresponsiveness, that results in wheezing and breathlessness. In the long run, functions of the lung in asthmatic individuals reduce quickly compared to that of healthy individuals, thus showing the progression of the diseases. When the disease is diagnosed, remodeling and inflammation of the airway cannot be treated as cause and effect since they are entwined in their involvement to the condition.


Creating awareness on how to identify symptoms and signs of asthma, optimize environmental controls, and how to use the peak flow meter is the primary prevention strategy. If one is asthmatic, they can stay away from the triggers such as pollen, sprays, strong odors, outdoor and indoor mold, and smoke. Patients should also avoid consuming junk foods, avoid getting a cold, drink plenty of fluids, and engage in regular exercises. Patients are also encouraged to receive vaccinations every year since asthma raises the risk of complications from respiratory illnesses like influenza and pneumonia. Medicine that is prescribed to control inflammation or relieving pain and preventing exacerbation both play a role in preventing chronic asthma attacks and improving general outcomes of the disease (Lugogo & MacIntyre, 2008).


Asthma is a chronic condition that is not curable, although specific treatment options are available to improve the patient's quality of life. Treatment of asthma includes pharmacologic intervention as well as patient awareness concerning their lifestyle changes and avoiding potential allergens. There are two groups of asthma medicines: quick-relief and long-term control remedies. Long-term medicines aid in controlling asthma attacks but are not used in case of an attack. Agents of long-term treatment include theophylline, inhaled corticosteroids, long-acting beta-agonists, and leukotriene modifiers, and (Lugogo & MacIntyre, 2008). Quick-relief medications, on the other hand, control the symptoms of an asthma attack. They are useful for around six hours only and include oral corticosteroids, beta2-agonists, and Atrovent (Lugogo & MacIntyre, 2008).

Clinical Relevance

Understanding the pathophysiology of asthma as a clinical condition characterized by anatomical changes and inflammation of the airways helps in the proper analysis and management of asthmatics. Allergy and IgE-related immunological airways are not successful in fully explaining the heterogeneity and natural history of the illness (Lugogo & MacIntyre, 2008). Clinicians thus ought to be well versed with the intricacy of the cellular system which connects to the pathophysiology of asthma. Knowledge into the pathophysiology of asthma has resulted in establishing diverse phenotypes which select and characterize patients more appropriately for innovative therapeutic interventions, particularly in severe asthma case.


In conclusion, asthma is a remitting, relapsing, chronic, episodic condition which affects the airways of the tracheobronchial structure that is brought about by the airway hyperresponsiveness to some stimuli, high mucus production, and mucosal edema. This results in a triad of persistent wheezing, cough, and paroxysmal dyspnea. Ingestion and inhalation of pollutants and allergens, environmental factors such as chemical and dust, infections, exercises, and exposure to cold weather are risk factors of asthma. For most patients, asthma begins from childhood. The pathophysiology of asthma is variable, redundant, interactive, and complex. Asthmatic exacerbations are usually short-term, resolving either due to pharmacological intervention or simultaneously and the individual is typically free of symptoms between the episodes. Asthma management involves both pharmacological intervention and patient awareness to keep the signs in check.


Barnes, P. J., & Drazen, J. M. (2002). Pathophysiology of asthma. In Asthma and COPD (pp. 343-359). Retrieved from

Bousquet, J., Mantzouranis, E., Cruz, A. A., Ait-Khaled, N., Baena-Cagnani, C. E., Bleecker, E. R., ... & Casale, T. B. (2010). Uniform definition of asthma severity, control, and exacerbations: document presented for the World Health Organization Consultation on Severe Asthma. Journal of Allergy and Clinical Immunology, 126(5), 926-938. Retrieved from

Lemanske Jr, R. F., & Busse, W. W. (2010). Asthma: clinical expression and molecular mechanisms. Journal of Allergy and Clinical Immunology, 125(2), S95-S102. doi:10.1016/j.jaci.2009.10.047

Lugogo, N. L., & MacIntyre, N. R. (2008). Life-threatening asthma: pathophysiology and management. Respiratory Care, 53(6), 726-739. Retrieved from

Zeeb, M., Schnapp, A., Pieper, M. P., & Lammert, E. (2014). Anatomy and Physiology of the Lung. Metabolism of Human Diseases: Organ Physiology and Pathophysiology, 207.

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Paper Example on Pathophysiology of Asthma. (2022, Aug 18). Retrieved from

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