The Pathophysiology, and Treatment of Asthma

As a child, I didn't like a smoky area, or dusty area, since it made my breathing difficult, but I can bet to say that no one likes a dusty or smoky area because it affects their breathing. That said, I didn't suffer from any respiratory condition, but there are a lot of people who suffer from respiratory conditions, and one of the conditions I will be discussing is Asthma. While I was in School, I had two friends who suffered from asthma. While one can smoke, the other always have an attack when around smoky, or dusty regions.

https://commons.wikimedia.org/wiki/File:Asthma_(Lungs)

Asthma Explained

Asthma is a respiratory disorder that affects both the young and the old, but it is non-communicable. According to the World Health Organization (WHO), about 262 million people have asthma, and in 2019, it caused the death of 455 thousand people. People with asthma usually present clinical symptoms such as shortness of breath (dyspnea), cough, wheezing and chest tightness, in an episodic manner. Asthmatic patients have Bronchial Hyper-Responsiveness, which literally means that their bronchial tree, responds to environmental stimuli and other stimuli that would not affect people who do not suffer from Asthma, as a result of the narrowing of the airways from inflammation.

Pathophysiology of Asthma

Asthma could be exacerbated, triggered, via Atopic or genetic causes, medications such as Aspirin-exacerbated respiratory disease (Samter's Triad), from chemicals, dust, pet hair/dander, common cold, smoke, exercise, and Viral upper respiratory tract infection.

Asthma starts with allergies, triggering the T helper cell type-2 (Th2) immune response in the airway to release cytokines such as interleukin (IL)-4, IL-5, IL-9 and IL-13. The interleukins, when released, act on plasma cells to produce eosinophilic inflammation and IGE antibodies to bind to mast cells. The binding of the mast cells and the IGE antibodies causes the Mast cells to produce inflammatory mediators, histamine, leukotrienes, and cysteinyl. The interleukin (IL)-5 is responsible for the activation of the white blood cell (eosinophil) which releases Leukotrienes and proteases which causes tissue damage to the tissue cells of the bronchiole. These cause bronchoconstriction of the smooth muscle, and the dilation of the capillary, increase in vascular permeability of the airway, and inflammation of the mucosa cell of the bronchial causing increase of mucus in it causing the airway to narrow.

Clinical Features and Diagnosis of Asthma

Asthma patients present symptoms such as cough, chest tightness, shortness of breath, difficulty in speech as a result of shortness of breathing, Use of Accessory muscles while respirating, and wheezing as a result of prolonged expiration. Clinically, in order to identify asthma, microscopic evaluation of sputum (in cases where sputum comes along with cough) is done to identify curschmann spiral, and Charcot-leyden crystals.

Diagnosis of Asthma would include a pulmonary function test (PFT) in symptomatic patients, to help identify the forced vital capacity (FVC), and forced expiratory volume in 1 second (FEV1). Patients with asthma will have low FVC and FEV1. BD bronchodilator which are short-acting beta 2 agonists (SABA), which binds to the smooth muscle of the bronchiole causing it to relax, or Long-acting beta 2-agonists (LABAs) (LABA) can be administered.

In cases where the patient is asymptomatic, a methacholine challenge test is done where methaholine is binds with the muscarinic receptors of the airway, causing broncho constriction where patients with asymptomatic asthma experience spasm. Thereby allowing for tests such as pulmonary function test (PFT) to be performed on the patient.

Treatment of Asthma

Depending on the diagnosis and the frequency of occurrence. In intermittent types of asthma, with occurrence less than twice a week in the daytime, or less than three times at night in a month, short-acting beta 2 agonists (SABA) can be administered. SABA medications include Albutero, and Levalbukol. In mild cases of Asthma, patients have attack more than 2 times in a week in daytime, and more than 4 times at night per month, short-acting beta 2 agonists (SABA) can be administered, as well as a low dose of Inhaled Corticosteroids. The Inhaled Corticosteroids include drugs such as fluticasone, Budenoside, and Mometasone. Inhaled Corticosteroids inhibit the release of cytokines, and reduce inflammation towards the airway. I moderate cases, which are patients with attack frequency up to 7 times a week, and more than once per week at night. Patients are administered SABA annd medium dose of Inhaled Corticosteroids, and Long-acting beta 2-agonists (LABAs). LABA drugs would include Formoterol, and Salmeterol. In severe case, where attack comes almost every other time, medications would include short-acting beta 2 agonists (SABA), Long-acting beta 2-agonists (LABA), and High doses of Inhaled Corticosteroids, and Intravenous Corticosteroids.

Conclusion

Asthma attacks are as a result of bronchospasm, which constricts the airway, Inflammation of the inside lining of the mucosa thereby thickening the mucosa lining, and the producing of excess mucus causing mucus plugs. These cause the physical signs that are noticed as cough, shortness of breath, and wheezing.

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Reference

https://www.who.int/news-room/fact-sheets/detail/asthma

https://www.nhs.uk/conditions/asthma/

https://www.msdmanuals.com/home/lung-and-airway-disorders/asthma/asthma

Pathophysiological Mechanisms of Asthma

National Library of Medicine - Asthma

American Academy of Allergy, Asthma and Immunology: Asthma Overview

Charcot-Leyden Crystals in Eosinophilic Inflammation: Active Cytolysis Leads to Crystal Formation

Section 2, Definition, Pathophysiology and Pathogenesis of Asthma, and Natural History of Asthma

Inhaled Corticosteroids