Bronchial Asthma: Etiology, Pathophysiology, Diagnosis and Management

Review Article

Austin J Pulm Respir Med. 2022; 9(1): 1085.

Bronchial Asthma: Etiology, Pathophysiology, Diagnosis and Management

Bereda G*

Department of Pharmacy, Negelle Health Science College, Guji, Ethiopia

*Corresponding author: Gudisa Bereda, Department of Pharmacy, Negelle Health Science College, Guji, Ethiopia; Email: gudisabareda95@gmail.com; Tel: +251913118492/+1919622717

Received: December 13, 2021; Accepted: January 21, 2022; Published: January 28, 2022

Abstract

Bronchial asthma is a disorder of the airways causing swelling and narrowing; which leads to wheezing, shortness of breath, chest tightness, and coughing. The impact of asthma in children depends on complex interaction between disease severity, reaction of children towards disease, treatment efficiency, social roles, and social environment. Most common asthma triggers of bronchial asthma are dust, animal dander, weather changes, pollution, mold, pollen, respiratory infections, stress, and tobacco smoke. The main pathophysiological characteristics of asthma are inflammation and airway remodeling, which include goblet cell hyperplasia, subepithelial fibrosis, collagen deposition, mucosal gland, hyperplasia, smooth muscle hypertrophy, and changes in the extracellular matrix. Spirometry (test lung function when diagnosing asthma), pulse oximetry (monitors oxygen saturation which used to measure amount of arterial hemoglobin that is combined with oxygen) used for diagnosis bronchial asthma. The goal of asthma treatment is to achieve normal respiratory function, with an absence of symptoms, exacerbations, or adverse effects. The beta 2 agonists are sympathomimetic drugs that produce “selective” activation of beta 2 adrenergic receptors, promote bronchodilation, and thereby relieve bronchospasm. The use of short actin beta 2 agonists as a reliever five or more times daily indicates controller agents need to be increased. Prednisone and prednisolone are preferred glucocorticoids for oral therapy of asthma. Methylxanthines are widely used in the treatment of asthma due its ability to inhibit phosphodiesterase causing bronchodilatation. The adverse effects of theophylline include gastrointestinal symptoms such as nausea and vomiting at initial oral administration. In addition, toxic symptoms may progress to tachycardia and arrhythmia.

Keywords: Bronchial asthma; Diagnosis; Etiology; Pathophysiology; Management

Abbreviations

BA: Bronchial Asthma; CysLT1: Cysteinyl Leukotriene 1; FEV1: Forced Expiratory Volume; GINA: Global Initiative for Asthma; GWA: Genome-Wide Association; HPA: Hypothalamic Pituitary Adrenocortical; ICS: Inhaled Corticosteroids; LABA: Long-Acting B2 Agonist; LAMA: Long-Acting Muscarinic Antagonist; LTRA: Leukotriene Receptor Antagonists; PDEI-5: Phosphodiesterase Inhibitors 5; PEF: Peak Expiratory Flow; QOL: Quality of Life; TGF: Transforming Growth Factor; TH-2: T-Helper Cell 2; SABA: Short- Acting B2 Agonist; SCIT: Specific Subcutaneous Immunotherapy; SNPs: Single Nucleotide Polymorphisms;

Introduction

Bronchial asthma is a chronic inflammatory disease of the respiratory passages, occurring with the participation of mast cells, eosinophils and T-lymphocytes, the release of a large number of inflammatory mediators. Inflammation of the respiratory passages causes their hyperreactivity, bronchial obstruction, and respiratory symptoms [1,2]. Airway obstruction in bronchial asthma is mainly caused by the following four mechanisms: i) contraction of bronchial smooth muscle; ii) edema of the airway walls; iii) mucous plugging of the bronchioles; iv) irreversible changes in the lungs (“remodeling”) [3]. Bronchial asthma is a major public health problem affecting a large number of individuals of all ages. Globally, 100-150 million people suffer from asthma [4]. In general, the prevalence of asthma is higher in developed countries than in developing countries, which is a serious public health problem in all ages [5]. Incidence of asthma in adults is 3.8%/1000 at-risk adults. Incidence of asthma in children is 12.5%/1000 at-risk children, especially among children 0-4 years old, the incidence is 23.4%/1000 children. The World Health Organization recognizes asthma as a major health problem. Asthma can occur at any age but children and young adults are the commonly affected age groups. Both sexes are affected almost equally though slight differences in prevalence between males and females have been reported. Although asthma cannot be ‘‘cured,’’ clinical episodes can largely be prevented and controlled by proper management [6]. The impact of asthma in children depends on complex interaction between disease severity, reaction of children towards disease, treatment efficiency, social roles, and social environment. Bronchial asthma, if a remains uncontrolled during childhood leads to continuous symptoms leading to limitations in physical activities and it can lead to development of chronic obstructive pulmonary disease during the later years of life [7-9]. Long-standing inflammation will damage airways, and induces airway remodelling, entailing subepithelial fibrosis under the basement membrane, smooth muscle hypertrophy, and submucosal gland hyperplasia. This results in intractable asthma, presenting irreversible airflow limitation and persistent airway hyperresponsiveness [10]. The airways of asthmatic individuals are characterized by a T-Helper cell (Th)-2-profile inflammation consisting of an overabundance of eosinophils, mast cells and Th2 lymphocytes. These inflammatory cells release mediators that trigger bronchoconstriction, mucous secretion and, possibly, remodeling. The number of infiltrating leukocytes, such as mast cells, eosinophils, CD8+ and CD45+ T cells, correlates with AHR in patients treated with Inhaled Corticosteroids (ICS). The inflammatory mediators that drive this process include the Th2 cytokines Interleukin (IL)- 4, IL-5, IL-9 and IL-13, Transforming Growth Factor (TGF)-beta, Granulocyte/Macrophage Colony Stimulating Factor (GM-CSF), lipid mediators and histamine. Some of these mediators, such as TGFbeta, IL-11 and IL-17, have potent remodelling properties. Histamine was recently proposed to participate in airway remodelling through increased fibroblast proliferation and connective tissue growth factor production [11-13] (Figure 1).