Respiratory Pathophysiology: Asthma.

Doreen Osiako

Kenyatta University.

Introduction

This essay is based on a case study of J.S is a 42-year-old man who lives in the Midwest and is known to be highly allergic to dust and pollen with a history of mild asthma, who was brought to the emergency room when his wheezing was unresponsive to fluticasone/salmeterol(Advair)inhaler. He was unable to lie down and was using accessory muscles to breathe hence started on 4litres of oxygen by nasal cannula and intravenous D5W at 75ml/hr. he appeared to be anxious and reports to have a shortage of breath. Arterial blood gas levels were as follows;

            pH = 7.31

            HCO3=26

            PaO2=55

The vital signs recorded were;

Blood pressure= 152/84

Heart rate=124beats per minute

Respiratory rate=42

Temperature=100.4° F

Pathophysiology

Asthma is a chronic inflammatory disease of the respiratory tract that results from bronchial hyperresponsiveness, airway inflammation, and reversible airflow obstruction (Webley C, Hahn L, 2017) This results in symptoms of wheezing, chest tightness, shortness of breath and cough. Inflammation results from airway edema and increased mucus secretion thereby contributing to airway obstruction. Principal cells involved are mast cells, eosinophils, epithelial cells, macrophages, and activated T lymphocytes, which help in the regulation through the release of cytokines. Constituent cells like fibroblast, endothelial cells contribute to the chronicity of the disease. The cell-derived mediators (Morris J., 2019) influence smooth muscle tone, structural changes, and remodeling of the airway. Bronchial hyperresponsiveness (hyperinflation) occurs as a compensation mechanism of airflow obstruction but limited when tidal volume approaches the volume of pulmonary dead space thereby causing a ventilation-perfusion mismatch. Hyperventilation triggered by hypoxia causes a decrease in the alveolar pressure of carbon(IV)oxide. Later increased work of breathing, oxygen consumption, and cardiac output results in metabolic acidosis (MorrisJ.2019).

Etiology

A definitive cause is unknown but can result from several factors. These risk factors are:

            Environmental allergens exposure such as house dust mites, plant pollen, animal allergen, and fungi.

Infections and infestations such as chronic sinusitis, Human Immunodeficiency Virus, virus infections (Respiratory Syncytial Virus)

            Tobacco smoking

Occupational exposures

Irritants such as house spray, smoke.

Drugs such as aspirin, non-steroidal inflammatory drugs, beta-adrenergic receptor blockers.

Combinations of these factors result in asthma that has varied subtypes may be allergic versus non-allergic asthma, late versus early-onset asthma, exercise-induced asthma, nocturnal asthma, and asthma with the prominent symptom of cough.

Clinical manifestation

Patient J.S presented with the following; Wheezing,

            Shortness of breath evidenced by the use of accessory muscles to breath and tachypnea of 42 breaths per minute.

            Chest tightness.

Other features are a cough that is non-productive and worse at night and recurrent croup or chest rattling.

Diagnosis

Diagnosis is done through the following ways:

            Detailed history consisting of the predisposing factors, family history, social history, physical examination, and systemic review of the respiratory tract.

            Laboratory investigations that entail lung function test (spirometer), arterial blood gas, complete blood count.

            Imaging studies; chest radiograph that shows hyperinflation.

Treatment

Management consists of supportive treatment and definitive or pharmacological treatment. Supportive therapy includes patient education, eliminating exposure to the allergen, administration of oxygen, and intravenous fluids. According to the 2019 global initiative for Asthma (GINA), severity is categorized as mild (well-controlled and requires reliever medication), moderate (well controlled with low dose inhaled corticosteroid) and severe (high dose inhaled corticosteroid with long-acting beta 2 agonists) treated using reliever drugs and controller dugs. Reliever medications include short-acting inhaled beta-agonist (SABA), low dose inhaled corticosteroids (ICS), and short-acting anticholinergic. Controller drugs are ICS, long-acting beta-agonist (LABA), leukotriene, longa acting anticholinergic, anti-IgE. The stepwise approach is as follows, step 1; as needed low dose ICS. Step 2; daily low dose ICS. Step 3; low dose ICS/LABA. Step 4; medium dose ICS-LABA, add on tiotropium. Step 5; high dose ICS-LABA with tiotropium or anti-IgE. The mediation can either be stepped up or down according to individual patient management while being monitored closely and frequently.

Reference list

Global initiative for asthma: Global strategy for asthma management and prevention. (2014). Bethsda, MD: U.S. Dept. of Health and Human Services, Public Health Service.

Michael J Morris, M. (2020, April 29). Asthma. Retrieved August 25, 2020, from https://emedicine.medscape.com/article/296301-overview

.

Webley, W. C., & Hahn, D. L. (2017). Infection-mediated asthma: etiology, mechanisms and treatment options, with focus on Chlamydia pneumoniae and macrolides. Respiratory research18(1), 1-12.

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