Dec 2, 2024
Topical therapy
Oral therapy
The upper and lower respiratory tract is a continuous passage. From nose to terminal bronchial, there is a simple ciliated columnar epithelium. Any mucosal disease in the nose could potentially involve the terminal bronchial as it is the continuation of the same mucosa. The lingual surface of the epiglottis, the upper surface of the vocal cords, and the anterior commissure do not have the ciliated columnar epithelium or the respiratory epithelium.
Any pathology in the nose can affect the lower airway. The relationship between the upper and lower respiratory tracts is quite evident in rhinitis and asthma. They essentially represent the same ends of the respiratory inflammatory spectrum. An issue in the nose is called rhinitis. If the same issue extends to the lower respiratory tract, it will result in asthma or a lower respiratory disease.
Most patients with asthma also have rhinitis, and treatment of coexisting rhinitis may improve asthma. However, when a patient is treated for any nasal pathology, auscultation of the chest is necessary to look for any rhonchi or wheeze (requiring a stethoscope) better to manage the two ends of the respiratory inflammatory spectrum. It is important to treat both the upper and lower respiratory tract, as it reduces the amount of therapy given or necessary and the amount of exacerbation that happens.
Treatments given through the above-mentioned information and awareness have shown that treatment for rhinitis improves asthma, too. The concept of 'one airway, one disease, and the unified airway' in which the upper and lower airways act as a whole unit has been proposed, with rhinitis and asthma representing manifestations of the same inflammatory process.
Also read: Understanding Objective Voice Evaluation and Acoustic Analysis Techniques
When it comes to the relationship between rhinitis and asthma, it is not just the allergic rhinitis associated with asthma but also the non-allergic rhinitis. The physiological basis is not just allergens or type 1 hypersensitivity reaction, but inflammatory mediators released in the mucosa of the nose leading to inflammation of the lower airways. The primary thing is the release of inflammatory mediators.
Rhinitis has also been observed as an independent, significant risk factor for asthma in both atopic and non-atopic individuals. Examples of diseases which affect the upper and lower
airways.
Bacterial enterotoxins, by acting as a superantigen, may assist in the development and/or add to the severity of asthma and allergic rhinitis. Upper respiratory tract viral infections often associated with the rhinovirus are strongly associated with asthma exacerbation in children as well as adults. Increased airway hyperreactivity and later asthmatic reactions after an allergen challenge are observed in allergic rhinitis patients having experimental induction of upper respiratory tract rhinovirus infection.
Allergens can be bacterial toxins or viral infections and can act on respiratory mucosa, which may result in rhinitis and asthma. The most common precipitant of occupational asthma is
occupational rhinitis. Exposure to wood dust, coal dust, or similar occupational exposure can lead to occupational asthma.
Also read: Management of Deformed Nasal Dorsum
Studies have shown that when the physician has diagnosed allergic rhinitis in infancy, there is a chance of doubling the risk of asthma by 11 years old. Though diagnosed in infancy, lower respiratory tract involvement in this disease typically occurs in later years due to inflammatory mediators causing airway remodeling, eventually leading to asthma.
Allergic rhinitis usually precedes asthma, and it is known as 'The Allergic March'. It is the term used to describe the progression of allergic nasal disease from the upper airway to the lower airway. It is not clear whether allergic rhinitis causes asthma or whether allergic rhinitis is just an earlier clinical manifestation of allergic disease in atopic patients who would in any case develop asthma
The nasal mucosa is highly vascular with an extensive subepithelial capillary and arterial system and venous cavernous sinusoids. In the nose, there are turbinates; the turbinates have blood
vessels or vascularity below the submucosa. Whenever there is an allergen, there is bogginess of the mucosa of the nose. It creates resistance to the flow of air, leading to symptoms of
nasal obstruction. Vascular dilation can result in increased upper airway resistance and subsequent nasal obstruction.
In contrast, bronchoconstriction happens because of the exposure of an allergen, which is not because of the mucosal or submucosal reaction. It is the result of the contraction of airway smooth muscle, which is present from the trachea to the bronchioles, rather than changes in the vasculature. Vasculature is responsible for airway resistance in the upper airway because the allergen acts on the vascularity of the submucosal flexes.
Airways smooth muscle is important in the pathogenesis of asthma not only by causing bronchoconstriction but also may be involved in increased proliferation and the expression and
secretion of a variety of proinflammatory mediators and cytokines.
In patients with both rhinitis and asthma, the degree of inflammation in the upper and lower airways may be different. Patients may have severe disease in the upper airway and
mild disease in the lower airway. So, the severity varies for the upper and lower airways.
Greater eosinophilic inflammation has been found in the bronchi compared to the nose in untreated asthmatic patients with rhinitis. So, when patients are not treated with asthma having rhinitis, there is a higher amount of eosinophilic inflammation in the lower airway in comparison to the upper airway.
Also read: Measurement Of The Nasal Airway
Bronchial inflammation and remodelling are observed in patients with allergic or non-allergic rhinitis. However, it is difficult to interpret if the inflammation is due to the rhinitis alone or is part of the bronchial disease, which is the result of exposure to the allergen irritant. Studies comprising endobronchial allergen challenge tests in patients with allergic rhinitis who never had asthma showed that exposure to allergens was the cause of bronchoconstriction.
Furthermore, the bronchial lavage taken from the patients after the test showed the occurrence of proinflammatory mediators and cytokines along with the recruitment of inflammatory cells.
Endobronchial allergen also induced nasal symptoms and impairment of nasal functions among the patients.
Glucocorticoids are most effective for rhinitis and asthma
Specific immunotherapy
Similarly, omalizumab can also be given to patients with severe symptoms.
The role of treatments is essentially the same for rhinitis or asthma. A little more vigilance is necessary about lower airway symptoms, and never rule out lower airway symptoms when there is an upper airway disease.
Also read: Mucoceles of the Paranasal Sinuses: Causes and Treatment
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