Pathophysiology Of Asthma
Pathophysiologyˌ(paTHəˌfizēˈäləjē/)- What happens to the body that creates the condition or illness.
So now that we know what pathophysiology is, let’s talk about the association with asthma. Asthma is a chronic illness of the lungs or more importantly the breathing tubes (bronchial tubes).
Asthma is a common, chronic inflammatory disorder of the airways of the lungs associated with a buildup of inflammatory cells, and characterized by airflow obstruction due to narrowing of the airways and bronchospasm as well as hyper mucus secretion.
The clinical manifestations of asthma include wheezing, coughing, shortness of breath and chest tightness. The risk factors for asthma are a combination of genetic and environmental factors.
Asthma can be triggered by air pollutants – irritants and allergens, medications like aspirin and beta blockers combined occasionally with a predisposition to a type 1 hypersensitivity reaction.
It has no cure, but can be managed with the use of inhaled or intravenous corticosteroids and long-acting Beta antagonists. Asthma has been classified in several ways.
One classification recorded asthma attacks according to the frequency of clinical manifestations, peak expiratory flow rate and forced expiratory volume in one second.
A widely adopted guideline classifies asthma attacks as intermittent asthma, mild persistent asthma, moderate persistent asthma and severe persistent asthma.
Most recently the Global Initiative for Asthma (GINA) simplifies it to three categories: Mild asthma, Moderate Asthma, and Severe asthma, based on the required treatment. Irrespective of classification, here is what we know about the Pathophysiology of asthma.
Pathophysiologic Features Of Asthma
The Pathophysiology of asthma can be best understood when we isolate the features of this chronic disease. Understanding just how much of the severity of a particular attack is due to muscle spasms, airway inflammation with edema or hyper mucus secretion is vital to correct diagnosis and subsequent treatment.
Airway inflammation and obstruction in asthma is mediated by hyperresponsive bronchial smooth muscle, secreted airway glycoproteins and inflammatory debris produced by airway goblet cells and other cells, as well as edema or swelling of the airway wall.
Two principal immune mechanisms lead to airway obstruction in the setting of allergic inflammation, both of which depend on the presence in our lungs of a terminally differentiated subset of T helper cells, the T helper cell type 2.
These cells secrete a highly characteristic cytokine cocktail that includes interleukin-4, interleukin-5, interleukin-9 and interleukin-13, this contribute to the various manifestations of allergy disease and inflammation..
Smooth Muscle Spasms
When you hear about patients dying of status Asthmaticus, those patients typically have a two-fold to three-fold increase of airway smooth muscle, especially in the medium-sized bronchi.
Smooth muscle thickness in asthmatic patients appears to increase with age. It had been proposed that myofibroblasts play a role in this smooth muscle thickening and also in the reticular basement membrane thickening because of the production and deposition of fibronectin in the bronchial mucosa.
The presence of myofibroblasts has been associated with local expression of TGF-Beta produced by eosinophils and fibroblasts; some studies show that basal TGF-Beta 1 levels in the airways are elevated in atopic asthma.
The TGF-Beta 1 is upregulated 24 hours after allergen stimulation. It is thought that these levels increase further in response to allergen exposure.
Airway inflammation together with smooth muscle spasms and hyper mucus secretion has helped us a great deal in understanding the Pathophysiology of asthma.
From experimental models in guinea pigs and rats to human clinical examinations, pulmonology is edging closer and closer to a cure. For now, though, the insights we have into how the three features above affect Pathophysiology and the clinical manifestation of the disease is heartwarming.
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