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The fundamental problem in asthma appears to be immunological: young children in the early stages of asthma show signs of excessive inflammation in their airways. Epidemiological findings give clues as to the pathogenesis : the incidence of asthma seems to be increasing worldwide, and asthma is now very much more common in affluent countries.
Asthma phenotyping and endotyping has emerged as a novel approach to asthma classification inspired by precision medicine which separates the clinical presentations of asthma, or asthma phenotypes, from their underlying causes, or asthma endotypes. The best-supported endotypic distinction is the type 2-high/type 2-low distinction.
Cardiac asthma is the medical condition of intermittent wheezing, coughing, and shortness of breath that is associated with underlying congestive heart failure (CHF). [1] Symptoms of cardiac asthma are related to the heart's inability to effectively and efficiently pump blood in a CHF patient. [ 2 ]
Figure showing the physiological changes in the respiratory tract during an asthma attack upon contact with a trigger. The pathophysiology for asthma mainly involves the inflammatory pathway, associated with several types of immune cells in the body, mainly T helper 2 cells (Th2 cells), B cells and mast cells.
Allergic inflammation is an important pathophysiological feature of several disabilities or medical conditions including allergic asthma, atopic dermatitis, allergic rhinitis and several ocular allergic diseases. Allergic reactions may generally be divided into two components; the early phase reaction, and the late phase reaction.
Bronchospasms can occur for a number of reasons. Lower respiratory tract conditions such as asthma, chronic obstructive pulmonary disease (COPD), and emphysema can result in contraction of the airways. Other causes are side effects of topical decongestants such as oxymetazoline and phenylephrine. Both of these medications activate alpha-1 ...
Overuse of β 2 agonists and asthma treatment without proper inhaled corticosteroid use has been associated with an increased risk of asthma exacerbations and asthma-related hospitalizations. [8] The excipients, in particular sulfite , could contribute to the adverse effects.
Asthma and COPD were once thought of as distinct entities; however, in some, there are clinical features of both asthma and COPD with significant overlap in pathophysiology and symptom profile. It is unclear whether ACO is a separate disease entity or a clinical subtype of asthma and COPD.
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