Pathophysiology of Bronchial Asthma - What happens in asthma

Bronchial asthma is a chronic inflammatory disorder of the small airways (bronchioles) associated with airway hyper-reactivity or bronchial hyper responsiveness, characterized by wide-spread but variable obstruction to the air-flow (leading to wheezing, cough, chest tightness and difficulty in breathing), which may be partially or completely reversible for a considerable period (evidenced by recurrent attacks of remissions and exacerbations) with or without specific therapy. This article is aimed at educating the medical professionals and medical students who are keen to learn about the pathophysiology of asthma.

Two main processes are seen in the pathophysiology of asthma in the airways.

1.      Inflammatory reaction

2.      Remodeling

The inflammatory reaction in bronchial asthma is brought about by four types of cells: namely the dendritic cells and macrophages, T-helper lymphocytes, mast cells and eosinophils. Dendritics cells and macrophages present antigens to T-helper cells and induce the switching of B lymphocytes to produce immunoglobulin E (IgE). These cells are influenced by corticosteroids (e.g. – beclamethasone, prednisolone) though beta receptor antagonists have no influence on them.

T helper lymphocyte is the key in the pathogenesis of bronchial asthma. They induce B cells to synthesize and secrete IgE through the production of interleukin 4 (IL-4) and induce eosinophilic inflammation via interleukin 5 (IL-5). T helper cells are also influenced by corticosteroids but not by the beta receptor agonists.

Mast cells contribute to the inflammatory reaction by the production and release of histamine, tryptase, prostaglandin D2 (PGD2) and leukotriene C4 (LTC4). These cells are involved in the early phases of asthma known as the early reaction. Unlike other types of cells mast cell membranes are stabilized by beta receptor agonists (such as salbutamol and terbutaline) and cromones (such as sodium cromoglycate).

Eosinophils are involved in the late phase reaction of bronchial asthma. They are attracted to the bronchial walls by interleukins 3 and 5 (IL-3, IL-5) and the granulocyte monocyte colony stimulating factor (GM-CSF) secreted by the T helper cells. Corticosteroids are effective in decreasing the entry of eosinophils as well as the number of eosinophils in circulation. In addition cortecosteroids prevent activation of eosinophils which have entered the bronchial walls.

Remodeling of the airways occurs when the inflammatory reaction goes on for a long period. Changes are seen to occur in epithelial cells, the basement membrane, smooth muscle cells and the neurons. Epithelial cells are damaged and the cilia are lost making them susceptible for infection by viruses. The number of goblet cells in the epithelium is increased leading to an increase in the secretions. With the loss of cilia, secretions tend to accumulate in the lungs as the normal function of the muco-ciliary escalator is lost. Basement membrane is thickened. Smooth muscle cells undergo division (hyperplasia) and acquire the ability to secrete. In addition, the contractility of the smooth muscles is also increased resulting in airway hyper-responsiveness. Local reflexes are developed due to the modification of the arrangement and synapses of neurons.

When a susceptible individual is exposed to a precipitating factor there can be several responses in the acute stage. These responses are classified as early reaction (immediate asthma), dual phase reaction, late phase reaction and recurrent asthmatic reaction. The early reaction is a result of mast cell activation and gives rise to bronshospasm within minutes of exposure. The response usually peaks within 15-20 minutes and subsides within 1 hour.  As the key cell involved is mast cell there is a good response to salbutamol and cromones. A late phase reaction may occur due to activation of eosinophils occurring 12-24 hours after exposure. Here the response to salbutamol is poor though cortecosteroids are very effective in the treatment as this phase is mediated by eosinophils. Dual phase reaction is the occurrence of the early reaction and the late phase reaction in the same individual. Sometimes the individual may exhibit airway hyper-responsiveness for the subsequent days after the exposure. This is known as the recurrent asthmatic reaction.

When a susceptible individual is exposed to one or more precipitating factors for a long period of time, a response is seen which includes bronchospasm, mucosal oedema and mucus plug formation. This leads to airway obstruction particularly during expiration resulting in decreased flow rates of air during expiration. This leads to trapping of air within the alveoli and hence the lungs leading to hyperinflation of the alveoli and lungs at the expense of proper ventilation. This leads to a ventilation perfusion mismatch in the lungs. Initially the blood gas analysis would show a hypoxaemia with normal or reduced carbon dioxide tensions due to compensatory hyperventilation. However, with the failure of these compensatory mechanisms retention of carbon dioxide occurs, giving rise to a respiratory acidosis.

Understanding of the pathophysiology of asthma is important to understand the disease process and the rationale of the pharmacological management in different situations and phases of asthma in the same individual. This basic knowledge may therefore be used as a foundation to learn the pharmacological management of asthma.

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Comments 7 comments

John Sarkis profile image

John Sarkis 5 years ago from Los Angeles, CA

Very nice hub - you're well versed in medicine....


Nadeeshan301 profile image

Nadeeshan301 5 years ago from Kandy - Sri Lanka Author

Thank you John Sarkis!!


effilnuc 5 years ago from eastern australia

thank you, very handy information, well presented.


Nadeeshan301 profile image

Nadeeshan301 5 years ago from Kandy - Sri Lanka Author

Thank you effilnuc!!


eveowl 5 years ago

Interesting & informative. I take medication for asthma & have been thinking of stopping the meds; There is two I take; One is the preventer and the other is the general Ventolin inhaler which I carry with me at all times.

I was thinking of stopping the preventer as it may not be necessary. I could give it a try & just use the other ventilator when necessary.


culit 5 years ago

it is better not to be drug dependent i suggest the best way is that you avoid those factors that could trigger your asthma attacks.like staying away from those people who smoke or uses perfumes and cologne that so strong....=)


Lugano Mwakipesile 3 years ago

thank 4 your notes,i gained a detailed knowledge on asthma that i failed to comprehend in famous textbooks of medicine i have read,it's my hope that i will be good in treating asthmatic cases once i completed my degree of medicine,and i liked the way you present the materials concisely and God bless you.

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