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Asthma is a predisposition to chronic inflammation of the lungs in which the airways (bronchi) are reversibly narrowed. Asthma affects 7% of the population of the United States,[1][2] and 300 million worldwide.[3] During asthma attacks (exacerbations of asthma), the smooth muscle cells in the bronchi constrict, the airways become inflamed and swollen, and breathing becomes difficult.

Asthma causes 4,000 deaths a year in the United States. Medicines such as inhaled short-acting beta-2 agonists may be used to treat acute attacks. Attacks can also be prevented by avoiding triggering factors such as allergens or rapid temperature changes and through drug treatment such as inhaled corticosteroids and then long-acting β2-agonists if necessary.[4][5] Leukotriene antagonists are less effective than corticosteroids, but have no side effects. Monoclonal antibodies, such as mepolizumab andomalizumab, are sometimes effective. Prognosis is good with treatment.

In contrast to chronic obstructive pulmonary disease and chronic bronchitis, the inflammation of asthma is reversible. In contrast to emphysema, asthma affects the bronchi, not the alveoli.

The National Heart, Lung and Blood Institute defines asthma as a common chronic disorder of the airways characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness (bronchospasm), and an underlying inflammation.[6]





Signs and symptoms

Because of the spectrum of severity within the asthma, some people with asthma only rarely experience symptoms, usually in response to triggers, where as other more severe cases may have marked airflow obstruction at all times.

Asthma exists in two states: the steady-state of chronic asthma, and the acute state of an acute asthma exacerbation. The symptoms are different depending on what state the patient is in.

Common symptoms of asthma in a steady-state include: nighttime coughing, shortness of breath with exertion but no dyspnea at rest, a chronic ‘throat-clearing’ type cough, and complaints of a tight feeling in the chest. Severity often correlates to an increase in symptoms. Symptoms can worsen gradually and rather insidiously, up to the point of an acute exacerbation of asthma. It is a common misconception that all people with asthma wheeze—some never wheeze, and their disease may be confused with another Chronic obstructive pulmonary disease such as emphysema or chronic bronchitis.

An acute exacerbation of asthma is commonly referred to as an asthma attack. The cardinal symptoms of an attack are shortness of breath (dyspnea), wheezing and chest tightness.[9] Although the former is often regarded as the primary symptom of asthma,[10] some patients present primarily with coughing, and in the late stages of an attack, air motion may be so impaired that no wheezing may be heard.[11] When present the cough may sometimes produce clear sputum. The onset may be sudden, with a sense of constriction in the chest, breathing becomes difficult, and wheezing occurs (primarily upon expiration, but can be in bothrespiratory phases). It is important to note inspiratory stridor without expiratory wheeze however, as an upper airway obstruction may manifest with symptoms similar to an acute exacerbation of asthma, with stridor instead of wheezing, and will remain unresponsive to bronchodilators.


Bronchial inflammation

The mechanisms behind allergic asthma—i.e., asthma resulting from an immune response to inhaled allergens—are the best understood of the causal factors. In both people with asthma and people who are free of the disease, inhaled allergens that find their way to the inner airways are ingested by a type of cell known as antigen-presenting cells, or APCs. APCs then “present” pieces of the allergen to other immune systemcells. In most people, these other immune cells (TH0 cells) “check” and usually ignore the allergen molecules. In asthma patients, however, these cells transform into a different type of cell (TH2), for reasons that are not well understood.

The resultant TH2 cells activate an important arm of the immune system, known as the humoral immune system. The humoral immune system produces antibodies against the inhaled allergen. Later, when a patient inhales the same allergen, these antibodies “recognize” it and activate a humoral response. Inflammation results: chemicals are produced that cause the wall of the airway to thicken, cells which produce scarring to proliferate and contribute to further ‘airway remodeling’, causes mucus producing cells to grow larger and produce more and thicker mucus, and the cell-mediated arm of the immune system is activated. Inflamed airways are more hyper-reactive, and will be more prone to bronchospasm.

The “hygiene hypothesis” postulates that an imbalance in the regulation of these TH cell types in early life leads to a long-term domination of the cells involved in allergic responses over those involved in fighting infection. The suggestion is that for a child being exposed to microbes early in life, taking fewer antibiotics, living in a large family, and growing up in the country stimulate the TH1 response and reduce the odds of developing asthma.[78]



Acute asthma exacerbation

When an asthma attack is unresponsive to a patient’s usual medication, other treatment options available for emergency management include:[135]



  1. ^ Merck Manual Home Edition
  2. ^ Merck Manual Professional Edition
  3. ^ Asthma, Christopher H. Fanta, N Engl J Med, 360:1002-1014, March 5, 2009
  4. ^ AAAAI article on avoiding asthma symptoms
  5. ^ Section in “The Asthma Sourcebook” discussing air temperature and asthma symptoms
  6. ^ Retrieved March 11, 2009
  7. ^ Lilly CM (2005). “Diversity of asthma: evolving concepts of pathophysiology and lessons from genetics”. J. Allergy Clin. Immunol. 115 (4 Suppl): S526–31. doi:10.1016/j.jaci.2005.01.028PMID 15806035.
  8. a b Yawn, BP (September 2008). “Factors accounting for asthma variability: achieving optimal symptom control for individual patients”Primary Care Respiratory Journal 17 (3): 138–147. doi:10.3132/pcrj.2008.00004PMID 18264646.
  9. ^ Kumar, Vinay; A. N. J., Abbas, Fausto, Aster (2010). Robbins and Cotran Pathologic Basis of Disease (8th ed.). Saunders. p. 688. ISBN 9781416031215.
  10. a b c d e Saunders (2005). “Asthma”. Mason: Murray & Nadel’s Textbook of Respiratory Medicine (Homer A. Boushey Jr. M.D. David B. Corry M.D. John V. Fahy M.D. Esteban G. Burchard M.D. Prescott G. Woodruff M.D. et al. (eds)) (4th ed.). Elsevier.
  11. a b c McFadden ER, Jr (2004). “Asthma”. Harrison’s Principles of Internal Medicine (Kasper DL, Fauci AS, Longo DL, et al. (eds)) (16th ed.). New York: McGraw-Hill. pp. 1508–16.
  12. a b Document on severe acute asthma and emergency management.. Guide for assessment of severity of exacerbation.
  13. ^ Longmore, Murray et al. (2007). Oxford Handbook of Clinical Medicine (7th ed.). Oxford University Press. ISBN 978-0198568377.

January 27, 2010 - Posted by | Blood, Cells, Heart, Lungs


  1. I find many Dr;s find it hard to come out and use the word asthma with children … my now 6 yr old was constanly having bouts of bronchilitis … since the age of two … then when school started her symptoms became more due to the exccesive running around … back to the drs we went all this time only being prescibed predmix liquid … finaly i found a dr … who told me repeated bounts of bronchilitis in children is basicly childrens asthma … she now has 2 puffers plus a liquid predmix …. why didnt they tell me this form the age of 2 till 5 that we struggled if they told me it was asthma .. then i would of treated it as more than just a cold or flu symptoms …

    Comment by Neema Shaw | January 27, 2010 | Reply

    • thanks for the comment. I do wish for the wellness of your daughter until she can run again and enjoy the life of an happy innocent children. Thanks & God bless you all.

      Comment by ardymotos | January 27, 2010 | Reply

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