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Asthma

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File:Inhaler girl.png
A young girl with asthma using an inhaler.

Asthma is a chronic inflammatory condition in which the airways develop increased responsiveness to various stimuli. Patients are usually symptom-free until exposed to the stimulus, causing a reversible narrowing of the airways. It is characterized by bronchial hyperresponsiveness (BHR), inflammation, mucus production and intermittent airway obstruction. A person with asthma may experience recurrent episodes of wheezing, shortness of breath, chest tightness, and cough. These episodes often happen in response to a "trigger," such as exposure to an allergen, cold air, exercise, or emotional stress. The symptoms of asthma, which can range from mild to life-threatening, can be controlled with a combination of drugs and lifestyle changes.

Public attention has become focused on asthma recently due to its rapidly increasing prevalence in the developed world, affecting up to 1 in 4 urban children. Susceptibility to asthma can be explained in part by genetic factors, but no clear pattern of inheritance has been found so far. Asthma is a complex disease, influenced by multiple genetic, developmental, and environmental factors, all interacting to produce the overall condition.

Asthma
SpecialtyPulmonology, immunology Edit this on Wikidata


Signs and symptoms

The main symptom of asthma is wheezing, caused by obstruction of the airways. A cough, sometimes with clear sputum, may also be present. The symptoms are variable, often with rapid onset, and are commonly associated with the triggers listed above. Symptoms can be worse during the night or upon waking. Asthma sometimes occurs with acid indigestion, especially amongst older patients.

Signs of asthma are wheezing, rapid breathing, expiratory phase of breathing longer than inspiratory, using accessory muscles of respiration - shown as in-drawing of tissues between ribs and above the sternum and clavicles, over-inflation of the chest, and rhonchi (wheezy noises heard with a stethoscope). During severe attacks, the asthma sufferer can turn blue from lack of oxygen, experience chest pain and even lose consciousness. However, between attacks, a person with asthma may show no symptoms of the disease at all.

Diagnosis

In most cases, the physician can make the diagnosis on the basis of the history of typical symptoms and examination signs. While measurement of airway function is possible for adults, most new cases are diagnosed in children who are unable to perform such tests. Diagnosis in children is based on careful compilation and analysis of the patient's medical history and subsequent improvement with an inhaled bronchodilator medication. Adults may perform peak flow meter testing of diurnal variation and/or measure the reversibility with inhaled bronchodilator medication as being greater than 15%. In making a diagnosis, asthma will be suspected particluarly if the patient has suffers from eczema (suggesting a general atopy condition), or has a family history of asthma.

If the diagnosis is in doubt, or chronic obstructive pulmonary disease is suspected, then more formal pulmonary lung function testing may carried out. Testing lung function at rest (or baseline) and after exercise can be helpful. Very occasionally, specialized tests after inhalation of methacholine, or less commonly histamine, may be performed. Other tests (for example chest X-ray or chest CT scan) may be required to exclude the possibility of other lung diseases after pulmonary function testing has been obtained.

In addition, many people with asthma have allergies. Positive allergy tests support a diagnosis of asthma and may help in identifying avoidable triggers of symptoms. In addition, some people with asthma have been diagnosed with gastroesophageal reflux disease (GERD in US, GORD in UK) and immune related disorders including atopic dermatitis.

Once the diagnosis is made, peak flow meter testing can be used to monitor the severity of the disease.

Pathology

During an asthma episode, inflamed airways react to environmental triggers such as smoke, dust, or pollen. The airways narrow and produce excess mucus, making it difficult to breathe.

In essence, asthma is an inflammatory disorder of the bronchial airways. The hypersensitization of asthma means that "trigger" factors may cause the bronchi to contract into spasm ("asthma attack"). The inflammation resulting from the "attack" leads to narrowing of the airway as well as excess mucus production, which leads to a cough.

Clues to the understanding of the mechanisms causing asthma come from its known risk factors [1],

  • Personal or family history of asthma or atopy
  • Triggers (see below)
  • Prematurity or low birth weight
  • Viral respiratory infection in early childhood
  • Maternal smoking
  • Male sex, for asthma in prepubertal children
  • Female sex, for persistence of asthma into adulthood
  • Reduced occurence in breast fed babies

and typical triggers of asthma attacks include:

Mechanisms

Primary exposure to a foreign antigen, such as pollen or cigarette smoke, can trigger the development of asthmatic symptoms. Once an inhaled antigen becomes trapped in the airway, it is enzymatically degraded into shorter peptides by antigen presenting cells (APCs) such as dendritic cells. APCs take the peptides derived from the antigen, and express them on the cell surface in the binding groove of the class II major histocompatiblity complex (MHC) molecule. Now located on the cell surface, the antigen-MHC complex is presented to T cells, which express a receptor specific for the MHC II peptide.

Presented with the antigen-MHC II complex, T helper 0 (TH0) cells become activated and begin to differentiate into either T helper type 1 (TH1) or T helper type 2 (TH2) cells. The selective differentiation of TH0 cells has profound consequences for the immune system: TH1 cell production leads to cell-mediated immunity, while the production of predominantly TH2 cells provides humoral immunity. The resulting balance of TH1 or TH2 cells is a crucial variable in the development of asthma. Studies indicate that the dominance of the TH2 cell type appears to be necessary for the development of asthma. In one study, mice that lack the ability to create TH1 cells displayed an asthma-like phenotype (Finotto and Glimcher, 2004). The variables that decide TH1 vs. TH2 cell fate are not well understood, but depend on many factors, including childhood exposure to infectious agents and the cytokines elicited by those agents.

One cytokine secreted by TH2 cells, IL-4, combined with the action of other cytokines, induces synthesis of IgE, an allergen-specific antibody, by antigen-stimulated B cells. IgE binds allergens, and then binds receptors on mast cells, basophils, and eosinophils in the airway epithelium. Subsequent exposure of the same antigen to these cells in the airway epithelium initiates the acute phase reaction of asthma. Stimulated mast cells in the airway release preformed granules of mediators such as histamine, eicosanoids, and cytokines. It is these molecules which are responsible for the symptoms of asthma. They affect the mucosa of the airways, increasing mucosal edema, mucus production, smooth muscle constriction, and recruit other immune cells, excacerbating the reaction.

The late phase of an asthmatic reaction is characterized by an influx of inflammatory and immune cells over the next several hours after antigen exposure. These cells, particularly eosinophils, secrete a series of cytokines, leukotrienes, and polypeptides which contribute to hyperresponsiveness, mucus secretion, bronchoconstriction, and sustained inflammation.

Pathogenesis

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. Epidemiology gives clues to the pathogenesis: the incidence of asthma seems to be increasing worldwide; asthma is more common in more affluent countries, and more common in higher socioeconomic groups within countries.

One theory is that asthma is a disease of hygiene. In nature, babies are exposed to bacteria soon after birth, "switching on" the TH1 lymphocyte cells of the immune system which deal with bacterial infection. If this stimulus is insufficient (as perhaps in modern clean environments) then TH2 cells predominate, and asthma and other allergic diseases may develop. This "Hygiene hypothesis" may explain the increase in asthma in affluent populations. The TH2 lymphocytes and eosinophil cells which protect us against parasites and other infectious agents are the same cells responsible for the allergic reaction. In the developed world these parasites are now rarely encountered but the immune response remains and is wrongly triggered in some individuals by certain allergens.

Another theory correlates the rise of asthma with increasing air pollution. Though it is well known that substantial exposures to certain industrial chemicals can cause acute episodes of asthma, it has not been proven that air pollution is responsible for the development of asthma. In Western Europe, most atmospheric pollutants have fallen significantly in the last forty years while the prevalence of asthma has risen.

Treatment

Triggers such as pets and aspirin should be identified and managed. While occasional symptom relievers may be used, a stepwise use of additional preventer medications is often used to control the disease.[2]

Relievers

A typical inhaler.

Symptomatic control of episodes of wheezing and shortness of breath is generally achieved with fast-acting bronchodilators. Ordinarily, these are provided in pocket-sized metered-dose inhalers (MDI). In younger sufferers, who may have difficulty with the coordination necessary to use inhalers, or those with a poor ability to hold their breath for 10 seconds after using an inhaler (generally the elderly), a device called an asthma spacer is used. An asthma spacer is an enclosed plastic cylinder that mixes the medication with air in a simple tube, making it easier for patients to recieve a full dose of the drug (see top image). For a minority of patients with severe asthma, a nebulizer, which provides a larger, continuous dose of drug to the patient, is sometimes needed.

Relievers include:

Long acting relievers

Long acting bronchodilators (LABD) give a 12 hour effect and are used to give a smoothed symptomatic effect during the day (used morning & night). While patients report improved symptom control, they do not replace the need for routine preventers and their slow onset of action means tha short-acting dilators may still be required.

Long acting relievers include:

Preventive

Current treatment protocols recommend an inhaled corticosteroid, which helps to suppress inflammation and reduce the swelling of the lining of the airway, for anyone who has frequent (greater than twice a week) need of relievers or who has severe symptoms. If symptoms persist, additional preventive drugs are added until the patient's asthma is controlled.

Preventive agents include:

Advanced

When an asthma attack is unresponsive to a patient's usual medication, other treatments are available to the physician or hospital:


Prognosis

Asthma prevalence in children has increased since 1980, especially in younger children.

Approximately half of the children that suffer of asthma during their childhood will "grow out" of their symptoms by the time they pass puberty. For those who continue to suffer from mild symptoms, corticosteroids can help most to live their lives with few disabilities.

Epidemiology

Asthma patients mostly present during childhood. The incidence of asthma seems to be increasing worldwide; asthma is more common in affluent countries, and more common in higher socioeconomic groups within countries.

References

  • ^ Diagnosing Childhood Asthma in Primary Care, Patient UK PatientPlus article written for doctors
  • ^ British guideline on the management of asthma - Scottish Intercollegiate Guidelines Network (SIGN) Online Full PDF Summary PDF
  • Asthma Prevention Program of the National Center for Environmental Health Center for Disease Control and Prevention. Asthma At-A-Glance. 1999.
  • Finotto S, Glimcher L. “T cell directives for transcriptional regulation in asthma.” Springer Semin. Immunopathology 2004, 25(3-4):281-94. PMID 15007632.
  • Inwald D, Roland M, Kuitert L, McKenzie SA, Petros A. Oxygen treatment for acute severe asthma. BMJ 2001;323:98-100. PMID 11451788.
  • Jenkins C, Costello J, Hodge L. Systematic review of prevalence of aspirin induced asthma and its implications for clinical practice. BMJ 2004;328:434. PMID 14976098.
  • Lilly CM, “Diversity of asthma: Evolving concepts of pathophysiology and lessons from genetics.” J Allergy Clin Immunol 2005, S526-31. PMID 15806035.
  • Maddox L, Schwartz DA. “The Pathophysiology of Asthma.” Annu. Rev. Med. 2002, 53:477-98. PMID 11818486.
  • Mujica VR, Rao SS. Recognizing atypical manifestations of GERD; asthma, chest pain, and otolaryngologic disorders may be due to reflux. Postgrad Med J 1999;105:53-55. PMID 9924493.

External links

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