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Thursday, April 19, 2007

Asthma (2)

Asthma

Asthma is a disease of the respiratory system in which the airways constrict, become inflamed, and are lined with excessive amounts of mucus, often in response to one or more "triggers," such as exposure to an environmental stimulant (or allergen ), cold air, exercise , or emotional stress. In children, the most common triggers are viral illnesses such as those that cause the common cold. This airway narrowing causes symptoms such as wheezing, shortness of breath , chest tightness, and coughing, which respond to bronchodilators. Between episodes, most patients feel fine.

Asthma - Diagnosis

In most cases, a physician can diagnose asthma on the basis of typical findings in a patient's clinical history and examination. Asthma is strongly suspected if a patient suffers from eczema or other allergic conditions—suggesting a general atopic constitution —or has a family history of asthma. 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 a careful compilation and analysis of the patient's medical history and subsequent improvement with an inhaled bronchodilator medication. In adults, diagnosis can be made with a peak flow meter (which tests airway restriction), looking at both the diurnal variation and any reversibility following inhaled bronchodilator medication .

Testing peak flow at rest (or baseline) and after exercise can be helpful, especially in young asthmatics who may experience only exercise-induced asthma. If the diagnosis is in doubt, a more formal lung function test may be conducted. Once a diagnosis of asthma is made, a patient can use peak flow meter testing to monitor the severity of the disease.

Differential diagnosis

Before diagnosing someone as asthmatic, alternative possibilities should be considered. A physician taking a history should check whether the patient is using any known bronchoconstrictors (substances that cause narrowing of the airways, e.g., certain anti-inflammatory agents or beta-blockers).

Chronic obstructive pulmonary disease , which closely resembles asthma, is correlated with more exposure to cigarette smoke, an older patient, less symptom reversibility after bronchodilator administration (as measured by spirometry ), and decreased likelihood of family history of atopy.

Pulmonary aspiration , whether direct due to dysphagia (swallowing disorder) or indirect (due to acid reflux), can show similar symptoms to asthma. However, with aspiration, fevers might also indicate aspiration pneumonia . Direct aspiration (dysphagia) can be diagnosed by performing a Modified Barium Swallow test and treated with feeding therapy by a qualified speech therapist . If the aspiration is indirect (from acid reflux) then treatment directed at this is indicated.

Only a minority of asthma sufferers have an identifiable allergy trigger. The majority of these triggers can often be identified from the history; for instance, asthmatics with hay fever or pollen allergy will have seasonal symptoms, those with allergies to pets may experience an abatement of symptoms when away from home, and those with occupational asthma may improve during leave from work. Occasionally, allergy tests are warranted and, if positive, may help in identifying avoidable symptom triggers.

After pulmonary function has been measured, radiological tests, such as a chest X-ray or CT scan , may be required to exclude the possibility of other lung diseases. In some people, asthma may be triggered by gastroesophageal reflux disease , which can be treated with suitable antacids . Very occasionally, specialized tests after inhalation of methacholine - or, even less commonly, histamine — may be performed.

Asthma is categorized by the NIH Heart Lung and Blood Institute as falling into one of four categories: mild intermittent, mild persistent, moderate persistent and severe persistent. The diagnosis of "severe persistent asthma" occurs when symptoms are continual with frequent exacerbations and frequent nighttime symptoms, result in limited physical activity and when lung function as measured by PEV or FEV1 tests is less than 60% predicted with PEF variability greater than 30%.


Asthma - Pathophysiology

Bronchoconstriction

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 the result of an abnormal immune response in the bronchial airways. The airways of asthmatics are " hypersensitive " to certain triggers, also known as stimuli. In response to exposure to these triggers, the bronchi (large airways) contract into spasm (an "asthma attack"). Inflammation soon follows, leading to a further narrowing of the airways and excessive mucus production, which leads to coughing and other breathing difficulties.

There are seven categories of stimuli:

  • allergens , typically inhaled, which include waste from common household insects, such as the house dust mite and cockroach , grass pollen , mould spores and pet epithelial cells;
  • medications , including aspirin and ß-adrenergic antagonists (beta blockers);
  • air pollution , such as ozone , nitrogen dioxide , and sulfur dioxide , which is thought to be one of the major reasons for the high prevalence of asthma in urban areas;
  • various industrial compounds and other chemicals, notably sulfites; chlorinated swimming pools generate chloramines —monochloramine (NH 2 Cl), dichloramine (NHCl 2) and trichloramine (NCl 3)—in the air around them, which are known to induce asthma.
  • early childhood infections, especially viral respiratory infections. However, persons of any age can have asthma triggered by colds and other respiratory infections even though their normal stimuli might be from another category (e.g. pollen) and absent at the time of infection.
  • exercise, the effects of which differ somewhat from those of the other triggers; and
  • emotional stress, which is poorly understood as a trigger.

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 asthmatics and non-asthmatics, 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 system cells. In most people, these other immune cells ( T H 0 cells ) "check" and usually ignore the allergen molecules. In asthmatics, however, these cells transform into a different type of cell (T H 2), for reasons that are not well understood. The resultant T H 2 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 an asthmatic inhales the same allergen, these antibodies "recognize" it and activate a humoral response . Inflammation results: chemicals are produced that cause the airways to constrict and release more mucus, and the cell-mediated arm of the immune system is activated. The inflammatory response is responsible for the clinical manifestations of an asthma attack. The following section describes this complex series of events in more detail.

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. 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.

In 1968 Andor Szentivanyi first described The Beta Adrenergic Theory of Asthma; in which blockage of the Beta-2 receptors of pulmonary smooth muscle cells causes asthma. Szentivanyi's Beta Adrenergic Theory is a citation classic [10] and has been cited more times than any other article in the history of the Journal of Allergy.

In 1995 Szentivanyi and colleagues demonstrated that IgE blocks Beta2 receptors. Since overproduction of IgE is central to all atopic diseases, this was a watershed moment in the world of Allergy.

The Beta-Adrenergic Theory has been cited in the scholarship of such noted investigtors as Richard Lockey (former President of The American Academy of Allergy, Asthma, and Immunology), Charles Reed (Chief of Allergy at Mayo Medical School), and Craig Venter (Human Genome Project).

One theory of pathogenesis is that asthma is a disease of hygiene. In nature, babies are exposed to bacteria and other antigens soon after birth, "switching on" the T H 1 lymphocyte cells of the immune system that deal with bacterial infection. If this stimulus is insufficient—as it may be in modern, clean environments—then T H 2 cells predominate, and asthma and other allergic diseases may develop. This " hygiene hypothesis " may explain the increase in asthma in affluent populations. The T H 2 lymphocytes and eosinophil cells that 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 is based on the correlation of air pollution and the incidence of asthma. Although it is well known that substantial exposures to certain industrial chemicals can cause acute asthmatic episodes, it has not been proven that air pollution is responsible for the development of asthma. In Western Europe , most atmospheric pollutants have fallen significantly over the last 40 years, while the prevalence of asthma has risen.

Finally, it has been postulated that some forms of asthma may be related to infection, in particular by Chlamydia pneumoniae . This issue remains controversial, as the relationship is not borne out by meta-analysis of the research. The correlation seems to be not with the onset, but rather with accelerated loss of lung function in adults with new onset of non-atopic asthma. One possible explanation is that some asthmatics may have altered immune response that facilitates long-term chlamydia pneumonia infection.] The response to targeting with macrolide antibiotics has been investigated, but the temporary benefit reported in some studies may reflect just their anti-inflammatory activities rather than their antimicrobic action.

Asthma and Sleep Apnea

It is recognized with increasing frequency, that patients who have both obstructive sleep apnea (OSA) and bronchial asthma, often improve tremendously when the sleep apnea is diagnosed and treated. Individuals who have OSA have repetitive episodes of upper airway closure during sleep. Upper airway clossure results in low arterial oxygen levels and CO 2 retention, both of which stimulate the respiratory center. The patient makes increasingly stronger efforts to breathe, which only worsens the upper airway collapse ("like sucking a thick milkshake through a straw"). When the patient starts arousing and the pharyngeal muscles recover their tone, the airway suddenly opens up, airflow is suddenly restored (manifested as a loud "heroic" gasping breath), during which contents of the oropharynx may be aspirated. If gastro-esophageal reflux disease is present, the patient may have repetitive episodes of acid aspiration, which results in airway inflammation and "irritant-induced" asthma.

Treatment, Epidemiology.

To be continued . . .


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