Asthma
| Asthma | |
| Classification and external resources | |
 peak flow meter | |
| ICD-10 | J45. |
|---|---|
| ICD-9 | 493 |
| OMIM | 600807 |
| DiseasesDB | 1006 |
| MedlinePlus | 000141 |
| eMedicine | med/177 emerg/43 |
| MeSH | C08.127.108 |
Asthma is a chronic inflammation of the lungs in which the airways (bronchi) are reversibly narrowed. Asthma affects 7% of the population,[1][2] and 300 million worldwide.[3] During attacks (exacerbations), the smooth muscle cells in the bronchi constrict, and the airways become inflamed and swollen. Breathing becomes difficult, and asthma causes 4,000 deaths a year in the U.S. Attacks can be prevented by avoiding triggering factors and by drug treatment. Drugs are used for acute attacks, commonly inhaled β2-agonists. In more serious cases, drugs are used for long-term prevention, starting with inhaled corticosteroids, and then long-acting β2-agonists if necessary. Leukotriene antagonists are less effective than corticosteroids but have no side effects. Monoclonal antibodies such as mepolizumab and omalizumab 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.[4]
Public attention in the developed world has recently focused on asthma because of its rapidly increasing prevalence, affecting up to one in four urban children.[5]
Contents
|
Classification
Asthma is classified according to the frequency of symptoms, FEV1 and peak expiratory flow rate.[6]
| Severity | Symptom frequency | Nighttime symptoms | Peak expiratory flow rate or FEV1 of predicted | Variability of peak expiratory flow rate or FEV1 |
|---|---|---|---|---|
| Intermittent | <> | ≤ twice per month | ≥ 80% predicted | <> |
| Mild persistent | > once per week but <> | > twice per month | ≥ 80% predicted | 20–30% |
| Moderate persistent | Daily | > once per week | 60–80% predicted | > 30% |
| Severe persistent | Daily | Frequent | <> | > 30% |
Signs and symptoms
Because of the spectrum of severity within 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.[7] Although the former is "often regarded as the sine qua non of asthma.[8] 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.[9] 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 both respiratory 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.
| Sign/Symptom | Mild | Moderate | Severe | Imminent respiratory arrest |
|---|---|---|---|---|
| Alertness | May show agitation | Agitated | Agitated | Confused/Drowsy |
| Breathlessness | On walking | On talking | Even at rest | |
| Talks in | Sentences | Phrases | Words | |
| Wheeze | Moderate | Loud | Loud | Absent |
| Accessory muscle | Usually,not used | Used | Used | |
| Respiratory rate (/min) | Increased | Increased | Often >30 | |
| Pulse rate (/min) | 100 | 100-120 | >120 | <60> |
| PaO2 | Normal | >60 | <60> | |
| PaCO2 | <45 | <45 | >45 |
Signs of an asthmatic episode include wheezing, prolonged expiration, a rapid heart rate (tachycardia), and rhonchous lung sounds (audible through a stethoscope). During a serious asthma attack, the accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck) may be used, shown as in-drawing of tissues between the ribs and above the sternum and clavicles, and there may be the presence of a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest.
During very severe attacks, an asthma sufferer can turn blue from lack of oxygen and can experience chest pain or even loss of consciousness. Just before loss of consciousness, there is a chance that the patient will feel numbness in the limbs and palms may start to sweat. The person's feet may become cold. Severe asthma attacks which are not responsive to standard treatments, called status asthmaticus, are life-threatening and may lead to respiratory arrest and death.
Though symptoms may be very severe during an acute exacerbation, between attacks a patient may show few or even no signs of the disease.[10]
Cause
Asthma is caused by environmental and genetic factors,[11] which can influence how severe asthma is and how well it responds to medication.[12] Some environmental and genetic factors have been confirmed by further research, while others have not been.
Environmental
Many environmental risk factors have been associated with asthma development and morbidity in children, but a few stand out as well-replicated or that have a meta-analysis of several studies to support their direct association.
Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.[13] Poor air quality, from traffic pollution or high ozone levels, has been repeatedly associated with increased asthma morbidity and has a suggested association with asthma development that needs further research.[13][14]
Recent studies show a relationship between exposure to air pollutants (e.g. from traffic) and childhood asthma.[15] This research finds that both the occurrence of the disease and exacerbation of childhood asthma are affected by outdoor air pollutants.
Caesarean sections have been associated with asthma when compared with vaginal birth; a meta-analysis found a 20% increase in asthma prevalence in children delivered by Caesarean section compared to those who were not. It was proposed that this is due to modified bacterial exposure during Caesarean section compared with vaginal birth, which modifies the immune system (as described by the hygiene hypothesis).[16]
Psychological stress has long been suspected of being an asthma trigger, but only in recent decades has convincing scientific evidence substantiated this hypothesis. Rather than stress directly causing the asthma symptoms, it is thought that stress modulates the immune system to increase the magnitude of the airway inflammatory response to allergens and irritants.[13][17]
Viral respiratory infections at an early age, along with siblings and day care exposure, may be protective against asthma, although there have been controversial results, and this protection may depend on genetic context.[13][18][19]
Antibiotic use early in life has been linked to development of asthma in several examples; it is thought that antibiotics make one susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis).[20] The hygiene hypothesis is a hypothesis about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. For example, asthma prevalence has been increasing in developed countries along with increased use of antibiotics, c-sections, and cleaning products.[16][20][21] All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause increased risk for asthma and allergy.
Recently scientists connected the rise in prevalence of asthma, to the rise in use of paracetamol, suggesting the possibility that paracetamol can cause asthma.[22]
Genetic
Over 100 genes have been associated with asthma in at least one genetic association study.[23] However, such studies must be repeated to ensure the findings are not due to chance. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:[23]
|
|
|
|
|
Many of these genes are related to the immune system or to modulating inflammation. However, even among this list of highly replicated genes associated with asthma, the results have not been consistent among all of the populations that have been tested.[23] This indicates that these genes are not associated with asthma under every condition, and that researchers need to do further investigation to figure out the complex interactions that cause asthma. One theory is that asthma is a collection of several diseases, and that genes might have a role in only subsets of asthma. For example, one group of genetic differences (single nucleotide polymorphisms in 17q21) was associated with asthma that develops in childhood.[24]
Gene–environment interactions
Research suggests that some genetic variants may only cause asthma when they are combined with specific environmental exposures, and otherwise may not be risk factors for asthma.[11]
The genetic trait, CD14 single nucleotide polymorphism (SNP) C-159T and exposure to endotoxin (a bacterial product) are a well-replicated example of a gene-environment interaction that is associated with asthma. Endotoxin exposure varies from person to person and can come from several environmental sources, including environmental tobacco smoke, dogs, and farms. Researchers have found that risk for asthma changes based on a person’s genotype at CD14 C-159T and level of endotoxin exposure.[25]
| Endotoxin levels | CC genotype | TT genotype |
|---|---|---|
| High exposure | Low risk | High risk |
| Low exposure | High risk | Low risk |
Risk factors
Studying the prevalence of asthma and related diseases such as eczema and hay fever have yielded important clues about some key risk factors. The strongest risk factor for developing asthma is a family history of atopic disease;[26] this increases one's risk of hay fever by up to 5x and the risk of asthma by 3-4x.[27] In children between the ages of 3-14, a positive skin test for allergies and an increase in immunoglobulin E increases the chance of having asthma.[28] In adults, the more allergens one reacts positively to in a skin test, the higher the odds of having asthma.[29]
Because much allergic asthma is associated with sensitivity to indoor allergens and because Western styles of housing favor greater exposure to indoor allergens, much attention has focused on increased exposure to these allergens in infancy and early childhood as a primary cause of the rise in asthma.[30][31] Primary prevention studies aimed at the aggressive reduction of airborne allergens in a home with infants have shown mixed findings. Strict reduction of dust mite allergens, for example, reduces the risk of allergic sensitization to dust mites, and modestly reduces the risk of developing asthma up until the age of 8 years old.[32][33][34][35] However, studies also showed that the effects of exposure to cat and dog allergens worked in the converse fashion; exposure during the first year of life was found to reduce the risk of allergic sensitization and of developing asthma later in life.[36][37][38]
The inconsistency of this data has inspired research into other facets of Western society and their impact upon the prevalence of asthma. One subject that appears to show a strong correlation is the development of asthma and obesity. In the United Kingdom and United States, the rise in asthma prevalence has echoed an almost epidemic rise in the prevalence of obesity.[39][40] In Taiwan, symptoms of allergies and airway hyperreactivity increased in correlation with each 20% increase in body-mass index.[41]
Hygiene hypothesis
One theory for the cause of the increase in asthma prevalence worldwide is the so-called "hygiene hypothesis" — that the rise in the prevalence of allergies and asthma is a direct and unintended result of the success of modern hygienic practices in preventing childhood infections. Studies have shown repeatedly that children coming from environments one would expect to be less hygienic (East Germany vs. West Germany,[42] families with many children,[43][44][45] day care environments,[46][47]) tended to result in lower incidences of asthma and allergic diseases. This seems to run counter to the logic that viruses are often causative agents in exacerbation of asthma.[48][49][50] Additionally, other studies have shown that viral infections of the lower airway may in some cases induce asthma, as a history of bronchiolitis or croup in early childhood is a predictor of asthma risk in later life.[51] Studies which show that upper respiratory tract infections are protective against asthma risk also tend to show that lower respiratory tract infections conversely tend to increase the risk of asthma.[52]
Population disparities
Asthma prevalence in the US is higher than in most other countries in the world, but varies drastically between diverse US populations.[13] In the US, asthma prevalence is highest in Puerto Ricans, African Americans, Filipinos, Irish Americans, and Native Hawaiians, and lowest in Mexicans and Koreans.[53][54][55] Mortality rates follow similar trends, and response to Ventolin is lower in Puerto Ricans than in African Americans or Mexicans.[56][57] As with worldwide asthma disparities, differences in asthma prevalence, mortality, and drug response in the US may be explained by differences in genetic, social and environmental risk factors.
Asthma prevalence also differs between populations of the same ethnicity who are born and live in different places.[58] US-born Mexican populations, for example, have higher asthma rates than non-US born Mexican populations that are living in the US.[59] This probably reflects differences in social and environmental risk factors associated with acculturation to the US.[citation needed]
Asthma prevalence and asthma deaths also differ by gender. Males are more likely to be diagnosed with asthma as children, but asthma is more likely to persist into adulthood in females.[60] Sixty five percent more adult women than men will die from asthma.[citation needed] This difference may be attributable to hormonal differences, among other things. In support of this, girls who reach puberty before age 12 were found to have a later diagnosis of asthma more than twice as much as girls who reach puberty after age 12.[citation needed] Asthma is also the number one cause of missed days from school.[citation needed]
No comments:
Post a Comment