Asthma (from the Greek άσθμα, ásthma, "panting") is the common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm. Symptoms include wheezing, coughing, chest tightness, and shortness of breath.[ Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in 1 second (FEV1), and peak expiratory flow rate. Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic).
It is thought to be caused by a combination of genetic and environmental factors. Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as salbutamol).[6] Symptoms can be prevented by avoiding triggers, such as allergens and irritants, and by inhaling corticosteroids. Leukotriene antagonists are less effective than corticosteroids and thus less preferred.[9]
Its diagnosis is usually made based on the pattern of symptoms and/or response to therapy over time. The prevalence of asthma has increased significantly since the 1970s. As of 2010, 300 million people were affected worldwide. In 2009 asthma caused 250,000 deaths globally. Despite this, with proper control of asthma with step down therapy, prognosis is generally good.

Classification

Asthma is defined by the Global Initiative for Asthma as "a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at night or in the early morning. These episodes are usually associated with widespread, but variable airflow obstruction within the lung that is often reversible either spontaneously or with treatment".
Clinical classification of severity
Severity in patients ≥ 12 years of age 15 Symptom frequency Night time symptoms %FEV1 of predicted FEV1 Variability Use of short-acting beta2 agonist for symptom control (not for prevention of EIB)
Intermittent ≤2 per week ≤2 per month ≥80% <20% ≤2 days per week
Mild persistent >2 per week
but not daily 3–4 per month ≥80% 20–30% >2 days/week
but not daily
Moderate persistent Daily >1 per week but not nightly 60–80% >30% Daily
Severe persistent Throughout the day Frequent (often 7×/week) <60% >30% Several times per day
Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in 1 second (FEV1), and peak expiratory flow rate.[3] Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic), based on whether symptoms are precipitated by allergens (atopic) or not (non-atopic).
While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system. Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research.
Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructive pulmonary disease as this term refers specifically to combinations of disease that are irreversible such as bronchiectasis, chronic bronchitis, and emphysema. Unlike these diseases, the airway obstruction in asthma is usually reversible; however, if left untreated, the chronic inflammation from asthma can lead the lungs to become irreversibly obstructed due to airway remodeling. In contrast to emphysema, asthma affects the bronchi, not the alveoli.
[edit]Brittle asthma
Main article: Brittle asthma
Brittle asthma is a term used to describe two types of asthma, distinguishable by recurrent, severe attacks. Type 1 brittle asthma refers to disease with wide peak flow variability, despite intense medication. Type 2 brittle asthma describes background well-controlled asthma, with sudden severe exacerbations.
[edit]Asthma attack
An acute asthma exacerbation is commonly referred to as an asthma attack. The classic symptoms are shortness of breath, wheezing, and chest tightness. While these are the primary symptoms of asthma, some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.
Signs which occur during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest.A blue color of the skin and nails may occur from lack of oxygen.
In a mild exacerbation the peak expiratory flow rate (PEFR) is ≥200 L/min or ≥50% of the predicted best. Moderate is defined as between 80 and 200 L/min or 25% and 50% of the predicted best while severe is defined as ≤ 80 L/min or ≤25% of the predicted best.
[edit]Status asthmaticus
Main article: Status asthmaticus
Status asthmaticus is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and steroids. Nonselective beta blockers (such as Timolol) have caused fatal status asthmaticus.
[edit]Exercise-induced
Main article: Exercise-induced asthma
A diagnosis of asthma is common among top athletes. One survey of participants in the 1996 Summer Olympic Games, in Atlanta, Georgia, U.S., showed that 15% had been diagnosed with asthma, and that 10% were on asthma medication.
There appears to be a relatively high incidence of asthma in sports such as cycling, mountain biking, and long-distance running, and a relatively lower incidence in weightlifting and diving. It is unclear how much of these disparities are from the effects of training in the sport.
Exercise-induced asthma can be treated with the use of a short-acting beta2 agonist.
[edit]Occupational
Main article: Occupational asthma
Asthma as a result of (or worsened by) workplace exposures is a commonly reported occupational respiratory disease. Still most cases of occupational asthma are not reported or are not recognized as such. Estimates by the American Thoracic Society (2004) suggest that 15–23% of new-onset asthma cases in adults are work related.[28] In one study monitoring workplace asthma by occupation, the highest percentage of cases occurred among operators, fabricators, and laborers (32.9%), followed by managerial and professional specialists (20.2%), and in technical, sales, and administrative support jobs (19.2%). Most cases were associated with the manufacturing (41.4%) and services (34.2%) industries. Animal proteins, enzymes, flour, natural rubber latex, and certain reactive chemicals are commonly associated with work-related asthma. When recognized, these hazards can be mitigated, dropping the risk of disease.
[edit]Signs and symptoms


Wheezing

The sound of wheezing as heard with a stethoscope.
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Common symptoms of asthma include wheezing, shortness of breath, chest tightness and coughing, and use of accessory muscle. Symptoms are often worse at night or in the early morning, or in response to exercise or cold air. Some people with asthma only rarely experience symptoms, usually in response to triggers, whereas other may have marked persistent airflow obstruction.
[edit]Gastro-esophageal reflux disease
Gastro-esophageal reflux disease coexists with asthma in 80% of people with asthma, with similar symptoms. Various theories say that asthma could facilitate GERD and/or viceversa. The first case could be due to the effect of change in thoracic pressures, use of antiasthma drugs, could facilitate the passage of the gastric content back into the oesophagus by increasing abdominal pressure or decreasing the lower esophageal sphincter. The second by promoting bronchoconstriction and irritation by chronic acid aspiration, vagally mediated reflexes and others factors that increase bronchial responsiveness and irritation.
[edit]Sleep disorders
Due to altered anatomy of the respiratory tract: increased upper airway adipose deposition, altered pharynx skeletal morphology, and extension of the pharyngeal airway; leading to upper airway collapse.
[edit]Causes

Asthma is caused by environmental and genetic factors. These factors influence how severe asthma is and how well it responds to medication. The interaction is complex and not fully understood.
Studying the prevalence of asthma and related diseases such as eczema and hay fever have yielded important clues about some key risk factors.[36] The strongest risk factor for developing asthma is a history of atopic disease; this increases one's risk of hay fever by up to 5× and the risk of asthma by 3–4×. 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. In adults, the more allergens one reacts positively to in a skin test, the higher the odds of having asthma.
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. 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. 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.
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. In Taiwan, symptoms of allergies and airway hyper-reactivity increased in correlation with each 20% increase in body-mass index. Several factors associated with obesity may play a role in the pathogenesis of asthma, including decreased respiratory function due to a buildup of adipose tissue (fat) and the fact that adipose tissue leads to a pro-inflammatory state, which has been associated with non-eosinophilic asthma.
Asthma has been associated with Churg–Strauss syndrome, and individuals with immunologically mediated urticaria may also experience systemic symptoms with generalized urticaria, rhino-conjunctivitis, orolaryngeal and gastrointestinal symptoms, asthma, and, at worst, anaphylaxis.[56Additionally, adult-onset asthma has been associated with periocular xanthogranulomas.
[edit]Environmental
Many environmental risk factors have been associated with asthma development and morbidity in children. Recent studies show a relationship between exposure to air pollutants (e.g. from traffic) and childhood asthma.[58] This research finds that both the occurrence of the disease and exacerbation of childhood asthma are affected by outdoor air pollutants. High levels of endotoxin exposure may contribute to asthma risk.
Viral respiratory infections are not only one of the leading triggers of an exacerbation but may increase one's risk of developing asthma especially in young children.
Respiratory infections such as rhinovirus, Chlamydia pneumoniae and Bordetella pertussis are correlated with asthma exacerbations.
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.
Beta blocker medications such as metoprolol may trigger asthma in those who are susceptible.
[edit]Tobacco
Maternal tobacco smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms, wheezing, and respiratory infections during childhood.Low 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.
[edit]Hygiene hypothesis
Antibiotic use early in life has been linked to development of asthma in several examples; it is thought that antibiotics make children who are predisposed to atopic immune responses susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis). The hygiene hypothesis (see below) is a hypothesis about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. 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 an increased risk for asthma and allergy.
Caesarean sections have been associated with asthma, possibly because of modifications to the immune system (as described by the hygiene hypothesis).
[edit]Volatile organic compounds
Observational studies have found that indoor exposure to volatile organic compounds (VOCs) may be one of the triggers of asthma, however experimental studies have not confirmed these observations. Even VOC exposure at low levels has been associated with an increase in the risk of pediatric asthma. Because there are so many VOCs in the air, measuring total VOC concentrations in the indoor environment may not represent the exposure of individual compounds.Exposure to VOCs is associated with an increase in the IL-4 producing Th2 cells and a reduction in IFN-γ producing Th1 cells. Thus the mechanism of action of VOC exposure may be allergic sensitization mediated by a Th2 cell phenotype.Different individual variations in discomfort, from no response to excessive response, were seen in one of the studies. These variations may be due to the development of tolerance during exposure. Another study has concluded that formaldehyde may cause asthma-like symptoms. Low VOC emitting materials should be used while doing repairs or renovations which decreases the symptoms related to asthma caused by VOCs and formaldehyde.[76] In another study "the indoor concentration of aliphatic compounds (C8-C11), butanols, and 2,2,4-trimethyl 1,3-pentanediol diisobutyrate (TXIB) was significantly elevated in newly painted dwellings. The total indoor VOC was about 100 micrograms/m3 higher in dwellings painted in the last year". The author concluded that some VOCs may cause inflammatory reactions in the airways and may be the reason for asthmatic symptoms.[
[edit]Phthalates
There is a significant association between asthma-like symptoms (wheezing) among preschool children and the concentration of DEHP (phthalates) in indoor environment.[79] DEHP (di-ethylhexyl phthalate) is a plasticizer that is commonly used in building material. The hydrolysis product of DEHP (di-ethylhexyl phthalate) is MEHP (Mono-ethylhexyl phthalate) which mimics the prostaglandins and thromboxanes in the airway leading to symptoms related to asthma. Another mechanism that has been studied regarding phthalates causation of asthma is that high phthalates level can "modulate the murine immune response to a coallergen". Asthma can develop in the adults who come in contact with heated PVC fumes.[81] Two main type of phthalates, namely n-butyl benzyl phthalate (BBzP) and di(2-ethylhexyl) phthalate (DEHP), have been associated between the concentration of polyvinyl chloride (PVC) used as flooring and the dust concentrations. Water leakage were associated more with BBzP, and buildings construction were associated with high concentrations of DEHP.[82] Asthma has been shown to have a relationship with plaster wall materials and wall-to wall carpeting. The onset of asthma was also related to the floor–leveling plaster at home. Therefore, it is important to understand the health aspect of these materials in the indoor surfaces.
[edit]Genetic
Over 100 genes have been associated with asthma in at least one genetic association study. 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:
GSTM1
IL10
CTLA-4
SPINK5
LTC4S
LTA
GRPA
NOD1
CC16
GSTP1
STAT6
NOS1
CCL5
TBXA2R
TGFB1
IL4
IL13
CD14
ADRB2 (β-2 adrenergic receptor)
HLA-DRB1
HLA-DQB1
TNF
FCER1B
IL4R
ADAM33
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.[84] 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.[citation needed] For example, one group of genetic differences (single nucleotide polymorphisms in 17q21) was associated with asthma that develops in childhood.
[edit]Gene–environment interactions
CD14-endotoxin interaction based on CD14 SNP C-159T
Endotoxin levels CC genotype TT genotype
High exposure Low risk High risk
Low exposure High risk Low risk
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.
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.
[edit]Exacerbation
Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Different asthmatic individuals react differently to various factors.[87] However, most individuals can develop severe exacerbation of asthma from several triggering agents.[87][88]
Home factors that can lead to exacerbation include dust, house mites, animal dander (especially cat and dog hair), cockroach allergens and molds at any given home.[87] Perfumes are a common cause of acute attacks in females and children. Both virus and bacterial infections of the upper respiratory tract infection can worsen asthma.
[edit]Hygiene hypothesis
Main article: Hygiene hypothesis
One theory for the cause of the increase in asthma prevalence worldwide is the "hygiene hypothesis" —that the rise in the prevalence of allergies and asthma is a direct and unintended result of reduced exposure to a wide variety of different bacteria and virus types in modern societies, or modern hygienic practices preventing childhood infections. Children living in less hygienic environments (East Germany vs. West Germany,[90] families with many children, day care environments tend to have 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. 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. 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.[99]
[edit]Socioeconomic factors
The incidence of asthma is highest among low-income populations worldwide[specify]. Asthma deaths are most common in low and middle income countries, and in the Western world, it is found in those low-income neighborhoods whose populations consist of large percentages of ethnic minorities.[101] Additionally, asthma has been strongly associated with the presence of cockroaches in living quarters; these insects are more likely to be found in those same neighborhoods.
Most likely due to income and geography, the incidence of and treatment quality for asthma varies among different racial groups. The prevalence of "severe persistent" asthma is also greater in low-income communities than those with better access to treatment.
[edit]Diagnosis

Severity of acute asthma exacerbations
Near-fatal asthma High PaCO2 and/or requiring mechanical ventilation
Life threatening asthma Any one of the following in a person with severe asthma:-
Clinical signs Measurements
Altered level of consciousness Peak flow < 33%
Exhaustion Oxygen saturation < 92%
Arrhythmia PaO2 < 8 kPa
Low blood pressure "Normal" PaCO2
Cyanosis
Silent chest
Poor respiratory effort
Acute severe asthma Any one of:-
Peak flow 33–50%
Respiratory rate ≥ 25 breaths per minute
Heart rate ≥ 110 beats per minute
Unable to complete sentences in one breath
Moderate asthma exacerbation Worsening symptoms
Peak flow 50–80% best or predicted
No features of acute severe asthma


Obstruction of the lumen of the bronchiole by mucoid exudate, goblet cell metaplasia, epithelial basement membrane thickening and severe inflammation of bronchiole in a patient with asthma.
There is currently not a precise physiologic, immunologic, or histologic test for diagnosing asthma. The diagnosis is usually made based on the pattern of symptoms (airways obstruction and hyperresponsiveness) and/or response to therapy (partial or complete reversibility) over time.
The British Thoracic Society determines a diagnosis of asthma using a ‘response to therapy’ approach. If the patient responds to treatment, then this is considered to be a confirmation of the diagnosis of asthma. The response measured is the reversibility of airway obstruction after treatment. Airflow in the airways is measured with a peak flow meter or spirometer, and the following diagnostic criteria are used by the British Thoracic Society:
≥20% difference on at least three days in a week for at least two weeks;
≥20% improvement of peak flow following treatment, for example:
10 minutes of inhaled β-agonist (e.g., salbutamol);
six weeks of inhaled corticosteroid (e.g., beclometasone);
14 days of 30 mg prednisolone.
≥20% decrease in peak flow following exposure to a trigger (e.g., exercise).
In contrast, the US National Asthma Education and Prevention Program (NAEPP) uses a ‘symptom patterns’ approach.[106] Their guidelines for the diagnosis and management of asthma state that a diagnosis of asthma begins by assessing if any of the following list of indicators is present.While the indicators are not sufficient to support a diagnosis of asthma, the presence of multiple key indicators increases the probability of a diagnosis of asthma. Spirometry is needed to establish a diagnosis of asthma.
Wheezing—high-pitched whistling sounds when breathing out—especially in children. (Lack of wheezing and a normal chest examination do not exclude asthma.)
history of any of the following:
Cough, worse particularly at night
Recurrent wheeze
Recurrent difficulty in breathing
Recurrent chest tightness
Symptoms occur or worsen in the presence of:
Exercise
Viral infection
Animals with fur or hair
House-dust mites (in mattresses, pillows, upholstered furniture, carpets)
Mold
Smoke (tobacco, wood)
Pollen
Changes in weather
Strong emotional expression (laughing or crying hard)
Airborne chemicals or dusts
Menstrual cycles
Symptoms occur or worsen at night, awakening the patient
The latest guidelines from the U.S. National Asthma Education and Prevention Program (NAEPP) recommend spirometry at the time of initial diagnosis, after treatment is initiated and symptoms are stabilized, whenever control of symptoms deteriorates, and every 1 or 2 years on a regular basis.[107] The NAEPP guidelines do not recommend testing peak expiratory flow as a regular screening method because it is more variable than spirometry. However, testing peak flow at rest (or baseline) and after exercise can be helpful, especially in young patients who may experience only exercise-induced asthma. It may also be useful for daily self-monitoring and for checking the effects of new medications.[107] Peak flow readings can be charted together with a record of symptoms or use peak flow charting software. This allows patients to track their peak flow readings and pass information back to their doctor or respiratory therapist.
[edit]Differential diagnosis
Differential diagnoses include:
Infants and Children
Upper airway diseases
Allergic rhinitis and allergic sinusitis
Obstructions involving large airways
Foreign body in trachea or bronchus
Vocal cord dysfunction
Vascular rings or laryngeal webs
Laryngotracheomalacia, tracheal stenosis, or bronchostenosis
Enlarged lymph nodes or tumor
Obstructions involving small airways
Viral bronchiolitis or obliterative bronchiolitis
Cystic fibrosis
Bronchopulmonary dysplasia
Heart disease
Other causes
Recurrent cough not due to asthma
Aspiration from swallowing mechanism dysfunction or gastroesophageal reflux
Medication induced
Adults
COPD (e.g., chronic bronchitis or emphysema)
Congestive heart failure
Pulmonary embolism
Mechanical obstruction of the airways (benign and malignant tumors)
Pulmonary infiltration with eosinophilia
Cough secondary to drugs (e.g., angiotensin-converting enzyme (ACE) inhibitors)
Vocal cord dysfunction
Before diagnosing asthma, alternative possibilities should be considered such as the use of known bronchoconstrictors (substances that cause narrowing of the airways, e.g. certain anti-inflammatory agents or beta-blockers). Among elderly people, the presenting symptom may be fatigue, cough, or difficulty breathing, all of which may be erroneously attributed to Chronic obstructive pulmonary disease(COPD), congestive heart failure, or simple aging
[edit]Chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease can coexist with asthma and can occur as a complication of chronic asthma. After the age of 65 most people with obstructive airway disease will have asthma and COPD. In this setting, COPD can be differentiated by increased airway neutrophils, abnormally increased wall thickness, and increased smooth muscle in the bronchi. However, this level of investigation is not performed due to COPD and asthma sharing similar principles of management: corticosteroids, long acting beta agonists, and smoking cessation.[110] It closely resembles asthma in symptoms, is correlated with more exposure to cigarette smoke, an older age, less symptom reversibility after bronchodilator administration (as measured by spirometry), and decreased likelihood of family history of atopy
[edit]Others
The term "atopy" was coined to describe this triad of atopic eczema, allergic rhinitis and asthma
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. If the aspiration is indirect (from acid reflux), then treatment is directed at this is indicated.[citation needed]
Prevention
Tips for asthma patient:-Medication used to treat high blood pressure can cause life threatening complication in people with asthma. Both blood pressure and asthma can be treated with home remedies.