Lungs and Lung Diseases

Lungs

2007-08-07T18:56:00.000-07:00

Lung
From Wikipedia, the free encyclopedia

Human respiratory system
Air enters and leaves the lungs via a conduit of cartilaginous passageways — the bronchi and bronchioles. In this image, lung tissue has been dissected away to reveal the bronchioles[1]The lung is the essential respiration organ in air-breathing vertebrates, the most primitive being the lungfish. Its principal function is to transport oxygen from the atmosphere into the bloodstream, and to excrete carbon dioxide from the bloodstream into the atmosphere. This exchange of gases is accomplished in the mosaic of specialized cells that form millions of tiny, exceptionally thin-walled air sacs called alveoli. The lungs also have non respiratory functions.

Medical terms related to the lung often begin with pulmo-, from the Latin pulmonarius ("of the lungs"), or with pneumo- (from Greek πνεύμω "lung")[2][3]

Respiratory function

The lungs flank the heart and great vessels in the chest cavity.[1]

Energy production from aerobic respiration requires oxygen and produces carbon dioxide as a by-product, creating a need for an efficient means of oxygen delivery to cells and excretion of carbon dioxide from cells. In small organisms, such as single-celled bacteria, this process of gas exchange can take place entirely by simple diffusion. In larger organisms, this is not possible; only a small proportion of cells are close enough to the surface for oxygen from the atmosphere to enter them through diffusion. Two major adaptations made it possible for organisms to attain great multicellularity: an efficient circulatory system that conveyed gases to and from the deepest tissues in the body, and a large, internalized respiratory system that centralized the task of obtaining oxygen from the atmosphere and bringing it into the body, whence it could rapidly be distributed to all the circulatory system.

In air-breathing vertebrates, respiration occurs in a series of steps. Air is brought into the animal via the airways — in reptiles, birds and mammals this often consists of the nose; the pharynx; the larynx; the trachea (also called the windpipe); the bronchi and bronchioles; and the terminal branches of the respiratory tree. The lungs of mammals are a rich lattice of alveoli, which provide an enormous surface area for gas exchange. A network of fine capillaries allows transport of blood over the surface of alveoli. Oxygen from the air inside the alveoli diffuses into the bloodstream, and carbon dioxide diffuses from the blood to the alveoli, both across thin alveolar membranes.

The drawing and expulsion of air is driven by muscular action; in early tetrapods, air was driven into the lungs by the pharyngeal muscles, whereas in reptiles, birds and mammals a more complicated musculoskeletal system is used. In the mammal, a large muscle, the diaphragm (in addition to the internal intercostal muscles), drive ventilation by periodically altering the intra-thoracic volume and pressure; by increasing volume and thus decreasing pressure, air flows into the airways down a pressure gradient, and by reducing volume and increasing pressure, the reverse occurs. During normal breathing, expiration is passive and no muscles are contracted (the diaphragm relaxes).

Another name for this inspiration and expulsion of air is ventilation. Vital capacity is the maximum volume of air that a person can exhale after maximum inhalation. A person's vital capacity can be measured by a spirometer (spirometry). In combination with other physiological measurements, the vital capacity can help make a diagnosis of underlying lung disease.

Non respiratory functions
In addition to respiratory functions such as gas exchange and regulation of hydrogen ion concentration, the lungs also:

influence the concentration of biologically active substances and drugs used in medicine in arterial blood
filter out small blood clots formed in veins
serve as a physical layer of soft, shock-absorbent protection for the heart, which the lungs flank and nearly enclose.
filter out gas micro-bubbles occurring in the venous blood stream during SCUBA diving decompression.[4]

Mammalian lungs
Further information: Human lung
The lungs of mammals have a spongy texture and are honeycombed with epithelium having a much larger surface area in total than the outer surface area of the lung itself. The lungs of humans are typical of this type of lung.

Breathing is largely driven by the muscular diaphragm at the bottom of the thorax. Contraction of the diaphragm pulls the bottom of the cavity in which the lung is enclosed downward. Air enters through the oral and nasal cavities; it flows through the larynx and into the trachea, which branches out into bronchi. Relaxation of the diaphragm has the opposite effect, passively recoiling during normal breathing. During exercise, the diaphragm contracts, forcing the air out more quickly and forcefully. The rib cage itself is also able to expand and contract to some degree, through the action of other respiratory and accessory respiratory muscles. As a result, air is sucked into or expelled out of the lungs, always moving down its pressure gradient. This type of lung is known as a bellows lung as it resembles a blacksmith's bellows.

Anatomy
In humans, it is the two main bronchi (produced by the bifurcation of the trachea) that enter the roots of the lungs. The bronchi continue to divide within the lung, and after multiple divisions, give rise to bronchioles. The bronchial tree continues branching until it reaches the level of terminal bronchioles, which lead to alveolar sacks. Alveolar sacs are made up of clusters of alveoli, like individual grapes within a bunch. The individual alveoli are tightly wrapped in blood vessels, and it is here that gas exchange actually occurs. Deoxygenated blood from the heart is pumped through the pulmonary artery to the lungs, where oxygen diffuses into blood and is exchanged for carbon dioxide in the hemoglobin of the erythrocytes. The oxygen-rich blood returns to the heart via the pulmonary veins to be pumped back into systemic circulation.

Bronchi, bronchial tree, and lungs (Cardiac notch labeled at bottom left).Human lungs are located in two cavities on either side of the heart. Though similar in appearance, the two are not identical. Both are separated into lobes, with three lobes on the right and two on the left. The lobes are further divided into lobules, hexagonal divisions of the lungs that are the smallest subdivision visible to the naked eye. The connective tissue that divides lobules is often blackened in smokers and city dwellers. The medial border of the right lung is nearly vertical, while the left lung contains a cardiac notch. The cardiac notch is a concave impression molded to accommodate the shape of the heart. Lungs are to a certain extent 'overbuilt' and have a tremendous reserve volume as compared to the oxygen exchange requirements when at rest. This is the reason that individuals can smoke for years without having a noticeable decrease in lung function while still or moving slowly; in situations like these only a small portion of the lungs are actually perfused with blood for gas exchange. As oxygen requirements increase due to exercise, a greater volume of the lungs is perfused, allowing the body to match its CO2/O2 exchange requirements.

The environment of the lung is very moist, which makes it hospitable for bacteria. Many respiratory illnesses are the result of bacterial or viral infection of the lungs.

Asthma

2007-08-07T08:54:00.000-07:00

Asthma
From Wikipedia, the free encyclopedia

Bronchial Asthma
Classification & external resources
ICD-10
J 45.
ICD-9
493
OMIM
600807
DiseasesDB
1006
MedlinePlus
000141
eMedicine
med/177 emerg/43
MeSH
C08.127.108

Asthma is a chronic disease of the respiratory system in which the airway occasionally constricts, becomes inflamed, and is lined with excessive amounts of mucus, often in response to one or more triggers. These episodes may be triggered by such things as exposure to an environmental stimulant (or allergen), cold air, warm air, moist air, exercise or exertion, or emotional stress. In children, the most common triggers are viral illnesses such as those that cause the common cold.[1] This airway narrowing causes symptoms such as wheezing, shortness of breath, chest tightness, and coughing. The airway constriction responds to bronchodilators. Between episodes, most patients feel well but can have mild symptoms and they may remain short of breath after exercise for longer periods of time than the unaffected individual.

The symptoms of asthma, which can range from mild to life threatening, can usually be controlled with a combination of drugs and environmental changes.

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.[2]

History
The word 'asthma' is derived from the Greek aazein, meaning "sharp breath." The word first appears in Homer's Iliad;[3] Hippocrates was the first to use it in reference to the medical condition, in 450 BC. Hippocrates thought that the spasms associated with asthma were more likely to occur in tailors, anglers, and metalworkers. Six centuries later, Galen wrote much about asthma, noting that it was caused by partial or complete bronchial obstruction. In 1190 AD, Moses Maimonides, an influential medieval rabbi, philosopher, and physician, wrote a treatise on asthma, describing its prevention, diagnosis, and treatment.[4] In the 17th century, Bernardino Ramazzini noted a connection between asthma and organic dust. The use of bronchodilators started in 1901, but it was not until the 1960s that the inflammatory component of asthma was recognized, and anti-inflammatory medications were added to the regimens.

Signs and symptoms
In some individuals asthma is characterized by chronic respiratory impairment. In others it is an intermittent illness marked by episodic symptoms that may result from a number of triggering events, including upper respiratory infection, stress, airborne allergens, air pollutants (such as smoke or traffic fumes), or exercise.

An acute exacerbation of asthma is referred to as an asthma attack. The clinical hallmarks of an attack are shortness of breath (dyspnea) and either wheezing or stridor. Although the former is "often regarded as the sine qua non of asthma,"[5] 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. 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).

Signs of an asthmatic episode include wheezing, rapid breathing (tachypnea), prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), and over-inflation of the chest. 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 the presence of a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation).

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. Feet may become icy cold. Severe asthma attacks, which may not be responsive to standard treatments (status asthmaticus), are life-threatening and may lead to respiratory arrest and death. Despite the severity of symptoms during an asthmatic episode, between attacks an asthmatic may show few signs of the disease.[6]

Diagnosis
Asthma is defined simply as reversible airway obstruction. Reversibility occurs either spontaneously or with treatment. The basic measurement is peak flow rates and the following diagnostic criteria are used by the British Thoracic Society:[7]

≥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 week of inhaled corticosteroid (e.g., beclometasone);
14 days of 30mg prednisolone.

≥20% decrease in peak flow following exposure to a trigger (e.g., exercise).

In many 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.

In the Emergency Department doctors may use a capnography PMID 16187465 which measures the amount of exhaled carbon dioxide along with pulse oximetry which shows the amount of oxygen dissolved in the blood, to determine the severity of an asthma attack as well as the response to treatment.

Differential diagnosis
Before diagnosing someone as asthmatic, alternative possibilities should be considered. A clinician 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.
A majority of children who are asthma sufferers have an identifiable allergy trigger. Specifically, in a 2004 study, 71% had positive test results for more than 1 allergen, and 42% had positive test results for more than 3 allergens.[8]

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 a pulmonary function test has been carried out, 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 United States National 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%.

There is no cure for asthma. Doctors have only found ways to prevent attacks and relieve the symptoms such as tightness of the chest and trouble breathing.

Pathophysiology

Inflamed airways and bronchoconstriction in asthma. Airways narrowed as a result of the inflammatory response cause wheezing.

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 immune response in the bronchial airways.[9]
The airways of asthmatics are "hypersensitive" to certain triggers, also known as stimuli (see below). 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.

Stimuli
There are many different categories of stimuli:

Allergenic air pollution,
from nature, typically inhaled, which include waste from common household pests,
such as the house dust mite and cockroach, grass pollen, mould spores, and pet epithelial cells; [citation needed]
Indoor allergenic air pollution from volatile organic compounds, including perfumes and perfumed products. Examples include:
soap dishwashing liquid,
laundry detergent,
fabric softener,
paper tissues,
paper towels,
toilet paper,
shampoo,
hairspray
hair gel,
cosmetics,
facial cream,
sun cream,
deodorant,
cologne,
shaving cream,
aftershave lotion,
air freshener and candles,
and products such as oil-based paint. [citation needed]
Medications, including aspirin,[10] β-adrenergic antagonists (beta blockers), and penicillin.[citation needed]
Food allergies such as milk, peanuts, and eggs. However, asthma is rarely the only symptom, and not all people with food or other allergies have asthma.[citation needed]
Use of fossil fuel related allergenic air pollution, such as ozone, smog, summer smog, nitrogen dioxide, and sulfur dioxide, which is thought to be one of the major reasons for the high prevalence of asthma in urban areas; [citation needed]
Various industrial compounds and other chemicals, notably sulfites; chlorinated
swimming pools generate chloramines—monochloramine (NH2Cl), dichloramine (NHCl2) and trichloramine (NCl3)—in the air around them, which are known to induce asthma.[11]
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. 80% of asthma attacks in adults and 60% in children are caused by respiratory viruses. [citation needed]
Exercise, the effects of which differ somewhat from those of the other triggers [citation needed]
Allergenic indoor air pollution from newsprint & other literature such as, junk mail leaflets & glossy magazines (in some countries).[citation needed]
Hormonal changes in adolescent girls and adult women associated with their menstrual cycle can lead to a worsening of asthma. Some women also experience a worsening of their asthma during pregnancy whereas others find no significant changes, and in other women their asthma improves during their pregnancy. [citation needed]
Emotional stress which is poorly understood as a trigger.[citation needed]

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 (TH0 cells) "check" and usually ignore the allergen molecules. In asthmatics, 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 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.[12] Szentivanyi's Beta Adrenergic Theory is a citation classic[13] 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 beta-2 receptors.[14] Since overproduction of IgE is central to all atopic diseases, this was a watershed moment in the world of allergy.[15]
The Beta-Adrenergic Theory has been cited in the scholarship of such noted investigators as Richard F. Lockey (former President of the American Academy of Allergy, Asthma, and Immunology),[16] Charles Reed (Chief of Allergy at Mayo Medical School),[17] and Craig Venter (Human Genome Project).[18]

Causes
Many studies have linked asthma, bronchitis, and acute respiratory illnesses to air quality experienced by children.[19] One of the largest of these studies is the California Children's Health Study.[20] From the press release [1]

The study showed that children in the high ozone communities who played three or more sports developed asthma at a rate three times higher than those in the low ozone communities. Because participation in some sports can result in a child drawing up to 17 times the “normal” amount of air into the lungs, young athletes are more likely to develop asthma.
Note that concentrations of ozone have risen steadily in Europe since 1870. [2]
Another 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 TH1 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 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 that protect us against parasites and other infectious agents are the same cells responsible for the allergic reaction. Charcot-Leyden crystals are formed when crystalline material in eosinophils coalesce. These crystals are significant in sputum samples of people with asthma. In the developed world, the parasites that eosinophils are programmed to combat are now rarely encountered, but the immune response remains and is wrongly triggered in some individuals by certain allergens.
It has been postulated that some forms of asthma may be related to infection, in particular by Chlamydia pneumoniae.[21] This issue remains controversial, as the relationship is not borne out by meta-analysis of the research.[22] 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.[23] One possible explanation is that some asthmatics may have altered immune response that facilitates long-term chlamydia pneumonia infection.[24] 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.[22]
One group of researchers suggested that, in part, asthma has a neurogenic paroxysmal component,[25] and that several anti-eleptic drugs have an effect. However only one paper[26] has been published as listed by PubMed and its conclusions criticized.[27]
A study conducted by the National Jewish Medical and Research Center concluded that overweight and obesity are associated with a dose-dependent increase in the odds of incident asthma in men and women, suggesting asthma incidence could be reduced by interventions targeting overweight and obesity. [28]
Asthma and sleep apnea
Main article: 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.[29] CPAP is not effective in patients with nocturnal asthma only.[30]
Asthma and gastro-esophageal reflux disease
Main article: gastro-esophageal reflux disease
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.[citation needed] GERD may be common in difficult-to-control asthma, but generally speaking, treating it does not seem to affect the asthma.[31]

Treatment
The most effective treatment for asthma is identifying triggers, such as pets or aspirin, and limiting or eliminating exposure to them. Desensitization to allergens has been shown to be a treatment option for certain patients.[32]

Desesitization to Allergens
As is common with respiratory disease, smoking is believed to adversely affect asthmatics in several ways, including an increased severity of symptoms, a more rapid decline of lung function, and decreased response to preventive medications.[33] Automobile emissions are considered an even more significant cause and aggravating factor.[3] Asthmatics who smoke or who live near traffic [4] typically require additional medications to help control their disease. Furthermore, exposure of both non-smokers and smokers to wood smoke, gas stove fumes and second-hand smoke is detrimental, resulting in more severe asthma, more emergency room visits, and more asthma-related hospital admissions.[34] Smoking cessation and avoidance of second-hand smoke is strongly encouraged in asthmatics.[35]
Medical Treatment
The specific medical treatment recommended to patients with asthma depends on the severity of their illness and the frequency of their symptoms. Specific treatments for asthma are broadly classified as relievers, preventers and emergency treatment. The Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma (EPR-2)[35] of the U.S. National Asthma Education and Prevention Program, and the British Guideline on the Management of Asthma[36] are broadly used and supported by many doctors. A new draft Full Report of Expert Panel: Guidelines for the Diagnosis and Management of Asthma (EPR-3) was posted on the NHLBI web site for public review and comment but has been withdrawn from the NIH website pending formal dissemination, although comments submitted by the American College of Allergy, Asthma and Immunology about the proposed revised NHLBI asthma guidelines are still available online. Bronchodilators are recommended for short-term relief in all patients. For those who experience occasional attacks, no other medication is needed. For those with mild persistent disease (more than two attacks a week), low-dose inhaled glucocorticoids or alternatively, an oral leukotriene modifier, a mast-cell stabilizer, or theophylline may be administered. For those who suffer daily attacks, a higher dose of glucocorticoid in conjunction with a long-acting inhaled β-2 agonist may be prescribed; alternatively, a leukotriene modifier or theophylline may substitute for the β-2 agonist. In severe asthmatics, oral glucocorticoids may be added to these treatments during severe attacks.

For those in whom exercise can trigger an asthma attack (exercise-induced asthma), higher levels of ventilation and cold, dry air tend to exacerbate attacks. For this reason, activities in which a patient breathes large amounts of cold air, such as skiing and running, tend to be worse for asthmatics, whereas swimming in an indoor, heated pool, with warm, humid air, is less likely to provoke a response.[5]

Researchers at Harvard Medical School (HMS) have come up with convincing evidence that the answer to what causes asthma lies in a special type of natural "killer" cell. This finding means that physicians may not be treating asthma sufferers with the right kinds of drugs. For example, natural killer T cells seem to be resistant to the corticosteroids in widely used inhalers.[37]
Relief medication

Symptomatic control of episodes of wheezing and shortness of breath is generally
achieved with fast-acting bronchodilators. These are typically provided in pocket-sized, metered-dose inhalers (MDIs). In young 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 inhaler use (generally the elderly), an asthma spacer . The spacer is a plastic cylinder that mixes the medication with air in a simple tube, making it easier for patients to receive a full dose of the drug and allows
for the active agent to be dispersed into smaller, more fully inhaled bits.
A nebulizer
which provides a larger, continuous dose can also be used. Nebulizers work by
vaporizing a dose of medication in a saline solution into a steady stream of
foggy vapour, which the patient inhales continuously until the full dosage is
administered. There is no clear evidence, however, that they are more effective
than inhalers used with a spacer. Nebulizers may be helpful to some patients
experiencing a severe attack. Such patients may not be able to inhale deeply, so
regular inhalers may not deliver medication deeply into the lungs, even on
repeated attempts. Since a nebulizer delivers the medication continuously, it is
thought that the first few inhalations may relax the airways enough to allow the
following inhalations to draw in more medication.

Relievers include:

Short-acting, selective beta2-adrenoceptor agonists, such as salbutamol (albuterol USAN), levalbuterol, terbutaline and bitolterol.Tremors, the major side effect, have been greatly reduced by inhaled delivery, which allows the drug to target the lungs specifically; oral and injected medications are delivered throughout the body. There may also be cardiac side effects at higher doses (due to Beta-1 agonist activity), such as elevated heart rate or blood pressure; with the advent of selective agents, these side effects have become less common. Patients must be cautioned against using these medicines too frequently, as with such use their efficacy may decline, producing desensitization resulting in an exacerbation of symptoms which may lead to refractory asthma and death.
Older, less selective adrenergic agonists, such as inhaled epinephrine and ephedrine tablets, have also been used. Cardiac side effects occur with these agents at either similar or lesser rates to albuterol.[38] [39] When used
solely as a relief medication, inhaled epinephrine has been shown to be an
effective agent to terminate an acute asthmatic exacerbation.[38] In
emergencies, these drugs were sometimes administered by injection. Their use via injection has declined due to related adverse effects.
Anticholinergic medications, such as ipratropium bromide may be used instead. They have no cardiac side effects and thus can be used in patients with heart disease; however, they take up to an hour to achieve their full effect and are not as powerful as the β2-adrenoreceptor agonists.
Inhaled glucocorticoids are usually considered preventive medications; however, a randomized controlled trial has demonstrated the benefit of 250 microg beclomethasone when taken as an as-needed combination inhaler with 100 microg of albuterol.[40]
Prevention medication
Current treatment protocols recommend prevention medications such as an inhaled corticosteroid, which helps to suppress inflammation and reduces the swelling of the lining of the airways, in 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 asthma is controlled. With the proper use of prevention drugs, asthmatics can avoid the complications that result from overuse of relief medications.
Asthmatics sometimes stop taking their preventive medication when they feel fine and have no problems breathing. This often results in further attacks, and no long-term improvement.

Preventive agents include the following:

Inhaled glucocorticoids are the most widely used of the prevention medications and normally come as inhaler devices (ciclesonide, beclomethasone, budesonide, flunisolide, fluticasone, mometasone, and triamcinolone). Long-term use of corticosteroids can have many side effects including a redistribution of fat, increased appetite, blood glucose problems and weight gain. In particular high doses of steroids may cause osteoporosis. For this reasons inhaled steroids are generally used for prevention, as their smaller doses are targeted to the lungs unlike the higher doses of oral preparations. Nevertheless, patients on high doses of inhaled steroids may still require prophylactic treatment to prevent osteoporosis. Deposition of steroids in the mouth may cause a hoarse voice or oral thrush (due to decreased immunity). This may be minimised by rinsing the mouth with water after inhaler use, as well as by using a spacer which increases the amount of drug that reaches the lungs.
Leukotriene modifiers (montelukast, zafirlukast, pranlukast, and zileuton).
Mast cell stabilizers (cromoglicate (cromolyn), and nedocromil).
Antimuscarinics/anticholinergics (ipratropium, oxitropium, and tiotropium), which have a mixed reliever and preventer effect. (These are rarely used in preventive treatment of asthma, except in patients who do not tolerate beta-2-agonists.)
Methylxanthines (theophylline and aminophylline), which are sometimes considered if sufficient control cannot be achieved with inhaled glucocorticoids and long-acting β-agonists alone.
Antihistamines, often used to treat allergic symptoms that may underlie the chronic inflammation. In more severe cases, hyposensitization ("allergy shots") may be recommended.
Omalizumab, an IgE blocker; this can help patients with severe allergic asthma that does not respond to other drugs. However, it is expensive and must be injected.
Methotrexate is occasionally used in some difficult-to-treat patients.
If chronic acid indigestion (GERD) contributes to a patient's asthma, it should also be treated, because it may prolong the respiratory problem.
Additionally, the antidepressant tianeptine
has shown significant efficacy in children with asthma.

Long-acting β2-agonists
A typical inhaler, of Serevent (salmeterol), a long-acting bronchodilator.
Long-acting bronchodilators (LABD) are similar in structure to short-acting selective beta2-adrenoceptor agonists, but have much longer sidechains resulting in a 12-hour effect, and are used to give a smoothed symptomatic relief (used morning and night). While patients report improved symptom control, these drugs do not replace the need for routine preventers, and their slow onset means the short-acting dilators may still be required. In November of 2005, the American FDA released a health advisory alerting the public to findings that show the use of long-acting β2-agonists could lead to a worsening of symptoms, and in some cases death.[41]
Currently available long-acting beta2-adrenoceptor agonists include salmeterol, formoterol, bambuterol, and sustained-release oral albuterol. Combinations of inhaled steroids and long-acting bronchodilators are becoming more widespread; the most common combination currently in use is fluticasone/salmeterol (Advair in the United States, and Seretide in the United Kingdom).

A recent meta-analysis of the roles of long-acting beta-agonists may indicate a danger to asthma patients. "These agents can improve symptoms through bronchodilation at the same time as increasing underlying inflammation and bronchial hyper-responsiveness, thus worsening asthma control without any warning of increased symptoms," said Shelley Salpeter in a Cornell study. The study goes on to say that "Three common asthma inhalers containing the drugs salmeterol or formoterol may be causing four out of five US asthma-related deaths per year and should be taken off the market".[42] This assertion has drawn criticism from many asthma specialists for being inaccurate. As Dr. Hal Nelson points out in a recent letter to the Annals of Internal Medicine,"Salpeter and colleagues also assert that salmeterol may be responsible for 4000 of the 5000 asthma-related deaths that occur in the United States annually. However, when salmeterol was introduced in 1994, more than 5000 asthma-related deaths occurred per year. Since the peak of asthma deaths in 1996, salmeterol sales have increased about 5-fold, while overall asthma mortality rates have decreased by about 25%, despite a continued increase in asthma diagnoses. In fact, according to the most recent data from the National Center for Health Statistics, U.S. asthma mortality rates peaked in 1996 (with 5667 deaths) and have decreased steadily since. The last available data, from 2004, indicate that 3780 deaths occurred. Thus, the suggestion that a vast majority of asthma deaths could be attributable to LABA use is inconsistent with the facts."
Dr. Salpeter has since tempered her comments regarding LABAs.[citation needed]

Emergency treatment
When an asthma attack is unresponsive to a patient's usual medication, other treatments are available to the physician or hospital:[43]

oxygen to alleviate the hypoxia (but not the asthma per se) that results from extreme asthma attacks;
nebulized salbutamol or terbutaline (short-acting beta-2-agonists), often combined with ipratropium (an anticholinergic);
systemic steroids, oral or intravenous (prednisone, prednisolone, methylprednisolone, dexamethasone, or hydrocortisone). Some research has looked into an alternative inhaled route.[44]
other bronchodilators that are occasionally effective when the usual drugs fail:
intravenous salbutamol;
nonspecific beta-agonists, injected or inhaled (epinephrine, isoetharine, isoproterenol, metaproterenol);
anticholinergics, IV or nebulized, with systemic effects (glycopyrrolate, atropine, ipratropium);
methylxanthines (theophylline, aminophylline);
inhalation anesthetics that have a bronchodilatory effect (isoflurane, halothane, enflurane);
the dissociative anaesthetic ketamine, often used in endotracheal tube induction
magnesium sulfate, intravenous; and

intubation and mechanical ventilation, for patients in or approaching
respiratory arrest.
Heliox, a mixture of helium and oxygen, may be used in a hospital setting. It
has a more laminar flow than ambient air and moves more easily through
constricted airways

Alternative and complementary medicine
Many asthmatics, like those who suffer from other chronic disorders, use alternative treatments; surveys show that roughly 50% of asthma patients use some form of unconventional therapy.[45][46] There are little data to support the effectiveness of most of these therapies. A Cochrane systematic review of acupuncture for asthma found no evidence of efficacy.[47] A similar review of air ionisers found no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.[48] A study of "manual therapies" for asthma, including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic manoeuvers, found there is insufficient evidence to support or refute their use in treating asthma;[49] these manoeuvers include various osteopathic and chiropractic techniques to "increase movement in the rib cage and the spine to try and improve the working of the lungs and circulation"; chest tapping, shaking, vibration, and the use of "postures to help shift and cough up phlegm." On the other hand, one meta-analysis found that homeopathy has a potentially mild benefit in reducing symptom intensity;[50] however, the number of patients involved in the analysis was small, and subsequent studies have not supported this finding.[51] Several small trials have suggested some benefit from various yoga practices, ranging from integrated yoga programs[52] —"yogasanas, Pranayama, meditation, and kriyas"—to sahaja yoga,[53] a form of meditation. Ayurveda recommends use of herbs such as Ajwain, Harad, Hing, Ajamoda, Lavanga, Sunthi and others.[54]
The Buteyko method, a Russian therapy based on breathing exercises, has been investigated. A randomized, controlled trial of just 39 patients in 1998 showed a substantial reduction in the need for beta-agonists and a 50% reduction in the need for inhaled steroids. Lung function remained the same despite the decrease in medication.[55] A trial in New Zealand in 2003 showed an 85% reduction in the use of beta-agonist medication and a 50% reduction in inhaled steroid use after six months.[56]
Given that some research has identified a negative association between helminth infection (hookworm) and asthma and hay fever,[57] some have suggested that hookworm infestation, although not medically sanctioned, would cure asthma. There is both anectdotal evidence[58] and peer-reviewed research to support this viewpoint. [59]
Guaifenesin, an expectorant available over the counter, may have a small effect in managing thickened bronchial mucus.

Prognosis
The prognosis for asthmatics is good, especially for children with mild disease. For asthmatics diagnosed during childhood, 54% will no longer carry the diagnosis after a decade. The extent of permanent lung damage in asthmatics is unclear. Airway remodelling is observed, but it is unknown whether these represent harmful or beneficial changes.[9] Although conclusions from studies are mixed, most studies show that early treatment with glucocorticoids prevents or ameliorates decline in lung function as measured by several parameters.[60] For those who continue to suffer from mild symptoms, corticosteroids can help most to live their lives with few disabilities. The mortality rate for asthma is low, with around 6000 deaths per year in a population of some 10 million patients in the United States.[5] Better control of the condition may help prevent some of these deaths.

Epidemiology

The prevalence of childhood asthma has increased since 1980, especially in younger children.
More than 6% of children in the United States have been diagnosed with asthma, a 75% increase in recent decades. The rate soars to 40% among some populations of urban children.[citation needed]

Asthma is usually diagnosed in childhood. The risk factors for asthma include:[citations needed]

a personal or family history of asthma or atopy;
triggers (see Pathophysiology above);
premature birth or low birth weight;
viral respiratory infection in early childhood;
maternal smoking;
being male, for asthma in prepubertal children; and
being female, for persistence of asthma into adulthood.

There is a reduced occurrence of asthma in people who were breast-fed as babies. Current research suggests that the prevalence of childhood asthma has been increasing. According to the Centers for Disease Control and Prevention's National Health Interview Surveys, some 9% of US children below 18 years of age had asthma in 2001, compared with just 3.6% in 1980 (see figure). The World Health Organization (WHO) reports that some 8% of the Swiss population suffers from asthma today, compared with just 2% some 25–30 years ago.[61] Although asthma is more common in affluent countries, it is by no means a problem restricted to the affluent; the WHO estimate that there are between 15 and 20 million asthmatics in India. In the U.S., urban residents, Hispanics, and African Americans are affected more than the population as a whole. Globally, asthma is responsible for around 180,000 deaths annually.[61] On the remote South Atlantic island Tristan da Cunha, 50% of the population are asthmatics due to heredity transmission of a mutation in the gene CC16.[citation needed]

Socioeconomic factors
The incidence of asthma is higher among low-income populations within a society (it is not more common in developed countries than developing countries [5]), which in the western world are disproportionately ethnic minorities, and more likely to live near industrial areas. Additionally, asthma has been strongly associated with the presence of cockroaches in living quarters, which is more likely in such neighborhoods.[62]

Asthma incidence and quality of treatment varies among different racial groups, though this may be due to correlations with income (and thus affordability of health care) and geography. For example, Black Americans are less likely to receive outpatient treatment for asthma despite having a higher prevalence of the disease. They are much more likely to have emergency room visits or hospitalization for asthma, and are three times as likely to die from an asthma attack compared to whites. The prevalence of "severe persistent" asthma is also greater in low-income communities compared with communities with better access to treatment.[63][64]

Asthma and athletics
Asthma appears to be more prevalent in athletes than in the general population. 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. [65] These statistics have been questioned on at least two bases. Athletes with mild asthma may be more likely to be diagnosed with the condition than non-athletes, because even subtle symptoms may interfere with their performance and lead to pursuit of a diagnosis. It has also been suggested that some professional athletes who do not suffer from asthma claim to do so in order to obtain special permits to use certain performance-enhancing drugs.

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, and from self-selection of sports that may appear to minimize the triggering of asthma.[65][66]
In addition, there exists a variant of asthma called exercise-induced asthma that shares many features with allergic asthma. It may occur either independently, or concurrent with the latter. Exercise studies may be helpful in diagnosing and assessing this condition.

See also

Wikimedia Commons has media related to:
Asthma
Reactive airway disease
Atopy
Hopkins syndrome
Hygiene hypothesis
Immune response
Asthma and Allergy Foundation of America

References
^ Zhao J, Takamura M, Yamaoka A, Odajima Y, Iikura Y. Altered eosinophil levels as a result of viral infection in asthma exacerbation in childhood. J Pediatr Allergy Immunol. 2002 Feb;13(1):47–50. PMID 12000498
^ Lilly CM. Diversity of asthma: Evolving concepts of pathophysiology and lessons from genetics. J Allergy Clin Immunol. 2005;115 (4 Suppl):S526-31. PMID 15806035
^ Marketos SG, Ballas CN. Bronchial asthma in the medical literature of Greek antiquity. J Asthma. 1982;19(4):263-9. PMID 6757243
^ Rosner F. Moses Maimonides' treatise on asthma. Thorax. 1981;36:245–251. PMID 7025335
^ a b c McFadden ER, Jr. "Asthma". In Kasper DL, Fauci AS, Longo DL, et al (eds). Harrison's Principles of Internal Medicine, 16th ed., pp. 1508–1516. New York: McGraw-Hill;2004.
^ Longmore, Murray et al (2007). Oxford Handbook of Clinical Medicine, 7th ed., Oxford University Press. ISBN 978-0198568377.
^ Pinnock H, Shah R (2007). "Asthma". Br Med J 334 (7598): 847–50. DOI:10.1136/bmj.39140.634896.BE.
^ Vargas, PA (September 2004). "Characteristics of children with asthma who are enrolled in a Head Start program". J Allergy Clin Immunol: 499–504. PMID 15356547.
^ a b Maddox L, Schwartz DA. The Pathophysiology of Asthma. Annu. Rev. Med. 2002, 53:477-98. PMID 11818486
^ 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
^ Nemery B, Hoet PH, Nowak D. Indoor swimming pools, water chlorination and respiratory health. Eur Respir J. 2002;19(5):790-3. PMID 12030714
^ Szentivanyi, Andor (1968). "The Beta Adrenergic Theory of the Atopic Abnormality in Asthma".
^ Lockey, Richard, In lasting tribute: Andor Szentivanyi, MD. J. Allergy and Clinical Immunology, January, 2006
^ Szentivanyi A., Ali K., Calderon EG., Brooks SM., Coffey RG., Lockey RF. (1993). "The in vitro effect of Imunnoglobulin E {IgE} on cyclic AMP concentrations in A549 human pulmonary epithelial cells with or without beta adrenergic stimulation". J. Allergy Clin Immunol. 91: 379. - Part of Abstracts from:(1993) "50th Anniversary of the American Academy of Allergy and Immunology. 49th Annual Meeting. Chicago, Illinois, March 12–17, 1993. Abstracts.". J Allergy Clin Immunol 91 (1 Pt 2): 141–379. PMID 8421135.
^ (2001) in Kowalak JP, Hughes AS et al (eds): Professional Guide To Diseases, 7th ed., Springhouse.
^ Lockey, Richard F. (2006-04-28). Anaphylaxis: Synopsis. Allergic Diseases Resource Center. World Allergy Organization. Retrieved on September 23, 2006.
^ Ouellette, J. J.; C. E. Reed (March 1967). "The effect of partial beta adrenergic blockade on the bronchial response of hay fever subjects to ragweed aerosol.". Journal of Allergy 39 (3): 160-6. PubMed.
^ Fraser, Claire M.; J. Craig Venter (May 14, 1980). "The synthesis of beta-adrenergic receptors in cultured human lung cells: induction by glucocorticoids." (PDF). Biochemical and Biophysical Research Communications 94 (1): 390–397. DOI:10.1016/S0006-291X(80)80233-6. PubMed. Retrieved on 2006-09-23.
^ Asthma and Air Quality.
^ California Children's Health Study.
^ Terttu HH, Leinonen M, Nokso-Koivisto J, Korhonen T, Raty R, He Q, Hovi T, Mertsola J, Bloigu A, Rytila P, Saikku P (2006). "Non-random distribution of pathogenic bacteria and viruses in induced sputum or pharyngeal secretions of adults with stable asthma". Thorax. PMID 16517571.
^ a b Richeldi L, Ferrara G, Fabbri LM, Lasserson TJ, Gibson PG (2005). "Macrolides for chronic asthma". Cochrane Database Syst Rev (4): CD002997. PMID 16235309.
^ Pasternack R, Huhtala H, Karjalainen J (2005). "Chlamydophila (Chlamydia) pneumoniae serology and asthma in adults: a longitudinal analysis". J Allergy Clin Immunol 116 (5): 1123–8. PMID 16275386.
^ Ronchetti R, Biscione GL, Ronchetti F, Ronchetti MP, Martella S, Falasca C, Casini C, Barreto M, Villa MP (2005). "Why Chlamydia pneumoniae is associated with asthma and other chronic conditions? Suggestions from a survey in unselected 9 years old schoolchildren". Pediatr Allergy Immunol 16 (2): 145-50. PMID 15787872.
^ Lomia M (March 20, 2006). Bronchial asthma as neurogenic paroxysmal and inflammatory disease -- Scientific background of effective use of anticonvulsants for pharmacotherapy of bronchial asthma.
^ Lomia M, Tchelidze T, Pruidze M (2006). "Bronchial asthma as neurogenic paroxysmal inflammatory disease: a randomized trial with carbamazepine". Respiratory medicine 100 (11): 1988-96. DOI:10.1016/j.rmed.2006.02.018. PMID 16597501.
^ Singh N (2007). "Carbamazepine in asthma: first do no harm!". Respiratory medicine 101 (3): 676; author reply 677-8. DOI:10.1016/j.rmed.2006.11.025. PMID 17223330. Related warnings:
Lee T, Cochrane GM, Amlot P (1981). "Pulmonary eosinophilia and asthma associated with carbamazepine" (Scanned image). British medical journal (Clinical research ed.) 282 (6262): 440. PMID 6780065.
Lewis IJ, Rosenbloom L (1982). "Glandular fever-like syndrome, pulmonary eosinophilia and asthma associated with carbamazepine". Postgraduate medical journal 58 (676): 100-1. PMID 7100019.
^ journal=American Journal of Respiratory and Critical Care Medicine volume=175 pages=661-666 year=2007
^ University of Michigan Health System (May 25, 2005). Breathing disorders during sleep are common among asthmatics, may help predict severe asthma. Press release. Retrieved on 2006-09-23.
^ Basner, Robert C. (2006-07-25). Asthma and OSA. ASAA Resources > Publications. American Sleep Apnea Association. Retrieved on September 23, 2006.
^ Leggett, Julian J.; Brian T. Johnston, Moyra Mills, Jackie Gamble, and Liam G. Heaney (April 2005). "Prevalence of Gastroesophageal Reflux in Difficult Asthma". Chest 127 (4): 1227–1231. PubMed. Retrieved on 2006-09-23.
^ American Journal of Respiratory and Critical Care Medicine 1995;151:969–74.
^ Thomson NC, Spears M. The influence of smoking on the treatment response in patients with asthma. Curr Opin Allergy Clin Immunol. 2005;5(1):57–63. PMID 15643345
^ Eisner MD, Yelin EH, Katz PP, et al. Exposure to indoor combustion and adult asthma outcomes: environmental tobacco smoke, gas stoves, and wood-smoke. Thorax. 2002;57(11):973-8. PMID 12403881
^ a b National Asthma Education and Prevention Program. Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma. National Institutes of Health pub no 97–4051. Bethesda, MD, 1997. (PDF)
^ British Thoracic Society & Scottish Intercollegiate Guidelines Network (SIGN). British Guideline on the Management of Asthma. Guideline No. 63. Edinburgh:SIGN; 2004. (HTML, Full PDF, Summary PDF)
^ Cromie, William J.. "Researchers uncover cause of asthma", Harvard University Gazette, Harvard News Office, 2006-03-16. Retrieved on 2006-09-23.
^ a b Hendeles L, Marshik PL, et al. Response to nonprescription epinephrine inhaler during nocturnal asthma. Ann Allergy Asthma Immunol. 2005 Dec;95(6):530-4. PMID 16400891
^ Rodrigo GJ, Nannini LJ. Comparison between nebulized adrenaline and beta2 agonists for the treatment of acute asthma. A meta-analysis of randomized trials. Am J Emerg Med. 2006 Mar;24(2):217-22. PMID 16490653
^ Papi A, Canonica GW, Maestrelli P, Paggiaro P, Olivieri D, Pozzi E, Crimi N, Vignola AM, Morelli P, Nicolini G, Fabbri LM; BEST Study Group. Rescue use of beclomethasone and albuterol in a single inhaler for mild asthma. N Engl J Med. 2007;356:2040-52. PMID 17507703
^ Serevent Diskus, Advair Diskus, and Foradil Information (Long Acting Beta Agonists) - Drug information. FDA (2006-03-03).
^ Ramanujan, Krishna (2006-06-09). Common asthma inhalers cause up to 80 percent of asthma-related deaths, Cornell and Stanford researchers assert. Cornell Chronicle Online. Cornell News Service. Retrieved on 2006-09-23.
^ Rodrigo GJ, Rodrigo C, Hall JB. Acute asthma in adults: a review. Chest. 2004;125(3):1081-102. PMID 15006973
^ Rodrigo G (2005). "Comparison of inhaled fluticasone with intravenous hydrocortisone in the treatment of adult acute asthma". Am J Respir Crit Care Med 171 (11): 1231–6. PMID 15764724.
^ Blanc PD, Trupin L, Earnest G, et al. Alternative therapies among adults with a reported diagnosis of asthma or rhinosinusitis: data from a population-based survey. Chest. 2001;120(5):1461–7. PMID 11713120
^ Shenfield G, Lim E, Allen H. Survey of the use of complementary medicines and therapies in children with asthma. J Paediatr Child Health. 2002;38(3):252-7. PMID 12047692
^ McCarney RW, Brinkhaus B, Lasserson TJ, et al. Acupuncture for chronic asthma. Cochrane Database Syst Rev. 2004;(1):CD000008. PMID 14973944
^ Blackhall K, Appleton S, Cates CJ. Ionisers for chronic asthma. Cochrane Database Syst Rev. 2003;(3):CD002986 PMID 12917939
^ Hondras MA, Linde K, Jones AP. Manual therapy for asthma. Cochrane Database Syst Rev. 2005;(2):CD001002. PMID 15846609
^ Reilly D, Taylor MA, Beattie NG, et al. Is evidence for homoeopathy reproducible? Lancet. 1994;344(8937):1601–6. PMID 7983994
^ White A, Slade P, Hunt C, et al. Individualised homeopathy as an adjunct in the treatment of childhood asthma: a randomised placebo controlled trial. Thorax. 2003;58(4):317-21. PMID 12668794
^ Nagendra HR, Nagarathna R. An integrated approach of yoga therapy for bronchial asthma: a 3-54-month prospective study. J Asthma. 1986;23(3):123-37. PMID 3745111
^ Manocha R, Marks GB, Kenchington P, et al. Sahaja yoga in the management of moderate to severe asthma: a randomised controlled trial. Thorax. 2002;57(2):110-5. PMID 11828038
^ Asthma Treatment
^ Bowler SD, Green A, Mitchell CA. Buteyko breathing techniques in asthma: a blinded randomised controlled trial. Med J Aust. 1998;169(11-12):575-8. PMID 9887897. Free full text
^ McHugh P, Aitcheson F, Duncan B, Houghton F. Buteyko Breathing Technique for asthma: an effective intervention. NZ Med J. 2003;116:1187 PMID 14752538. Free full text
^ Huang SL, Tsai PF, Yeh YF (2002). "Negative association of Enterobius infestation with asthma and rhinitis in primary school children in Taipei". Clin. Exp. Allergy 32 (7): 1029-32. PMID 12100049.
^ "Worm infestation 'beats asthma'", BBC News, 2001-11-02.
^ Leonardi-Bee J, Pritchard D, Britton J (2006). "Asthma and current intestinal parasite infection: systematic review and meta-analysis". Am. J. Respir. Crit. Care Med. 174 (5): 514-23. DOI:10.1164/rccm.200603-331OC. PMID 16778161.
^ Beckett PA, Howarth PH. Pharmacotherapy and airway remodelling in asthma? Thorax. 2003;58(2):163-74. PMID 12554904
^ a b World Health Organization. Bronchial asthma: scope of the problem. Retrieved on 2005-08-23.
^ Patient/Public Education: Fast Facts - Asthma Demographics/Statistics. American Academy of Allergy Asthma & Immunology. Retrieved on 2006-05-02.
^ National Heart, Lung, and Blood Institute (May 2004). Morbidity & Mortality: 2004 Chart Book On Cardiovascular, Lung, and Blood Diseases. National Institutes of Health.
^ National Center for Health Statistics (07 April 2006). Asthma Prevalence, Health Care Use and Mortality, 2002. Centers for Disease Control and Prevention.
^ a b Weiler JM, Layton T, Hunt M. Asthma in United States Olympic athletes who participated in the 1996 Summer Games. J Allergy Clin Immunol. 1998;102(5):722-6. PMID 9819287
^ Helenius I, Haahtela T. Allergy and asthma in elite summer sport athletes. J Allergy Clin Immunol. 2000;106(3):444-52 PMID 10984362

External links
World Health Organization site on asthma
World Health Organization fact sheet on asthma
National Heart, Lung, and Blood Institute — Asthma – U.S. NHLBI Information for Patients and the Public page.
National Heart, Lung, and Blood Institute — Asthma – U.S. NHLBI Information for Health Professionals page.
MedLinePlus: Asthma – a U.S. National Library of Medicine page.
American Academy of Allergy, Asthma, and Immunology – a U.S. organization of medical professionals with a special interest in treating and researching conditions such as allergic rhinitis, asthma, atopic dermatitis/eczema, and anaphylaxis.
Asthma and Allergy Foundation of America – national nonprofit patient advocacy organization with information about asthma.
Asthma UK – a patient-oriented site with information on asthma and ways that UK residents can help improve asthma-related policy.
Asthma Foundation of Queensland Information and education for Australian asthma sufferers.
Case Studies in Environmental Medicine (CSEM): Environmental Triggers of Asthma – Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services.
Asthma as Neurogenic Inflammatory Disease Neurogenic aspects of asthma. Pathophysiological links with other inflammatory disorders.
Asthma and Socio-economic Status
India Asthma Care Society Easy to understand asthma information site for patients.
The Segal Guide to Asthma by Michael Segal MD PhD.

COPD Chronic Obstructive Pulmonary Disease

2007-08-05T21:32:00.000-07:00

Chronic obstructive pulmonary disease
From Wikipedia, the free encyclopedia

For COPD occuring in horses, see recurrent airway obstruction.
Chronic obstructive pulmonary disease

Classification & external resources
ICD-10
J 40. - J 44., J 47.
ICD-9
490 - 496
OMIM
606963
DiseasesDB
2672
MedlinePlus
000091
eMedicine
med/373 emerg/99
MeSH
C08.381.495.389

Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive airway disease (COAD), is a group of diseases characterized by limitation of airflow in the airway that is not fully reversible. COPD is the umbrella term for chronic bronchitis, emphysema and a range of other disorders. It is most often due to tobacco smoking [1] but can be due to other airborne irritants such as coal dust, asbestos or solvents, as well as preserved meats containing nitrites [1].

Signs and symptoms
The main symptoms of COPD include dyspnea (shortness of breath) lasting for months or perhaps years, possibly accompanied by wheezing, and a persistent cough with sputum production.[2] It is possible the sputum may contain blood (hemoptysis), usually due to damage of the blood vessels of the airways. Severe COPD could lead to cyanosis (bluish decolorization usually in the lips and fingers) caused by a lack of oxygen in the blood. In extreme cases it could lead to cor pulmonale due the extra work required by the heart to get blood to flow through the lungs.[3]

COPD is particularly characterised by a ratio of forced expiratory volume over 1 second (FEV1) to forced vital capacity (FVC) being < class="new" title="FEV1" href="http://en.wikipedia.org/w/index.php?title=FEV1&action=edit">FEV1 < title="" href="http://en.wikipedia.org/wiki/Lung_disease#_note-2">[4] (see Spirometry). Other signs include a rapid breathing rate (tachypnea) and a wheezing sound heard through a stethoscope. Pulmonary emphysema is NOT the same as subcutaneous emphysema, which is a collection of air under the skin that may be detected by the crepitus sounds produced on palpation.[5]

Causes

Cigarette smoking
A primary factor of COPD is chronic tobacco smoking. In the United States, around 90% of cases of COPD are due to smoking.[6] Not all smokers will develop COPD, but continuous smokers have at least a 25% risk.[7]
Occupational pollutants
Some occupational pollutants, such as cadmium and silica, have shown to be a contributing risk factor for COPD. The people at highest risk for these pollutants include coal workers, construction workers, metal workers and cotton workers, amongst others. However, in most cases these pollutants are combined with cigarette smoking further increasing the chance of developing COPD.[6] These occupations are commonly associated with other respiratory diseases, particularly pneumoconiosis (black lung disease).
Air pollution
Urban air pollution may be a contributing factor for COPD as it is thought to impair the development of the lung function. In developing countries indoor air pollution, usually due to biomass fuel, has been linked to COPD, especially in women.[1]
Genetics
Very rarely, there may be a deficiency in an enzyme known as alpha 1-antitrypsin which causes a form of COPD.[8]
Other risk factors
Increasing age, male gender, allergy, repeated airway infection and general impaired lung function are also related to the development of COPD.

Pathophysiology

Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years.
Chronic bronchitis is hallmarked by hyperplasia (increased number) and hypertrophy (increased size) of the goblet cells (mucous gland) of the airway, resulting in an increase in secretion of mucus which contributes to the airway obstruction. Microscopically there is infiltration of the airway walls with inflammatory cells, particularly neutrophils. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airway. Further progression leads to metaplasia (abnormal change in the tissue) and fibrosis (further thickening and scarring) of the lower airway. The consequence of these changes is a limitation of airflow.[10].
Emphysema
Main article: Emphysema
Emphysema is defined histologically as the enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.[9]
The enlarged air sacs (alveoli) of the lungs reduces the surface area available for the movement of gases during respiration. This ultimately leads to dyspnea in severe cases. The exact mechanism for the development of emphysema is not understood, although it is known to be linked with smoking and age.

Diagnosis
The diagnosis of COPD is usually suggested by symptoms; it is a clinical diagnosis and no single test is definitive. A comprehensive history from the patient is very important with regard to smoking and occupation. Physical examination with a plethysmograph can reveal the true extent of COPD.

Management
Although COPD is not curable, it can be controlled in a variety of ways.

Smoking cessation
Main article: Smoking cessation
Smoking cessation is one of the most important factors in slowing down the progression of COPD. Even at a late stage of the disease it can reduce the rate of deterioration and prolong the time taken for disability and death.[10]
Occupational change
Workers may be able to transfer to a significantly less contaminated area of the company depending on circumstances. Often however, workers may need complete occupational change.
Pharmacotherapy
Bronchodilators
There are several types of bronchodilators used clinically with varying efficacy: β2 agonists, M3 antimuscarinics, leukotriene antagonists, cromones and xanthines.[11] These drugs relax the smooth muscles of the airway allowing for improved airflow. The change in FEV1 may not be substantial, but changes in the vital capacity are significant. Many patients feel less breathless after taking bronchodilators.
β2 agonists
There are several highly specific β2 agonists available. Salbutamol (Ventolin) is the most widely used short acting β2 agonist to provide rapid relief and should be prescribed as a front line therapy for all classes of patients. Other β2 agonists are Bambuterol, Clenbuterol, Fenoterol, and Formoterol. Longer acting β2 agonists such as Salmeterol act too slowly to be used as relief for dypsnea so these drugs should be used as a secondary therapy. An increased risk is associated with long acting β2 agonists due to decreased sensitivity to inflammation so generally the use of a concomitant corticosteroid is indicated[2][3][4].
M3 muscarinic antagonists (anticholinergics)
Derived from the deadly agaric Amanita muscaria, specific antimuscarinics were found to provide effective relief to COPD. Inhaled antimuscarinics have the advantage of avoiding endocrine and exocrine M3 receptors. The quaternary M3 muscarinic antagonist Ipratropium is widely prescribed with the β2 agonist salbutamol. [5]. Ipratropium is offered combined with salbutamol (Combivent) and with fenoterol (Duovent). Tiotropium provides improved specificity for M3 muscarinic receptors.
Cromones
Cromones are mast cell stabilizers that are thought to act on a chloride channel found on mast cells that help reduce the production of histamine and other inflammatory factors. Chromones are also thought to act on IgE-regulated calcium channels on mast cells. Cromoglicate and Nedocromil, which has a longer half-life, are two chromones available.[12]
Leukotriene antagonists
More recently leukotriene antagonists block the signalling molecules used by the immune system. Montelukast, Pranlukast, Zafirlukast are some of the leukotrienes antagonists.[13]
Xanthines
Theophylline is the prototype of the xanthine [14] class of drug. Teas are natural sources of methylxanthines, xanthines and caffeine while chocolate is a source of theobromine. Caffeine is approximately 16% metabolized into theophylline. Nebulized theophylline is used in the EMR for treatment of dyspnea (Difficulty in breathing). Patients need continual monitoring as theophylline has a narrow therapeutic range. More aggressive EMR interventions include IV H1 antihistamines and IV dexamethasone.
Corticosteroids
Inhaled corticosteriods (specifically glucocorticoids) act in the inflammatory cascade and may improve airway function considerably,[10] however the long term value has not been proven. Corticosteroids are often combined with bronchodilators in a single inhaler. Some of the more common inhaled steroids in use are beclomethasone, mometasone, and fluticasone.
Salmeterol and fluticasone are combined (Advair), however the reduction in death from all causes among patients with COPD in the combination therapy group did not reach the predetermined level of statistical significance.[15][16]
TNF antagonists
Tumor necrosis factor antagonists (TNF) are the most recent class of medications designed to deal with refractory cases. Tumor necrosis factor-alpha is a cachexin or cachectin and is considered a so-called biological drug. They are considerered immunosopressive with attendant risks. These rather expensive drugs include infliximab, adalimumab and etanercept.[17]
Vaccination
Patients with COPD should be routinely vaccinated against influenza, pneumococcus and other diseases to prevent illness and the possibility of death.[11]
Pulmonary rehabilitation
Pulmonary rehabilitation is a program of disease management, counseling and exercise coordinated to benefit the individual.[18] Pulmonary rehabilitation has been shown to relieve difficulties breathing and fatigue. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.[19]
Diet
A recent French study conducted over 12 years with almost 43,000 men concluded that eating a Mediterranean diet "halves the risk of serious lung disease like emphysema and bronchitis". [6]

Prognosis
A good prognosis of COPD relies on an early diagnosis and prompt treatment. Most patients will have improvement in lung function once treatment is started, however eventually signs and symptoms will worsen as COPD progresses. The median survival is about 10 years if two-thirds of expected lung function was lost by diagnosis.

Bronchitis
Acute bronchitis usually resolves in 7-10 days with no underlying lung disease. Chronic bronchitis however is dependent on early recognition and smoking cessation which improves the outcome significantly.

Emphysema
The outcome is better for patients with less damage to the lung who stop smoking immediately. Still, patients with extensive lung damage may live for many years so predicting prognosis is difficult. Death may occur from respiratory failure, pneumonia, or other complications.

Asbestosis
The outcome is clouded by the many complications associated with asbestosis. Malignant mesothelioma is refractory to management affording patients with 6-12 months of life expectancy upon clinical presentation.

Pneumoconiosis
The outcome is good for patients with minimal damage to the lung. However, patients with extensive lung damage may live for many years so predicting prognosis is difficult. Death may occur from respiratory failure, pneumonia, cor pulmonale or other complications.

Pulmonary neoplasms
The stage of the tumor(s) has a major impact on neoplasm prognosis. Staging is the process of determining tumor size, growth rate, potential metastasis, lymph node involvement, treatment options and prognosis. Two-year prognosis for limited small cell pulmonary neoplasms is twenty percent and for extensive disease five percent. The average life expectancy for someone with recurrent small cell pulmonary neoplasms is two to three months.[7]
The 5-year overall survival rate for pulmonary neoplasms is 14%.[20]

Epidemiology
According to the World Health Organization (WHO), 80 million people suffer from moderate to severe COPD and 3 million died due to it in 2005. The WHO predicts that by 2030, it will be the 4th largest cause of mortality worldwide.[21]

Since COPD is not diagnosed until it becomes clinically apparent, prevalence and mortality data greatly underestimate the socioeconomic burden of COPD.[11] In the UK, COPD accounts for about 7% of all days of sickness related absence from work.[10]

Smoking rates in the industrialized world have continued to fall, causing rates of emphysema and pulmonary neoplasms to slowly decline.

References
^ a b Devereux G. ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors. BMJ 2006;332:1142-1144. PMID 16690673
^ U.S. National Heart Lung and Blood Institute - Signs and Symptoms
^ MedicineNet.com - COPD signs & symptoms
^ PatientPlus - Spirometry
^ eMedicine - Barotrauma
^ a b MedicineNet.com - COPD causes
^ Lokke A, Lange P, Scharling H, Fabricius P, Vestbo J. Developing COPD: a 25 year follow up study of the general population. Thorax. 2006 Nov;61(11):935-9. PMID 17071833
^ MedlinePlus Medical Encyclopedia
^ a b Longmore M, Wilkinson I, Rajagopalan S (2005). Oxford Handbook of Clinical Medicine, 6ed. Oxford University Press. pp 188-189. ISBN 0-19-852558-3.
^ a b c d Kumar P, Clark M (2005). Clinical Medicine, 6ed. Elsevier Saunders. pp 900-901. ISBN 0702027634.
^ a b c American Thoracic Society / European Respiratory Society Task Force (2005). Standards for the Diagnosis and Management of Patients with COPD. Version 1.2. New York: American Thoracic Society. http://www.thoracic.org/go/copd
^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=4166895&dopt=Abstract
^ available.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=13804592&amp;amp;dopt=Citation
^ http://www.chemistry.org/portal/a/c/s/1/acsdisplay.html?DOC=HomeMolecule\archive\motw_xanthine_arch.html
^ http://content.nejm.org/cgi/content/short/356/8/775
^ http://clinicaltrials.gov/show/NCT00268216
^ http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/C/CellSignaling.html
^ U.S. National Heart Lung and Blood Institute - Treatment
^ Lacasse Y, Goldstein R, Lasserson T J, Martin, S. Pulmonary rehabilitation for chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews. (4):CD003793, 2006. PMID 12137716
^ John D. Minna, "Neoplasms of the Lung," in Harrison's Principles of Internal Medicine, 16th ed. (2005), p. 506
^ WHO - COPD

External links
National Heart, Lung and Blood Institute - COPD U.S. NHLBI Information for Patients and the Public page.

v • d • e Pathology of respiratory system (J, 460-519)
Acute upper respiratory infections
Upper respiratory tract infection · Common cold · Rhinitis · Sinusitis · Pharyngitis (Strep throat) · Tonsillitis · Laryngitis · Tracheitis · Croup · Epiglottitis

Influenza and Pneumonia
Influenza · Pneumonia (Viral, Bacterial, Bronchopneumonia)

Other acute lower respiratory infections
Bronchitis · Bronchiolitis

Other diseases of upper respiratory tract
Vasomotor rhinitis · Hay fever · Atrophic rhinitis · Nasal polyp · Adenoid hypertrophy · Peritonsillar abscess · Vocal fold nodule · Laryngospasm

Chronic lower respiratory diseases
Emphysema · COPD · Asthma · Status asthmaticus · Bronchiectasis

Lung diseases due to external agents
Pneumoconiosis (Coalworker's pneumoconiosis, Asbestosis, Silicosis, Bauxite fibrosis, Berylliosis, Siderosis) · Byssinosis · Hypersensitivity pneumonitis (Farmer's lung, Bird fancier's lung)

Other, principally affecting the interstitium
Acute respiratory distress syndrome · Pulmonary edema · Hamman-Rich syndrome · Interstitial lung disease

Suppurative and necrotic conditions of lower respiratory tract
Lung abscess · Pleural effusion · Empyema

Other
Pneumothorax · Hemothorax · Hemopneumothorax · Mendelson's syndrome · Respiratory failure · Atelectasis · Mediastinitis

Retrieved from "http://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_disease"
Categories: Pulmonology Occupational diseases

This page was last modified 14:47, 1 August 2007.
All text is available under the terms of the GNU Free Documentation License. (See Copyrights for details.)

ILD Interstitial Lung Disease

2007-08-04T19:59:00.000-07:00

Interstitial lung disease
From Wikipedia, the free encyclopedia
(Redirected from Diffuse parenchymal lung disease)

Interstitial lung diseaseClassification & external resources

End-stage pulmonary fibrosis of unknown origin, taken from an autopsy in the 1980s.
ICD-10
J 84.9
ICD-9
506.4, 508.1, 515, 516.3, 714.81, 770.7
DiseasesDB
31509
eMedicine
ped/1950
MeSH
D017563

Interstitial lung disease (ILD), also known as diffuse parenchymal lung disease (DPLD), refers to a group of lung diseases (including idiopathic pulmonary fibrosis), affecting the alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues. The term ILD is used to distinguish these diseases from obstructive airways diseases. Most types of ILD involve fibrosis, but this is not essential; indeed fibrosis is often a later feature. Hence the term pulmonary fibrosis has fallen out of favor.

Causes
ILD may be classified according to the cause: -

Investigation

Patients with pneumocystis pneumonia can present with interstitial lung disease, as seen in the reticular markings on this AP chest x-ray
Investigation is tailored towards the symptoms and signs. Most patients have blood testing, chest x-ray, pulmonary function testing, and high resolution CT thorax.

Treatment
ILD is not a single disease, but encompasses many different pathological processes. Hence treatment is different for each disease.
If a specific occupational exposure cause is found, the person should avoid that environment. If a drug cause is suspected, that drug should be discontinued.
Many idiopathic and connective tissue-based causes of ILD are treated with prednisolone. Some patients respond to immunosuppressant treatment. Patients with hypoxemia may be given supplemental oxygen.

External links
Coalition for Pulmonary Fibrosis - Research, Education, Support & Hope
What is Pulmonary Fibrosis?
00736 at CHORUS
1476788304 at GPnotebook
MeSH Pulmonary+Fibrosis
MedlinePlus Overview pulmonaryfibrosis
AIMIP - Italian Association for IPF - Associazione Italiana
Dorothy P. and Richard P. Simmons Center for Interstitial Lung Diseases
University of Chicago Interstitial Lung Disease Program

v • d • e Pathology of respiratory system (J, 460-519)
Acute upper respiratory infections
Upper respiratory tract infection · Common cold · Rhinitis · Sinusitis · Pharyngitis (Strep throat) · Tonsillitis · Laryngitis · Tracheitis · Croup · Epiglottitis
Influenza and Pneumonia
Influenza · Pneumonia (Viral, Bacterial, Bronchopneumonia)
Other acute lower respiratory infections
Bronchitis · Bronchiolitis
Other diseases of upper respiratory tract
Vasomotor rhinitis · Hay fever · Atrophic rhinitis · Nasal polyp · Adenoid hypertrophy · Peritonsillar abscess · Vocal fold nodule · Laryngospasm
Chronic lower respiratory diseases
Emphysema · COPD · Asthma · Status asthmaticus · Bronchiectasis
Lung diseases due to external agents
Pneumoconiosis (Coalworker's pneumoconiosis, Asbestosis, Silicosis, Bauxite fibrosis, Berylliosis, Siderosis) · Byssinosis · Hypersensitivity pneumonitis (Farmer's lung, Bird fancier's lung)
Other, principally affecting the interstitium
Acute respiratory distress syndrome · Pulmonary edema · Hamman-Rich syndrome · Interstitial lung disease
Suppurative and necrotic conditions of lower respiratory tract
Lung abscess · Pleural effusion · Empyema
Other
Pneumothorax · Hemothorax · Hemopneumothorax · Mendelson's syndrome · Respiratory failure · Atelectasis · Mediastinitis
Retrieved from "http://en.wikipedia.org/wiki/Interstitial_lung_disease"
Categories: Disease stubs Pulmonology

This page was last modified 04:22, 7 August 2007.
All text is available under the terms of the GNU Free Documentation License.