Emphysema is a long-term, progressive disease of the lung that primarily causes shortness of breath. In people with emphysema, the tissues necessary to support the physical shape and function of the lungs are destroyed. It is included in a group of diseases called chronic obstructive pulmonary disease or COPD (pulmonary refers to the lungs). Emphysema is called an obstructive lung disease because the destruction of lung tissue around smaller airways, called alveoli, makes these airways unable to hold their functional shape upon exhalation.

The term means swelling and comes from the Greek emhysan meaning inflate, itself composed of en meaning in and physa meaning breath, blast. [1]

Contents

[hide] 1 Classification

o 1.1 Congenital lobar emphysema

2 Signs and symptoms

3 Causes

4 Pathophysiology

5 Diagnosis

6 Prognosis and treatment

7 Research

8 Notable cases

9 Additional images

10 See also

11 Footnotes

12 External links

[edit] Classification

Emphysema can be classified into primary and secondary color. However, it is more commonly classified by location.

Emphysema can be subdivided into panacinary and centroacinary (or panacinar and centriacinar,[2] or centrilobular and panlobular).[3]

Panacinar (or panlobular) emphysema: The entire respiratory acinus, from respiratory bronchiole to alveoli, is expanded. Occurs more commonly in the lower lobes, especially basal segments, and anterior margins of the lungs.[2]

Centriacinar (or centrilobular) emphysema: The respiratory bronchiole (proximal and central part of the acinus) is expanded. The distal acinus or alveoli are unchanged. Occurs more commonly in the upper lobes.[2]

Other types include distal acinar and irregular.[2]

A special type is congenital lobar emphysema (CLE).

[edit] Congenital lobar emphysema

CLE results in overexpansion of a pulmonary lobe and resultant compression of the remaining lobes of the ipsilateral lung, and possibly also the contralateral lung. There is bronchial narrowing because of weakened or absent bronchial cartilage.[4]

There may be congenital extrinsic compression, commonly by an abnormally large pulmonary artery. This causes malformation of bronchial cartilage, making them soft and collapsible.[4]

CLE is potentially reversible, yet possibly life-threatening, causing respiratory distress in the neonate.[4]

[edit] Signs and symptoms

Emphysema is a disease of the lung tissue caused by destruction of structures feeding the alveoli, in some cases owing to the action of alpha 1-antitrypsin deficiency. This causes the small airways to collapse during forced exhalation, as alveolar collapsibility has decreased. As a result, airflow is impeded and air becomes trapped in the lungs, in the same way as other obstructive lung diseases. Symptoms include shortness of breath on exertion, and an expanded chest. However, the constriction of air passages isn't always immediately deadly, and treatment is available. Most of the people who have emphysema are smokers. Damage caused by emphysema is permanent even after the person stops smoking. People with this disease do not get enough oxygen and cannot eradicate the carbon dioxide, so they always have a shortage of breath.

[edit] Causes

The primary cause of emphysema is the smoking of cigarettes. In some cases it may be due to alpha 1-antitrypsin deficiency. Severe cases of A1AD may also develop cirrhosis of the liver, where the accumulated A1AT leads to a fibrotic reaction.

[edit] Pathophysiology

Pathology of lung showing centrilobular emphysema characteristic of smoking. Closeup of fixed, cut surface shows multiple cavities lined by heavy black carbon deposits. (CDC/Dr. Edwin P. Ewing, Jr., 1973)

In normal breathing, air is drawn in through the bronchi and into the alveoli, which are tiny sacs surrounded by capillaries. Alveoli absorb oxygen and then transfer it into the blood. When toxicants, such as cigarette smoke, are breathed into the lungs, the harmful particles become trapped in the alveoli, causing a localized inflammatory response. Chemicals released during the inflammatory response (e.g., elastase) can eventually cause the alveolar septum to disintegrate. This condition, known as septal rupture, leads to significant deformation of the lung architecture.[5] The large cavities left by the septal degeneration are known as bullae (sin. = bulla). These deformations result in a large decrease of alveoli surface area used for gas exchange. This results in a decreased Transfer Factor of the Lung for Carbon Monoxide (TLCO). To accommodate the decreased surface area, thoracic cage expansion (barrel chest) and diaphragm contraction (flattening) take place. Expiration increasingly depends on the thoracic cage and abdominal muscle action, particularly in the end expiratory phase. Due to decreased ventilation, the ability to exude carbon dioxide is significantly impaired. In the more serious cases, oxygen uptake is also impaired.

As the alveoli continue to break down, hyperventilation is unable to compensate for the progressively shrinking surface area, and the body is not able to maintain high enough oxygen levels in the blood. The body's last resort is vasoconstricting appropriate vessels. This leads to pulmonary hypertension, which places increased strain on the right side of the heart, the side responsible for pumping deoxygenated blood to the lungs. The heart muscle thickens in order to pump more blood. This condition is often accompanied by the appearance of jugular venous distension. Eventually, as the heart continues to fail, it becomes larger and blood backs up in the liver.

Patients with alpha 1-antitrypsin deficiency (A1AD) are more likely to suffer from emphysema. A1AT inhibits inflammatory enzymes (such as elastase) from destroying the alveolar tissue. Most A1AD patients do not develop clinically significant emphysema, but smoking and severely decreased A1AT levels (10-15%) can cause emphysema at a young age. The type of emphysema caused by A1AD is known as panacinar emphysema (involving the entire acinus) as opposed to centrilobular emphysema, which is caused by smoking. Panacinar emphysema typically affects the lower lungs, while centrilobular emphysema affects the upper lungs. A1AD causes about 2% of all emphysema. Smokers with A1AD are at the greatest risk for emphysema. Mild emphysema can often develop into a severe case over a short period of time (1–2 weeks).

While A1AD provides some insight into the pathogenesis of the disease, hereditary A1AT deficiency only accounts for a small proportion of the disease. Studies for the better part of the past century have focused mainly upon the putative role of leukocyte elastase (also neutrophil elastase), a serine protease found in neutrophils, as a primary contributor to the connective tissue damage seen in the disease. This hypothesis, a result of the observation that neutrophil elastase is the primary substrate for A1AT, and A1AT is the primary inhibitor of neutrophil elastase, together have been known as the "protease-antiprotease" theory, implicating neutrophils as an important mediator of the disease. However, more recent studies have brought into light the possibility that one of the many other numerous proteases, especially matrix metalloproteases might be equally or more relevant than neutrophil elastase in the development of non-hereditary emphysema.

The better part of the past few decades of research into the pathogenesis of emphysema involved animal experiments where various proteases were instilled into the trachea of various species of animals. These animals developed connective tissue damage, which was taken as support for the protease-antiprotease theory. However, just because these substances can destroy connective tissue in the lung, as anyone would be able to predict, doesn't establish causality. More recent experiments have focused on more technologically advanced approaches, such as ones involving genetic manipulation. One particular development with respect to our understanding of the disease involves the production of protease "knock-out" animals, which are genetically deficient in one or more proteases, and the assessment of whether they would be less susceptible to the development of the disease. Often individuals who are unfortunate enough to contract this disease have a very short life expectancy, often 0–3 years at most.

[edit] Diagnosis

A severe case of emphysema.

The diagnosis is usually confirmed by pulmonary function testing (e.g. spirometry); however, X-ray radiography may aid in the diagnosis.

[edit] Prognosis and treatment

Emphysema is an irreversible degenerative condition. The most important measure to slow its progression is for the patient to stop smoking and avoid all exposure to cigarette smoke and lung irritants. Pulmonary rehabilitation can be very helpful to optimize the patient's quality of life and teach the patient how to actively manage his or her care. Patients with emphysema and chronic bronchitis can do more for themselves than patients with any other disabling disease.

Emphysema is also treated by supporting the breathing with anticholinergics, bronchodilators, steroid medication (inhaled or oral), effective body positioning (High Fowlers), and supplemental oxygen as required. Treating the patient's other conditions including gastric reflux and allergies may improve lung function. Supplemental oxygen used as prescribed (usually more than 20 hours per day) is the only non-surgical treatment which has been shown to prolong life in emphysema patients. There are lightweight portable oxygen systems which allow patients increased mobility. Patients can fly, cruise, and work while using supplemental oxygen. Other medications are being researched.

Lung volume reduction surgery (LVRS) can improve the quality of life for certain carefully selected patients. It can be done by different methods, some of which are minimally invasive. In July 2006 a new treatment, placing tiny valves in passages leading to diseased lung areas, was announced to have good results, but 7% of patients suffered partial lung collapse. The only known "cure" for emphysema is lung transplant, but few patients are strong enough physically to survive the surgery. The combination of a patient's age, oxygen deprivation and the side-effects of the medications used to treat emphysema cause damage to the kidneys, heart and other organs. Surgical transplantation also requires the patient to take an anti-rejection drug regimen which suppresses the immune system, and can lead to microbial infection of the patient. Patients who think they may have contracted the disease are recommended to seek medical attention as soon as possible.

[edit] Research

A study published by the European Respiratory Journal suggests that tretinoin (an anti-acne drug commercially available as Retin-A) derived from vitamin A can reverse the effects of emphysema in mice by returning elasticity (and regenerating lung tissue through gene mediation) to the alveoli.[6][7]

While vitamin A consumption is not known to be an effective treatment or prevention for the disease, this research could in the future lead to a cure. A follow-up study done in 2010 found inconclusive results ("no definitive clinical benefits") using Vitamin A (retinoic acid) in treatment of emphysema in humans and stated that further research is needed to reach conclusions on this treatment.[8]

[edit] Notable cases

Notable cases of emphysema have included Ava Gardner, Don Cornell, Spencer Tracy,[9] Leonard Bernstein, Eddie Dean,[10] Dean Martin, Norman Rockwell, Samuel Beckett, Johnny Carson, Al Capp, T. S. Eliot, Tallulah Bankhead, Dick York, James Franciscus, R. J. Reynolds, R. J. Reynolds Jr., R. J. Reynolds, III,[11] Don Imus,[12] Ike Turner, Charlie Simpson, Yosef Hayim Yerushalmi, Elizabeth Dawn, Jerry Reed, Boris Karloff, Leonid Brezhnev and Paul Avery.[13]

[edit] Additional images

H&E (haematoxylin and eosin) stained lung tissue sample from an end-stage emphysema patient. RBCs are red, nuclei are blue-purple, other cellular and extracellular material is pink, and air spaces are white.

Micrograph demonstrating emphysema (left of image - large empty spaces) and lung tissue with relative preservation of the alveoli (right of image). H&E stain.

Air sac" redirects here. For the specialist air sacs found in birds, see bird anatomy. For the air sac in the throat of birds and other species, see throat sac."Alveolus" redirects here. For the sockets in which teeth are placed, see dental alveolus.

The alveoli

An alveolus (plural: alveoli, from Latin alveolus, "little cavity") is an anatomical structure that has the form of a hollow cavity. Found in the lung, the pulmonary alveoli are spherical outcroppings of the respiratory sites of gas exchange with the blood. Alveoli are particular to mammalian lungs. Different structures are involved in gas exchange in other vertebrates.[1] The alveolar membrane is the gas-exchange surface. The blood brings carbon dioxide from the rest of the body for release into the alveoli, and the oxygen in the alveoli is taken up by the blood in the alveolar blood vessels, to be transported to all the cells in the body.

Contents

[hide] 1 Location 2 Anatomy

3 Diseases

4 Additional images

5 References

6 External links

[edit] Location

The alveoli are located in the respiratory zone of the lungs, at the distal termination of the alveolar ducts and atria, forming the termination point of the respiratory tract. They provide total surface area of about 75 m2[2].

[edit] Anatomy

The alveoli contain some collagen and elastic fibres. The elastic fibers allow the alveoli to stretch as they fill with air when breathing in. They then spring back during breathing out in order to expel the carbon dioxide-rich air.

Each human lung contains about 300 million alveoli. Each alveolus is wrapped in a fine mesh of capillaries covering about 70% of its area. An adult alveolus has an average diameter of 200 to 300 microns, with an increase in diameter during inhalation.[citation needed]

The alveoli consist of an epithelial layer and extracellular matrix surrounded by capillaries. In some alveolar walls there are pores between alveoli called Pores of Kohn.

There are three major alveolar cell types in the alveolar wall (pneumocytes):

Type I (Squamous Alveolar) cells that form the structure of an alveolar wall Type II (Great Alveolar) cells that secrete pulmonary surfactant to lower the surface

tension of water and allows the membrane to separate, thereby increasing the capability to exchange gases. Surfactant is continuously released by exocytosis. It forms an underlying aqueous protein-containing hypophase and an overlying phospholipid film composed primarily of dipalmitoyl phosphatidylcholine.

Macrophages that destroy foreign material, such as bacteria.

Reinflation of the alveoli following exhalation is made easier by pulmonary surfactant, which is a phospholipid and protein mixture that reduces surface tension in the thin fluid coating within all alveoli. The fluid coating is produced by the body in order to facilitate the transfer of gases between blood and alveolar air. The surfactant is produced by great alveolar cells (granular pneumonocytes, a cuboidal epithelia), which are the most numerous cells in the alveoli, yet do not cover as much surface area as the squamous alveolar cells (a squamous epithelium).

Great alveolar cells also repair the endotheilium of the alveolus when it becomes damaged. Insufficient pulmonary surfactant in the alveoli can contribute to atelectasis (collapse of part or all of the lung). Without pulmonary surfactant, atelectasis is a certainty; however, there are other causes of lung collapse such as trauma (pneumothorax), COPD, and pleuritis.[3]

[edit] Diseases

Acute respiratory distress syndrome (ARDS) is a severe inflammatory disease of the lung. Usually triggered by other pulmonary pathology, the uncontrolled inflammation leads to impaired gas exchange, alveolar flooding and/or collapse, and systemic inflammatory response syndrome. It usually requires mechanical ventilation in an intensive care unit setting.

Infant respiratory distress syndrome (IRDS) is a syndrome caused by lack of surfactant in the lungs of premature infants.

In asthma, the bronchioles, or the "bottle-necks" into the sac are restricted, causing the amount of air flow into the lungs to be greatly reduced. It can be triggered by irritants in the air, photochemical smog for example, as well as substances that a person is allergic to.

Emphysema is another disease of the lungs, whereby the elastin in the walls of the alveoli is broken down by an imbalance between the production of neutrophil elastase (elevated by cigarette smoke) and alpha-1-antitrypsin (the activity varies due to genetics or reaction of a critical methionine residue with toxins including cigarette smoke). The resulting loss of elasticity in the lungs leads to prolonged times for exhalation, which occurs through passive recoil of the expanded lung. This leads to a smaller volume of gas exchanged per breath.

Chronic bronchitis occurs when an abundance of mucus is produced by the lungs. The production of this substance occurs naturally when the lung tissue is exposed to irritants. In chronic bronchitis, the air passages into the alveoli, the broncholiotes, become clogged with mucus. This causes increased coughing in order to remove the mucus, and is often a result of extended periods of exposure to cigarette smoke.

Cystic fibrosis is a genetic condition caused by the dysfunction of a transmembrane protein responsible for the transport of chloride ions. This causes huge amounts of mucus to clog the bronchiolites, similar to chronic bronchitis. The result is a persistent cough and reduced lung capacity.

Diffuse interstitial fibrosis

Lung cancer is a common form of cancer causing the uncontrolled growth of cells in the lung tissue. Due to the sensitivity of lung tissue, such malignant growth is often hard to treat effectively.

Pneumonia is an infection of the lung parenchyma, which can be caused by both viruses and bacteria. Cytokines and fluids are released into the alveolar cavity and/or interstitium in response to infection, causing the effective surface area of gas exchange in the lungs to be reduced. If this happens to such a degree that the patient cannot draw enough oxygen from his environment to maintain cellular respiration, then the victim may need supplemental oxygen.

Cavitary pneumonia is a process in which the alveoli are destroyed and produce a cavity. As the alveoli are destroyed, the surface area for gas exchange to occur becomes reduced. Further changes in blood flow can lead to decline in lung function.

Pulmonary contusion is a bruise of the lung tissue.

[edit] Additional images

Bronchial anatomy

Emphysema Causes

Cigarette smoking is by far the most dangerous behavior that causes people to develop emphysema, and it is also the most preventable cause. Other risk factors include a deficiency of an enzyme called alpha-1-antitrypsin, air pollution, airway reactivity, heredity, male sex, and age.

The importance of cigarette smoking as a risk factor for developing emphysema cannot be overemphasized. Cigarette smoke contributes to this disease process in two ways. It destroys lung tissue, which results in the obstruction of air flow, and it causes inflammation and irritation of airways that can add to air flow obstruction.

o Destruction of lung tissue occurs in several ways. First, cigarette smoke directly affects the cells in the airway responsible for clearing mucus and other secretions. Occasional smoking temporarily disrupts the sweeping action of tiny hairs called cilia that line the airways. Continued smoking leads to longer dysfunction of the cilia. Long-term exposure to cigarette smoke causes the cilia to disappear from the cells lining the air passages. Without the constant sweeping motion of the cilia, mucous secretions cannot be cleared from the lower respiratory tract. Furthermore, smoke causes mucous secretion to be increased at the same time that the ability to clear the secretions is decreased. The resulting mucous buildup can provide bacteria and other organisms with a rich source of food and lead to infection.

o The immune cells in the lung, whose job it is to prevent and fight infection, are also affected by cigarette smoke. They cannot fight bacteria as effectively or clear the lungs of the many particles (such as tar) that cigarette smoke contains. In these ways cigarette smoke sets the stage for frequent lung infections. Although these infections may not even be serious enough to require medical care, the

inflammation caused by the immune system constantly attacking bacteria or tar leads to the release of destructive enzymes from the immune cells.

o Over time, enzymes released during this persistent inflammation lead to the loss of proteins responsible for keeping the lungs elastic. In addition, the tissue separating the air cells (alveoli) from one another also is destroyed. Over years of chronic exposure to cigarette smoke, the decreased elasticity and destruction of alveoli leads to the slow destruction of lung function.

Alpha-1-antitrypsin (also known as alpha-1-antiprotease) is a substance that fights a destructive enzyme in the lungs called trypsin (or protease). Trypsin is a digestive enzyme, most often found in the digestive tract, where it is used to help the body digest food. It is also released by immune cells in their attempt to destroy bacteria and other material. People with alpha-1-antitrypsin deficiency cannot fight the destructive effects of trypsin once it is released in the lung. The destruction of tissue by trypsin produces similar effects to those seen with cigarette smoking. The lung tissue is slowly destroyed, thus decreasing the ability of the lungs to perform appropriately. The imbalance that develops between trypsin and antitrypsin results in an “innocent bystander” effect. Foreign objects (e.g. bacteria) are trying to be destroyed but this enzyme destroys normal tissue since the second enzyme (antiprotease) responsible for controlling the first enzyme (protease) is not available or is poorly functioning. This is referred to as the “Dutch” hypothesis of emphysema formation.

Air pollution acts in a similar manner to cigarette smoke. The pollutants cause inflammation in the airways, leading to lung tissue destruction.

Close relatives of people with emphysema are more likely to develop the disease themselves. This is probably because the tissue sensitivity or response to smoke and other irritants may be inherited. The role of genetics in the development of emphysema, however, remains unclear.

Abnormal airway reactivity, such as bronchial asthma, has been shown to be a risk factor for the development of emphysema.

Men are more likely to develop emphysema than women. The exact reason for this is unknown, but differences between male and female hormones are suspected.

Older age is a risk factor for emphysema. Lung function normally declines with age. Therefore, it stands to reason that the older the person, the more likely they will have enough lung tissue destruction to produce emphysema.

It is important to emphasize that COPD is often not purely emphysema or bronchitis, but varying combinations of both.

Emphysema Symptoms

Shortness of breath is the most common symptom of emphysema. Cough, sometimes caused by the production of mucus, and wheezing may also be symptoms of emphysema. You may notice that your tolerance for exercise decreases over time. Emphysema usually develops slowly. You may not have any acute episodes of shortness of breath. Slow deterioration is the rule, and it may go unnoticed. This is especially the case if you are a smoker or have other medical problems that limit your ability to exercise.

One of the hallmark signs of emphysema is "pursed-lipbreathing." The person with emphysema struggles to exhale completely, in an attempt to empty trapped air. They purse their lips, leaving only a small opening. Then, when they exhale, the lips block the flow of air, increasing pressure in the collapsed airways, and opening them, allowing the trapped air to empty.

People with emphysema may develop a "barrel chest," where the distance from the chest to the back, which is normally less than the distance side to side, becomes more pronounced. This is a direct result of air becoming trapped behind obstructed airways.

Exams and Tests

When a doctor suspects you have emphysema, based on your complaints, a physical examination will be performed. The doctor will pay particular attention to your breathing sounds, your heart sounds, and your general physical appearance. A number of tests may be ordered or performed in the office or in the Emergency Department. These tests serve to clarify the extent of the disease, the remaining lung function, and the presence of lung infections.

A chest X-ray helps the doctor to identify changes in your lung that may indicate emphysema. The X-ray also may show the presence of an infection or a mass in the lung (such as a tumor) that could explain your symptoms. Shortness of breath has many causes. The chest X-ray is considered by most doctors to be the quickest and easiest test to begin to separate the different possible causes and formulate a diagnosis.

Lung function tests can give the doctor specific information about how the lungs work mechanically. These tests involve having you breathe into a tube that is connected to a computer or some other monitoring device, which can record the necessary information. The tests measure how much air your lungs can hold, how quickly your lungs can expel air during expiration, and how much reserve capacity your lungs have for increased demand, such as during exercise.

If you have a family history of alpha-1-antitrypsin deficiency, the doctor may wish to send a blood test to evaluate for this genetic disease.

Blood tests may also be used to check your white blood cell count, which can sometimes indicate an acute infection. This information can be used with the chest X-ray to evaluate for pneumonia, bronchitis, or other respiratory infections that can make emphysema worse.

Another blood test that may be helpful, especially in the hospital setting, is called the arterial blood gas. This test helps doctors determine how much oxygen and carbon dioxide are in your blood.

Medical Treatment

Treatment for emphysema can take many forms. Different approaches to treatment are available. Generally, a doctor will prescribe these treatments in a step-wise approach, depending on the severity of your condition.

Stop smoking: Although not strictly a treatment, most doctors make this recommendation for people with emphysema (and everyone). Quitting smoking may halt the progression of the disease and should improve the function of the lungs to some extent. Lung function deteriorates with age. In those susceptible to developing COPD, smoking can result in a five-fold deterioration of lung function. Smoking cessation may return lung function from this rapid deterioration to its normal rate after smoking is stopped. A doctor may be able to prescribe medications to help in breaking the addiction and can also recommend behavioral therapies, such as support groups. You and your doctor should work to find an approach that results in the successful end to cigarette smoking and, in the process, the beginning of improved lung function and quality of life.

Bronchodilating medications: These medications, which cause the air passages to open more fully and allow better air exchange, are usually the first medications that a doctor will prescribe for emphysema. In very mild cases, bronchodilators may be used only as needed, for episodes of shortness of breath.

o The most common bronchodilator for mild cases of emphysema is albuterol (Proventil or Ventolin). It acts quickly, and 1 dose usually provides relief for 4-6 hours. Albuterol is most commonly available as a metered-dose inhaler or MDI, and this is the form that is used most often for patients with mild emphysema, with intermittent shortness of breath. When used for this purpose, some people refer to their albuterol inhaler as a "rescue" medication. It acts to rescue them from a more serious attack of shortness of breath.

o If you have some degree of shortness of breath at rest, a doctor may prescribe the albuterol to be given at regularly scheduled intervals, either through the MDI, or by nebulization. Nebulization involves breathing in liquid medication that has been vaporized by a continuous flow of air (in much the same way a whole-room vaporizer causes liquid droplets to enter the air by the flow of air through water). Nebulized albuterol may be prescribed once scheduled doses via inhaler are no longer adequate to alleviate shortness of breath.

o Ipratropium bromide (Atrovent) is another bronchodilating medication that is used for relatively mild emphysema. Similar to albuterol, it is available in both an inhaler and as a liquid for nebulization. Unlike albuterol, however, ipratropium bromide is usually given in scheduled intervals. Therefore, it is not usually prescribed for "rescue" purposes. Atrovent lasts longer than albuterol, however,

and often provides greater relief. Tiotropium (Spiriva) is a long acting form of ipratropium. This once a day medicine has shown to result in a fewer hospitalizations and possible increased survival in some patients with COPD.

o Methylxanthines (Theophylline) and other bronchodilating medications are available that have varying properties that may make them useful in certain cases. Theophylline (Theo-Dur, Uniphyl) is a medication given orally (tablets). It can have a sustained effect on keeping air passageways open. Theophylline levels must be monitored by blood tests. This medicine is used less frequently today due to its narrow therapeutic window. Too much theophylline can produce an overdose; too little, and there will not be enough relief of shortness of breath. In addition, other drugs can interact with theophylline, altering the blood level without warning. For this reason, doctors now prescribe theophylline after very carefully considering its potential for other drug interactions. If you take theophylline, take the medication as prescribed and check with your doctor before starting any new medication. Some new studies are suggesting that very low dose theophylline may have anti-inflammatory properties as well. Theophylline used to be widely prescribed; currently it is prescribed infrequently and usually only in special circumstances because of its narrow range of effectiveness, necessity of blood level monitoring and its interactions with other drugs.

Steroid medications: They decrease inflammation in the body. They are used for this effect in the lung and elsewhere and have been shown to be of some benefit in emphysema. However, not all people will respond to steroid therapy. Steroids may either be given orally or inhaled through an MDI or another form of inhaler.

Antibiotics: These medications are often prescribed for people with emphysema who have increased shortness of breath. Even when the chest x-ray does not show pneumonia or evidence of infection, people treated with antibiotics tend to have shorter episodes of shortness of breath. It is suspected that infection may play a role in an acute bout of emphysema, even before the infection worsens into a pneumonia or acute bronchitis.

o Data now suggests that when patients with COPD have a sudden worsening of their symptoms of cough and shortness of breath (also termed an exacerbation), brief and immediate use of steroids and antibiotics can reduce hospitalizations.

Oxygen: If you have shortness of breath and go to a hospital's emergency department, you often are given oxygen. It may even be necessary to give oxygen by placing a tube in your windpipe and allowing a machine to assist your breathing (also termed tracheal intubation). In some cases, it may be necessary for you to receive oxygen at home as well. There are home-based oxygen tanks available and portable units that enable you to be mobile and engage in normal day-to-day activities.

Surgery

Surgical options are available to some people with advanced emphysema.

Lung Volume Reduction surgery (LVRS): Although it may not make sense that reducing the size of the lung could help the shortness of breath from emphysema, it is important to remember that emphysema causes an abnormal expansion of the chest wall, which decreases the efficiency of breathing. This surgery is only effective if both upper lobes of the lungs are involved. Removal of this involved lung allows for better expansion of the lower portion of lungs. In a select group of emphysema patients this can improve quality of life for a period of years. Newer studies are underway using one way valves placed in the airways to simulate this volume reduction. The effectiveness of this less invasive procedure is undergoing study at this time.

Lung transplant: For people with the most advanced disease, transplantation of either one or both lungs can produce a near-cure. Transplantation brings with it another set of risks and benefits. People who undergo transplantation, however, will have to take medication to prevent the rejection of the transplant by the body. Also, not everyone qualifies for transplantation, and those who do are limited by the short supply of available organs.

_____________________________________________________________

ntroduction to emphysema

The lungs are a pair of organs in the chest that are primarily responsible for the exchange of oxygen and carbon dioxide between the air we breathe and the blood.

The lung is composed of clusters of small air sacs (alveoli) divided by thin, elastic walls or membranes. Capillaries, the tiniest of blood vessels, run within these walls between the alveoli and allow blood and air to come near each other. The distance between the air in the lungs and the blood in the capillaries is very small, and allows molecules of oxygen and carbon dioxide to transfer across the membranes.

Air reaches the alveoli via the bronchial tree. The trachea splits into the right and left mainstem bronchi, which branch further into bronchioles and finally ends in the alveolar air sacs.

When we breathe in, air enters the lung and the alveoli expand. Oxygen is transferred onto hemoglobin molecules in the red blood cells to be transported to the rest of the body for use. As oxygen attaches to the red blood cell, carbon dioxide, the waste product of metabolism, detaches and crosses into the alveoli to be exhaled. When we breathe out, the alveoli get squeezed by the elasticity in their walls and air is pushed out of the lungs.

Emphysema

Emphysema is a chronic lung condition that is a major cause of death and disability in the United States. Two million Americans are affected, largely those who are over age 50. With emphysema, breathing becomes difficult as the fine architecture of the lung is destroyed, leading to large holes in the lung, obstruction of the airways, trapping of air, and difficulty

exchanging oxygen because of reduced elasticity of the lungs.In the United States, cigarette smoking is by far the most important risk factor for emphysema. Emphysema costs more than $2.5 billion in annual health care expenses and causes or contributes to 100,000 deaths in the U.S. each year.Current medical treatments include smoking cessation for those who still smoke, exercise rehabilitation, oxygen therapy for those with low blood oxygen levels, supportive and preventive measures such as flu shots, pneumonia vaccine, medications such as bronchodilators to help open airways, prompt treatment of

respiratory infections, and lung transplantation.Emphysema is one form of chronic obstructive pulmonary disease (COPD) -- a slowly progressive disease of the airways that is characterized by a gradual loss of lung function. Chronic bronchitis, chronic obstructive bronchitis, or a combination of these conditions with emphysema also are forms of COPD. COPD is the fourth most common and the most rapidly increasing cause of death in the United States.SOURCE: National Heart, Lung and Blood Institute

Medical/Legal DisclaimerCopyright © 2003 Nucleus Medical Art, Inc. All Rights Reserved.

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This follows the pages about Introduction to the Respiratory System and the Anatomy of the Upper Respiratory Tract.

It is not possible to completely describe the lower respiratory tract in a single diagram because this part of the body consists of several layers. However, the main components of the lower respiratory tract are shown below. These include the requirements of most first-level courses in anatomy and physiology. The diagram is followed by descriptions of the parts shown and links to pages that explain specific features in more detail.

 

Diagram of the Structureof the Lower Respiratory Tract

 

Most textbooks describe the larynx as part of the upper respiratory tract, it is also shown in the diagram above to make clear the position of the structures described here relative to those of the upper respiratory tract.

The trachea (also known as the windpipe) extends from below the larynx towards the lungs. It is reinforced by a column of C-shaped rings of hyaline cartilage that support the trachea in the open position when thoracic pressure falls. The trachea is also coated with mucous membranes and cilia (ciliated epithelium) that trap minute dust particles and sweep them upwards. The C-shaped cartilage merges with the submucosa.

Outer Structures of the Lower Respiratory Tract:

The external intercostal muscles contract to raise the rib cage upwards and outwards. For more about the function of these muscles, see the page about external respiration.

Two continuous layers of epithelium called "pleurae" cover the lungs, chest wall, and mediastinum*. The inner pleura (covering the lung) is called the visceral pleura and the outer pleura (covering the chest wall) is called the parietal pleura. These two pleurae are separated by a thin layer of liquid called the pleural effusion this fluid occupies the space between the pleurae (which is called the pleural cavity). The pleural effusion acts as a lubricant, allowing the surfaces of the two pleurae to slip over each other during breathing.The pleural membranes are also described on the page about components of the respiratory system.

Inner Structures of the Lower Respiratory Tract:

Inside the pleural membranes are the structures that perform the functions of the lungs - their main functions being the gaseous exchange that oxygenates blood. This involves 3 main groups of structures:

1. Structures delivering deoxygenated blood to the lungs :The pulmonary artery conveys blood to the lungs after it has passed around the body delivering oxygen and nutrients to tissues. This blood is therefore low in oxygen but high in carbon dioxide (CO2) when it is returned to the lungs. The pulmonary artery divides into many arterioles that carry blood further into the structures of the lung. These continue to sub-divide until they eventually form capillaries.

2. Structures that re-oxygenate the bloodby removing carbon dioxide (CO2) from it and replacing the CO2 removed with oxygen (O2) :

These structures perform the specialised functions that re-oxygenate blood. Only some of the bronchial structures are illustrated above - to show their position relative to other structures of the lower respiratory tract. The diagram on this page shows the main bronchus, an example of a terminal bronchiole (there are many in each lung), and some alveoli (sing. = "alveolus"), in each lung. These structures are all part of the main bronchial structure of each lung, which is called the tracheobronchial tree. To show this in more detail, the tracheobronchial tree is illustrated on it's own page.

3. Structures that return the re-oxygenated blood to the heart:The pulmonary vein and the network of venules that lead to it convey newly oxygenated blood from the capillaries of the lung to the heart (from which that oxygenated blood is pumped around the body for supply to the rest of the body, via the blood vessels of the systemic circulation system).

 

* The mediastinum is located in the midline of the body between the lungs. It contains the heart, trachea, oesophagus, major blood vessels to/from the heart (aorta and vena cava), phrenic and vagus nerves, and some lymph nodes.

 

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Definition of Antielastase

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Antielastase: An inhibitor of the action of the enzyme elastase. Alpha-1 antitrypsin is an antielastase. Also called an elastase inhibitor.

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