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What Is Emphysema?

Edited by Guy Slowik MD FRCS. Last updated on June 28th 2011

Emphysema is a lung disease that reduces the ability of the lungs to expel air, a process

which depends upon the natural rubber-band-like quality or elastic properties of the

lungs. Damage occurs to the tiny airways in the lungs called bronchioles. Bronchioles arejoined to alveoli, tiny grape-like clusters of sacs in the lungs where oxygen from the air is

exchanged for carbon dioxide from the body. The elastic properties of the lung reside in

the tissue around the alveoli.

In emphysema:

Because the lungs lose elasticity they become less able to contract.

This prevents the alveoli from deflating completely, and the person has difficulty

exhaling.

Hence, the next breath is started with more air in the lungs. The trapped "old" air takes up space, so the alveoli are unable to fill with enough

fresh air to supply the body with needed oxygen.

A person with emphysema may feel short of breath during exertion and, as the diseaseprogresses, even while at rest.

Emphysema is one of several irreversible lung diseases that diminish the ability to exhale.

This group of diseases is called chronic obstructive pulmonary disease (COPD). The

two major diseases in this category are emphysema and chronic bronchitis, which oftendevelop together.

For more information about bronchitis, go to Bronchitis.

Facts About Emphysema

Nearly two million Americans have emphysema.

Emphysema ranks 15th among chronic conditions that force people to limit their

activities.

Cigarette smoking is the primary cause of emphysema.

Most people with emphysema are older men. As with lung cancer and other smoking-

related diseases, however, the incidence of emphysema is increasing among women.

Emphysema doesn't develop suddenly. Instead, it comes on gradually, usually after
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years of exposure to cigarette smoke or some other inhaled irritant.

Typically, symptoms of emphysema appear only after 30 to 50 percent of lung tissue

is lost.

Emphysema rates are highest for men age 65 and older.

More people in the Midwest have emphysema than in any other region in the country.

Emphysema is an irreversible disease that can be slowed but not reversed or stopped.

What Causes Emphysema?


Generally, lungs become damaged because of reactions to irritants entering the airways

and alveoli. Researchers continue to investigate the factors that may make some peoplemore susceptible to emphysema than others. But there are some clear causes for

emphysema:

Cigarette smoking

Alpha-1 antitrypsin deficiency

Cigarette Smoking

Cigarette smoking is the major cause of emphysema. When exposed to cigarette smoke,the air sacs of the lungs produce defensive cells, called macrophages, which "eat" the

inhaled particles. But macrophages are stimulated to release materials which can destroy

the proteins that let the lungs expand and contract, called elastin and collagen.

Cigarette smoke also damages the cilia, tiny hair-like projections in the bronchi that"sweep" foreign bodies and bacteria out of the lungs.

Alpha-1 Antitrypsin Deficiency

People who a deficiency of a protein called alpha-1 antitrypsin (AAT) are at a higher risk

of developing severe emphysema. Alpha-1 antitrypsin deficiency (AAT deficiency) is an

inherited condition and occurs in varying degrees.

AAT is thought to protect against some of the damage caused by macrophages. In AAT

deficiency-related emphysema, the walls of the bronchial tubes and the alveoli are both

damaged, often leading to severe disease.

Need To Know:
http://www.ehealthmd.com/library/Emphysema/EMP_causes.html#cigshttp://www.ehealthmd.com/library/Emphysema/EMP_causes.html#alphahttp://www.ehealthmd.com/library/Emphysema/EMP_causes.html#cigshttp://www.ehealthmd.com/library/Emphysema/EMP_causes.html#alpha


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About 2 out of every 1,000 people have an alpha-1 antitrypsin deficiency. People who smoke

and have AAT deficiency are almost certain to develop emphysema.

What Are The Symptoms OfEmphysema?


The first sign of emphysema is shortness of breath when you are exerting yourself.

Eventually, this shortness of breath may occur even when you are at rest.

As the disease progresses, the following symptoms which are related to one of the other

major lung diseases also caused by smoking - bronchitis - may occur:

Difficulty breathing (dyspnea - this can also be caused by emphysema)

Coughing (with or without sputum)

Wheezing (this can also be caused by emphysema itself)

Excess mucus production

A bluish tint to the skin (cyanosis)

Nice To Know:

If wheezing occurs, it helps to know whether it is found while breathing in or out (or both).

Wheezing at the end of a complete exhalation is usually due to bronchitis. Wheezing that

begins early in expiration is usually due to emphysema or the combination of bronchitis and

emphysema - COPD.

If you only wheeze when you breathe in, you probably have asthma (or, very rarely, a

narrowing of your windpipe in your neck). Asthma and emphysema sometimes are confused

with each other. One way to tell the difference is to try asthma medications prescribed by your

doctor and see if they make a difference. While people with asthma often respond

dramatically to medications, people with emphysema usually do not respond to asthma

medications and those with COPD may respond somewhat. In some people bronchitis may

lead to asthma which is difficult, even for physicians, to distinguish from asthma due toallergy.

Nice To Know:

Emphysema may affect the brain, too. Low oxygen levels in the blood may mean that the

brain is not getting enough oxygen. The end result can be grumpiness, irritability, impaired

mental ability. High carbon dioxide levels in the blood can lead to headaches and
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sleeplessness.

Emphysema

Definition

Emphysema is a chronic respiratory disease where there is over-inflation of the air sacs(alveoli) in the lungs, causing a decrease in lung function, and often, breathlessness.

Description

Emphysema is the most common cause ofdeath from respiratory disease in the United

States, and is the fourth most common cause of death overall. There are 1.8 million

Americans with the disease, which ranks fifteenth among chronic conditions that causelimitations of activity. The disease is usually caused by smoking, but a small number of

cases are caused by an inherited defect.Normally functioning lungs are elastic, efficiently expanding and recoiling as air passesfreely through the bronchus to the alveoli, where oxygen is moved into the blood and

carbon dioxide is filtered out. When a person inhales cigarette smoke or certain other

irritants, his or her immune system responds by releasing substances that are meant to

defend the lungs against the smoke. These substances can also attack the cells of thelungs, but the body normally inhibits such action with the release of other substances. In

smokers and those with the inherited defect, however, no such prevention occurs and the

lung tissue is damaged in such a way that it loses its elasticity. The small passageways(bronchioles) leading to the alveoli collapse, trapping air within the alveoli. The alveoli,

unable to recoil efficiently and move the air out, over expand and rupture. As the disease

progresses, coughing and shortness of breath occur. In the later stages, the lungs cannotsupply enough oxygen to the blood. Emphysema often occurs with other respiratory

diseases, particularly chronicbronchitis. These two diseases are often referred to as one

disorder called chronic obstructive pulmonary disease (COPD).Emphysema is most common among people aged 50 and older. Those with inherited

emphysema may experience the onset as early as their thirties or forties. Men are more

likely than women to develop emphysema, but female cases are increasing as the number

of female smokers rises.

Causes and symptoms

Heavy cigarette smoking causes about 80-90% of all emphysema cases. However a few

cases are the result of an inherited deficiency of a substance called alpha-1-antitrypsin(AAT). The number of Americans with this deficiency is relatively small, probably nogreater than 70,000. Pipe, cigar, andmarijuana smoking can also damage the lungs.

While a person may be less likely to inhale cigar and pipe smoke, these types of smoke

can also impair lung function. Marijuana smoke may be even more damaging because it

is inhaled deeply and held in by the smoker.The symptoms of emphysema develop gradually over many years. It is a common

occurrence for many emphysema patients to have lost over half of their functioning lung
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tissue before they become aware that something is wrong. Shortness of breath, a chronic

mild cough (which may be productive of large amounts of dark, thick sputum, and often

dismissed as "smoker's cough"), and sometimes weight loss are associated withemphysema. Initially, a patient may only notice shortness of breath when he or she is

exercising. However, as the disease progresses, it will occur with less exertion or no

exertion at all. Emphysema patients may also develop an enlarged, or "barrel,", chest.Other symptoms may be skipped breaths, difficulty sleeping, morning headaches,

increased difficulty breathing while lying down, chronic fatigue, and swelling of the feet,

ankles, or legs. Those with emphysema are at risk for a variety of other complicationsresulting from weakened lung function, includingpneumonia.

Diagnosis

A variety of pulmonary function tests may be ordered. In the early stages of emphysema,

the only result may be dysfunction of the small airways. Patients with emphysema may

show an increase in the total amount of air that is in the lungs (total lung capacity), but adecrease in the amount of air that can be breathed out after taking a deep breath (vital

capacity). With severe emphysema, vital capacity is substantially below normal.Spirometry, a procedure that measures air flow and lung volume, helps in the diagnosis ofemphysema.

A chest x ray is often ordered to aid in the diagnosis of emphysema, though patients in

the early stages of the disease may have normal findings. Abnormal findings on the chest

x ray include over-inflation of the lungs and an abnormally increased chest diameter. Thediaphragm may appear depressed or flattened. In addition, patients with advanced

emphysema may show a smaller or vertical heart. The physician may observe blisters in

the lungs and bulging of the accessory muscles of the respiratory system. Late in thedisease, an EKG will show signs of right ventricular failure in the heart and increased

hemoglobin due to lower levels of oxygen in the patient's blood.

Treatment

Treatment methods for emphysema do not cure or reverse the damage to the lungs.However, they may slow the progression of the disease, relieve symptoms, and help

control possibly fatal complications. The first step in treatment for smokers is to quit, so

as to prevent any further deterioration of breathing ability. Smoking cessation programs

may be effective. Consistent encouragement along with the help of health careprofessionals as well as family and friends can help increase the success rate of someone

attempting to quit.

If the patient and the health care team develop and maintain a complete program ofrespiratory care, disability can be decreased, acute episodes of illness may be prevented,

and the number of hospitalizations reduced. However, only quitting smoking has beenshown to slow down the progression of the disease, and among all other treatments, onlyoxygen therapy has shown an increase in the survival rate.

Home oxygen therapy may improve the survival times in those patients with advanced

emphysema who also have low blood oxygen levels. It may improve the patient's

tolerance of exercise, as well as improve their performance in certain aspects of brainfunction and muscle coordination. The functioning of the heart may also improve with an

increased concentration of oxygen in the blood. Oxygen may also decreaseinsomnia and
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headaches. Some patients may only receive oxygen at night, but studies have illustrated

that it is most effective when administered at least 18, but preferably 24 hours per day.

Portable oxygen tanks prescribed to patients carry a limited supply and must be refilledon a regular basis by a home health provider. Medicare and most insurance companies

cover a large proportion of the cost of home oxygen therapy. Patients should be

instructed regarding special safety issues involving the transport and presence of oxygenin the home.

A variety of medications may be used in the treatment of emphysema. Usually the patient

responds best to a combination of medicines, rather than one single drug.Bronchodilatorsare sometimes used to help alleviate the patient's symptoms by relaxing

and opening the airways. They can be inhaled, taken by mouth, or injected. Another

category of medication often used is corticosteroids or steroids. These help to decrease

the inflammation of the airway walls. They are occasionally used if bronchodilators areineffective in preventing airway obstruction. Some patients' lung function improves with

corticosteroids, and inhaled steroids may be beneficial to patients with few side effects. A

variety ofantibioticsare frequently given at the first sign of a respiratory infection, such

as increased amounts of sputum, or if there has been a change in the color of the sputum.Expectorants can help to loosen respiratory secretions, enabling the patient to more easily

expel them from the airways.Many of the medications prescribed involve the use of a metered dose inhaler (MDI) that

may require special instruction to be used correctly. MDIs are a convenient and safe

method of delivering medication to the lungs. However, if they are used incorrectly the

medication will not get to the right place. Proper technique is essential for the medicationto be effective.

For some patients, surgical treatment may be the best option. Lung volume reduction

surgery is a surgical procedure in which the most diseased parts of the lung are removedto enable the remaining lung and breathing muscles to work more efficiently. Preliminary

studies suggest improved survival rates and better functioning with the surgery. Another

surgical procedure used for emphysema patients islung transplantation. Transplantationmay involve one or both lungs. However, it is a risky and expensive procedure, and donor

organs may not be available.

For those patients with advanced emphysema, keeping the air passages reasonably clearof secretions can prove difficult. Some common methods for mobilizing and removing

secretions include:

Postural drainage. This helps to remove secretions from the airways. The patient

lies in a position that allows gravity to aid in draining different parts of the lung.This is often done after the patient inhales an aerosol medication. The basic

position involves the patient lying on the bed with his chest and head over the side

and the forearms resting on the floor.

Chest percussion. This technique involves lightly clapping the back and chest, andmay help to loosen thick secretions.

Coughing and deep breathing. These techniques may aid the patient in bringing

up secretions.

Aerosol treatments. These treatments may involve solutions of saline, often mixed

with a bronchodilator, which are then inhaled as an aerosol. The aerosols thin and
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loosen secretions. A treatment normally takes 10 to 15 minutes, and is given three

or four times a day.

Patients with COPD can learn to perform a variety of self-help measures that may helpimprove their symptoms and their ability to participate in everyday activities. These

measures include:

Avoiding any exposure to dusts and fumes.

Avoiding air pollution, including the cigarette smoke of others.

Avoiding other people who have infections like the cold or flu. Get a pneumonia

vaccinationand a yearly flu shot.

Drinking plenty of fluids. This helps to loosen respiratory secretions so they can

be brought up more easily through coughing. Avoiding extreme temperatures of heat or cold. Also avoiding high altitudes.

(Special precautions can be taken that may enable the emphysema patient to fly

on a plane.)

Maintaining adequate nutritional intake. Normally a high protein diet taken inmany small feedings is recommended.

Alternative treatment

Many patients are interested in whether any alternative treatments for emphysema areavailable. Some practitioners recommend supplements of antioxidant nutrients. There

have also been some studies indicating a correlation between a low Vitamin A levels and

COPD, with suggestions that supplements of vitamin A might be beneficial.Aromatherapists have used essential oils like eucalyptus, lavender, pine, and rosemary to

help relieve nasal congestion and make breathing easier. The herb elecampane may act as

an expectorant to help patients clear mucus from the lungs. The patient should discuss

these remedies with their health care practitioner prior to trying them, as some mayinteract with the more traditional treatments that are already being used.

Prognosis

Emphysema is a serious and chronic disease that cannot be reversed. If detected early, the

effects and progression can be slowed, particularly if the patient stops smokingimmediately. Complications of emphysema include higher risks for pneumonia and acute

bronchitis. Overall, the prognosis for patients with emphysema is poor, with a survival

rate for all those with COPD of four years, and even less for emphysema. However,individual cases vary and many patients can live much longer with supplemental oxygen

and other treatment measures.

Prevention

The best way to prevent emphysema is to avoid smoking. Even patients with inherited

emphysema should avoid smoking, as it especially worsens the onset and severity. Ifpatients quit smoking as soon as evidence of small airway obstruction begins, they can

significantly improve their prognosis.
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Key terms

Alveoli Small cells or cavities. In the lungs, these are air sacs where oxygen enters the

blood and carbon dioxide is filtered out.

Pulmonary Related to or associated with the lungs.

Resources

Books

Beers, Mark H., and Robert Berkow, editors. The Merck Manual of Diagnosis andTherapy. Whitehouse Station, NJ: Merck and Company, Inc., 2004.

Periodicals

"Data Mounting on Merits of Lung Volume ReductionSurgery."Family Practice News

February 15, 2001: 5.

Lewis, Laurie. "Optimal Treatment for COPD."PatientCare May 30, 2000: 60.

Organizations

American Lung Association. 1740 Broadway New York, NY 10019. (212) 315-8700.

http://www.lungusa.org.National Emphysema Foundation. 15 Stevens St. Norwalk, CT 06856.

http://www.emphysemafoundation.org.

National Heart, Lung and Blood Institute. http://www.nhlbi.nih.gov.Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights

reserved.

emphysema /emphysema/ (emf-semah)

1. a pathologic accumulation of air in tissues or organs.

2.pulmonary e.emphysematousatrophic emphysema senile e.

bullous emphysema single or multiple large cystic alveolar dilatations of lung tissue.

centriacinar emphysema , centrilobular emphysema focal dilatations of respiratory

bronchioles rather than alveoli, throughout the lung among normal lung tissue.

congenital lobar emphysema overinflation of a lung, usually in early life in one of the

upper lobes, with respiratory distress.

hypoplastic emphysema pulmonary emphysema due to a developmental anomaly, withfewer and abnormally large alveoli.

infantile lobar emphysema congenital lobar e.

interlobular emphysema air in the septa between lung lobules.

interstitial emphysema air in the peribronchial and interstitial tissues of the lungs.intestinal emphysemapneumatosis cystoides intestinalis.

mediastinal emphysemapneumomediastinum.

obstructive emphysema that associated with partial bronchial obstruction that interfereswith exhalation.

panacinar emphysema , panlobular emphysema a type characterized by enlargement

of air spaces throughout the acini.
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pulmonary emphysema abnormal increase in size of lung air spaces distal to the

terminal bronchioles.

pulmonary interstitial emphysema (PIE) a condition seen mostly in premature infants,in which air leaks from lung alveoli into interstitial spaces, often because of underlying

lung disease or use of mechanical ventilation.

senile emphysema overdistention and stretching of lung tissues due to atrophic changes.subcutaneous emphysema air or gas in subcutaneous tissues, usually caused by

intrathoracic injury.

surgical emphysema subcutaneous emphysema following surgery.

vesicular emphysemapanacinar e.

Dorland's Medical Dictionary for Health Consumers. 2007 by Saunders, an imprint of

Elsevier, Inc. All rights reserved.

emphysema ( mf -s m , -z -)n.

1. A pathological condition of the lungs marked by an abnormal increase in the size of the

air spaces, resulting in labored breathing and an increased susceptibility to infection. It canbe caused by irreversible expansion of the alveoli or by the destruction of alveolar walls.

Also calledpulmonary emphysema.

2. An abnormal distention of body tissues caused by retention of air.

em physem atous (-s m -t s, -s m -, -z m -, -z m -) adj.

em physe mic adj. & n.

The American Heritage Medical Dictionary Copyright 2007, 2004 by Houghton

Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.

emphysema

[emfsm]

Etymology: Gk, en +physema, a blowingan abnormal condition of the pulmonary system, characterized by overinflation and

destructive changes in alveolar walls. It results in a loss of lung elasticity and decreased

gas exchange. When emphysema occurs early in life, it is usually related to a rare geneticdeficiency of serum alpha-1-antitrypsin, which inactivates the enzymes leukocyte

collagenase and elastase. More common causes are air pollution and cigarette smoking.

Acute emphysema may be caused by the rupture of alveoli during severe respiratory

efforts, as may occur in acute bronchopneumonia, suffocation, whooping cough, and,occasionally, labor. Patients with chronic emphysema may also have a component of

chronic bronchitis. Emphysema also occurs after asthma or tuberculosis, conditions in

which the lungs are overstretched until the elastic fibers of the alveolar walls are

destroyed. In old age the alveolar membranes atrophy and may collapse, producing large,air-filled spaces and a decreased total surface area of the pulmonary membranes. There

are three primary types: centriacinar emphysema, distal acinar emphysema, and panacinaremphysema. -emphysematous,adj.

observations The patient may have dyspnea on exertion or at rest, cough, orthopnea,

unequal chest expansion, tachypnea, tachycardia, diminished breath sounds caused by airtrapping, or, atypically, an elevated temperature and breath sounds if there is an infection.

Anxiety, increased PaCO2, restlessness, confusion, weakness, anorexia, hypoxemia, and
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respiratory failure are common in advanced cases. Chronic emphysema is characterized

by increased anterior-posterior chest diameter secondary to hyperinflation and air

trapping and use of accessory muscles.

interventions The primary treatment consists of breathing exercises, oxygen

administration, and avoiding infection. The airway is kept open, and oxygen is

administered to maintain an arterial oxygen saturation of 92%. Bronchodilators,antibiotics, expectorants when bronchitis is also present, methylxanthines, and

corticosteroids may be prescribed. Sedation is to be avoided because sedatives depress

respiratory function.

nursing considerations The patient is taught breathing exercises and encouraged to

drink between 2 and 3 L of fluids daily, if not contraindicated by cardiac function.

Activity is encouraged to the limit of the patient's tolerance. Fatigue, constipation, and

upper respiratory tract infection and irritation are to be avoided. Mechanical ventilationand oxygen therapy may be prescribed for use at home. The patient is taught the adverse

role that smoking plays in the disease and is encouraged to stop smoking.

Mosby's Medical Dictionary, 8th edition. 2009, Elsevier.

emphysema (emfizm ),n1. a swelling caused by air in the tissue spaces. In the oral and facial regions it may be

caused either by air introduced into a tooth socket or gingival crevice with the air syringe,or by blowing of the nose.

n2. a permanent dilation of the respiratory alveoli.

Mosby's Dental Dictionary, 2nd edition. 2008 Elsevier, Inc. All rights reserved.

emphysema

a pathological accumulation of air in tissues. The air may derive from a skin laceration

and be drawn in by the movements of muscles. A discontinuity of the tracheal mucosa isa common cause, either by way of laceration or ulceration. Extension from a pulmonary

lesion is also common. The syndrome resulting depends on the location of the air. See

also pulmonary emphysema and subcutaneous emphysema (below).acute bovine pulmonary emphysema

see atypical interstitial pneumonia.

alveolar emphysema

see pulmonary emphysema (below).

bullous emphysema

emphysema in which bullae form in areas of lung tissue so that these areas do notcontribute to respiration.

conjunctival emphysema

may occur after head trauma which permits escape of air from the paranasal sinuses.

fetal emphysema

see emphysematous/putrescent fetus.generalized emphysemawidespread distribution of air, including subcutaneous tissues, seen with

pneumomediastinum.

hypoplastic emphysema

pulmonary emphysema due to a developmental abnormality, resulting in a reduced

number of alveoli, which are abnormally large.

interlobular emphysema
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accumulation of air in the septa between lobules of the lungs.

interstitial emphysema

presence of air in the peribronchial and interstitial tissues of the lungs.

intestinal emphysema

a condition marked by accumulation of gas under the tunica serosa of the intestine.

lobar emphysemaemphysema involving less than all the lobes of the affected lung.

mediastinal emphysema

seepneumomediastinum.

orbital emphysema

may occur after trauma to the head which permits escape of air from the paranasal

sinuses; appears as swelling with crepitus under the conjunctiva or periocular skin.

panacinar emphysema, panlobular emphysema

generalized obstructive emphysema affecting all lung segments, with atrophy and

dilatation of the alveoli and destruction of the vascular bed.

pulmonary emphysema

distention of the lung caused by overdistention of alveoli and rupture of alveolar walls(alveolar emphysema) and in some cases escape of air into the interstitial spaces

(interstitial emphysema). It is a common pathological finding in many diseases of thelung in all species, but also occurs independently, especially in horses, as a principal

lesion in chronic obstructive pulmonary disease. It is also a prominent lesion in bovine

atypical interstitial pneumonia. It is always secondary to a primary lesion which

effectively traps an excessive amount of air in the alveoli. It is characterized clinically bycough, dyspnea, forced expiratory effort and poor work tolerance. A double expiratory

effort is a characteristic signhence broken wind.

subconjunctival emphysema

occurs with fractures involving the paranasal sinuses.

subcutaneous emphysema

air or gas in the subcutaneous tissues. The characteristic lesion is a soft, mobile swellingwhich crackles like stiff paper when palpated. There is no pain, nor heat and no ill effects

unless the pharyngeal area is sufficiently involved to cause asphyxia.

surgical emphysema

subcutaneous emphysema following operation.

unilateral emphysema

emphysema affecting only one lung, frequently due to congenital defects in circulation.

vesicular emphysema

see panacinar emphysema (above).

Saunders Comprehensive Veterinary Dictionary, 3 ed. 2007 Elsevier, Inc. All rights

reserved

emphysema

Internal medicine Accumulation of air in tissueeg, lungs, dermis; pulmonary

emphysema is characterized by size of air spaces distal to terminal bronchioles, vitalcapacity and airway resistance, often with alveolar wall destruction and fibrosis;

emphysema commonly is often associated with chronic bronchitis and COPD

Mechanisms Atrophy, bronchitis, bronchiolitis, scarring. See Centriacinar emphysema,
http://medical-dictionary.thefreedictionary.com/pneumomediastinumhttp://medical-dictionary.thefreedictionary.com/atypical+interstitial+pneumoniahttp://medical-dictionary.thefreedictionary.com/pneumomediastinumhttp://medical-dictionary.thefreedictionary.com/atypical+interstitial+pneumonia


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Coal workers' pneumoconiosis,COPD, Distal acinar emphysema, Giant bullous

emphysema, Panacinar emphysema, Senile emphysema. Cf Focal emphysema.

McGraw-Hill Concise Dictionary of Modern Medicine. 2002 by The McGraw-HillCompanies, Inc.

Patient discussion about emphysema.

Q. Does smoking cause emphysema? I know it sounds like a silly question, as you can

read everywhere that smoking damages your lung and cause emphysema and lung cancer,but I know a family with 4 brothers,2 of them not smoking and by the age of 50 both of

them had emphysema, and another brothers that doesn't stop smoking but is completely

healthy. How can than happen?

A. When doctors say that smoking cause emphysema, they doesn't say that you mustsmoke to get emphysema and that everyone that smokes will eventually develop the

disease. You can smoke and never have emphysema, and you can never smoke and haveemphysema. The numbers (i.e. the risk) is what makes all the difference...

Q. can you ever get better from emphysema?

A. Emphysema is a chronic state where the lungs pathologically expand and cause them

to lose their compliance during breathing. This is not a reversible state, and usually the

lung pathological changes will continue to deteriorate if the lungs are exposed to the

same pathogens that caused the initial damage (for example- smoking). However,smoking cessation is known to have benefitial results in slowing down the progress of

lung disability and somewhat reversing part of the damage by regression of the

inflammatory processes that are related to the emphysema.

Q. EMPHYSEMA what type of disease is it?

A. It's a chronic lung disease, characterized by destruction of the walls of the air sacs (alveoli) where

blood exchange oxygen and CO2 with the air. The disease leads to obstruction of the airflow, air trap

inside the lungs, and to many long term complications, and eventually to death. It's caused mainly bysmoking.

Emphysema is a long-term, progressive disease of thelungs that primarily causes

shortness of breath. In people with emphysema, the tissues necessary to support thephysical 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 sacs, calledalveoli, makes these air sacs unable to hold theirfunctional shape upon exhalation. It is often caused by long-term exposure toair

pollution orsmoking.
http://medical-dictionary.thefreedictionary.com/COPDhttp://medical-dictionary.thefreedictionary.com/COPDhttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Exhalationhttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Smokinghttp://medical-dictionary.thefreedictionary.com/COPDhttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Exhalationhttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Smoking


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The term emphysema meansswellingand comes from the Greek emphysan

meaning inflate, itself composed of en meaning in and physan meaning breath,

blast.[1]

Classification and external resources

A lateral chest x-ray of a person with emphysema.

Note the barrel chest and flat diaphragm.

ICD-10 J43.

ICD-9 492

DiseasesDB 4190

MedlinePlus 000136

eMedicine med/654

MeSH D011656
http://en.wikipedia.org/wiki/Greek_languagehttp://en.wikipedia.org/wiki/Emphysema#cite_note-0http://en.wikipedia.org/wiki/Emphysema#cite_note-0http://en.wikipedia.org/wiki/International_Statistical_Classification_of_Diseases_and_Related_Health_Problemshttp://en.wikipedia.org/wiki/ICD-10http://en.wikipedia.org/wiki/ICD-10_Chapter_Jhttp://apps.who.int/classifications/apps/icd/icd10online/?gj40.htm+j43http://apps.who.int/classifications/apps/icd/icd10online/?gj40.htm+j43http://en.wikipedia.org/wiki/International_Statistical_Classification_of_Diseases_and_Related_Health_Problemshttp://en.wikipedia.org/wiki/List_of_ICD-9_codeshttp://www.icd9data.com/getICD9Code.ashx?icd9=492http://en.wikipedia.org/wiki/Diseases_Databasehttp://www.diseasesdatabase.com/ddb4190.htmhttp://en.wikipedia.org/wiki/MedlinePlushttp://www.nlm.nih.gov/medlineplus/ency/article/000136.htmhttp://en.wikipedia.org/wiki/EMedicinehttp://www.emedicine.com/med/topic654.htmhttp://en.wikipedia.org/wiki/Medical_Subject_Headingshttp://www.nlm.nih.gov/cgi/mesh/2011/MB_cgi?field=uid&term=D011656http://en.wikipedia.org/wiki/File:Barrowchest.JPGhttp://en.wikipedia.org/wiki/Greek_languagehttp://en.wikipedia.org/wiki/Emphysema#cite_note-0http://en.wikipedia.org/wiki/International_Statistical_Classification_of_Diseases_and_Related_Health_Problemshttp://en.wikipedia.org/wiki/ICD-10http://en.wikipedia.org/wiki/ICD-10_Chapter_Jhttp://apps.who.int/classifications/apps/icd/icd10online/?gj40.htm+j43http://en.wikipedia.org/wiki/International_Statistical_Classification_of_Diseases_and_Related_Health_Problemshttp://en.wikipedia.org/wiki/List_of_ICD-9_codeshttp://www.icd9data.com/getICD9Code.ashx?icd9=492http://en.wikipedia.org/wiki/Diseases_Databasehttp://www.diseasesdatabase.com/ddb4190.htmhttp://en.wikipedia.org/wiki/MedlinePlushttp://www.nlm.nih.gov/medlineplus/ency/article/000136.htmhttp://en.wikipedia.org/wiki/EMedicinehttp://www.emedicine.com/med/topic654.htmhttp://en.wikipedia.org/wiki/Medical_Subject_Headingshttp://www.nlm.nih.gov/cgi/mesh/2011/MB_cgi?field=uid&term=D011656


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Contents

[hide]

1 Classification

o 1.1 Congenital lobar emphysema

o 1.2 Paraseptal emphysema

2 Signs and symptoms

3 Causes

4 Pathophysiology

5 Diagnosis

6 Management

7 Notable cases

8 Footnotes

9 External links

Classification

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

classified by location into panacinary and centroacinary (or panacinar and centriacinar, [2]

or centrilobular and panlobular).[3]

Panacinar(orpanlobular) emphysema: The entire respiratory acinus, from

respiratory bronchioleto alveoli, is expanded. Occurs more commonly in thelower lobes, especially basal segments, and anterior margins of the lungs.[2]

Centriacinar(orcentrilobular) 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).
http://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Emphysema#Classificationhttp://en.wikipedia.org/wiki/Emphysema#Congenital_lobar_emphysemahttp://en.wikipedia.org/wiki/Emphysema#Paraseptal_emphysemahttp://en.wikipedia.org/wiki/Emphysema#Signs_and_symptomshttp://en.wikipedia.org/wiki/Emphysema#Causeshttp://en.wikipedia.org/wiki/Emphysema#Pathophysiologyhttp://en.wikipedia.org/wiki/Emphysema#Diagnosishttp://en.wikipedia.org/wiki/Emphysema#Managementhttp://en.wikipedia.org/wiki/Emphysema#Notable_caseshttp://en.wikipedia.org/wiki/Emphysema#Footnoteshttp://en.wikipedia.org/wiki/Emphysema#External_linkshttp://en.wikipedia.org/wiki/Emphysema#cite_note-urlEmphysema-1http://en.wikipedia.org/wiki/Emphysema#cite_note-pmid4784376-2http://en.wikipedia.org/wiki/Respiratory_bronchiolehttp://en.wikipedia.org/wiki/Respiratory_bronchiolehttp://en.wikipedia.org/wiki/Emphysema#cite_note-urlEmphysema-1http://en.wikipedia.org/wiki/Emphysema#cite_note-urlEmphysema-1http://en.wikipedia.org/wiki/Emphysema#cite_note-urlEmphysema-1http://en.wikipedia.org/wiki/Emphysema#cite_note-urlEmphysema-1http://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Emphysema#Classificationhttp://en.wikipedia.org/wiki/Emphysema#Congenital_lobar_emphysemahttp://en.wikipedia.org/wiki/Emphysema#Paraseptal_emphysemahttp://en.wikipedia.org/wiki/Emphysema#Signs_and_symptomshttp://en.wikipedia.org/wiki/Emphysema#Causeshttp://en.wikipedia.org/wiki/Emphysema#Pathophysiologyhttp://en.wikipedia.org/wiki/Emphysema#Diagnosishttp://en.wikipedia.org/wiki/Emphysema#Managementhttp://en.wikipedia.org/wiki/Emphysema#Notable_caseshttp://en.wikipedia.org/wiki/Emphysema#Footnoteshttp://en.wikipedia.org/wiki/Emphysema#External_linkshttp://en.wikipedia.org/wiki/Emphysema#cite_note-urlEmphysema-1http://en.wikipedia.org/wiki/Emphysema#cite_note-pmid4784376-2http://en.wikipedia.org/wiki/Respiratory_bronchiolehttp://en.wikipedia.org/wiki/Emphysema#cite_note-urlEmphysema-1http://en.wikipedia.org/wiki/Emphysema#cite_note-urlEmphysema-1http://en.wikipedia.org/wiki/Emphysema#cite_note-urlEmphysema-1


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[edit] Congenital lobar emphysema

CLE results in overexpansion of apulmonary lobeand resultant compression of the

remaining lobes of the ipsilateral lung, and possibly also the contralaterallung. There isbronchial narrowing because of weakened or absent bronchial cartilage.[4] There may be

congenital extrinsic compression, commonly by an abnormally largepulmonary artery.This causes malformation of bronchial cartilage, making them soft and collapsible.[4] CLEis potentially reversible, yet possibly life-threatening, causing respiratory distress in the

neonate.[4]

[edit] Paraseptal emphysema

Paraseptal emphysema is a type of emphysema which involves the alveolar ducts andsacs at the lung periphery. The emphysematous areas are subpleural in location and often

surrounded by interlobular septa (hence the name). It may be an incidental finding in

young adults, and may be associated with spontaneouspneumothorax. It may also be

seen in older patients with centrilobular emphysema. Both centrilobular and paraseptalemphysema may progress to bullous emphysema. A bulla is defined as being at least

1 cm in diameter, and with a wall less than 1mm thick. Bullae are thought to arise by air

trapping in emphysematous spaces, causing local expansion.[5]

[edit] Signs and symptoms

Emphysema is a disease of the lungtissue caused by destruction of structures feeding the

alveoli, in some cases owing to the action ofalpha 1-antitrypsin deficiency. Smoking is

one major cause of this destruction, which causes the small airways in the lungstocollapse during forced exhalation. As a result, airflow is impeded and air becomes

trapped, just as in other obstructive lung diseases. Symptoms include shortness of breathon exertion, and an expanded chest.

People with this disease do not get enough oxygen and cannot remove carbon dioxidefrom their blood; they therefore exhibit dyspnea (shortness of breath). At first this occurs

only during physical activity. Eventually it will occur after any physical exertion. Later

the patient may be dyspneic all the time, even when relaxing. Because breathing isdifficult, the patient must use accessory muscles to help them breathe; tachypnea (rapid

breathing) may occur when they try to extend their exertion. They may have trouble

coughing and lowered amounts ofsputum. They may also lose weight.

The anteroposteriordiameter of their chest may increase; this symptom is sometimesreferred as "barrel chest." The patient may lean forward with arms extended or resting on

something to help them breathe.

When lung auscultation and chestpercussionis performed a hyperresonant sound is

heard.
http://en.wikipedia.org/w/index.php?title=Emphysema&action=edit&section=2http://en.wikipedia.org/wiki/Pulmonary_lobehttp://en.wikipedia.org/wiki/Pulmonary_lobehttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Emphysema#cite_note-Wood-3http://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Emphysema#cite_note-Wood-3http://en.wikipedia.org/wiki/Emphysema#cite_note-Wood-3http://en.wikipedia.org/w/index.php?title=Emphysema&action=edit&section=3http://en.wikipedia.org/wiki/Pneumothoraxhttp://en.wikipedia.org/wiki/Pneumothoraxhttp://en.wikipedia.org/wiki/Air_trappinghttp://en.wikipedia.org/wiki/Air_trappinghttp://en.wikipedia.org/wiki/Air_trappinghttp://en.wikipedia.org/wiki/Emphysema#cite_note-4http://en.wikipedia.org/wiki/Emphysema#cite_note-4http://en.wikipedia.org/w/index.php?title=Emphysema&action=edit&section=4http://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Lungshttp://en.wikipedia.org/wiki/Lungshttp://en.wikipedia.org/wiki/Shortness_of_breathhttp://en.wikipedia.org/wiki/Expanded_chesthttp://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Tachypneahttp://en.wikipedia.org/wiki/Sputumhttp://en.wikipedia.org/wiki/Anteroposterior#Anterior_and_posteriorhttp://en.wikipedia.org/wiki/Anteroposterior#Anterior_and_posteriorhttp://en.wikipedia.org/wiki/Auscultationhttp://en.wikipedia.org/wiki/Percussion_(medicine)http://en.wikipedia.org/wiki/Percussion_(medicine)http://en.wikipedia.org/w/index.php?title=Emphysema&action=edit&section=2http://en.wikipedia.org/wiki/Pulmonary_lobehttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Emphysema#cite_note-Wood-3http://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Emphysema#cite_note-Wood-3http://en.wikipedia.org/wiki/Emphysema#cite_note-Wood-3http://en.wikipedia.org/w/index.php?title=Emphysema&action=edit&section=3http://en.wikipedia.org/wiki/Pneumothoraxhttp://en.wikipedia.org/wiki/Air_trappinghttp://en.wikipedia.org/wiki/Air_trappinghttp://en.wikipedia.org/wiki/Emphysema#cite_note-4http://en.wikipedia.org/w/index.php?title=Emphysema&action=edit&section=4http://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Lungshttp://en.wikipedia.org/wiki/Shortness_of_breathhttp://en.wikipedia.org/wiki/Expanded_chesthttp://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Tachypneahttp://en.wikipedia.org/wiki/Sputumhttp://en.wikipedia.org/wiki/Anteroposterior#Anterior_and_posteriorhttp://en.wikipedia.org/wiki/Auscultationhttp://en.wikipedia.org/wiki/Percussion_(medicine)


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The patient may also exhibit symptoms ofhypoxia-inducedcyanosis, or the appearance

of a blue to purplish discoloration of the skin, due to increased levels of

deoxyhemoglobin in the blood.

[edit] Causes

The majority of all emphysema cases are caused by smoking tobacco. Emphysema cases

that are caused by other etiologies are referred to as secondary emphysema.

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 fibroticreaction.

Some types of emphysema are considered a normal part of aging and are found in the

elderly whose lungs have deteriorated due to age. At about 20 years of age, people stop

developing new alveoli tissue. In the years following the cessation of the development of

new alveoli, lung tissue can start to deteriorate. This is a normal, natural part of aging inhealthy people. Alveoli will die, the number of lung capillaries will decline and the

elastin of the lungs will begin to break down causing a loss of pulmonary elasticity. Aspeople age, they will also lose strength and mass in their chest muscles causing these

muscles to become weaker. In addition, bones can start to deteriorate and a persons

posture can change. Together, all of these age-related manifestations can cause thedevelopment of emphysema. Though not all elderly people will develop emphysema,

they are all at risk of having decreased respiratory function.

Other causes of emphysema can be anything that causes the body to be unable to inhibit

proteolytic enzymes in the lung. This could be exposure to air pollution, second hand

smoke or other chemicals and toxins.

[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 thebronchi and into thealveoli, which aretiny sacs surrounded by capillaries. Alveoli absorb oxygenand then transfer it into the

blood. When toxicants, such as cigarette smoke, are breathed into the lungs, the harmful
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particles become trapped in the alveoli, causing a localized inflammatoryresponse.

Chemicals released during the inflammatory response (e.g.,elastase) can eventually

cause the alveolar septum to disintegrate. This condition, known as septal rupture, leadsto significant deformations of the lung architecture[6][7](video) that have important

functional consequences. The key mechanical event consequent to septal rupture is that

the resulting cavity is larger than the sum of the two alveolar spaces (see side figure);

An elastic net distended on finite surface may offer a bidimensional model useful for

understanding the pure mechanical consequences of septal rupture. In red is the extra

space of the new cavity after septal rupture due to the lung elastic recoil re-arrangement,necessarily at the expenses of the space of the surrounding healthy meshes (alveoli)

(VIDEO)[8]

in fact because of the lacking mechanical support of the broken septa the lung elasticrecoil further enlarges this new space, necessarily at the expenses of the surrounding

healthy parenchyma. In other words, as immediate and spontaneous consequence of

septal rupture, the elastic lung recoil resets healthy parenchyma expansion at a lowerlevel, in proportion to the amount of septal disruption.

The large cavities left by the septal rupture are known as bullae (sin. = bulla). These

deformations result in a large decrease of alveoli surface area used for gas exchange, aswell as decreased ventilation of the surrounding healthy parenchyma. This results in adecreased 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, which physiologically depends completelyon lung elastic recoil, 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, oxygenuptake 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 placesincreased 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.
http://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Elastasehttp://en.wikipedia.org/wiki/Elastasehttp://en.wikipedia.org/wiki/Alveolar_septumhttp://en.wikipedia.org/wiki/Emphysema#cite_note-5http://en.wikipedia.org/wiki/Emphysema#cite_note-6http://www.fondazionecarrel.org/carrel/thorac/files/enphys/new/emphysema1.htmlhttp://en.wikipedia.org/wiki/Emphysema#cite_note-7http://en.wikipedia.org/wiki/TLCOhttp://en.wikipedia.org/wiki/File:Rete1.pnghttp://en.wikipedia.org/wiki/File:Rete1.pnghttp://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Elastasehttp://en.wikipedia.org/wiki/Alveolar_septumhttp://en.wikipedia.org/wiki/Emphysema#cite_note-5http://en.wikipedia.org/wiki/Emphysema#cite_note-6http://www.fondazionecarrel.org/carrel/thorac/files/enphys/new/emphysema1.htmlhttp://en.wikipedia.org/wiki/Emphysema#cite_note-7http://en.wikipedia.org/wiki/TLCO


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Patients withalpha 1-antitrypsin deficiency (A1AD) are more likely to suffer from

emphysema. A1AT inhibits inflammatory enzymes (such as elastase) from destroying the

alveolartissue. 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 aspanacinaremphysema

(involving the entire acinus) as opposed to centrilobularemphysema, which is caused bysmoking. 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 developinto a severe case over a short period of time (12 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 ofleukocyteelastase(also neutrophil elastase), a serineproteasefound 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 A1ATis 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 equallyor 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 ofvarious species of animals. These animals developed connective tissue damage, which

was taken as support for the protease-antiprotease theory. However, just because thesesubstances 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 theproduction 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 03 years at most

Diagnosis

The diagnosis is usually confirmed bypulmonary function testing (e.g. spirometry);

however, X-ray radiographymay aid in the diagnosis. A DLCO test may be used to

differentiate Emphysema from other types of Obstructive disorders such as ChronicBronchitis and Asthma. DLCO is a test that measures the ability of gases to diffuse across
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the alveolar-capillary membrane. A DLCO will be decreased in Emphysema whereas it

will be normal or increased in Asthma and Chronic Bronchitis.

H&E stained lung tissue of end-stage emphysema. RBCs are red, nucleiare

purple, other material is pink, and air spaces are white.

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

Axial CT image of the lung of a person with end-stage bullus emphysema.

A severe case of emphysema.

Lung bulla as seen on CXR in a person with severe COPD
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[edit] Management

Emphysema is an irreversible degenerative condition. Patients who think they may have

contracted the disease are recommended to seek medical attention as soon as possible.The most important measure to slow its progression is for the patient to stop smoking and

avoid all exposure to cigarette smoke and lungirritants. Pulmonary rehabilitation can bevery helpful to optimize the patient's quality of life and teach the patient how to actively

manage his or her care.

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 conditionsincludinggastric reflux andallergies 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 beingresearched.

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 areminimally 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 islung 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 causedamage to the kidneys, heart and otherorgans. Surgical transplantation also requires thepatient to take an anti-rejection drug regimen which suppresses the immune system, and

can lead to microbial infection of the patient.

With the discovery ofmultipotent lung stem cells in 2011, a new treatment option may

soon become available. Scientists injected human lung stem cells into mice with damagedlungs. The stem cells formed human bronchioles, alveoli, and pulmonary vessels

integrated structurally and functionally with the damaged mouse organ. The May 2011

report in the New England Journal of Medicine [9] concluded that human lung stem cells"have the undemonstrated potential to promote tissue restoration in patients with lung

disease".

[edit] Notable cases

Amy Winehouse[10]

Paul Avery[11]

Don Imus[12]

Leonard Nimoy[13]
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R. J. Reynolds, R. J. Reynolds Jr., R. J. Reynolds, III,[14]

Spencer Tracy[15]

Johnny Carson[16] [17]

Dick York[18]

Occupational dust exposure and chronic

obstructive pulmonary disease. A

systematic overview of the evidence.

Oxman AD, Muir DC,Shannon HS, Stock SR, Hnizdo E,Lange HJ.

Source

Department of Family Medicine, Clinical Epidemiology & Biostatistics, and Medicine,

Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada.

Abstract

The object of this study was to assess the relationship between occupational dust

exposure and chronic obstructive pulmonary disease (COPD). Studies were identified

using MEDLINE (January 1966 to July 1991), SCISEARCH, manual review of reference

lists, and personal contact with more than 30 international experts. Studies of COPD,

lung function, emphysema, chronic bronchitis, or mortality in workers exposed tononorganic dust were retrieved. Studies were included if dust exposure was measured

quantitatively, and a quantitative relationship between dust exposure and one of theoutcomes of interest was calculated while controlling at least for smoking and age.

Methodological rigor was assessed, and data regarding the study populations, prognostic

factors, and outcomes were extracted independently by two reviewers. Thirteen reportsderived from four cohorts of workers met our inclusion criteria. Three of the cohorts were

of coal miners and one was of gold miners. All of the studies found a statistically

significant association between loss of lung function and cumulative respirable dust

exposure. It was estimated that 80 (95% CI, 34 to 137) of 1,000 nonsmoking coal minerswith a cumulative respirable dust exposure of 122.5 gh/m3 (considered equivalent to 35

years of work with a mean respirable dust level of 2 mg/m3) could be expected todevelop a clinically important (> 20%) loss of FEV1 attributable to dust. Among 1,000smoking miners the comparable estimate was 66 (95% CI, 49 to 84). The risk of a

clinically important loss of lung function attributable to dust among nonsmoking gold

miners was estimated to be three times as large as for coal miners at less than one fifth ofthe cumulative respirable dust exposure (21.3 gh/m3), the maximal exposure observed

among the cohort of gold miners. We conclude that occupational dust is an important

cause of COPD, and the risk appears to be greater for gold miners than for coal miners.
http://en.wikipedia.org/wiki/R._J._Reynoldshttp://en.wikipedia.org/wiki/Emphysema#cite_note-13http://en.wikipedia.org/wiki/Spencer_Tracyhttp://en.wikipedia.org/wiki/Spencer_Tracyhttp://en.wikipedia.org/wiki/Emphysema#cite_note-14http://en.wikipedia.org/wiki/Emphysema#cite_note-14http://en.wikipedia.org/wiki/Johnny_Carsonhttp://en.wikipedia.org/wiki/Johnny_Carsonhttp://en.wikipedia.org/wiki/Emphysema#cite_note-15http://en.wikipedia.org/wiki/Emphysema#cite_note-15http://en.wikipedia.org/wiki/Emphysema#cite_note-15http://en.wikipedia.org/wiki/Emphysema#cite_note-16http://en.wikipedia.org/wiki/Emphysema#cite_note-15http://en.wikipedia.org/wiki/Dick_Yorkhttp://en.wikipedia.org/wiki/Emphysema#cite_note-17http://en.wikipedia.org/wiki/Emphysema#cite_note-17http://www.ncbi.nlm.nih.gov/pubmed?term=%22Oxman%20AD%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Muir%20DC%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Muir%20DC%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Shannon%20HS%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Stock%20SR%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Hnizdo%20E%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Hnizdo%20E%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Lange%20HJ%22%5BAuthor%5Dhttp://en.wikipedia.org/wiki/R._J._Reynoldshttp://en.wikipedia.org/wiki/Emphysema#cite_note-13http://en.wikipedia.org/wiki/Spencer_Tracyhttp://en.wikipedia.org/wiki/Emphysema#cite_note-14http://en.wikipedia.org/wiki/Johnny_Carsonhttp://en.wikipedia.org/wiki/Emphysema#cite_note-15http://en.wikipedia.org/wiki/Emphysema#cite_note-16http://en.wikipedia.org/wiki/Dick_Yorkhttp://en.wikipedia.org/wiki/Emphysema#cite_note-17http://www.ncbi.nlm.nih.gov/pubmed?term=%22Oxman%20AD%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Muir%20DC%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Shannon%20HS%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Stock%20SR%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Hnizdo%20E%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Lange%20HJ%22%5BAuthor%5D


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One possible explanation of the greater risk among gold miners is the higher silica

content in gold mine dust.

Comment in

DefinitionBy Mayo Clinic staff

Emphysema

Emphysema occurs when the air sacs in your lungs are gradually destroyed, making youprogressively more short of breath. Emphysema is one of several diseases known

collectively as chronic obstructive pulmonary disease (COPD). Smoking is the leading

cause of emphysema.

As it worsens, emphysema turns the spherical air sacs clustered like bunches of grapes

into large, irregular pockets with gaping holes in their inner walls. This reduces the

surface area of the lungs and, in turn, the amount of oxygen that reaches your

bloodstream.

Emphysema also slowly destroys the elastic fibers that hold open the small airways

leading to the air sacs. This allows these airways to collapse when you breathe out, so the

air in your lungs can't escape. Treatment may slow the progression of emphysema, but it

can't reverse the damage.

Risk factors

By Mayo Clinic staff

Factors that increase your risk of developing emphysema include:

Smoking. Emphysema is most likely to develop in cigarette smokers, but cigarand pipe smokers also are susceptible. The risk for all types of smokers increases

with the number of years and amount of tobacco smoked.

Age. Although the lung damage that occurs in emphysema develops gradually,most people with tobacco-related emphysema begin to experience symptoms of

the disease between the ages of 40 and 60.

Exposure to secondhand smoke. Secondhand smoke, also known as passive or

environmental tobacco smoke, is smoke that you inadvertently inhale fromsomeone else's cigarette, pipe or cigar. Being around secondhand smoke increases

your risk of emphysema.
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Occupational exposure to fumes or dust. If you breathe fumes from certain

chemicals or dust from grain, cotton, wood or mining products, you're more likely

to develop emphysema. This risk is even greater if you smoke.

Exposure to indoor and outdoor pollution. Breathing indoor pollutants, such as

fumes from heating fuel, as well as outdoor pollutants car exhaust, for instance

increases your risk of emphysema.

Complications

By Mayo Clinic staff

People who have emphysema are also more likely to develop:

Collapsed lung (pneumothorax). A collapsed lung can be life-threatening inpeople who have severe emphysema, because the function of their lungs is

already so compromised.

Heart problems. Emphysema can increase the pressure in the arteries that

connect the heart and lungs. This can cause a condition called cor pulmonale, inwhich a section of the heart expands and weakens.

Large holes in the lungs (giant bullae). Some people with emphysema develop

empty spaces in the lungs called bullae. Giant bullae can be as large as half thelung. In addition to reducing the amount of space available for the lung to expand,

giant bullae can become infected and are more prone to causing a collapsed lung

(pneumothorax).

Complications

COPD affects an estimated 9 - 10% of people worldwide in both developed and

underdeveloped countries. It is the 4th most common cause of death in the United States,but experts predict that it will be the third leading cause of death in the world by 2020 as

the population ages and people continue to smoke.

Although COPD has traditionally been considered a man's disease, an increase in women

who smoke has caused COPD to skyrocket in women. Women with COPD tend to fareworse than men -- they are more likely to be hospitalized and to die from COPD. They

also report more severe symptoms, greater depression, and a worse quality of life than

men.
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Women appear to be more susceptible to the effects of smoking and pollution, possibly

because of hormones or other genetic differences. The good news is that women who

stop smoking get their lung function back more quickly than men.

The leading cause of death from COPD is respiratory failure. However, patients with

mild-to-moderate COPD tend to succumb to cardiovascular disease or lung cancer. Thislikely occurs from chronic low-grade inflammation, which is involved in all three COPD

diseases.

Traditionally, physicians have measured the severity of COPD by the amount of air that a

person can forcibly exhale in one second (FEV1). The amount decreases as COPD

worsens. However, COPD affects other systems and body parts, which provide clues

about the severity of the disease. Many physicians now use the BODE index to categorizeCOPD and predict outcome. BODE stands for body-mass index, degree of airflow

obstruction, dyspnea (breathlessness), and exercise capacity as measured in a 6-minute

walk test.

Outlook for Patients with Emphysema. If emphysema is detected before causing

symptoms, there may be some chance of reversing it, although permanent changes

in the alveoli usually occur, even in young smokers. Patients with the inherited

form of early-onset emphysema are at risk for early death, unless the disease istreated and its progression halted or slowed. Emphysema patients who experience

severe involuntary weight loss (which indicates muscle wasting) have a poorer

outlook, regardless of their lung function.

Outlook for Patients with Chronic Bronchitis. Chronic bronchitis does not cause

as much lung damage as emphysema, although the airways become blocked by

mucus plugs, and narrow due to inflammation. Thus poor air exchange causes

reduced levels of oxygen, and high carbon dioxide levels. This state of poor gasexchange can lead to serious, life-threatening conditions that include severe

breathing difficulty and heart failure.

Acute Exacerbations

Acute exacerbations are episodes that occur when airways suddenly become obstructed

and symptoms worsen. Such events are associated with inflammation in the airways and

are generally triggered by an infection in the airway or throughout the body.

Other factors that can trigger serious lung events:

Certain medications Exposure to irritants in the air

Seasonal changes

Acute exacerbations include the following symptoms:

Increased volume of sputum


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Sputum that is thicker and darker

Worsened shortness of breath that causes the patient to breathe faster and harder.

This is the most common and distressing acute symptom.

Acute exacerbations occur, on average, between two and three times a year in patients

with moderate-to-severe COPD. In about 80% of the cases, they are triggered byinfections. Smokers have more episodes than nonsmokers.

Acute exacerbations get better on their own, but they are still the most common cause ofhospitalization in these patients, and often require different medications to improve.

Frequent acute exacerbations of COPD cause lung function to deteriorate quickly, and

patients never recover to the condition they were in before the last exacerbation. In

COPD patients who are hospitalized, mortality rates are 11%. Survivors of a firsthospitalization have a 50% chance of rehospitalization within 6 months.

Reduced Quality of Life and Mood

Nearly half of patients with COPD report a limitation in daily activities. They havetrouble walking up stairs or carrying even small packages. Breathing becomes hard work.

More than half of patients with COPD have insomnia. Such impairment in quality of life

can negatively affect mood.

Almost half of patients with COPD have anxiety, depression, or another psychiatricdisorder, compared with 31% of people in the general population. Women with COPD

are more susceptible to psychological problems than men. If patients with COPD become

anxious or depressed, they may have a poorer outlook than those without these emotional

problems. COPD patients with moderate-to-severe depression face a greater 3-year

mortality rate than those who experience less depression. Low oxygen levels also canimpair mental function and short-term memory. Psychological interventions may be

particularly helpful for people with COPD.

Malnourishment

People with COPD often lack good nutrition. Patients with chronic bronchitis tend to be

obese. Patients with emphysema tend to be underweight. Loss of weight and muscle mass

is associated with a poor outcome in COPD. Good nutrition improves the ability toexercise, which in turn builds muscle strength and lung function. Obese patients with

COPD who lose weight sleep better.

Heart Disease

Over time, COPD causes low levels of oxygen (hypoxia) and high levels of carbondioxide (hypercapnia) in the body. In order to boost oxygen delivery, the body

compensates in a number of ways:


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Blood vessels in the lung constrict to force blood and oxygen through the

circulatory system. This leads to high blood pressure in the lungs (pulmonary

hypertension).

More red blood cells are produced to increase the blood's oxygen-carrying

capacity.

The heart rate increases to pump more blood. The rate of breathing increases.

Eventually these activities can lead to very serious and even life-threatening conditions:

Abnormally high blood pressure in the lungs can cause a complication called corpulmonale, in which the right ventricle of the heart enlarges, eventually leading to

heart failure. Chronic bronchitis is associated with a 50% higher risk of death from coronary

artery disease, independent of the risks associated with smoking.

Patients with prolonged and severe hypoxia and hypercapnia are at risk foracute

respiratory failure, which can cause heart rhythm abnormalities or other life-threatening conditions.

Other Serious Medical Problems Associated with COPD

The smoking that causes COPD is associated with high risks of pneumonia, lung cancer,stroke, and heart attack. Tobacco smoke contains more than 400 substances, many of

which are oxidants, metals (such as lead, cadmium, and aluminum), and carcinogens.

Nicotine itself may not damage tissues, but it is the chemical that addicts the smoker totobacco.

Lung Cancer. Patients with a 30-year history of smoking and indications of airflowlimitation (in other words, most patients with COPD), are at high risk for lung cancer.

Sleep Disturbance. About half of all people with severe COPD experience sleep disorderssuch as sleep-related hypoxia or insomnia. Nocturnal hypoxia, a lack of oxygen during

sleep, occurs when breathing is shallowest during rapid-eye-movement (REM) sleep. It

may be due to suppression of the cough reflex and a build-up of mucus. Nocturnal

hypoxia is treated with overnight oxygen therapy. As COPD worsens, many patients havetrouble falling or staying asleep. COPD patients should not use sleep medications.

Nighttime oxygen or a change in COPD medications from beta-agonists to

anticholinergics can sometimes help restore restful sleep.

Osteoporosis. Osteoporosis is a significant problem in patients with COPD. Manyconditions associated with COPD, including smoking, vitamin D deficiency, sedentary

lifestyle, and the use of corticosteroid medications put people at risk for bone density loss

and osteoporosis.

Gastroesophageal Reflux (GERD). More than half of patients with severe COPD have

GERD, a condition in which stomach acids back up from the stomach into the esophagus.


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However, many COPD patients don't report experiencing GERD symptoms such as

heartburn.

More Information on This Topic

Background Causes

Symptoms

Diseases With Similar Symptoms

Complications

Risk Factors

Diagnostic Tests

Medications Treatment

Oxygen-Replacement Therapy

Lifestyle Changes

Surgical Procedures References

News & Features

Reporter's File

Expert Q & A

Questions for Your Doctor

Clinical Trials

Background

Chronic obstructive pulmonary disease (COPD) is a condition in which there is limited

airflow in the lungs. The disease develops and worsens over time, and although it is notreversible, its progress can be slowed with therapy.

Although patients can breathe in normally, changes in the small airways cause the walls

to narrow during expiration, making it hard to breathe out. In many patients with COPD,

the small sacs where oxygen and carbon dioxide are exchanged are destroyed, graduallystarving the body of oxygen.

COPD is associated with a set of breathing-related symptoms:

Being out of breath, at first when doing physical activities, but as lung function

deteriorates, also at rest Chronic cough Spitting or coughing mucus (phlegm)

The ability to exhale (breathe out) gets worse over time.
http://health.nytimes.com/health/guides/disease/emphysema/background.htmlhttp://health.nytimes.com/health/guides/disease/emphysema/causes.htmlhttp://health.nytimes.com/health/guides/disease/emphysema/symptoms.htmlhttp://health.nytimes.com/health/guides/disease/emphysema/diseases-with-similar-symptoms.htmlhttp://health.nytimes.com/health/guides/disease/emphysema/risk-factors.htmlhttp://health.nytimes.com/health/guides/disease/emphysema/diagnostic-tests.htmlhttp://health.nytimes.com/health/guides/disease/emphysema/medications.htmlhttp://health.nytimes.com/health/guides/disease/emphysema/treatment.htmlhttp://health.nytimes.

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