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This was the exhibit at the Hunterian museum that my presentation was
inspired by
What is emphysema?
Spirometry
To assess how well your lungs work, a breathing test called spirometry is
carried out. You will be asked to breathe into a machine called a
spirometer.
The spirometer takes two measurements: the volume of air you can
breathe out in one second (called the forced expiratory volume in one
second or FEV1) and the total amount of air you breathe out (called the
forced vital capacity or FVC).
You may be asked to breathe out a few times to get a consistent reading.
The readings are compared with normal measurements for your age,
which can show if your airways are obstructed.
Other tests
You may have other tests as well as spirometry. Often, these other tests
will help the doctor rule out other conditions that cause similar symptoms.
Chest X-ray
Phlegm sample
tested to check for signs of a chest infection
Tar stimulates goblet cells and mucus glands to enlarge, producing more
mucus. It destroys the cilia inhibiting the cleaning of the airways and
mucus (containing dirt, bacteria and viruses) builds up blocking the
smallest bronchioles. Makes you very prone to infections. Infections cause
the accumulation scar tissue, which results in thicker alveolar walls and
they increase the diffusion pathway of oxygen and carbon dioxide,
therefore decreasing the rate of diffusion.
Large air spaces appear, reducing the surface area for gas exchange and
making sufferers breathe more rapidly. As it progresses, patients become
breathless and wheezy - they may need a constant supply of oxygen to
stay alive.
Although it happens less than 1% of the time, emphysema can also be
caused by a genetic condition. It happens where there is a fault with a
persons alpha-1-antitrypsin.
one of its functions is to protect the lungs from elastase, an enzyme that can disrupt
connective tissue (acts as a competitive inhibitor)
Treatment options
Medication cannot cure COPD and cannot reverse the damage caused by
smoking, but medication can help in a variety of ways. It may help:
Your doctor may prescribe more than one type of medication. Here are the
most common types used to treat COPD:
If you have severe COPD, you may have low levels of oxygen in your
blood. This means your body doesn't get enough oxygen from your
damaged airways and lungs. Your doctor may recommend oxygen
treatment to protect your organs, enhance your sleep, improve your daily
activity and help you live longer.
Latest in Research
Tests on mice have found that damaged lungs have been repaired to
normal by the compound, which is already used to treat chronic acne.
Trials are now being carried out to see if it could have similar success if
used on humans.
He said the retinoic acid compound worked on tissue cells in the lungs,
causing them to regenerate.
Emphysema begins with the destruction of tiny air sacs (alveoli), which
creates permanent "holes" in the walls of the lungs.
As the air sacs are destroyed the lungs are able to transfer less and less
oxygen to the bloodstream.
Prof Maden said that during the tests on mice his compound made the
alveoli grow back again until they returned to normal levels.
He said: "We saw quite dramatic results. It is potentially hopeful for
emphysema sufferers, and for premature babies who often suffer from
loss of alveoli because of treatments given to stimulate lung growth."
Preliminary studies show the coil procedure gives results that are comparable to the lung
volume reduction surgery. However, because there are no incisions or tissue removal, the
recovery process is much quicker, with patients returning home after an overnight stay in the
hospital.
A new study found this lung coil procedure significantly improved quality
of life for people with emphysema improving exercise capacity (versus
patients who did not receive the therapy).
While the treatment is not yet approved by the Food and Drug
Administration, doctors hope that it will be approved to treat emphysema
by next year.
Study details
The coils are believed to bring elasticity back to the lungs and may help
tether airways open to provide better airflow.
The results showed that coil treatment was associated with improved
quality of life. Patients who received coils also showed greater
improvement in a walking test when
compared to the group that didnt get coils.
Fibrosis is the accumulation of scar tissue as a result of damage or bacterial
infection
Introduction
This was the exhibit at the hunterian museum that my presentation was inspired
by
What is emphysema?
Surprisingly it's the third biggest killer worldwide behind heart disease and stroke
emphysema, the inner walls of the air sacs weaken and eventually rupture
creating one larger air space instead of many small ones. This reduces the surface
area of the lungs and, in turn, the amount of oxygen that reaches your bloodstream.
Due to constant infection, phagocytes are attracted to the lungs where they release
elastase - an enzyme that breaks down the elastin in the alveoli walls, to enable them to
reach the surface where the bacteria are. Without adequate elastin, the alveoli cannot
stretch, so they recoil and many burst.
Large air spaces appear, reducing the surface area for gas exchange and making sufferers
breath more rapidly. As it progresses, patients become breathless and wheezy - they may
need a constant supply of oxygen to stay alive.
Fibrosis occurs in the lungs, which results in thicker alveolar walls which increase the
diffusion pathway of oxygen and carbon dioxide, therefore decreasing the rate of
diffusion. Another side effect is a loss of elasticity which makes breathing out more
difficult.
Scar tissue is fibrous connective tissue and prevents good lung function, therefore
symptoms caused are coughing and shortness of breath. Damaged alveoli will not
contribute to the diffusion of oxygen into red blood cells.
TREATMENT
Medication cannot cure COPD and cannot reverse the damage caused by smoking, but
medication can help in a variety of ways. It may help:
Your doctor may prescribe more than one type of medication. Here are the most common types
used to treat COPD:
Bronchodilators. This class of drugs relaxes muscles around airways. They may make
breathing easier and reduce the number of episodes when the disease becomes acutely worse.
Your doctor is likely to first prescribe an inhaled bronchodilator. To take it, you breathe in using a
device such as a metered-dose inhaler, dry-powder inhaler or nebuliser. Metered-dose inhalers
(MDIs) use a chemical to push medication out of the inhaler. The common propellant is
heptafluoropropane (HFA). The harmful CFCs that were damaging to the ozone layer have now
been phased out.
You may also take these types of medications as a tablet, or in rare cases, into a vein
(intravenously). You may need to combine more than one bronchodilator or use a combination
product for the best results.
Examples of bronchodilators used as COPD treatment include:
sym block acetylcholine, a chemical messenger that makes airways constrict. They may
help you breathe easier and lower the number of acute episodes you have.
Using oxygen treatment
If you have severe COPD, you may have low levels of oxygen in your blood. This means
your body doesn't get enough oxygen from your damaged airways and lungs. Your doctor
may recommend oxygen treatment to protect your organs, enhance your sleep, improve
your daily activity and help you live longer.
Oxygen can be supplied in a large, heavy oxygen cylinder. These can be prescribed by
your doctor and delivered to your home. There are also small portable cylinders that you
can take out of the house. The oxygen is delivered through a flexible nasal tube or a face
mask. If you have a long-term need for constant oxygen, you can be provided free of
charge with an oxygen concentrator, a device that extracts oxygen from room air. An
NHS oxygen concentrator may have to be authorised by a hospital specialist. Do not
smoke when you are using an oxygen concentrator. The increased level of oxygen that is
produced is highly flammable, and a lit cigarette could trigger a fire or an explosion.
Emphysema gradually damages the air sacs (alveoli) in your lungs, making you
progressively more short of breath. Emphysema is one of several diseases known
collectively as chronic obstructive pulmonary disease (COPD).
Your lungs' alveoli are clustered like bunches of grapes. In emphysema, the inner
walls of the air sacs weaken and eventually rupture creating one larger air space
instead of many small ones. This reduces the surface area of the lungs and, in turn,
the amount of oxygen that reaches your bloodstream.
When you exhale, the damaged alveoli don't work properly and old air becomes
trapped, leaving no room for fresh, oxygen-rich air to enter. Treatment may slow the
progression of emphysema, but it can't reverse the damage.
Surgery
If you have severe COPD with significant lung damage, you may need surgery, especially if you
have severe symptoms, can't control your COPD with medication or have trouble breathing most
of the time. Surgery may involve:
Emphysema
Emphysema is a long-term, progressive disease of the lungs that primarily causes shortness of
breath. In people with emphysema the lung tissues necessary to support the physical shape and
function of the lung are damaged. It is included in a group of diseases calledchronic 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 bronchioles,
makes these airways unable to hold their shape properly when you exhale. This makes them
inefficient at transferring oxygen into the blood, and in taking carbon dioxide out of the blood.
The NHS says around 900,000 people in the UK have been diagnosed with COPD and about two
million people have the condition but have not been diagnosed. COPD causes 25,000 deaths a year.
Emphysema changes the anatomy of the lung in several important ways.
Normally, the lungs are very spongy and elastic. When a breath is taken, the chest wall expands,
expanding the sponge. Just as a squeezed sponge will draw water into it when released, suction
draws air into the lungs when the chest wall expands. Air is brought though the trachea (windpipe)
and bronchi (the main air tubes going to right and left lungs). These tubes divide into smaller and
smaller tubes, finally ending in alveoli. Alveoli, the tiniest structures in the lung, are very small air sacs
that are arranged like a bunch of grapes. The alveoli are at the ends of the smallest tubes called
bronchioles. The alveoli and the bronchioles are very important structures for the lungs to function
properly. It is these structures that are damaged by emphysema.
A sponge works to pick up water because all the tiny little holes expand at once after being squeezed.
If the holes were larger, the sponge would not pick up as much water. This is because a larger hole
cannot expand enough by itself to equal the action of multiple smaller ones. Thinking of the lungs as a
sponge in this way, it becomes easier to see how emphysema acts to cause impaired lung function.
Lungs require an elastic quality, so that they can expand and contract well. Also, as with the holes of
the sponge, the lungs need many alveoli (hundreds of millions, in fact) to draw enough air into them.
The fewer and the bigger the alveoli, the less effectively they perform.
Emphysema causes
Cigarette smoking is by far the biggest culprit for people developing 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
overemphasised. Cigarette smoke contributes to this disease process in two ways. It destroys lung
tissue, which is the cause of the obstruction, and it causes inflammation and irritation of airways that
can cause the disease to get worse.
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 damage to the cilia that prevents them working properly to clear secretions. Long-
term exposure to cigarette smoke causes the cilia to disappear completely from the cells lining the air
passages. Without the constant sweeping motion of the cilia, mucus secretions cannot be cleared
from the lower respiratory tract. Furthermore, smoke causes mucus secretion to be increased at the
same time that the ability to clear the secretions is decreased. The resulting mucus build-up can
provide bacteria with a rich source of food and lead to infection.
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.
Over time, enzymes released during this persistent inflammation leads to the loss of proteins
responsible for keeping the lungs elastic. In addition, the tissue separating the air cells (alveoli) from
one another is also destroyed. Over years of chronic exposure to cigarette smoke, the decreased
elasticity and destruction of alveoli leads to the slow destruction of lung function. And if that isnt
enough of a reason to stop, remember that cigarette smoke is also carcinogenic, meaning that it leads
to lung cancer. In the UK, cigarette smoking causes 90% of lung cancer in men and 83% in women,
according to Cancer Research UK. It is also responsible for most cancers of the larynx, oral cavity
and pharynx, oesophagus and bladder.
Alpha-1-antitrypsin is a substance that fights a destructive enzyme in the lungs called trypsin.
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.
Air pollution acts in a similar manner to cigarette smoke. The pollutants cause inflammation in
the airways, leading to the destruction of lung tissue.
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, although the number of women
developing COPD is increasing.
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 it is that they will have enough
lung tissue destruction to produce emphysema.
http://www.who.int/respiratory/copd/en/
Introduction
Chronic obstructive pulmonary disease
(COPD) is the name for a collection of lung
diseases including chronic bronchitis,
emphysema and chronic obstructive airways
disease.
People with COPD have difficulties breathing,
primarily due to the narrowing of their airways,
this is called airflow obstruction.
Typical symptoms of COPD include:
increasing breathlessness when active
a persistent cough with phlegm
frequent chest infections
Who is affected?
COPD is one of the most common respiratory
diseases in the UK. It usually only starts to affect
people over the age of 35, although most people
are not diagnosed until they are in their 50s.
It is thought there are more than 3 million people
living with the disease in the UK, of which only
about 900,000 have been diagnosed. This is
because many people who develop symptoms of
COPD do not get medical help because they
often dismiss their symptoms as a smokers
cough.
COPD affects more men than women,
although rates in women are increasing.
Diagnosis
It is important that COPD is diagnosed as early
as possible so treatment can be used to try to
slow down the deterioration of your lungs. You
should see your GP if you have any of the
symptoms mentioned above.
COPD is usually diagnosed after a consultation
with your doctor, which may be followed by
breathing tests.
Read more about diagnosing chronic obstructive
pulmonary disease.
Treating COPD
Although the damage that has already occurred
to your lungs cannot be reversed, you can slow
down the progression of the disease. Stopping
smoking is particularly effective at doing this.
Treatments for COPD usually involve relieving
the symptoms with medication, for example by
using an inhaler to make breathing easier.
Pulmonary rehabilitation may also help increase
the amount of exercise you are capable of doing.
Surgery is only an option for a small number of
people with COPD.
Read more about treating chronic obstructive
pulmonary disease.
FUTURE
http://www.dailymail.co.uk/health/article-204532/Vitamin-cure-emphysema.html
British scientists have found that retinoic acid, a derivative of vitamin A, can reverse damage caused to the lungs by the previously
incurable disease.
Tests on mice have found that damaged lungs have been repaired to normal by the compound, which is already used to treat chronic
acne.
Trials are now being carried out to see if it could have similar success if used on humans.
Professor Malcolm Maden, of the Medical Research Centre for Developmental Neurobiology at King's College, London, said his team's
research held out "great hope" for the development of a treatment for emphysema in humans.
He said the retinoic acid compound worked on tissue cells in the lungs, causing them to regenerate.
Emphysema begins with the destruction of tiny air sacs (alveoli), which creates permanent "holes" in the walls of the lungs.
As the air sacs are destroyed the lungs are able to transfer less and less oxygen to the bloodstream.
Prof Maden said that during the tests on mice his compound made the alveoli grow back again until they returned to normal levels.
He said: "We saw quite dramatic results. It is potentially hopeful for emphysema sufferers, and for premature babies who often suffer
from loss of alveoli because of treatments given to stimulate lung growth."
https://www.sciencedaily.com/releases/2016/05/160515183719.htm
https://www.sciencedaily.com/releases/2016/07/160705135135.htm
Researchers have developed a new strategy using lung-targeted gene
therapy that may lead to improved treatments for inherited diseases
including emphysema.
The current treatment for patients affected by AATD involves weekly intravenous infusion of the
normal AAT protein -- an inconvenient, invasive and expensive option. Delivery of a normal copy
of the gene, known as gene therapy, is an experimental approach to treating some genetic
conditions including AATD. Because patients with AATD have low levels of AAT protein in their
lungs, researchers at the Center for Regenerative Medicine (CReM) of Boston University and
Boston Medical Center have focused their recent efforts on evaluating whether targeting gene
therapy directly to the lungs may have promise as a treatment for AATD.
Using an experimental model, the researchers delivered a copy of the normal gene to cells in the
lung and found this corrected gene persisted in lung cells for at least one year. These findings
appear in the journal Molecular Therapy -- Methods & Clinical Development.
Additionally, the study demonstrated that multiple cell types in the lungs and also the liver are
affected by these changes and that once the normal gene incorporated into DNA, normal alpha 1
antitrypsin protein was produced in quantities sufficient to lessen the severity of lung disease.
"These results support direct transgene delivery to the lung as a potential alternative approach to
achieve the goal of developing a gene therapy for AATD," explained corresponding author
Andrew Wilson, MD, assistant professor of medicine at BUSM and a physician in the department
of pulmonary, allergy, sleep & critical care medicine at BMC.