CHRONIC OBSTRUCTIVE AIRWAYS DISEASE
Table of contents
1). Introduction……………………………………………………………………………….4
2 Pathophysiology and pathology…………………………………………………………….4
i) Pathophysiology…………………………………………………………………….4
ii) Mechanisms responsible……………………………………………………………6
a) Smoking…………………………………………………………………….6
b) Industrial exposures………………………………………………………...6
c) Air pollution………………………………………………………………...7
d) Genetic factor……………………………………………………………….7
e) Autoimmunity………………………………………………………………8
iii) Clinical characteristics……………………………………………………………..8
a) Symptoms…………………………………………………………………...8
3) Medical management……………………………………………………………………….9
i) Diagnosis……………………………………………………………………………9
a) Patient’s medical history……………………………………………………9
b) Chronic smoking……………………………………………………………9
c). X-ray and CT scans……………………………………………………….10
d) Pulmonary function tests………………………………………………….10
e) Carbon dioxide and oxygen levels
in the blood…………………………...11
f) 6MWT……………………………………………………………………..11
ii) Historical development of
therapeutics/medical treatments………………………11
iii) Current management practices/therapies…………………………………………12
a) Smoking cessation…………………………………………………………12
Benefit………………………………………………………………..12
Limitation…………………………………………………………….12
b) Medications………………………………………………………………13
Benefits……………………………………………………………...13
Limitations…………………………………………………………...13
c) Oxygen therapy……………………………………………………………13
Limitation…………………………………………………………….14
Benefit………………………………………………………………..14
iii) Development of new therapies and future
perspectives………………………….14
4) Conclusion………………………………………………………………………………...14
5) References…………………………………………………………………………………15
6) Appendices………………………………………………………………………………...16
1. Introduction
Chronic obstructive airways disease refers to
the incidence of chronic bronchitis or emphysema. These two are common diseases
affecting the lungs that most of the times coexist making the airways to get
narrowed. A person suffering from this disease has limitation in the amount of
air flowing to and from his or her lungs, resulting in breath shortness, also
known as (dyspnea). In medical practice, the disorder, the definition of the
disorder is through its typically low flow of air into the lung. As opposed to
other related conditions such as asthma, the limitation resulting from this
disorder is inadequately reversible and tends to get worse over time. According
to Simpson, Hippisley-Cox and Sheikh (2010), in the United Kingdom it is approximated
that 842,100 of 50 million individuals are diagnosed with the disorder. Internationally,
chronic obstructive airways disease was ranked among the six major causes of
death in the year 1990. Projections reveal that it might be the fourth major
cause of death by 2030 because of the higher rates of smoking as well as
demographic changes in the world.
2. Pathophysiology and pathology
i) Pathophysiology
In an event where one is suffering from COAD,
the normal functioning of the lungs is affected. The lung is the body organ
that is responsible for gaseous exchange. It is responsible for ensuring that
there is enough air rich in oxygen entering the body and that air rich in
carbon dioxide is exhaled from the body. COAD affects the optimal exchange of
these gases. There are various risk factors for the disorder that affect the
lungs and tampers with the smooth exchange of gases in and out of the body. However,
research has not completely revealed the process that take place to cause the
damage to the lungs by smoke and other pollutants. However, some of the known
processes that result in the damage to the lungs include: oxidative stress generated
by high levels of free radicals in smoke; release of cytokine because of inflammation
in the lungs due to the response by the body to particles in the airways; the
functioning of antiprotease enzymes like alpha 1-antitrypsin is affected by the
irritants (Simpson, Hippisley-Cox and Sheikh, 2010).
Following the damaging of the lungs and the
airways, there is reduction in the rate of flow of air to and from the alveoli.
With the effects of the disorder, higher reductions in the rate of flow of air
happen when one is breathing out. This is due to the fact that the force in the
chest compresses instead of expanding the lungs. Theoretically, the rate of the
flow of air is enhanced when one breathes with a lot of force, augmenting the
force of the chest while the air is being breathed out. With individuals
suffering from the disorder, there is normally a restriction in the manner in
which the pressure can augment the flow of air. Calverley and Koulouris (2005)
refer to this situation as expiratory flow limitation. In case of very low rate
in breathing, an individual may fail to complete the expiration before the need
to catch another breath. Hyperinflation, an increase in the amount of air
inside the lungs, resulting from some of the air from the preceding breath is
left in the lungs when the next is begun.
Shortness of breath also results from the
decrease in the surface area in the people suffering from the disorder. There
is a limit in the amount of surface area available for gaseous exchange with
emphysema. The effect of the loss of surface area lowers the speed of exchange
between the lungs and the atmosphere and can result to higher CO2
and lower O2 levels. Such a situation may require more rapid and
deep breathing to make up for the insufficiency of oxygen, which can be hard
because of the limitation in the flow. Some of the patients may manage to
breathe faster and deeper to make up, but dyspnea may develop as a result. For
others, it is possible to have less shortness in breath, tolerate high levels
of carbon dioxide and low levels of oxygen in the body, but may suffer other
compilations such as headaches, drowsiness and even heart failure. The disorder
can cause complications in other parts of the body like cachexia or weight loss,
pulmonary hypertension and cor pulmonale or right-sided heart failure.
ii) Mechanisms responsible
a) Smoking
The primary risk factor for COPD is chronic smoking.
It is estimated that about 80-90 percent of he disorder is as a result of
chronic smoking. The measurement of the exposure to cigarette smoking is done
in pack-years. This is by taking the average number of cigarette packs used in
a day and multiplying the number by the number of years the person has been
smoking. The chances of getting the disorder increase as the person ages as
well as increasing exposure to smoke. According to Rennard and Vestbo (2006), approximately
every one of life-long cigarette smokers will get the disorder provided other
extrapulmonary disorders (cardiovascular, diabetes, cancer) related to smoking
do not kill the person ahead of time.
b) Industrial exposures
Another risk factor for the disorder is
industrial exposure. Extreme and long-drawn-out exposure to work-related dust
and other pollutants present in gold-mining, coal-mining and textile industries
as well as chemicals like isocyanates, cadmium, and fumes resulting from welding
have been suggested to increase the chances of developing the disorder. Obstruction
of airways results under these kinds of exposures even among people who do not
smoke (Rennard and Vestbo, 2006). Those who work in these kinds of environment
and also smoke are at a higher risk of developing the disorder. Severe exposure
to silica dust has been known to cause silicosis, which is a limiting lung
disorder that is different from COAD, but exposure to less severe silica dust
has been related to incidences of COAD-like conditions. Nevertheless, the risk
of exposure to industrial dusts has been found to be less significant compared
to the risk resulting from cigarette smoking.
c). Air pollution
Researchers have suggested air pollution as
another risk factor for COAD. Studies have showed that those who reside in
large cities are at a greater risk of developing the disorder compared to those
who reside in rural regions (Halbert, et al 2006). This is because air
pollution in the large cities is a contributing factor for the disorder. It is
suggested that the pollution affects the ordinary development of the lungs.
However, there has not been thorough research to establish this relationship. Research
carried out on work-related waste gas as well as COAD/asthma-aggravating
compounds, sulphur dioxide, and the opposite connection to the occurrence of
the blue lichen Xanthoria have suggested that combustive manufacturing activities
do not assist those suffering from COAD. In the developing world, air pollution
happening indoors such as smoke from cooking fire is related to the occurrence
of the disorder, particularly among women.
d) Genetic factor
Genetic predisposition is a factor that has
been found necessary to cause the disorder in addition to heavy smoking. It has
been established that the disorder is common among individuals with a family
history of the disorder. This is because of the genetic dissimilarities that
render some lungs vulnerable to the effects of cigarette smoke and other
pollutants. However, these genetic differences are not very well known. Insufficiency
in Alpha 1-antitrypsin is a genetic factor that has been showed to be
responsible for approximately 2 percent of the suffering from the disorder. Individuals
with this genetic predisposition have their bodies failing to produce protein,
alpha 1-antitrypsin. This chemical offers protection to the lungs from being
damaged by protease enzymes, like elastase and trypsin, which can be produced
as a response of inflammatory reaction to smoke (Mahler, 2006).
e) Autoimmunity
Studies have suggested that there might be an autoimmune
element to the development of the disorder, set off by life-long cigarette
smoking (Mahler, 2006). Most of the people suffering from the disorder who have
quit smoking tend to have active lung inflammation. Because of the continuing inflammation
on the lungs, the disease may continue worsening even after one quits smoking. Autoantibodies
and autoreactive T cells are suggested to be the mediating factors of the
ongoing inflammation (Mahler, 2006).
iii) Clinical characteristics
Past studies have revealed dual character of
the pathology. Additionally, more recent studies have showed that a patient
diagnosed with the disorder could be categorized as having a principally bronchial
or emphysematous phenotype. This is through the analysis of medical,
functional, and radiological results or carrying out studies on remarkable
biomarkers (Kitaguchi et al 2006).
a). Symptoms
According to Kitaguchi et al (2006), essentials
of diagnosis of COAD include: a long history of smoking; chronic cough
accompanied by sputum production; dyspnea; rhonchi which is the decrease in the
strength of breath sounds, as well as long-drawn-out expiration on physical
test; and limitation in the flow of air revealed on lung function test. The
limitation should be poorly reversible and progressing over time.
The most common indication of the disorder is
shortness of breath, also known as dyspnea. Individuals with the disorder
normally describe this occurrence as: “My breathing requires effort,” “I feel
out of breath,” or “I can't get enough air in” (Mahler, 2006: 234-235). Such
people notice this symptom (shortness of breath) following long and vigorous
activities as this is where the demand of air to the lung is highest. As it
progresses with time, it gets worse such that patients can experience shortness
of breath even folk owing minor activities, even household chores. In the
advanced stages of the disorder, the problem can worsen such that it happens
even when one is resting and is constantly present.
There are other symptoms of the disorder such
as persistent coughing, production of mucus or sputum, wheezing, tightness of
the chest, and tiredness. Respiratory failure has been noted among individuals
during the advanced stages of the disorder or for people with severe COAD. This
can be indicated by cyanosis. Cyanosis refers to a bluish staining of the lips as
a result of the inadequacy of oxygen reaching the blood. Headaches, twitching
(asterixis) or drowsiness can result from the increase of carbon dioxide levels
in the blood. Cor pulmonale is a complication that happens at the advanced
stage of the disorder which is a staining of the heart because of the extra
demand in pumping blood through the affected lungs. Some of the symptoms of
this complication include dyspnea and peripheral edema, indicated by the
swelling of ankles (Kitaguchi et al, 2006).
3) Medical management
i) Diagnosis
a) Patient’s medical history
The disorder is normally diagnosed based on the patient’s medical
history. Such history forms the basis for disclosing various symptoms of the
disorder. The signs of the disorder are disclosed through physical tests. Some
of the tests that diagnose the disorder include chest X-ray, CAT or CT chest
scan, lung function test and tests to measure the levels of oxygen and carbon
dioxide levels in the blood (Rabe et al 2007).
b) Chronic smoking
Doctors normally suspect COAD in smokers
exhibiting signs such as shortness of breath, in the presence or absence of
exertion, those with chronic unrelenting cough producing sputum, and recurrent
lung infections like bronchitis or pneumonia. Some cases of the disorder are
diagnosed in patients developing respiratory infections requiring hospitalization.
Practically, the disorder to be suspected in all chronic smokers whether or not
they have the symptoms as some of the symptoms of the disorder appear after
significant lung damage. Some of the physical findings that are used in the
diagnosis of the disorder are wheezing and enlargement of the chest cavity. A
stethoscope is used in listening to the chest where faint and distant breath can
be heard (Rabe et al 2007).
c). X-ray and CT scans
According to Mahler et al (2006), the X-ray on the chest can reveal
enlargement in chest cavity and enlarged lung markings among patients with
principally emphysema, revealing damaging of tissues in the lungs and increase
in air-sacs. The X-ray reveals an increase in lung markings for patients
suffering from chronic bronchitis only. CT or CAT chest scan can more
accurately than X-ray reveal damages in lung tissue and airways in a patient
with the disorder. X-rays and CT scans are used as a way of ruling out other
lung infections with similar symptoms as COAD. However, CT scans are not
required for regular tests and management of the disorder, but they are
important in the evaluation of the level of change in emphysematous and in detecting
initial stages of lung cancer.
d) Pulmonary function tests
According to Nathell et al (2007) lung or pulmonary function tests are
also useful in the diagnosis of COAD. One such test is spirometry, which is a
test that quantitates the level of the obstruction of the airway. The test is
used in determining the severity of the disorder (see appendix 1). During the test, the individual is asked to
take complete breath and exhale rapidly and vehemently into a tube. The tube is
normally attached to a machine used for measuring the amount of exhaled air.
The volume of air exhaled per second (the FEV1) has proven a reliable and significant
measure of the amount of obstruction in the flow of air. The normal ratio of FEV1
to the FVC is typically 70 percent. There is reduction in the ratio where there
is occurrence of obstruction. The test is normally repeated after treatment
using bronchodilators. Improvement in the second test reveals that the
obstruction of the airway is reversible (Mahler et al 2006).
e) Carbon dioxide and oxygen levels
in the blood
Samples of blood drawn from the patient’s
artery are used in testing the level of carbon dioxide and oxygen in the blood.
Pulse oximetry is an alternative to inserting a needle into the artery to draw
blood. This test operates from the point of view that the extent of redness of
the haemoglobin is relative to the level of oxygen. This means that the blood
becomes redder with the amount of oxygen present. The patient has a probe
(oximeter) put around his or her finger. Different shades of red are
transmitted through the tip of the finger on the basis of the amount of oxygen
present in the blood (Rabe et al 2007).
f) 6MWT
Nathell et al (2007) posits that 6MWT or six
minute walking test is a simple and effective test for the disorder. This is
where the individual is required to take a six minutes walk on a level ground
at his own speed. A standard script is used by the healthcare worker performing
the test. Besides being kept up to date on the amount of time remaining to
complete the task, there is no other kind of engorgement given. The patient is
allowed to stop and take a rest at any point. There is measurement of distance
covered. It is normally an extremely precise index (Rabe et al 2007).
ii) Historical development of
therapeutics/medical treatments
Research has been carried towards the development of treatment for COAD,
but there is still no cure for the disorder. However, the years of research
have produced preventive and treatment methods for managing it. Research on
COAD and its treatment can be traced back to the 18th century with
descriptio of cases where the lungs did not function optimally. Contemporary
diagnosis started with the development of the stethoscope by René Laennec in
1837. However, thorough research and understanding of the disorder did not
start until the past century.
iii) Current management practices/therapies
According to Rabe et al (2007) the main present directions of the
management of the disorder are assessment and monitoring of the disease in
order to lower the risk factors, management of stable COAD, prevention of acute
damage and management of comorbidity. Two measures have been found to lower
mortality, which are smoking cessation and supplemental oxygen.
a) Smoking cessation
This ha been revealed to be the most effective
factor in reversing the progression of the disorder once diagnosed. Even at the
advanced stages, quitting smoking can lower the rate of damage to the lungs,
thus delaying the start of disability or death. This process starts with a
personal decision to quit smoking. There are other management therapies that
involve the use a second or third party in helping the individual to quit
smoking. Such strategies that can help include social support, smoking
cessation programme. Medications like nicotine replacement therapy, varenicline
and bupropion can also be used. Reduction or elimination of workplace exposure
would decrease the risk of developing COAD and can also lower the progression
of the disorder for those who are already diagnosed (Paoletti et al 2009).
Benefits: The main benefit of this method is reduction
in the rate of progression of the disorder once it is diagnosed. Those people
who are diagnosed early and quit smoking on time tend to have higher chances of
longer life than those who continue to smoke. Studies show that long-term
sustained smoking cessation can cause a decrease in the progression of the
disorder. Reduction or elimination of industrial exposure also works in the
same wary.
Limitations: Particularly for individuals living
in an environment that encourages smoking it is hard to avoid or quit smoking.
Even if cessation, even following many years of smoking, lowers the risk of
developing COAD, ex-smokers never reasonably lower their risk when compared to
non-smokers. Additionally there is the risk of relapse. For industrial exposure
it is hard to avoid toxins while working in industries where they are produced.
Additionally, some people are forced to loose their source of income to manage
the disorder (Rabe et al 2007).
b) Medications
There are various medications that are used in
the treatment and management of the disorder. Bronchodilators are drugs used
for the relaxation of smooth muscle in the airways, thus improving the flow of
air. Normally used with inhaler or through a nebulizer. Two kinds of
bronchodilators are presently used: β2 agonists and
anticholinergics. Anticholinergics
medications block the stimulation of cholinergic nerves causing
relaxation of airway muscles (Paoletti et al 2009).
Benefits: Medications are used to lower the
symptoms of the disorder such as shortness of breath, wheeze as well exercise
limitation. They help in enhancing the quality of life for those with the
disorder. Ipratropium has been linked to higher cardiovascular morbidity.
Limitations: Drugs are known to cause other
negative side effects such as cardiovascular problems. Additionally, the drugs
used in the management of the disorder help in alleviating the symptom and the
patient may have to use them for a long time without the possibility of being
cured of the disorder.
c) Oxygen therapy
The current research is centred on the use of oxygen in therapy. People
with low oxygen in the body are given supplementary oxygen. Some of the equipments that can be used
include oxygen cylinder or oxygen concentrator. This is important in allowing
individuals with the disorder to carry on with their daily duties (Rabe et al
2007).
Benefits: Oxygen therapy has been proven to
improve the ability of the patient to carry on with the normal duties without
suffering shortness of breath. It has also been known to increase the chances
of survival in the patient.
Limitations: A high level of oxygen
supplementation is capable of causing accumulation of carbon dioxide as well as
respiratory acidosis for a number of individuals with the disorder.
iii) Development of new therapies and future
perspectives
The current development is headed towards development of pulmonary
rehabilitation which will combine exercise program, disease management with the
use of the other kinds of therapies, and counseling, all coordinated to for the
good of the patient. This will provide a sense of control for the patient in
addition to improving the quality of life and chances of survival.
4) Conclusion
Chronic obstructive airways disease has been defined as the occurrence
of chronic bronchitis or emphysema. It is a common disease especially among
cigarette smokers. Various advancements have been made in the diagnosis and
management of the disorder, but there is still no cure. All the therapies and
treatment programs that are currently available are used in the management of
the symptoms and slowing down the progression of the disorder. it is thus
important that more research is made into more effective treatments or
therapies, possibly those that can cure the disorder.
5) References:
Calverley PM, Koulouris NG (2005). "Flow limitation and dynamic
hyperinflation: key
concepts in modern respiratory
physiology". Eur Respir J 25
(1): 186–199.
Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM
(September 2006).
"Global burden of COPD: systematic review
and meta-analysis". Eur. Respir. J.
28 (3): 523–32.
Kitaguchi Y, Fujimoto K, Kubo K, Honda T (October 2006).
"Characteristics of COPD
phenotypes classified according to the findings
of HRCT". Respir Med 100 (10):
1742–52.
Mahler DA (2006). "Mechanisms and measurement of dyspnea in chronic
obstructive
pulmonary disease". Proceedings of the American Thoracic Society 3 (3): 234–8.
Nathell, L.; Nathell, M.; Malmberg, P.; Larsson, K. (2007). "COPD
diagnosis related to
different guidelines and spirometry
techniques". Respiratory research
8 (1): 89.
Paoletti M, Camiciottoli G, Meoni E, et al. (December 2009).
"Explorative data analysis
techniques and unsupervised clustering methods
to support clinical assessment of Chronic Obstructive Pulmonary Disease (COPD) phenotypes". J Biomed Inform 42 (6): 1013–21
Rabe KF, Hurd S, Anzueto A, et al. (2007). "Global Strategy for the
Diagnosis, Management,
and Prevention of Chronic Obstructive Pulmonary
Disease: GOLD Executive Summary". Am.
J. Respir. Crit. Care Med. 176 (6): 532–55.
Rennard, S. I.; Vestbo, J. R. (2006). "COPD:
the dangerous underestimate of 15%". The
Lancet 367
(9518): 1216.
Simpson CR, Hippisley-Cox J, Sheikh A (2010). "Trends in the
epidemiology of chronic
obstructive pulmonary disease in England:
a national study of 51 804 patients". Brit
J Gen Pract 60 (576): 483–488.
6) Appendices
|
Severity of COPD (GOLD scale)
|
FEV1 % predicted
|
|
Mild (GOLD 1)
|
≥80
|
|
Moderate (GOLD 2)
|
50–79
|
|
Severe (GOLD 3)
|
30–49
|
|
Very severe (GOLD 4)
|
<30 or chronic respiratory failure
symptoms
|
Appendix 1
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