You are on page 1of 10

BACHELOR MEDICAL AND HEALTH SCIENCES WITH HONOURS

SEMESTER 1 TAHUN 1

NBMS2402

PATHOPHYSIOLOGY

NO. MATRIKULASI : 930216025268001

NO. KAD PENGNEALAN : 930216025268

NO. TELEFON : 011-10161602

E-MEL : kimu_taku93@yahoo.co.uk

PUSAT PEMBELAJARAN : OUM PETALING JAYA


1.0 INTRODUCTION

What is Chronic Obstructive Pulmonary Disease ( COPD)? Chronic Obstructive


Pulmonary Disease (COPD) is a term used to describe progressive lung diseases including
chronic bronchitis, refractory or non-reversible asthma and emphysema(Viegi,2007). This
disease is characterized by increasing breathlessness.COPD is a progressive and incurable
disease, but with the right diagnosis and treatment, there are many things you can do to
manage your COPD and breathe better. The human can live for many years with COPD and
enjoy life. COPD prevalence, morbidity, and mortality vary across the world and across
different ethnic groups within countries (Rosell A,2005) . The prevalence and burden of
COPD are projected to increase in the coming decades due to continued exposure to COPD
risk factors and the changing age structure of the world's population. According to WHO
estimates in 2007, 210 million people have COPD worldwide with 80 million of them
experiencing moderate to severe chronic disease.COPD was ranked as the twelfth leading
cause of disability in 1990, but it is projected to rank fifth in 2020, behind ischaemic heart
disease, major depression, traffic accidents and cerebrovascular disease as a leading cause of
disability. It is second only to heart disease as a cause of disability that forces people to stop
working. The number of deaths from COPD has increased more than 60% over the last 20
years, and more than 95% of all COPD related deaths occur in people older than age 55.
COPD will become the third leading cause of death worldwide by 2030. In this writing, we
can know more about the pathophysiologic changes triggered by lifestyle practices that
increase the risk of COPD.

2.0 Discussion of pathophysiologic changes that can be triggered by common lifestyle


practices to increase the risk of COPD.

Chronic obstructive pulmonary disease (COPD), a preventable and treatable


respiratory disorder largely caused by smoking, is characterized by progressive, partially
reversible airflow obstruction and lung hyperinflation with significant extrapulmonary
(systemic) manifestations and comorbid conditions all of which may contribute to the
severity of the disease in individual patients(Lundbäck B,2003). The co-morbid conditions
associated with COPD include ischaemic heart disease; osteopenia, osteoporosis and bone
fractures; cachexia and malnutrition; normochromic normocytic anaemia; skeletal muscle
wasting and peripheral muscle dysfunction; diabetes mellitus; sleep disorders; cataracts and
glaucoma; lung cancer; and anxiety and depression both of which increase in incidence with
disease severity (Buist AS,2007). Chronic Obstructive Pulmonary Disease (COPD) is a term
used to describe progressive lung diseases including chronic bronchitis, refractory or non-
reversible asthma and emphysema.Chronic bronchitis is an inflammation of the breathing
tubes (bronchial airways) inside your lungs. Tiny hair-like structures (cilia) line your airways
and sweep mucus up, keeping your airways clean. When cilia are damaged, they can't do this,
and it becomes harder for you to cough up mucus. This can make your airways swollen and
clogged. These changes limit airflow in and out of your lungs, making it hard to breathe.
Meanwhile, In Emphysema the tiny, delicate air sacs (alveoli) in your lungs are damaged.
The walls of the damaged air sacs become stretched out and your lungs actually get bigger,
making it harder to move your air in and out. Old air gets trapped inside the alveoli so there is
little or no room for new air to go. In emphysema, it is harder to get oxygen in and carbon
dioxide (the waste product of your breathing) out. Also, Refractory (non-reversible) asthma is
a type of asthma that does not respond to usual asthma medications. In an asthma attack,
bronchial airways tighten up and swell. Medications can usually reverse this, opening up the
airways and returning them to how they were before the asthma attack. In refractory asthma,
medications cannot reverse the tightening and swelling of the airways. There is a lot of
examples of common lifestyle practices to increase the risk of COPD which is can be
triggered and make changes of pathophysiologic such as smoking(Silverman EK,2009). The
main risk factor for COPD is smoking. It causes up to 90 percent of COPD deaths, according
to the American Lung Association (ALA). People who smoke are 13 times more likely to die
from COPD than those who never smoked.Long-term exposure to tobacco smoke is
dangerous. The longer you smoke and the more packs you smoke, the greater your risk is of
developing the disease. Pipe smokers and cigar smokers are also at risk.Exposure to
secondhand smoke also increases your risk. Secondhand smoke includes both the smoke from
burning tobacco and smoke exhaled by the person smoking.

3.0 Discussion on clinical manifestation of COPD

As we know , there is a lot of clinical manifestation of COPD that can be know.


Clinical manifestation also can be seen as signs and symptoms. The definition of clinical
manifestations that can be either objective when observed by a physician or subjective when
perceived by the patient. There is a lot of clinical manifestation of COPD. The most common
symptoms of COPD include sputum production,cough, and dyspnea, particularly dyspnea on
exertion(Vestbo J,2013). These symptoms may arise from a variety of diverse etiologies, and
therefore the diagnosis of COPD requires confirmation with spirometry.COPD develops
slowly over many years and clinical features may be subtle. Since patients develop exertional
dyspnea, many limit their level of activity or adjust their expectations to a lower level of
functioning and thus have no complaints. The clinician must inquire not only about dyspnea
but also about habitual levels of exertional activity to determine which levels precipitate
dyspnea. The same is true for non-smokers with COPD (Svanes C ,2010.) COPD should be
suspected in all individuals with reduced exertional activity, particularly 2010if it is
associated with dyspnea.A cough and sputum production may be the defining features of
chronic bronchitis, although airflow limitation can result from small airways in the absence of
a cough and sputum (Barnes PJ,2009). Therefore, a clinical diagnosis cannot distinguish
emphysema from airways disease with much reliability. Signs that may be present in late
disease include prolongation of expiratory airflow, signs related to hyperinflation of the chest,
and if airways disease is present, adventitial lung sounds, including rhonchi and wheezes.
However, these findings are neither sensitive nor reliable, and definitive diagnosis requires
spirometry. While COPD is defined by expiratory airflow limitation (of which there are
several causes), not all expiratory airflow limitation is due to COPD.COPD develops slowly
over many years and clinical features may be subtle. Since patients develop exertional
dyspnea, many limit their level of activity or adjust their expectations to a lower level of
functioning and thus have no complaints. The clinician must inquire not only about dyspnea
but also about habitual levels of exertional activity to determine which levels precipitate
dyspnea. The same is true for non-smokers with COPD. COPD should be suspected in all
individuals with reduced exertional activity, particularly if it is associated with dyspnea.A
cough and sputum production may be the defining features of chronic bronchitis, although
airflow limitation can result from small airways in the absence of a cough and sputum.
Therefore, a clinical diagnosis cannot distinguish emphysema from airways disease with
much reliability. Signs that may be present in late disease include prolongation of expiratory
airflow, signs related to hyperinflation of the chest, and if airways disease is present,
adventitial lung sounds, including rhonchi and wheezes. However, these findings are neither
sensitive nor reliable, and definitive diagnosis requires spirometry. While COPD is defined
by expiratory airflow limitation (of which there are several causes), not all expiratory airflow
limitation is due to COPD.
4.0 Discussion of the diagnostic criteria and basic treatment options for COPD.

COPD is commonly misdiagnosed for former smokers may sometimes be told they
have COPD, when in reality they may have simple deconditioning or another less common
lung condition. Likewise, many people who have COPD may not be diagnosed until the
disease is advanced and interventions are less effective.To diagnose your condition, your
doctor will review your signs and symptoms, discuss your family and medical history, and
discuss any exposure you've had to lung irritants especially cigarette smoke. Your doctor may
order several tests to diagnose your condition.

The tests may include such as lung (pulmonary) function tests. Pulmonary function tests
measure the amount of air you can inhale and exhale, and if your lungs are delivering enough
oxygen to your blood.Next is spirometry.Spirometry is the most common lung function test.
During this test, you'll be asked to blow into a large tube connected to a small machine called
a spirometer. This machine measures how much air your lungs can hold and how fast you can
blow the air out of your lungs.Spirometry can detect COPD even before you have symptoms
of the disease. It can also be used to track the progression of the disease and to monitor how
well treatment is working. Spirometry often includes measurement of the effect of
bronchodilator administration. Other lung function tests include measurement of lung
volumes, diffusing capacity and pulse oximetry.Next is to do chest X-ray. A chest X-ray can
show emphysema, one of the main causes of COPD. An X-ray can also rule out other lung
problems or heart failure.Next is to do CT scan. A CT scan of your lungs can help detect
emphysema and help determine if you might benefit from surgery for COPD. CT scans can
also be used to screen for lung cancer.Next is to take arterial blood gas analysis. This blood
test measures how well your lungs are bringing oxygen into your blood and removing carbon
dioxide.Also we can do laboratory tests. Laboratory tests aren't used to diagnose COPD, but
they may be used to determine the cause of your symptoms or rule out other conditions. For
example, laboratory tests may be used to determine if you have the genetic disorder alpha-1-
antitrypsin (AAT) deficiency, which may be the cause of some cases of COPD. This test may
be done if you have a family history of COPD and develop COPD at a young age, such as
under age 45.The treatment can be given to COPD patients is many.We must control and
treat them.A diagnosis of COPD is not the end of the world. Most people have mild forms of
the disease for which little therapy is needed other than smoking cessation. Even for more
advanced stages of the disease, effective therapy is available that can control symptoms,
reduce your risk of complications and exacerbations, and improve your ability to lead an
active life.

Smoking cessation is the most best way to reduce the risk of disease.The most essential step
in any treatment plan for COPD is to stop all smoking. It's the only way to keep COPD from
getting worse which can eventually reduce your ability to breathe. But quitting smoking isn't
easy. And this task may seem particularly daunting if you've tried to quit and have been
unsuccessful.Talk to your doctor about nicotine replacement products and medications that
might help, as well as how to handle relapses (Oberg M,2011). Your doctor may also
recommend a support group for people who want to quit smoking. It's also a good idea to
avoid secondhand smoke exposure whenever possible.There also be help by giving good
medications to the patients.Doctors use several kinds of medications to treat the symptoms
and complications of COPD. You may take some medications on a regular basis and others as
needed such as bronchodilators which usually come in an inhaler that can relax the muscles
around your airways (Hurst JR,2010). This can help relieve coughing and shortness of breath
and make breathing easier. Depending on the severity of your disease, you may need a short-
acting bronchodilator before activities, a long-acting bronchodilator that you use every day or
both.Short-acting bronchodilators include albuterol (ProAir HFA, Ventolin HFA, others),
levalbuterol (Xopenex HFA), and ipratropium (Atrovent). The long-acting bronchodilators
include tiotropium (Spiriva), salmeterol (Serevent), formoterol (Foradil, Perforomist),
arformoterol (Brovana), indacaterol (Arcapta) and aclidinium (Tudorza) and many
mores.And antibiotics also help.Respiratory infections, such as acute bronchitis, pneumonia,
and influenza, can aggravate COPD symptoms. Antibiotics help treat acute exacerbations, but
they aren't generally recommended for prevention. However, a recent study shows that the
antibiotic azithromycin prevents exacerbations, but it isn't clear whether this is due to its
antibiotic effect or its anti-inflammatory properties.Next is pulmonary rehabilitation program.
These programs generally combine education, exercise training, nutrition advice, and
counseling. You'll work with a variety of specialists, who can tailor your rehabilitation
program to meet your needs.Pulmonary rehabilitation may shorten hospitalizations, increase
your ability to participate in everyday activities and improve your quality of life. Talk to your
doctor about a referral to a program.Patients also have to manage exacerbations.Even with
ongoing treatment, you may experience times when symptoms become worse for days or
weeks. This is called an acute exacerbation, and it may lead to lung failure if you don't
receive prompt treatment.Exacerbations may be caused by a respiratory infection, air
pollution or other triggers of inflammation (Frostad A,2006). Whatever the cause, it's
important to seek prompt medical help if you notice a sustained increase in coughing, a
change in your mucus or if you have a harder time breathing.When exacerbations occur, you
may need additional medications (such as antibiotics, steroids or both), supplemental oxygen
or treatment in the hospital. Once symptoms improve, your doctor will talk with you about
measures to prevent future exacerbations, such as quitting smoking, taking inhaled steroids,
long-acting bronchodilators or other medications, getting your annual flu vaccine, and
avoiding air pollution whenever possible(Geelhoed EA,2007) Also,lung volume reduction
surgery. In this surgery, your surgeon removes small wedges of damaged lung tissue from the
upper lungs. This creates extra space in your chest cavity so that the remaining healthier lung
tissue can expand and the diaphragm can work more efficiently. In some people, this surgery
can improve quality of life and prolong survival.And lung transplant. Lung transplantation
may be an option for certain people who meet specific criteria. Transplantation can improve
your ability to breathe and to be active. However, it's a major operation that has significant
risks, such as organ rejection, and it's necessary to take lifelong immune-suppressing
medications.

5.0 Conclusion

A complex and interrelated set of risk factors influences functional decline,


exacerbations, and early mortality in patients with COPD (Jensen HH,2006). Most cases of
COPD are due to environmentally related disease. Unlike cardiovascular disease in which
90% of the population attributable risk is due to nine conventional risk factors , in the case of
COPD, about 80% of the population-attributable disease is due to smoking, and 15% is due to
work-related conditions. This message can empower clinicians in justifying the cost of
treating COPD, a public disease, to policymakers and governments.With limited health care
resources, efficient and effective management of COPD ideally involves identifying and
focusing efforts on individuals who are at particular risk. It is essential that there is some way
of identifying individuals at risk to be able to optimize appropriate intervention. Although
FEV1 has been mooted as an objective means of identifying individuals at greatest risk for
exacerbations and early mortality, in much the same way cholesterol is used in cardiology, a
more sophisticated risk profile beyond the measurement of FEV1 is required. The body-mass
index, airflow obstruction dyspnea, and exercise capacity (BODE) index is a useful step in
this direction (Mathers CD,2002). In the development of an appropriate multimodal strategy,
lessons could be learned from the evolution of guidelines and management of cardiovascular
disease, in particular, heart failure, which has many parallels with COPD in terms of
prevalence, prognosis, and impact on patient quality of life.The cardiovascular trials also
demonstrate that there are many obstacles when translating trial findings to clinical practice.
Education of clinicians and their patients is essential. For example, despite extensive trial
evidence that convincingly demonstrated the efficacy and safety of the statins to clinicians,
patients may be less well informed and convinced, which may affect compliance. This can
also be seen for COPD; compliance can be an issue with inhaled corticosteroids because
patients cannot usually detect an immediate treatment-associated benefit. Side effects can
also deter clinicians from using treatments shown to be effective in large clinical trials. For
example, the β-blocker trials showed that it was necessary to titrate very slowly after the
initiation of treatment due to problems with tolerability. However, this influenced the
perception of the tolerability of β-blockers in practice, reducing uptake of an effective
therapy.There is a need for large prospective trials in COPD, based on hard clinical
outcomes, such as death, to drive improvements in clinical management. The toward a
Revolution in COPD Health (TORCH) trial is the largest study to date in COPD, comparing
the effect of salmeterol/fluticasone propionate with placebo, in which the primary outcome is
total mortality. The TORCH trial is the first major outcome trial in COPD, and it will be
interesting to observe whether its impact on guideline recommendations and hence clinical
practice is similarly dramatic to the major cardiovascular disease outcome trials.
References

Rosell A, Monso E, Soler N, Torres F, Angrill J, Riise G, Zalacain R, Morera J, Torres A.


Microbiologic determinants of exacerbation in chronic obstructive pulmonary
disease. Arch Intern Med2005;165:891–897.

Viegi G, Pistelli F, Sherill DL, et al. Definition, epidemiology and natural history of COPD.
Eur Respir J 2007; 30: 993–1013

Buist AS, McBurnie MA, Vollmer WM, et al. International variation in the prevalence of
COPD (the BOLD Study): a population-based prevalence study. Lancet 2007; 370:
741–750.

Eide GE. Attributable fractions for partitioning risk and evaluating disease prevention: a
practical guide. Clin Respir J 2008; 2: 92–103.

Lundbäck B, Lindberg A, Lindström M, et al. Not 15 but 50% of smokers develop COPD? –
report from the Obstructive Lung Disease in Northern Sweden studies. Respir Med
2003; 97: 115–122.

Oberg M, Jaakkola MS, Woodward A, et al. Worldwide burden of disease from exposure to
second-hand smoke: a retrospective analysis of data from 192 countries. Lancet 2011;
377: 139–146.

Silverman EK, Spira A, Paré PD. Genetics and genomics of chronic obstructive pulmonary
disease. Proc Am Thorac Soc 2009; 6: 539–542.

Svanes C, Sunyer J, Plana E, et al. Early life origins of chronic obstructive pulmonary
disease. Thorax 2010; 65: 14–20

Vestbo J, Hurd SS, Agustí AG, et al. Global strategy for the diagnosis, management, and
prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am
J Respir Crit Care Med 2013; 187: 347–365. Comorbidity, exacerbations and
mortality

Barnes PJ, Celli BR. Systemic manifestations and comorbidities of COPD. Eur Respir J 2009;
33: 1165–1185.

Frostad A, Søyseth V, Andersen A, et al. Respiratory symptoms as predictors of all-cause


mortality in an urban community: a 30-year follow-up. J Intern Med 2006; 259: 520–
529.

Geelhoed EA, Brameld KJ, Holman CD, et al. Readmission and survival following
hospitalization for chronic obstructive pulmonary disease: long-term trends. Intern
Med J 2007: 37: 87–94.

Hurst JR, Vestbo J, Anzueto A, et al. Susceptibility of exacerbation in chronic obstructive


pulmonary disease. N Engl J Med 2010; 363: 1128–1138.
Jensen HH, Godtfredsen NS, Lange P, et al. Potential misclassification of causes of death
from COPD. Eur Respir J 2006; 28: 781–785.

Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to
2030. PLoS Med2006; 3: e442.