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Time Allotment:1 hourTopic description:This topic provides an
overview of a disease condition of the respiratory system called
Chronic Obstructive Pulmonary Disease. Included hereinare its
definition, etiology, manifestations, pathophysiology and
management. It is also about the complications that might arise in
the long run, if COPD is notcontrolled.Central Objective: At the
end of the 1hour ward class, the learners shall have gained
knowledge, enhanced skills and develop appropriate values in caring
for
patients with COPD in the hospital setting as well as in the
community setting.
Specific Objectives Content T. A. T-L Strategies Evaluation
Given the necessaryinformation about COPD, thelearners
shall:
1) Define COPD in theirown words accurately.
2) Give three examples ofobstructive diseasesthat can co-exist
withCOPD.
PRAYER VIDEO
I. IntroductionThe Global Initiative for Chronic Obstructive
LungDisease (GOLD) has defined COPD as apreventable and treatable
disease with some
significant extrapulmonary effects that maycontribute to the
severity in individual patients. Its
pulmonary component is characterized by airflowlimitation that
is not fully reversible. The airflowlimitation is usually
progressive and associated withan abnormal inflammatory response of
the lungs tonoxious partcles or gases.(GOLD, 2008)
COPD may include diseases that cause airflowobstruction (eg.
Emphysema, chronic bronchitis) orany combination of these
disorders. While mortality
from other major cause of death has been decreasing,deaths from
COPD have continued to rise.
Socialized Discussion
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3) Explain the risk factorsfor developing COPDconcisely.
4) Determine the role ofsmoking in thedevelopment of COPD.
People with COPD commonly become symptomaticduring the middle
adult years, and the incidence ofthe disease increases with age.
Although certainaspects of lung function decrease with age,
COPD
accentuates and accelerates these physiologicchanges. (Smeltzer,
et. al., 2010)
II. Risk FactorsA. Exposure to tobacco smoke
Smoking depresses the activity of scavenger cellsand affects the
respiratory tracts ciliary cleansing
mechanism, which keeps breathing passages free of
inhaled irritants, bacteria and other foreign matter.When
smoking damages this cleansing mechanism,airflow is obstructed and
air becomes trapped behindthe obstruction. The alveoli greatly
distend,diminishes lung capacity.
Smoking also irritates the goblet cells and mucousglands,
causing an increased accumulation of mucus,which in turn produces
more irritation, infection, and
damage to the lung.
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Carbon monoxide (a byproduct of smoking),combines with
hemoglobin to formcarboxyhemoglobin. Hemoglobin that is bound
bycarboxyhemoglobin cannot carry oxygen efficiently.(Smeltzer, et.
al., 2010)
B. Occupational exposure--- dust, chemicalsOther environmental
risk factors for COPD include
prolonged and intense exposure to occupationaldusts and
chemicals, indoor air pollution, andoutdoor air pollution. (GOLD,
2008)
In the United States, it has been estimated that
COPD in 19% of smokers and in as many as 31% ofnonsmokers may be
attributable to such exposure.
C. Air PollutionStudies in many countries have found people
wholive in large cities have a higher rate of COPDcompared to
people who live in rural areas. Urbanair pollution may be a
contributing factor for COPD,as it is thought to slow the normal
growth of thelungs, although the long-term research needed
toconfirm the link has not been done.
Studies of the industrial waste gas andCOPD/asthma-aggravating
compound,sulfur
http://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Sulfur_dioxidehttp://en.wikipedia.org/wiki/Sulfur_dioxidehttp://en.wikipedia.org/wiki/Air_pollution
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5) Trace thepathophysiology ofCOPD on the concept
dioxide,and the inverse relation to the presence ofthe blue
lichenXanthoria(usually found abundantlyin the countryside, but
never in towns or cities) have
been seen to suggest combustive industrial processesdo not aid
COPD sufferers.
In manydeveloping countries,indoor air pollutionfrom cooking
fire smoke (often usingbiomass fuelssuch as wood and animal dung)
is a common causeof COPD, especially in women.
D. Genetic abnormalities(alpha1- antitrypsin)This deficiency of
alpha1- antitrypsin, an enzymeinhibitor that protects the lung
parenchyma frominjury, predisposes young people to the
rapiddevelopment of lobular emphysema, even if theydont smoke.
Genetically susceptible people are
sensitive to environmental factors (eg, smoking, airpollution,
infectious agents, allergens) andeventually develop chronic
obstructive symptoms.(Smeltzer, et. al., 2010)
III. PathophysiologyNarrowing of the airways reduces the rate at
whichair can flow to and from the air sacs (alveoli)andlimits the
effectiveness of the lungs. In COPD, the
greatest reduction in airflow occurs when breathingout (during
expiration) because the pressure in thechest tends to compress
rather than expand the
http://en.wikipedia.org/wiki/Sulfur_dioxidehttp://en.wikipedia.org/wiki/Xanthoriahttp://en.wikipedia.org/wiki/Xanthoriahttp://en.wikipedia.org/wiki/Xanthoriahttp://en.wikipedia.org/wiki/Developing_countrieshttp://en.wikipedia.org/wiki/Biomass_fuelhttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Biomass_fuelhttp://en.wikipedia.org/wiki/Developing_countrieshttp://en.wikipedia.org/wiki/Xanthoriahttp://en.wikipedia.org/wiki/Sulfur_dioxide
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map provided for.
6) Determine the effect ofobstruction in patientswith COPD.
airways. In theory, airflow could be increased bybreathing more
forcefully, increasing the pressure inthe chest during expiration.
In COPD, there is oftena limit to how much this can actually
increaseairflow, a situation known as expiratory flow
limitation.If the rate of airflow is too low, a person with
COPDmay not be able to completely finish breathing out(expiration)
before he or she needs to take another
breath. This is particularly common during exercise,when
breathing has to be faster. A little of the air ofthe previous
breath remains within the lungs whenthe next breath is started,
resulting in an increase inthe volume of air in the lungs, a
process calleddynamichyperinflation.
Dynamic hyperinflation is closely linked todyspneain COPD. It is
less comfortable to breathe withhyperinflation because it takes
more effort to movethe lungs andchest wall when they are
alreadystretched by hyperinflation.
Another factor contributing to shortness of breath inCOPD is the
loss of thesurface area available for theexchange of oxygen
andcarbon dioxide withemphysema. This reduces the rate of transfer
ofthese gases between the body and the atmosphere
and can lead to low oxygen and high carbon dioxidelevels in the
body. A person with emphysema mayhave to breathe faster or more
deeply to compensate,
http://en.wikipedia.org/wiki/Hyperaerationhttp://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Chest_wallhttp://en.wikipedia.org/wiki/Surface_areahttp://en.wikipedia.org/wiki/Carbon_dioxidehttp://en.wikipedia.org/wiki/Carbon_dioxidehttp://en.wikipedia.org/wiki/Surface_areahttp://en.wikipedia.org/wiki/Chest_wallhttp://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Hyperaeration
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which can be difficult to do if there is also flowlimitation or
hyperinflation.
Some people with advanced COPD do manage tobreathe fast to
compensate, but usually have dyspneaas a result. Others, who may be
less short of breath,
tolerate low oxygen and high carbon dioxide levelsin their
bodies, but this can eventually lead toheadaches, drowsiness and
heart failure.
Advanced COPD can lead to complications beyondthe lungs, such as
weight loss (cachexia),pulmonaryhypertension and right-sided heart
failure (cor
pulmonale).Osteoporosis,heart disease,musclewasting
anddepression are all more common in
people with COPD.
Several molecular signatures associated to lung
function decline and corollaries of disease severityhave been
proposed, a majority of which arecharacterized in easily accessible
surrogate tissue,including blood derivatives such as serum and
plasma.
A recent 2010 clinical study proposes alpha 1B-glycoprotein
precursor/A1BG,alpha 2-antiplasmin,apolipoprotein A-IV
precursor/APOA4,andcomplement component 3precursor,
amongothercoagulation andcomplement systemproteins
as corollaries of lung function decline, althoughambiguity
between cause and effect is unresolved.
http://en.wikipedia.org/wiki/Cachexiahttp://en.wikipedia.org/wiki/Pulmonary_hypertensionhttp://en.wikipedia.org/wiki/Pulmonary_hypertensionhttp://en.wikipedia.org/wiki/Cor_pulmonalehttp://en.wikipedia.org/wiki/Cor_pulmonalehttp://en.wikipedia.org/wiki/Osteoporosishttp://en.wikipedia.org/wiki/Heart_diseasehttp://en.wikipedia.org/wiki/Muscle_wastinghttp://en.wikipedia.org/wiki/Muscle_wastinghttp://en.wikipedia.org/wiki/Major_depressive_disorderhttp://en.wikipedia.org/w/index.php?title=A1BG&action=edit&redlink=1http://en.wikipedia.org/wiki/Alpha_2-antiplasminhttp://en.wikipedia.org/wiki/APOA4http://en.wikipedia.org/wiki/Complement_component_3http://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Complement_systemhttp://en.wikipedia.org/wiki/Complement_systemhttp://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Complement_component_3http://en.wikipedia.org/wiki/APOA4http://en.wikipedia.org/wiki/Alpha_2-antiplasminhttp://en.wikipedia.org/w/index.php?title=A1BG&action=edit&redlink=1http://en.wikipedia.org/wiki/Major_depressive_disorderhttp://en.wikipedia.org/wiki/Muscle_wastinghttp://en.wikipedia.org/wiki/Muscle_wastinghttp://en.wikipedia.org/wiki/Heart_diseasehttp://en.wikipedia.org/wiki/Osteoporosishttp://en.wikipedia.org/wiki/Cor_pulmonalehttp://en.wikipedia.org/wiki/Cor_pulmonalehttp://en.wikipedia.org/wiki/Pulmonary_hypertensionhttp://en.wikipedia.org/wiki/Pulmonary_hypertensionhttp://en.wikipedia.org/wiki/Cachexia
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7) Explain correctly thesigns and symptomsmanifested by a
patientwith COPD.
IV. Clinical ManifestationsAlthough the natural history of COPD
is variable, itis generally a progressive disease characterized
by
three primary symptoms: chronic cough, sputumproduction, and
dyspnea on exertion. (GOLD, 2008)
The cough may be intermittent and may beunproductive in some
patients. Dyspnea may besevere and often interferes with patients
activities. It
is usually progressive, is worse with exercise, and
ispersistent. As COPD progresses, dyspnea may occurat rest. Weight
loss is common, because dyspneainterferes with eating and the work
of breathing isenergy depleting.
As the work of breathing increases over time, theaccessory
muscles are recruited in an effort to
breathe. In patients with COPD that has primaryemphysematous
component, chronic hyperinflationleads to the barrel chest thorax
configuration.
Retraction of the supraclavicular fossae occurs oninspiration,
causing the shoulders to heave upward.In advanced emphysema, the
abdominal musclesmay also contract on inspiration. (Smeltzer, et.
al.,
2010)
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8) Give a brief andaccurate description of
the diagnostic testsdone to a patient withCOPD.
9) Analyze a certainblood gas resultcorrectly.
V. Diagnostic TestsA. Spirometry
Spirometry is used to evaluate airflow obstruction,which is
determined by the ratio of FEV1 to forcedvital capacity (FVC).
Spirometric results are
expressed as an absolute volume and as a percentageof the
predicted value using appropriate normalvalues for gender, age, and
height. With obstruction,the patient either has difficulty exhaling
or cannotforcibly exhale air from the lungs, reducing theFEV1.
B. Arterial Blood Gas (ABG) analysisArterial blood gas
measurements may also beobtained to assess baseline oxygenation and
gasexchange and are especially important in advanced
COPD. (Smeltzer, et. al., 2010)
C. Chest X- rayOnchest x-ray,the classic signs of COPD
areoverexpanded lung (hyperinflation), a flatteneddiaphragm,
increased retrosternal airspace, and
bullae. It can be useful to help exclude other lungdiseases,
such aspneumonia,pulmonary edema orapneumothorax.
4 Stages of COPD
1) Mild- defined by an FEV1/ FVC < 70% andFEV1 greater than
or equal to 80%
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10)Briefly discuss the 4stages of COPD
concisely.
11)Give 2 examples ofeach of the medicationsunder
theclassifications of drugsthat were discussed.
- without cough and sputumproduction
2) Moderate- defined by an FEV1/ FVC
