Download Example of Graduate Work - Allison miller, RN, FNP-S

Allison Miller
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COPD refers to a group of lung diseases that
block airflow during exhalation and result in
dyspnea.
COPD is a progressive disease that results
from a chronic inflammatory response.
It is characterized by airflow limitation that is
not fully reversible.
There is no cure for COPD
80 to 90 % of all cases of COPD are due to
cigarette smoking.
(Winland-Brown & Porter, 2011)
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Chronic bronchitis and emphysema are the two
diseases present with COPD.
Chronic bronchitis is defined by a recurrent
cough and increased mucus production that is
present for at least two years and occurs on most
days for at least three months.
Emphysema is a disease process that affects the
alveoli. Emphysema is characterized by the
destruction of the alveolar walls due to an
imbalance of proteinase and anti-proteinase
enzymatic activity.
(Winland-Brown & Porter, 2011)
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Chronic bronchitis is the most common
disease process that occurs in COPD, but
most people with COPD have both chronic
bronchitis and emphysema.
(Winland-Brown & Porter, 2011)
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Chronic irritation of the airway epithelium can
result in:
Increased inflammation and mucus production
increased number and size of mucus glands and goblet cells
Secretion of thick mucus
Decrease in ciliary function
Thick mucus in the bronchi can facilitate bacterial
growth and infection.
Chronic Inflammation can lead to bronchospasm
and permanent narrowing of the airways.
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(Williams & Bourdet, 2008)
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Alveoli walls are weakened and broken down by
increased protease activity that is a result of
chronic inflammation.
The increased protease activity causes the
breakdown of elastin within the alveolar walls.
Results in the destruction of the alveolar walls,
loss of elastic recoil within the alveoli, and a
decrease in the alveolar surface area.
Results in retained carbon dioxide, increased
residual lung volume, reduced expiratory flow,
and hypoxemia.
(Brashers, 2010)
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Rare genetic disease in which individuals have
low or absent levels of alpha one antitrypsin.
Alpha 1 antitrypsin is a major anti-proteinase
enzyme that is normally produced in the liver.
Without this protective anti-proteinase
enzyme, the alveolar walls can be broken
down by protease activity (Brashers, 2010).
Only accounts for 1-2% of all cases of COPD.
(Devereux, 2006)
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COPD is typically caused by long-term exposure
to airborne irritants such as;
Tobacco smoke
Dust
Chemical Fumes
Air pollution
Alpha-1-antitrypsin deficiency
The most significant risk factor for COPD is long
term cigarette smoking.
People over 40 are at greater risk because COPD
generally develops slowly
(Mayo Clinic, 2011)
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COPD is the fourth leading cause of death in the
world and is projected to be the third leading cause
of death by 2020 (GOLD: The Global Initiative for Chronic Obstructive Lung Disease, 2011).
More than 120,000 Americans die due to COPD each
year. This equals one death every four minutes
within the United States (Centers for Disease Control and Prevention, 2012).
More than 12 million people are currently diagnosed
with COPD and an additional 12 million likely have
the disease but have not been diagnosed (U.S Department of Health
and Human Services).
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The total deaths from COPD are projected to increase
by more than 30% in the next ten years if there are no
interventions placed to cut this risk (World Health Organization, 2011).
Around 10-20% of cigarette smokers will develop
clinically significant COPD (Devereux, 2006).
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Shortness of breath
Wheezing
Chest tightness
Chronic cough
Fatigue
Frequent respiratory infections
(Mayo Clinic, 2011)
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For most people COPD is not diagnosed until
at least 50% of their lung function is lost (Freeman &
Price, 2006).
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Spirometry is the gold standard for the diagnosis and
assessment of COPD (GOLD, 2011).
The spirometer is a machine that measures the total
amount of air exhaled or Forced Vital Capacity (FVC) and
the amount of air that is exhaled in the first second, which
is the forced expiratory volume in one second (FEV1).
Spirometry can be used to detect COPD before symptoms
occur and can be used to monitor the progression of the
disease (Mayo Clinic, 2011).
The hallmark of COPD is an FEV1/ FVC ratio of less than
seventy percent, which indicates airway obstruction, and a
post bronchodilator FEV1 of less than 80% of the predicted
value, which confirms the presence of airflow limitation
that is not fully reversible (Williams & Bourdet, 2008).
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Physical exam: cyanosis, wheezing, weight
gain, diminished breath sounds, and distant
heart sounds.
Arterial blood gases may show elevated
carbon dioxide and decreased oxygen levels.
X-ray: May show increased bronchovascular
markings and cardiomegaly.
(Winland-Brown & Porter, 2011)
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Physical exam: Barrel chest, use of accessory
muscles for breathing, pursed lip breathing, may
have slight cyanosis, breath sounds may be
diminished. As the disease progresses they may
have significant weight loss, increasing dyspnea,
and increased episodes of acute exacerbations.
Chest x-ray and CT scan may show
hyperinflation of the lungs, hypovascularity, and
large air spaces within the lung parenchyma.
Arterial Blood Gas may show decreased oxygen
levels.
(Winland-Brown & Porter, 2011)
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Treatment and medications are given for
COPD in order to:
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Dilate the airways
Decrease bronchoconstriction
Improve oxygenation
Decrease levels of carbon dioxide within the body
Prevent exacerbations
Prevent or Fight Infections
Improve quality of life
Medications and treatments for COPD include:
 Inhaled beta-2 agonists: long and short acting
 Inhaled Anticholinergic bronchodilators
 Corticosteroids
 Xanthines
 Antibiotics
 Diuretics
 Mucolytics
 Home oxygen
 Surgery
 Pulmonary Rehabilitation
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Stage 1 or mild COPD: short acting bronchodilator as
needed.
Stage 2- moderate COPD: short acting bronchodilator as
needed, regular treatments with one or more long acting
bronchodilators, and pulmonary rehabilitation.
Stage 3- severe COPD: short acting bronchodilator as
needed, regular treatments with one or more long-acting
bronchodilators, inhaled glucocorticosteriods if having
repeated exacerbations, and pulmonary rehab.
Stage 4- very severe COPD: short acting bronchodilator as
needed, regular treatments with one or more long acting
bronchodilators, inhaled glucocorticosteriods if having
repeated exacerbations, treatment of complications,
rehabilitation, long term oxygen therapy for respiratory
failure, and surgical consideration
(GOLD: The Global Initiative for Chronic Obstructive Lung Disease, 2011).
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Short acting beta agonist: Albuterol
Anticholinergics: Atrovent (ipratropium) and
Spiriva (tiotropium).
Long Acting Beta agonists: Servent
(salmeterol), Foradil (formoterol), Brovana
(aformoterol, and Perforomist (formoterol)
(Cropp, 2012).
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Dyspnea, fatigue, malnutrition, insomnia,
infections, pneumothorax, arrhythmias,
weight loss, cor pulmonale, osteoporosis,
edema, pulmonary hypertension, heart
attack, anemia, depression, and anxiety.
(GOLD: The Global Initiative for Chronic Obstructive Lung Disease, 2011).
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The most important intervention for decreasing
the progression of COPD is smoking cessation.
If there are no contraindications, people with
COPD should receive the flu and pneumonia
vaccines.
Avoid second hand smoke
Avoid travel at high altitudes.
Create an advanced health directive
Discuss end of life care for those with advanced
COPD.
(Cropp, 2012)
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Health care professionals that are involved with
treating people with COPD include:
Pulmonologists
Respiratory therapists
Dieticians
Cardiologist
Mental health workers
Surgeons
General practitioners
Social workers
Physical and occupational therapists
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COPD is a disease that results in airway obstruction
and a decreased ability to exhale air and carbon
dioxide out of the lungs.
Chronic bronchitis and emphysema are two forms of
COPD and usually occur together.
There is no cure for COPD
COPD is the fourth leading cause of death in the U.S.
Primary symptoms of COPD are dyspnea and chronic
cough
Treatments are aimed at increasing bronchodilation,
decreasing bronchial constriction, and maintaining
appropriate oxygen and carbon dioxide levels within
the body.
Brashers, V. L. (2010). Alterations of pulmonary function. In L. K. McCance, S. E. Huether, V. L. Brashers, & N. S. Rote (Eds.),
Pathophysiology: the biologic basis for disease in adults and children (6 ed., pp. 1266-1309). Maryland Heights,
MS: Mosby.
Centers for Disease Control and Prevention (2012, March). Chronic obstructive pulmonary disease. Retrieved September 26,
2012, from http://www.cdc.gov/copd.
Cropp, A. J. (2012). Chronic obstructive pulmonary disease and emphysema. In F. J. Domino, R. A. Baldor, J. Golding, J. A.
Grimes, & J. S. Taylor (Eds.), The 5-minute clinical consult 2013 (21ed., pp. 264-265). Philadelphia, PA:
Liippincott, Williams, & Wilkins.
Devereux, G. (2006). Abc of chronic obstructive pulmonary disease: Definition, epidemiology, and risk factors. British Medical
Journal, 332 (7550), 1142-1144.
GOLD: The Global Initiative for Chronic Obstructive Lung Disease (2011, December). Global strategy for diagnosis,
management, and prevention of COPD. Retrieved September 26, 2012, from http://goldcopd.org/guidelines-globalstrategy-for –diagnosis.
Mayo Clinic (2011, March). COPD. Retrieved September 26,2012, from http://www.mayoclinic.com/health/copd.
Williams, D. M., & Bourdet, S. V. (2008). Chronic obstructive pulmonary disease. In J. T. Dipiro, R. L. Talbert, G. C. Yee, G. R.
Matzke, B. G. Wells, & L. M. Posey (Eds.), Pharmacotherapy: a pathophysiologic approach (7 ed.), pp. 495-517).
New York, NY: McGraw Hill.
Winland-Brown, J. E., & Porter, B. O. (2011). Respiratory problems. In L. M. Dunphy, J. E. Winland, B. O. Porter, & D. J.
Thomas
(Eds.), Primary care: the art and science of advanced practice nursing (3 ed., pp. 331-417). Philadelphia, PA: F. A. Davis
Co.
World Health Organization (2011, November). Chronic obstructive pulmonary disease. Retrieved September 26, 2012 from
http://who.int/mediacentre/factsheets/fs315/en/index.html.