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Lecture 7

NURSING 2LA2 Lecture Notes - Lecture 7: Innate Immune System, Elastin, Passive Smoking


Department
Nursing
Course Code
NURSING 2LA2
Professor
Ruth Hannon
Lecture
7

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Module 2b: COPD
COPD
This is the second of two modules on obstructive airway diseases. This module will cover the
disease of Chronic Obstructive Pulmonary Disease (COPD). Learning about the disease of
COPD requires you to have a basic understanding of the anatomy and physiology of the
respiratory system. You may also find it helpful to review concepts related to genetics and
inflammation. I have not included any specific readings on these topics but you can find content
related to inflammation and genetics Porth Pathophysiology textbook. I will briefly review the
pharmacological agents used to treat COPD and highlight key points related to
pharmacotherapies for COPD. There is a lot of content in this module, some of it should be a
review from previous science courses and some of it will be new or add on to previous learning.
The overall aim of this module is to provide basic science content related to COPD so that you
are then able to apply it to clinical practice.
Additional Resources
Barnes, P.J. & Celli, B.R. (2009). Systemic manifestations and comorbidities of COPD.
European Respiratory Journal, 33, 1165-1185.
Canadian Lung Association, http://www.lung.ca/diseases-maladies/copd-mpoc_e.php
oUp to date information on lung diseases in Canada including COPD.
oIntended audience of the website are patients and the general public, however,
you will find much of the information helpful as nursing students.
oSpecifically, you may want to look at the personal stories of COPD patients and
health care professionals. Also, there is information on community supports and
the BreathWorks program is worth checking out.
Kuebler, K.K., Buchsel, P.C. & Balkstra, C.R. (2008). Differentiating chronic obstructive
airway disease from asthma. Journal of the American Academy of Nurse Practitioners,
20, 445-454.
oCompares COPD and asthma in terms of epidemiology, etiology,
pathophysiology, clinical manifestations, disease evaluation, and pharmacologic
interventions. This article should supplement your readings about drugs for
obstructive airway diseases by identifying and providing rationale for which drugs
are used for asthma and for which drugs are used for COPD
RNAO. (2010). Nursing Care of Dyspnea: The 6th Vital Sign in Individuals with Chronic
Obstructive Pulmonary. Available online:
http://www.rnao.org/Storage/67/6135_REVISED_BPG_COPD.pdf
Learning Outcomes
1. Describe current Canadian epidemiology related to COPD.
2. Describe the etiology of COPD.
3. Compare asthma and COPD.
4. Describe the pathophysiology of COPD.
I will discuss chronic bronchitis, emphysema, and inflammation.
5. Link the pathogenesis of COPD to the clinical manifestations and evaluation of the disease.
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6. Provide scientific rationale for interventions.
Specifically, oxygen therapy, pharmacotherapy, and pulmonary rehabilitation.
7. Provide scientific rationale for patient teaching.
COPD in Canada
COPD underdiagnosed, affects at least 700 000 adults, app. 4.4% Canadians aged 35
years or older
4th leading cause of death in females, 5th in males
Higher prevalence in women except for the > or =75 years age group
Mortality rates increasing
Mortality rates higher in men (4.5/100 000) than females (2.8/100 000)
COPD is a major respiratory disease in Canada that is often preventable and can be treated but
remains underdiagnosed. It is thought that the prevalence of COPD is underestimated because
those with early symptoms of COPD are not recognized and/or do not seek treatment. COPD
affects at least 700 000 adults which is approximately 4.4% of Canadians aged 35 years or older.
In contrast, COPD affects a much higher percentage of off-reserve Aboriginal people at 7.9%.
COPD is the 4th leading cause of death in females and 5th in males. There is a higher prevalence
in women except for the aged 75 years and older group. Over the past 15 years, mortality rates
have increased, especially for women. Mortality rates are higher in males (4.5/100 000) than
females (2.8/100 000). Mortality rates may be actually higher than reported because two
complications of COPD, pneumonia and congestive heart failure, may be listed as the cause of
death instead of COPD. Also, it is predicted that as new epidemiological data emerges, the
mortality rates in women will be higher than for men.
COPD is also a major cause of death worldwide. In the United States, it is the 4th leading cause
of death and it is the 6th leading cause of death worldwide. Like Canada, the mortality and
morbidity are increasing around the world. The burden of COPD from a health, economical, and
societal cost is significant. Hospitalizations, ER visits, pharmacotherapy, pulmonary
rehabilitation, oxygen therapy, missed work days are but a few of the items that were studied in
the confronting COPD survey in North America and Europe which studied the burden of COPD
in different countries. Among major chronic illnesses in Canada, COPD now accounts for the
highest rating of hospital admissions. Hospitalization for an acute exasperation of COPD are on
average 10 days in length and cost about $10 000. A conservative estimate of the total cost of
COPD hospitalizations in Canada is 1.5 billion dollars per year. It is beyond the scope of this
lecture to go into further detail about the actual costs of care. But I have listed the reference from
the confronting COPD survey as well as a more recent report from the Canadian Thoracic
Society for those who may be interested.
Etiology
Cigarette smoking
o#1 cause of COPD, 15-20% smokers -> COPD dx; 80-90% dx COPD have hx of
smoking
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oToxic to cells in lungs + impairs mechanisms responsible for lung tissue repair
Genetics
oGenetic susceptibilities – polymorphisms of genes that code for TNF, surfactant,
proteases and antiproteases
oInherited mutation in alpha-1 antitrypsin gene -> AAT deficiency
oHeterogeneous nature of COPD attributed to multiple genetic & environmental
factors as well as gene-gene & gene-environment interactions (i.e. epigenetics)
Cigarette smoking is the leading cause of COPD. 15-20% of smokers will be diagnosed with
COPD. This does not take into account smokers who have yet to be diagnosed with COPD. An
average smoker loses lung function at twice the rate of a non-smoker. This means that smoking
adults lose lung function at a more rapid rate as they age in comparison to non-smokers. Loss of
lung function is associated with an increased mortality. Adolescents who begin smoking before
they are finished growing will inhibit maximal lung development. Smoking is common in people
diagnosed with COPD as 80-90% of them have a history of smoking. Smoking is toxic to cells in
the lungs and also impairs the mechanisms that are responsible for lung tissue repair. It is
important to note that both active and passive smoking have been implicated in COPD.
Genetics also play a contributory factor to developing COPD. Genetic susceptibilities have been
identified. Polymorphisms of genes that code for Tumour Necrosis Factor (TNF), surfactant,
proteases and antiproteases are examples. Also, a hereditary deficiency of alpha-1 antitrypsin
may result in early onset of severe COPD. The onset and severity is worsened by smoking.
Alpha-1 antitrypsin will be discussed further when I describe the pathophysiology of
emphysema. The heterogeneous nature of COPD can be attributed to multiple genetic and
environmental factors as well as gene-to-gene and gene-to-environment interactions, known as
epigenetics. We will be looking at different phenotypes of COPD after the next slide. Genetics
have a role in how these phenotypes are expressed and how gene-environment interactions
contribute to disease manifestations such as exacerbations.
Environmental
oLong-term inhalational exposure to: occupational dusts/chemicals; indoor
pollution from heating and cooking with biomass fuels; outdoor pollution
Other risk factors
oSevere childhood respiratory infections, asthma, airway hyper-responsiveness,
nutritional compromise, impairment of fetal development resulting in low birth
weight, infants who develop bronchopulmonary dysplasia
Environmental risk factors include long-term inhalational exposure to: occupational dusts or
chemicals, indoor pollution from heating and cooking with biomass fuels, and outdoor pollution.
Other risk factors include: severe childhood respiratory infections, asthma, airway hyper-
responsiveness, nutritional compromise, impairment of fetal development resulting in low birth
weight, and infants who develop bronchopulmonary dysplasia. Although the risk factors listed on
this slide are relevant to the etiology of COPD, the most important etiologic factor is cigarette
smoking.
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