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Lecture 6

NURSING 2LA2 Lecture Notes - Lecture 6: Anaphylaxis, Cell Adhesion Molecule, Microsoft Powerpoint

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Ruth Hannon

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Module 2: Alteraons in Respiratory Funcon- Asthma
This is the first of two modules on obstructive airway diseases. This module will cover the
disease of asthma. Learning about the disease of asthma requires you to have a basic
understanding of the anatomy and physiology of the respiratory system and inflammation. I
recommend that you review chapter 23 in the Tortora and Derrickson A&P textbook. I will cover
the drugs used for asthma in this module. To supplement this information please review chapter
29 of the Adams pharmacology textbook, specifically pages 369-379. Required readings for this
lecture from your Forth pathophysiology textbook are in chapters 17, 18, 19, 27 and 29. Specific
pages and further required readings are listed on the next 2 slides. There is a brief tutorial on
asthma available to you on the CD that came with your Porth pathophysiology textbook. 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 asthma so that you are then able to apply it to clinical
practice. Remember, you will have further opportunity to discuss and apply this content in
tutorial sessions and in the clinical setting. Please note that there is a reference list at the end of
the power point presentation, specific references for each slide are found in the notes section of
each slide. Also, the term asthma attack and acute exacerbation of asthma are used
interchangeably throughout the module.
Concepts in Action Animations - Asthma
The respiratory system is composed of airway passages, the lungs, and the associated
blood vessels. The purpose of the respiratory system is to provide for oxygen and carbon
dioxide exchange between air and blood. Respiration consists of three distinct processes.
Ventilation is the movement of air from the atmosphere into and out of the lungs. Air
must be taken in through the upper airway passages comprising the nose, nasal passages,
mouth, pharynx, and larynx. The air then proceeds from there into the lower airway
consisting of the trachea, the bronchi, and bronchioles of the lungs. The process of taking
air in is called inspiration. Perfusion is the movement of blood through the lungs.
Diffusion is the movement of gases between the roughly one million alveoli or air-filled
sacs within the lungs and the capillaries that supply the alveoli. In diffusion, gases move
across the alveolar capillary membrane. Oxygen moves from the air that is in the alveoli
into the blood flowing through the pulmonary capillaries. Carbon dioxide passes from the
blood into the alveoli. Completing the respiration process, the carbon dioxide is expelled
through expiration. If respiration is impeded, gas exchange cannot occur. The bodys
supply of oxygen becomes insufficient for its needs and carbon dioxide cannot be
expelled from the blood.
Asthma is a chronic reactive airway disorder characterized by increased resistance to
airflow due to episodic airway obstruction. Asthma involves inflammation of the airways,
bronchospasm, increased mucus secretion and injury to the mucosal lining of the airways.
Asthma can be characterized as extrinsic or intrinsic, based on the factors that trigger the

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Extrinsic, atopic asthma is initiated by a type one hypersensitivity response to an extrinsic
antigen. An antigen binds with a mast cell, and causes mast cell degranulation with
release of histamine, leukotrienes, interleukins, and prostaglandins, resulting in
inflammation and bronchospasm. This airway inflammation in turn produces airway
edema, epithelial injury, and impaired mucociliary function.
Intrinsic, non-atopic asthma is initiated by diverse non-immune mechanisms; however,
many people have overlapping symptoms. Intrinsic asthma is triggered by irritant
receptors and vagal reflex. Intrinsic asthma is often triggered by viral infections, inhaled
irritants, NSAIDs, sulfites, and emotional stress.
Asthma usually has its onset in childhood or adolescence; however, adults may develop
asthma without a previous history of the disease. Asthma arises from a complex
interaction between heredity and environmental factors, and manifests as acute attacks.
The early phase or acute responsive asthma occurs within 10-20 minutes of exposure to a
trigger. Mast cells, which in people with asthma, are in a pre-sensitized state, react to
antigens and release histamine, leukotrienes, interleukins, and prostaglandins. With
airborne antigens, the antigen binds to the mast cells on the mucosal surface of the
airway. The release of inflammatory mediators leads to infiltration of inflammatory cells
and allows the antigens to reach the sub-mucosal mast cells. In addition, direct
stimulation of parasympathetic receptors causes bronchospasm, and increased vascular
permeability causes mucosal edema and increased mucus secretions. As airway
obstruction progresses, expiration becomes prolonged.
Late phase response develops 4-8 hours after exposure to an asthmatic trigger. Release of
inflammatory mediators induces the migration and activation of other inflammatory cells,
basophils, eosinophils, and neutrophils. The late phase response involves inflammation,
increased airway responsiveness, and renewed bronchospasm. These symptoms lead to
further airflow limitations and continued heightened airway responsiveness. This
sequence prolongs the asthma attack and sets into motion a vicious cycle of exacerbations
including additional edema, epithelial injury, and impaired mucociliary function.
Treatment for all asthma patients is approached in two ways: through control of factors
contributing to asthma severity and through pharmacologic treatment. If exposure to
triggers can’t be avoided, then pharmacologic treatment is usually needed. This can
include corticosteroids, bronchodilators, mast cell stabilizers, beta-agonists, and
anticholinergic drugs.
In summary, asthma is a chronic reactive airway disorder characterized by increased
resistance to airflow due to obstruction of the airway passages. Asthma involves a
hypersensitivity reaction to stimuli and the release of chemical mediators from pre-
sensitized mast cells, leading to a vicious cycle of edema, epithelial injury, and impaired
mucociliary function.

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Learning Outcomes
1. Describe current Canadian trends in the prevalence of asthma.
2. Describe the etiology of asthma.
3. Describe the pathophysiology of asthma.
4. Link the pathogenesis of asthma to the clinical manifestations and evaluation of the disease.
Clinical manifestations are the signs and symptoms of the disease.
Evaluation of the disease includes assessment findings, laboratory results, radiological
findings, pulmonary function texts, and peak flow measurement. Remember that the
evaluation findings are objective signs of a disease.
5. Provide scientific rationale for interventions.
Specifically understanding the mechanism of action of the various drugs used to treat
6. Provide scientific rationale for patient teaching.
Provide key points.
Prevalence: The Faces of Asthma
Canadians >12 y.o. (Statistics Canada)
o2,362,902 (2008)
o2 249 703(2005)
NLSCY data 2000/01:
o586 000 (13.4%) children aged 11 and under
Higher prevalence in boys and women
Childhood asthma rates highest in Atlantic provinces, lowest in British Columbia and
Prairie Provinces
Rates are steadily increasing around the world
The prevalence of physician diagnosed asthma among Canadians 12 years and older has
increased from over 2.2 million in 2005 to over 2.3 million in 2008. This represents between 8
and 9 percent of the Canadian population aged 12 and over. It is important to identify
populations where the prevalence of asthma is different than that of the general population. In
Canada, the prevalence of asthma of off-reserve aboriginal people 12 years of age and over is
higher than that of the general population at 11.9%.
The National Longitudinal Survey in Children and Youth (NLSCY) is a longitudinal study of
Canadian children that began in 1994. The study provides information about health,
development, and social environments of the participants from birth to early adulthood. Data
from the NLSCY found that 586 000 Canadian children aged 11 and under had been diagnosed
with asthma. This represents 13.4% of Canadian children aged 11 and under. Overall, this is a
statistically significant increase from 1994/95 data where 11.1% of Canadian children under 11
years of age had been diagnosed with asthma. However, when broken down into age groups, the
increase was only significant for children aged 5 and younger and children aged 10 and 11.
Despite the increase in childhood asthma, the prevalence of asthma attacks has decreased from
51% to 39% between 1994/95 and 2000/01 data of 0-11 year old Canadian children.
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