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Lecture

Asthma.docx

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Department
Nursing
Course Code
NURSING 2LA2
Professor
Jennifer Ostovich

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Asthma
Prevalence: The Faces of Asthma
- Canadians > 12 years old
o2,362,902 (2008)
o2,249,703 (2005)
oThis represents between 8-9% of the Canadian population aged 12 years
of age and older
- 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%
- NLSCY data 2000/01
o586 000 (13.4%) children aged 11 and under have been diagnosed with
asthma
13.4% of Canadian children aged 11 and under
owhen broken down into age groups the increase was only significant for
children aged 5 and younger and children aged 10 and 11
othe prevalence of asthma attacks has decreased from 51% to 39% between
1994/95 and 2000/2001 date of 0-11 year old Canadian children
- Higher prevalence in boys and women
oThere has been a 60% increase in women aged 35 – 44 years
o80% increase in women aged 45 – 64 years and 41% increase in men aged
35 – 44 years between 1994/95 and 2005
- Childhood asthma rates highest in Atlantic provinces, lowest in BC and Prairie
provinces
- Rates are steadily increasing around the world
- Despite increasing prevalence, asthma mortality rates have steadily declined in
Canada since 1987
oThis is consistent with other developed nations
- Hospitalization rates have also decreased in children and adults along with ER
visits
oThis is attributed to appropriate use of Asthma Practice Guidelines and
active involvement of patients and their families
Etiology
- Longitudinal studies suggest that in childhood asthma, susceptibility is
determined during fetal development and the first 3 – 5 years of life.
- Risk factors for developing childhood asthma include:
oFamily history of allergy and allergic disorders
Family history of allergy and allergic disorders including hay
fever, asthma and eczema
The genetic basis of asthma is complicated and multifactorial as
there have been several genetic loci on a variety of different
chromosomes implicated in the pathogenesis of asthma
There have actually been more than 100 genes identified that may
play a role in the susceptibility and pathogenesis of asthma
Some of these genes influence the production of IL-4, IL-5, IL-13,
IgE, eosinophils, mast cells, adrenergic receptors, leukotrienes and
bronchial hyper-responsiveness
In particular, the gene ADAM 33 has been associated with asthma
and bronchial hyperresponsiveness
oHigh exposure to airborne allergens
High exposure of susceptible children to airborne allergens such as
pets, house dust mites, cockroaches and mould in the first years of
life
oExposure to tobacco smoke
In utero or early years of life
The NLSCY found that Canadian children living in households
where either parent smoked daily were significantly more likely to
be diagnosed with asthma than children in non-smoking
households
oLow birth weight and RDA
RDA = respiratory distress syndrome
- The NLSCY has not found any relationship between household income and
childhood asthma
oIt is important to note that the NLSCY has not found a difference in the
prevelance of asthma between urban and rural areas
In contrast to other countries, specifically the USA
Prevalence of asthma is higher in urban areas
- In adult onset risk factors include:
oOccupational exposures to low molecular weight sensitizers (i.e.
isocyanates)
oExposure to infectious agents, allergens or pollution
Although, atmospheric pollution itself is unlikely to be the primary
cause of asthma in the absence of other risk factors
oFor women: smoking, obesity and hormonal infulences
- The etiology of asthma is multi-modal and most often without one singular cause
Definition of Asthma
- Asthma is characterized by paroxysmal or persistent symptoms, such as
dyspnea, chest tightness, wheezing, sputum production and cough associated with
variable airflow limitation and airway hyperresponsiveness to endogenous or
exogenous stimuli. Inflammation and its resultant effects on airway structure are
considered the main mechanism leading to the development and persistence of
asthma”.
- The descriptive definition is used in both adult and pediatric Canadian asthma
consensus guidelines and has not changed in over a decade
- Asthma can also be classified as mild, moderate or severe
oIt can vary from one patient to another and symptoms may be transient,
intermittent and persistent
- Other definitions often include that the lower airway obstruction is usually
reversible which is in contract to other obstructive airway disease such as COPD
Pathophysiology
- Inflammation
oSpecific inflammatory mediators involved
- Bronchospasm
oCauses and effects of hyperresponsiveness of bronchial smooth muscle
resulting in bronchspasm
- Increased mucous production
- Airway remodeling
- Extrinsic vs intrinsic asthma
- Early and late phases
Triggers
- Extrinsic Asthma (atopic/allergy asthma): type I hypersensitivity reaction
oExposure to allergen/antigen
oType I IgE mediated hypersensitivity reaction
- Intrinsic Asthma (non-atopic asthma)
oRespiratory tract infection (*viral)
oExercise
oHyperventilation
oCold air, weather changes
oDrugs and chemicals
oIrritants
oOrmonal changes and emotional upsets
oAirborne pollutants
oGERD
- Most individuals with asthma have a combination of extrinsic and intrinsic
asthma
- The pathophysiology of intrinsic asthma is not as well understood or
straightforward as extrinsic asthma
oThere are different explanations for why a non-atopic trigger may cause
bronchospasm and subsequently an acute asthma exacerbation
oEx. Its thought that bronchospasm by way of parasympathetic stimulation
through vagal pathways may initiate an exacerbation of asthma and
asthma symptoms for triggers such as inhaled irritants, emotional factors
and hormonal changes
- Intrinsic asthma generally has the same cell involvement including mast cell and
immune activation
Early Phase Response
- Occurs within 10 – 20 min of triggering stimuli and can last up to 2 hours
- Allergen binds to preformed IgE on sensitized mast cells on mucosal surface of
airways

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Description
Asthma Prevalence: The Faces of Asthma ­ Canadians > 12 years old o 2,362,902 (2008) o 2,249,703 (2005) o This represents between 8­9% of the Canadian population aged 12 years  of age and older ­ In Canada, the prevalence of asthma of off­reserve Aboriginal people 12 years of  age and over is higher than that of the general population at 11.9% ­ NLSCY data 2000/01 o 586 000 (13.4%) children aged 11 and under have been diagnosed with  asthma  13.4% of Canadian children aged 11 and under o when broken down into age groups the increase was only significant for  children aged 5 and younger and children aged 10 and 11 o the prevalence of asthma attacks has decreased from 51% to 39% between  1994/95 and 2000/2001 date of 0­11 year old Canadian children ­ Higher prevalence in boys and women o There has been a 60% increase in women aged 35 – 44 years o 80% increase in women aged 45 – 64 years and 41% increase in men aged  35 – 44 years between 1994/95 and 2005 ­ Childhood asthma rates highest in Atlantic provinces, lowest in BC and Prairie  provinces ­ Rates are steadily increasing around the world ­ Despite increasing prevalence, asthma mortality rates have steadily declined in  Canada since 1987 o This is consistent with other developed nations ­ Hospitalization rates have also decreased in children and adults along with ER  visits o This is attributed to appropriate use of Asthma Practice Guidelines and  active involvement of patients and their families Etiology ­ Longitudinal studies suggest that in childhood asthma, susceptibility is  determined during fetal development and the first 3 – 5 years of life.  ­ Risk factors for developing childhood asthma include: o Family history of allergy and allergic disorders  Family history of allergy and allergic disorders including hay  fever, asthma and eczema  The genetic basis of asthma is complicated and multifactorial as  there have been several genetic loci on a variety of different  chromosomes implicated in the pathogenesis of asthma  There have actually been more than 100 genes identified that may  play a role in the susceptibility and pathogenesis of asthma  Some of these genes influence the production of IL­4, IL­5, IL­13,  IgE, eosinophils, mast cells, adrenergic receptors, leukotrienes and  bronchial hyper­responsiveness   In particular, the gene ADAM 33 has been associated with asthma  and bronchial hyperresponsiveness o High exposure to airborne allergens   High exposure of susceptible children to airborne allergens such as  pets, house dust mites, cockroaches and mould in the first years of  life  o Exposure to tobacco smoke  In utero or early years of life  The NLSCY found that Canadian children living in households  where either parent smoked daily were significantly more likely to  be diagnosed with asthma than children in non­smoking  households o Low birth weight and RDA  RDA = respiratory distress syndrome ­ The NLSCY has not found any relationship between household income and  childhood asthma o It is important to note that the NLSCY has not found a difference in the  prevelance of asthma between urban and rural areas  In contrast to other countries, specifically the USA • Prevalence of asthma is higher in urban areas ­ In adult onset risk factors include: o Occupational exposures to low molecular weight sensitizers (i.e.  isocyanates) o Exposure to infectious agents, allergens or pollution  Although, atmospheric pollution itself is unlikely to be the primary  cause of asthma in the absence of other risk factors o For women: smoking, obesity and hormonal infulences  ­ The etiology of asthma is multi­modal and most often without one singular cause Definition of Asthma ­ “ Asthma is characterized by paroxysmal or persistent symptoms, such as  dyspnea, chest tightness, wheezing, sputum production and cough associated with  variable airflow limitation and airway hyperresponsiveness to endogenous or  exogenous stimuli. Inflammation and its resultant effects on airway structure are  considered the main mechanism leading to the development and persistence of  asthma”. ­ The descriptive definition is used in both adult and pediatric Canadian asthma  consensus guidelines and has not changed in over a decade ­ Asthma can also be classified as mild, moderate or severe o It can vary from one patient to another and symptoms may be transient,  intermittent and persistent ­ Other definitions often include that the lower airway obstruction is usually  reversible which is in contract to other obstructive airway disease such as COPD Pathophysiology ­ Inflammation o Specific inflammatory mediators involved ­ Bronchospasm o Causes and effects of hyperresponsiveness of bronchial smooth muscle  resulting in bronchspasm ­ Increased mucous production ­ Airway remodeling ­ Extrinsic vs intrinsic asthma ­ Early and late phases Triggers ­ Extrinsic Asthma (atopic/allergy asthma): type I hypersensitivity reaction  o Exposure to allergen/antigen o Type I IgE mediated hypersensitivity reaction ­ Intrinsic Asthma (non­atopic asthma) o Respiratory tract infection (*viral) o Exercise o Hyperventilation o Cold air, weather changes o Drugs and chemicals o Irritants o Ormonal changes and emotional upsets o Airborne pollutants o GERD ­ Most individuals with asthma have a combination of extrinsic and intrinsic  asthma ­ The pathophysiology of intrinsic asthma is not as well understood or  straightforward as extrinsic asthma o There are different explanations for why a non­atopic trigger may cause  bronchospasm and subsequently an acute asthma exacerbation o Ex. Its thought that bronchospasm by way of parasympathetic stimulation  through vagal pathways may initiate an exacerbation of asthma and  asthma symptoms for triggers such as inhaled irritants, emotional factors  and hormonal changes  ­ Intrinsic asthma generally has the same cell involvement including mast cell and  immune activation Early Phase Response ­ Occurs within 10 – 20 min of triggering stimuli and can last up to 2 hours ­ Allergen binds to preformed IgE on sensitized mast cells on mucosal surface of  airways ­ Mast cell activation releasing inflammatory mediators o Histamine, chemotactic chemokines, interleukins and tumor necrosis  factor alpha  This immediate response if called mast cell degranulation o Mast cells also begin synthesizing leukotrienes, prostaglandin D2,  cytokines, further tumor necrosis factor alpha and platelet activating factor  for release in the late phase response ­ Increase mucous secretion, increased vascular permeability and  bronchoconstriction o These inflammatory mediators cause infiltration of inflammatory cells,  opening of mucosal intercellular junctions allowing access to submucosal  mast cells which results in further inflammation as well as increased  mucous secretion, increased vascular permeability and  bronchoconstriction ­ It should also be noted that dendritic cells may receive antigen at this time that  will be processed and presented later in the late phase response to naïve T  lymphocytes in the lymph nodes or memory Th2 cells in the airway mucosa o This will result in further immune activation Late Phase Response ­ Occurs 4 – 8 hours after triggering stimuli, may persist for days or even weeks ­ Release of inflammatory mediators causes recruitment of neutrophils, eosinophils,  basophils, T lymphocytes (specifically TH2*)  o Triggered earlier by chemotactic factors and upregulation of endothelial  adhesion molecules ­ These inflammatory cells cause epithelial injury and edema, increased mucous,  changes in mucociliary function resulting in the accumulation of mucous and  increased airway responsiveness and bronchospasm o Epithelial damage and impaired mucociliary function is caused because of  direct toxic effects of cellular products, specifically from eosinophils such  as major basic protein ­ This injury causes local nerve endings to be stimulated through automatic  pathways which may cause further bronchoconstriction and mucous sectretion o Macrophages are also activated in the respiratory tract during the late  phase Inflammatory Cells ­ Mast cells o Are cellular bags of granules found in large numbers in the skin and  linings of the GI and respiratory tract o They are activated by several means including physical injury, chemical  agents, immunologic and infectious means o When they degranulate they release:  Histamine  Chemotactic chemokines  Cytokines o They also begin synthesizing inflammatory mediators derived from  plasma membrane lipids such as  Platelet activating factor  Prostaglandin D2  Leukotrienes  Cytokines and growth factors o This results in long­term response ­ Histamine o Potent vasodilator that causes increased vascular permeability through  retraction of endothelial cells o Also causes smooth muscle to contract causing bronchoconstriction when  stimulated in the bronchi  Particularily importantin the pathogenesis of asthma ­ Leukotrienes  o Functions are similar and omplementary to that of histamine o More potent and stimulate slower and more prolonged effects compared to  histamine o Cysteinyl leukotrienes (LLTC4, LTD4 & LTE4) cause slow and sustained  constriction of the bronchioles  ­ Prostaglandin D2 o Causes vasodilation, increased vascular permeability and  bronchoconstriction ­ Chemotactic chemokines o Cytokines that attract immune and inflammatory cells o They primarily function to attract leukocytes ­ Cytokines (i.e. TNF­alpha, IL­4, IL­5) o Proteins that modulate the function of other cells o TNF­alpha, IL­4, 5, 8 and 13 are key mediators in the pathogenesis of  asthma o TNF­alpha   Increase the activation and migration of inflammatory cells  (specifically eosinophils and neutrophils)  Contributes to airway remodeling  Causes endothelial cells to express adhesion molecules o TNF­alpha and IL­1 alter muscarinic receptor function resulting in  increased levels of acetylcholine which causes bronchial smooth muscle  contraction and mucous secretion o IL­4, 5, 8 and 13 are T­helper 2 cytokines  IL­4 stimulates activation, proliferation and production of antigen­ specific, IgE by B cells  IL­5 activates and promotes eosinophil activity  IL­8 causes a more exaggerated inflammatory response through  activation of basophils, neutrophils and eosinophils  IL­13 impairs the clearance of mucous, contributes to  bronchoconstriction and increase fibroblast secretion ­ PAF o Induces platelet aggregation, increases vascular permeability through  endothelial cell retraction o Activates neutrophils  o Potent eosinophil chemoattractant o In the respiratory tract, PAF causes bronchospasm, eosinophil infiltration  and nonspecific bronchial hyperreactivity ­ Cysteinyl leukotrienes o Important to note that they are the leukotrienes that play a major role in  the pathophysiology of asthma o They were initially called “slow reacting substance of anaphylaxis” due to  their effect on bronchial smooth muscle of slow and prolonged contraction  and hence bronchoconstriction ­ T Lymphocytes (Th2) o Play an important role in the pathogenesis of extrinsic asthma o TH2 lymphocytes act as growth factors for mast cells as well as recruiting  and activating eosinophils by stimulating the differentiation of B cells into  IgE – producing plasma cells o In asthmatic patients, T cell differentiation is skewed towards TH2  phenotype cells ­ Leukocytes (i.e. eosinophils, basophils, neutrophils, lymphocytes, macrophages) o Known as white blood cells o Neutrophils, eosinophils and basophils are also known as granulocytes o Neutrophils are first on scene and the predominant phagocytes in the early  inflammatory phase o Eosinophils control the release of specific mediators from mast cells o Basophils bind to IgE which is secreted by plasma cells and release  histamine and mediators of inflammation such as IL­4 o Remember that lymphocytes are T & B cells o Macrophages arrive after neutrophils, which means that in the  pathogenesis of asthma they arrive in the late phase response Bronchospasm ­ Bronchospasm is the result of the action of several mediators listed: o Histamine (early phase) o Leukotienes (late phase) o PAF o Prostaglandins ­ Autonomic nervous system dysregulation (PNS) o Cholinergic mediators responsiveness increase  The parasympathetic control of airway function appears to not  function appropriately due to heightened responsiveness to  cholinergic mediators  This is caused by an alteration of muscarinic receptor function by  TNF­alpha and IL­1 leading to an increase in acetylcholine which  causes bronchial smooth muscle contraction and further mucous  secretion Mucus Hypersecretion  ­ Mucous secretion is a major pathophysiological feature of asthma  ­ Goblet cell hyperplasia and submucosal gland hypertrophy o Submucosal glands and goblet cells produce mucous in the airways o Both sources are affected in patients with asthma resulting in goblet cell  hyperplasia and submucosal gland hypertrophy ­ Mucous secretion triggered by the inflammatory response ­ Leukotrienes stimulate increased mucous secretion ­ Th2 release IL­9 & IL­13  ▯upregulate mucous production in asthmatic patients o Interleukin­9 and 13 are the two most relevant cytokines that upregulate  mucus secretion o Other mediators that have a role in mucous hypersecretion are TNF­alpha,  IL­1 beta and ligands of the epidermal growth factor receptor ­ Airway obstruction by mucous plugs d/t mucous hypersecretion + increased  plasma exudation  ▯increased airway hyperresponsiveness o The most damaging effect of mucous hypersecretion is airway obstruction  by mucous hypersecretion and increased plasma exudation o Mucous hypersecretion may also increase airway hyperresponsiveness  ­ Furthermore, impaired mucociliary function worsens the situation as the ability to  clear the mucous is impaired Airway Remodeling  ­ Airway remodeling is recognized as one of the major contributors in the  pathogenesis of asthma ­ Appears to occur in parallel with inflammation o Meaning that more inflammation equals more airway remodeling o Therefore, airway remodeling begins early on in the disease process of  asthma and declining lung function which is attributed to airway  remodeling is found in young children as well as new asthmatics o Changes to the airway due to inflammation may include submucosal  infiltration with activa
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