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400815 – ABWM
(Alterations in Breathing, Work / Leisure & Mobility)
Lecture 2
Asthma
Spring 2010
Asthma is a chronic inflammatory disorder of the airways characterised by hyperresponsiveness and bronchospasmleading to airway limitation (obstruction) which manifests as coughing, wheezing, shortness of breath and chest tightness.
How big is the problem?
It is estimated that asthma is a health problem affecting more than 300 million people worldwide.
The International Study of Asthma and Allergies in Childhood (ISAAC) epidemiological research programmewas established in 1991 to determine the prevalence of asthma in school age children worldwide.
In the 2007 phase III ISAAC study it was found that generally there has been no decline in asthma. For 6 to 7 year old children, Australia had the second highest prevalence of asthma.
Asthma in Australia 2008
•Australia has the second highest prevalence of asthma in the world.
•About 2 million Australians have asthma (10.2% of population).
•Indigenous Australians have a higher prevalence of asthma, have a higher mortality rate due to asthma and have higher rates of hospitalisation for asthma than non-Indigenous Australians.
•Compared with 2001, the prevalence of asthma decreased slightly in children and young adults but remained unchanged in older adults.
•Among those aged 0–14 years, the prevalence of asthma is higher among boys than girls, but among those aged 15 years and over, current asthma is more prevalent in females than males.
•The majority of children with asthma in Australia are classified as having infrequent episodic asthma while very few (less than 5%) have persistent asthma.
•There were 402 deaths attributed to asthma as the underlying cause in 2006.
•There was a 69% decrease in the mortality attributed to asthma between 1989 and 2006.
Causes of asthma
Interaction between genes and environmental factors.
Atopic asthma•Response mediated by IgE.
•Inflammatory triggers includepollendust mitesanimal hairinfections
Non atopic asthma
•Response not triggered by IgE.
•Bronchospasmic triggers includecold airexerciseenvironmental irritants e.g. cigarette smokeemotion
PathogenesisInitial antigen sensitization production of presensitized IgE‐coated mast cells.
Early phase•Antigen binds to IgE on sensitized mast cells of mucosal lining.•Mast cells release inflammatory mediators such as histamine, leukotrienes, interleukins and prostaglandins.•Stimulation of parasympathetic receptors causes bronchospasm and increased mucous production.
Late phase• Infiltration of inflammatory cells leads to release of inflammatory mediators such as cytokines and interleukins from mast cells, macrophages and epithelial cells.
• Increased vascular permeability leads to oedema.• Migration and activation of basophils, eosinophilsand neutrophils leads to impaired mucociliaryfunction and cell injury.
• Heightened responsiveness to cholinergic mediators leads to increased airway responsiveness and bronchospasm.
Pathogenesis – early and later phasestaken from Porth, fig 31.7, p.697
Airway remodelling
Chronic inflammation can lead to airway remodelling.
•airways become thickened•increased number of myofibroblasts•hypertrophy of smooth muscle•mucous gland hyperplasia
Summary of structural changes• Airways have hypertrophied smooth muscle.• Hypertrophy of bronchial mucous glands• Inflammation and oedema of bronchial wall• Extensive cellular infiltration – especially by eosinophils• Mucous is abnormal (thick, tenacious and slow moving)
• Sputum is typically scant and white.
• Subepithelial fibrosis is commonly seen in chronic asthma.
• In uncomplicated asthma, there is no‐destruction of alveolar walls (as in emphysema), and
• No copious purulent bronchial secretions (as in chronic bronchitis)
Functional consequences
• Narrowed airways due to– Bronchospasm– Oedema of bronchial mucosa– Mucous plugging
• Thick sputum• Impaired mucociliary function• Mucous plugs
• Air trapped behind occluded and narrowed airways
• More energy needed to overcome tension present in hyperinflated lungs
• Effectiveness of alveolar ventilation declines
Clinical manifestations
• Wheezing• Dyspnoea• Prolonged expiration• FVC reduced• FEV1 and peak expiratory flow rate decreased
• Dry non‐productive cough
• Hyperinflation of lungs • Residual volume increased
• Accessory muscles used • Dyspnoea• Fatigue• Anxiety
• Hypoxaemia and cyanosis• Hypercapnia
Pulmonary functions test in asthma
A spirometer measures lung volumes and capacities.
Best practice guidelines recommend that doctors managing asthma should use a spirometer to assess, diagnose and monitor the disease.
Revise lung volumes and capacities from UGH
During an asthma attack, all indices of expiratory flow rate are reduced significantly:
• Forced expiratory volume (FEV1)
• FEV/FVC%
Forced vital capacity is reduced due to premature airway closure during expiration (gas trapping)
Pulmonary functions test in asthma (cont’)
• Static lung volumes are increased.
• Remarkably high functional residual capacity (FRC)
and total lung capacity (TLC) during asthma attacks
have been reported.
1. Beta2‐ adrenergic agonists
e.g. Salbutamol (Ventolin)•Sympathomimetic•Activate beta 2 adrenergic receptors in smooth muscle of lung promoting bronchodilation.•Suppress histamine release and increase ciliarymotility. • Used to relieve acute bronchospasm and prevent exercise‐induced bronchospasm
Pharmacological management of asthma
e.g. BeclomethasonePulmicort
Suppress inflammation decrease synthesis and release of inflammatory mediatorsdecrease infiltration and activity of inflammatory cellsdecrease oedema of airway Used for prophylaxis
2 Anti inflammatory drugs
• Glucocorticoids
•Cromolyn (Intal)
•Stabilises cell membrane of mast cells preventing release of histamine.•Inhibits eosinophils, macrophages.•Used for prophylaxis.
•Leukotriene modifiers
•e.g. Montelukast (oral)•Suppress effects of leukotrienes
3. Anticholinergics
•e.g. Ipratropium (Atrovent)•Muscarinic antagonist•Blocks muscarinic cholinergic receptors in the bronchi promoting bronchodilation.
• Australia has a high prevalence of asthma and it is one of the National Health
Priorities
• Asthma is characterised by episodes of severe dyspnea that are often worse in
the spring and are sometimes exacerbated by exercise or cold air.
• Airways have hypertropied, contracted smooth muscle, oedema, mucous
gland hypertropy, and increased secretions.
• Pulmonary functions tests show increases in airway resistance and lung
volume.
• Pathogenesis is still not fully understood, but there is hyperresponsivnes and
inflammation.
Key Concepts
References Asher, M.I., Montefort, S., Bjorksten,B., Lai, C.K.W., Strachan, D., Weiland,H.W. and the
ISAAC Phase Three Study Group(2006). Worldwide time trends in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis and eczema in childhood: ISAAC Phases One and Three repeat multicountry cross‐sectional surveys. Lancet 368: 733‐743.
Copstead, L. C., & Banasik, J. L. (2005). Pathophysiology (3rd ed.). Philadelphia: Saunders.
Hockenberry, M.J., Wilson, D., Winkelstein, M.L., & Kline, N.E. (Eds.). (2003). Wong’s nursing care of infants and children (6th ed.). St Louis: Mosby.
Jenkins, G. W., Kemnitz, C. P., & Tortora, G. J. (2007). Anatomy and physiology from science to life. New Jersey: Wiley in/Cummings.
Lehne, R. A., Moore, L., Crosby, L., & Hamilton, D. (2007). Pharmacology for nursing care (6th ed.). Philadelphia: Saunders.
National Asthma Council Australia (NACA). (2006). Asthma management handbook 2006. Melbourne: NACA. Retrieved July 22, 2010 from http://www.nationalasthma.org.au/html/management/amh/index.asp
Porth, C. M. (2005). Pathophysiology: Concepts of altered health states (7th ed.). Philadelphia: Lippincott.