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    Obstructive lung disease

    Dr Rebecca ScholesApril [email protected]

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    COMMONWEALTH OF AUSTRALIACopyright Regulations 1969

    WARNINGThis material has been reproduced andcommunicated to you by or on behalf of

    Monash University pursuant to Part VB ofthe Copyright Act 1968 (the Act).

    The material in this communication may besubject to copyright under the Act. Any

    further reproduction or communication ofthis material by you may be the subjectof copyright protection under the Act.

    Do not remove this notice.

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    Learning objectives

    At the completion of this session it isexpected the student will be ableto:

    Describe the pathophysiologicalmechanisms responsible forasthma development and COPD

    Explain the role of environmental

    factors, exercise and geneticfactors in asthma development

    Describe the pathological andphysiological changes associatedwith asthma and COPD

    Discuss the impact of asthma andCOPD on the individual and thepopulation

    Examine the National Healthpriorities in relation to respiratorydisease

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    References

    PRYOR, J. & PRASAD, S. A. (2002)

    Physiotherapy for respiratory andcardiac problems, Edinburgh,Churchill Livingstone.

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    Asthma

    Definition

    Airways disease characterisedby episodic, reversiblebronchoconstriction resultingfrom hyper-reactivity of the

    airways to a variety of stimulior triggers

    Obstructive airways disease

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    Asthma

    Epidemiology

    Australias asthma problem

    10% of entire population

    30% of children & adolescents

    Most common illness in children

    Most common reason for timeoff school

    National Health Priority

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    Asthma

    Causes

    Atopy Pollen

    Animal danders

    House dust mites

    Weather

    Exercise

    Emotion

    Medications

    Moulds/Fungi URTIs

    Inhaled toxins e.g. cigarettesmoke

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    Asthma

    Pathology

    Inflammation of airway mucosa

    Oedema of airway wall

    Plasma exudation frombronchial microvessels

    Goblet cell hyperplasia

    Mucous hypersecretion

    Mucous plugging

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    Asthma

    Pathogenesis

    Inhaled proteins captured by dendriticcells which live just under theepithelium

    Dendritic cells trigger Helper T cellsbearing the CD4 surface marker

    Triggers TH2 immune deviation as a

    result of IL-4 signal TH2 secrete IL4/5/6/9/13 and GM-

    CSF

    Chronically (after a few years ofsensitisation) further antigeninhalation causes TH2 cytokinesecretion. IL-4 and IL-13 induce theadhesion molecule VCAM-1 onmicrovessels used by eosinophils toenter tissues

    Marked increase in eosinophilproduction secondary to IL-5

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    Asthma

    Pathogenesis

    IL-4 causes B cells to secrete IgEwhich sensitises mast cells and othercells so they can release massiveamounts of inflamm mediators whenIgE bound to their surface iscrosslinked by antigen.

    Tissue damage results from eosinophildegranulation products and theeffects of inflammatory mediators.

    Cysteinyl-leukotrines (inflammatorymediators) are also potent smoothmuscle constrictors.

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    Asthma

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    Asthma

    Chronic changes

    Caused by cycles of damage andrepair

    Hypertrophy and hyperplasia ofairway wall (smooth muscle)

    Submembrane deposition ofcollagen causingpseudothickening of basementmembrane

    Epithelial fragility Hyperinflation of lungs

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    Asthma

    S&S

    Wheeze (n.b. silent chest)

    SOBAR/SOBOE

    Cough (tight)

    Retractions (intercostal,

    supra/substernal)

    Use of accessory muscles ofrespiration

    Cyanosis

    Altered Conscious State

    Prolonged expiratory phase

    Reduced SpO2

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    Asthma

    S&S

    Diaphoretic

    Anxious

    Talk test

    Tripod Position

    Catatonic

    Tachycardia (Bradycardia)

    Hypotensive

    Tracheal tugging

    VEs

    Tremor

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    Asthma History taking

    Subjective Assessment Identify trigger

    PHx of exacerbations

    Medication

    Objective Assessment SpO2 Auscultation

    Respiratory rate

    Heart rate

    PEF

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    Asthma

    Treatment short term

    O2 therapy

    Fast acting bronchodilators e.g.Salbutamol (relievers vs. preventers)

    Corticosteroids e.g.Beclomethasone (mdi),prednisolone (oral)

    Anticholinergic bronchodilators

    Nebulisation and deposition ofdrugs

    Combined therapies e.g.Seretide

    Latent response

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    Asthma

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    Asthma

    Treatment long term

    1. Assess severity2. Achieve best lung function

    Exercise

    Breathing control

    3. Maintain best lung function Optimise medication

    Avoid triggers where possible

    4. Asthma management plan

    5. Educate and review

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    Emphysema

    Definition

    Derived from Greek and meansto blow into hence aircontaining or air inflated

    An abnormal, permanent

    enlargement of the air spacesdistal to the terminalbronchioles, accompanied bydestruction of their walls

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    Emphysema

    Causes

    Smoking Genetic

    Air Pollution

    Mining

    Asbestosis

    Farming

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    Emphysema

    Pathology

    Thinning and destruction ofalveolar walls

    Loss of elastic tissue and radialtraction in airways

    Early collapse of airways duringexpiration

    Hyperinflation of lungs

    Bullae

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    Emphysema

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    Emphysema

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    Emphysema

    S&S

    Dyspnoea partic. SOBOE Barrel shaped chest

    Pale & cyanosed

    Wheeze

    Cough Body wasting

    PLB

    Prolonged expiratory phase

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    Emphysema

    S&S

    Tripod position Talk test

    Anxious

    Indrawing of intercostal m.

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    Emphysema

    S&S

    Pink Puffers Maintain adequate ABGs and SpO2 Dyspnoeic

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    Emphysema

    S&S

    Blue Bloater Chronic bronchitis

    Purulent sputum

    CO2 retainers

    Hypoxic drive

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    Emphysema

    Treatment

    Remove cause (smoking) Optimise medication

    Education

    Exercise

    Breathing exercises

    O2 therapy

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    Chronic bronchitis

    Definition

    The presence of a chronic,productive cough for at least 3consecutive months over atleast 2 consecutive years

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    Chronic bronchitis

    Causes Cigarette smoking

    Hypertrophy of submucosalglands

    Increase in goblet cells

    Infection Smokers have more infections

    due to:

    a) Inhibition of ciliary action

    b) Direct damage to respiratoryepithelium

    c) Inhibition of leucocytes inclearance of bacteria

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    Chronic bronchitis

    Pathology

    Mucous gland enlargement Mucous hypersecretion

    Airways atrophy

    focal squamous metaplasia

    ciliary abnormalities

    airway smooth muscle hyperplasia

    inflammation

    bronchial wall thickening

    fibrosis and scarring

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    Chronic bronchitis

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    Chronic bronchitis

    S&S

    Cough Sputum

    SOB

    Cyanosed

    Over-weight

    Wheeze

    Abnormal blood gases Hypercapnia & hypoxaemia

    Cor pulmonale

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    Chronic bronchitis

    S&S

    Clubbing of fingers Anxious

    Talk test

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    Chronic bronchitis

    Treatment

    Pharmacological managementof infections

    Bronchodilators

    Education

    Exercise Breathing exercises

    O2 therapy