obstructive+lung+disease
TRANSCRIPT
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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