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Copd 2010

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pathophysiology
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Chronic Obstructive Pulmonary Disease
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Page 1: Copd 2010

Chronic Obstructive Pulmonary Disease

Page 2: Copd 2010

Chronic Obstructive Pulmonary DiseaseA disease state characterised by airway

obstruction that is not fully reversibleIncludes chronic bronchitis and

emphysemaMajor contributor to the overall burden of

disease & second only to stroke in NZ3rd cause of death for males & 4th for females

in NZ50% die within 10yrs of diagnosisSymptomatic during middle adult yearsIncidence increases with age

Page 3: Copd 2010

PathophysiologyIncludes inflammation & fibrosis of bronchial wall hypertrophy of submucosal glands hypersecretion of mucous loss of elastic lung fibres & alveolar tissue

leading to airway collapseAll of the above result in obstruction of

airflowdestruction of alveolar tissue decreases

surface area for gas exchange

Page 4: Copd 2010

Chronic BronchitisA disease of the airwaysPresence of cough & sputum production for

at least 3 months in each of 2 consecutive years

Smoke or other pollutants irritate airways, resulting in hypersecretion of mucous & inflammation

Constant irritation causes: mucous-secreting glands & goblet cells to

increase in number reduction of ciliary function Production of more mucous

Page 5: Copd 2010

Clinical Manifestations of Chronic BronchitisEarliest symptoms:Frequent productive cough during winterFrequent respiratory infectionsBronchospasm can occur at end of paroxysms

of coughingCough usually exacerbated by respiratory

irritants or cold airDyspnoea on exertionHistory of smoking is almost always presentNormal weightHypoxaemia and hypercapnia (Result from

hypoventilation and airway resistance in addition to problems with alveolar gas exchange)

Page 6: Copd 2010

EmphysemaCarbon dioxide elimination is impaired resulting in hypercapnoea (excess CO2 in the blood)

As alveolar walls break down, pulmonary capillary bed is reduced

Page 7: Copd 2010

Structural Changes in Emphysema1. Hyperinflation of alveoli2. Destruction of alveolar walls3. Destruction of alveolar capillary walls4. Narrowed, tortuous, small airways5. Loss of lung elasticity

Page 8: Copd 2010

Clinical Manifestations of EmphysemaDyspnoea- initially on exertion & then on restMinimal coughingNo sputum or small amts of mucoid sputumBarrel chest – alveoli over distended, air trappedPursed – lip breathing (expiration through

pursed lips). Increases the resistance to the outflow of air & helps to prevent airway collapse by increasing airway pressure

‘Chest breather’ – relying on intercostal & accessory muscles (ribs become fixed in inspiratory position)

Hypoxaemia (during exercise) & hypercapnoea later in disease

Underweight

Page 9: Copd 2010
Page 10: Copd 2010

Risk Factors for COPDExposure to

tobacco smoke (80%)

Passive smokingOccupational

exposureAir pollutionGenetic

abnormalities

Page 11: Copd 2010

Cigarette SmokingNicotine acts as a stimulant to the

sympathetic nervous system resulting in:Increased HRIncreased peripheral vasoconstrictionIncreased BP & cardiac workload

Page 12: Copd 2010

Cigarette SmokingDecreased ciliary activityPossible loss of ciliated cellsCellular hyperplasiaProduction of mucousReduction of airway diameterIncreased difficulty in clearing secretions

Page 13: Copd 2010

Clinical Manifestations of COPDCough, sputum production & dyspnoea on

exertionSymptoms worsen over timeChronic cough & sputum production often

precede development of airflow limitation by many years

Dyspnoea may be severe & interferes with ADLs

Weight loss – dyspnoea interferes with eating & work of breathing is energy depleting

Use of accessory muscles for breathing

Page 14: Copd 2010
Page 15: Copd 2010

Pathologies of COPDEmphysema• Hyperinflation of alveoli• Destruction of alveolar

walls• Destruction of alveolar

capillary walls• Narrow, small , tortuous

airways• Loss of lung elasticity

Chronic Bronchitis• Inflammation• ↑ in mucous-secreting

glands & goblet cells• ↓ ciliary function→ more mucous• Bronchial walls thicken &

narrow• Mucous can plug airway• Alveoli damaged →altered

function of macrophages → more susceptible to resp infections

Page 16: Copd 2010

Comparison of Emphysema & Chronic BronchitisEmphysemaOnset 30-40yrsThinMarked weight lossGenerally healthy,

insidious dyspnoea, smoking

Scanty mucoid sputumNegligible cough

Chronic BronchitisOnset 20-30yrsTendency towards

obesityNo weight lossRecurrent URTI,

smokingDyspnoea variable & lateCopious mucopurulent

sputumConsiderable cough

Page 17: Copd 2010

COPDEmphysemaDyspnoea- initially on

exertion & then on restMinimal coughingNo sputum or small amts of

mucoid sputumBarrel chest – alveoli over

distended, air trappedPursed – lip breathing ‘Chest breather’ – relying

on intercostal & accessory muscles

Hypoxaemia (during exercise) & hypercapnoea later in disease

Underweight

Chronic Bronchitis• Frequent productive

cough• Frequent respiratory

infections• Bronchospasm at

end of coughing• Dyspnoea on

exertion


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