copd 2010
DESCRIPTION
pathophysiologyTRANSCRIPT
Chronic Obstructive Pulmonary Disease
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
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
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
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)
EmphysemaCarbon dioxide elimination is impaired resulting in hypercapnoea (excess CO2 in the blood)
As alveolar walls break down, pulmonary capillary bed is reduced
Structural Changes in Emphysema1. Hyperinflation of alveoli2. Destruction of alveolar walls3. Destruction of alveolar capillary walls4. Narrowed, tortuous, small airways5. Loss of lung elasticity
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
Risk Factors for COPDExposure to
tobacco smoke (80%)
Passive smokingOccupational
exposureAir pollutionGenetic
abnormalities
Cigarette SmokingNicotine acts as a stimulant to the
sympathetic nervous system resulting in:Increased HRIncreased peripheral vasoconstrictionIncreased BP & cardiac workload
Cigarette SmokingDecreased ciliary activityPossible loss of ciliated cellsCellular hyperplasiaProduction of mucousReduction of airway diameterIncreased difficulty in clearing secretions
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
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
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
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