Transcript CHRONIC OBSTRUCTIVE PULMONARY DISEASE:

Chronic Obstructive Pulmonary Disease
Hou-haifeng
LUNG STRUCTURE
NORMAL VENTILATORY FUNCTION
• Diaphragm contracts and descends, rib cage moves
upwards and outward.
• Pressure in the thorax is less than in the mouth so air
flow into the lungs occurs.
• In expiration diaphragm relaxes and moves upwards, the
rib cage moves inward.
• Expiration is passive so no muscular contraction is
needed.
• Lung tissue is intrinsically elastic and has a natural ability
to recoil.
• During exercise expiration is aided by the contraction of
abdominal and thoracic expiratory muscles.
• Contractions generate positive pressure in the thorax
pushing air out.
COPD DISORDERS
– Chronic Bronchitis
– Emphysema
– Asthma (?)
Although not strictly a COPD disorder ASTHMA is often
linked with being a COPD disorder.
DEFINITION
 Progressive, non-reversible, obstructive airway
disease leading to damaged alveolar walls and
inflammation of the conducting airways
• Some part of the airway becomes obstructed or
no longer functions efficiently
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE:
Pathogenesis of COPD
NOXIOUS AGENT
(tobacco smoke, pollutants, occupational agent)
Genetic factors
Respiratory
infection
Other
COPD
Noxious particles
and gases
Host factors
Lung inflammation
Anti-oxidants
Oxidative stress
Anti-proteinases
Proteinases
Repair mechanisms
COPD pathology
MECHANISMS
Bronchial glands / cells inflame
Increased secretions
Inflammation spreads to smooth muscle (bronchiole)
Airway obstruction, decreased ciliary action
Air trapping / Collapse of small airways
Further air trapping
Hyperventilation
Increased pressure in airways
Weakened airway walls / wall destruction
Alveolar destruction
Overstressed right ventricle
MECHANISMS II
Increases in RBC, Blood viscosity, BP
Ventilation / Perfusion imbalances
Hypoxemia
Carbon dioxide retention
Bronchial hyperreactivity
Hyperinflation
CHRONIC BRONCHITIS
• Chronic bronchitis is defined as "persistent cough with sputum
production for at least 3 months in at least two consecutive
years".
• The most important cause of chronic bronchitis is recurrent
irritation of the bronchial mucosa by inhaled substances, as
occurs in cigarette smokers.
• The pathological hallmarks of chronic bronchitis are congestion
of the bronchial mucosa and a prominent increase in the number
and size of the bronchial mucus glands. Copious mucus may be
seen within airway lumens. The terminal airways are most
susceptible to obstruction by mucus.
CHRONIC BRONCHITIS
Aetiology
– Characterised by a chronic cough and excessive sputum
production.
– There is an enlargement and an increased density of
mucous glands.
– The airway becomes thickened and the surface irregular
– Bronchial inflammation. (ACSM, 1998)
– Reduced number of ciliated cells
– Causes an increase in air flow resistance
– In chronic severe cases right heart failure occurs
– Plugged airways and decreased ciliary action encourages
stagnant bronchial secretions and an increased risk of
infection.
CHRONIC BRONCHITIS
• Inflammatory cells produce elastase
• Destroys connective tissue of alveolar
walls
• Alpha-1 anti-trypsin (or alpha-1
protease inhibitor) is a protein produced
by the liver that circulates in the blood
and limits the action of elastase
MUCUS PRODUCTION
MUCUS PRODUCTION
CHANGES IN LUNG VOLUMES
VENTILATION COST
• In COPD work of breathing is greater for any given
level of ventilation than normal.
SEVERE COPD
WORK OF
BREATHING
The cost of work at a
MODERATE COPD
given ventilation for
‘normal’ and COPD
NORMAL COPD patients (ACSM,
1998)
VENTILATION
EMPHYSEMA
AETIOLOGY
 Can be caused by smoking, air pollution and
environmental and occupational hazards
 Main characteristic is loss of lung elasticity and
reduction of elastic recoil due to alveolar destruction
 Destruction of elastic tissue leads to loss of elastic
recoil of lungs during expiration and forced expiration
necessitated
 Eventual destruction of airway / capillary membranes
 Destruction due to increased protease production or a
deficiency in anti-protease
EFFECTS OF EMPHYSEMA ON
HEALTH
• Reduction in expiratory flow level
• Patients are thin with general muscle wastage.
• Lung diffusion capacity is reduced due to loss of
alveolar capillary units
• Lactic acid threshold is much lower in COPD
patients
• Exercise tolerance impaired
Diagnosis of COPD
EXPOSURE TO RISK
FACTORS
SYMPTOMS
cough
sputum
dyspnea
tobacco
occupation
indoor/outdoor pollution

SPIROMETRY
Spirometry: Normal and COPD
0
FEV1
Normal
COPD
1
Liter
2
FVC
FEV1/ FVC
4.150
5.200
80 %
2.350
3.900
60 %
FEV1
3
COPD
4
FVC
FEV1
Normal
5
1
2
3
FVC
4
5
6 Seconds
MEDICAL THERAPY
 BRONCHODILATORS
Adrenergic agents
• Beta-agonists bind to B2 receptors on airway and result in
smooth muscle relaxation and bronchodilation
• Inhaled route is preferred
• Acute relief of symptoms
Anti-cholinergic agents
 Bind to acetylcholine receptors and result in bronchodilation (of
mostly larger airways)
• Reduces sputum production
• Inhaled route is preferred
•
•
•
•
Methylxanthines (i.e. theophylline)
Weak bronchodilator
Delays respiratory muscle fatigue
Reduces trapped lung gas
Improves respiratory muscle mechanics
MEDICAL THERAPY
 Corticosteroids
• Reduce airway inflammation
 Mucolytics
• Alter viscosity of sputum
• May reduce symptoms in some patients
• Must be used carefully (i.e. avoiding hypotension)
EXERCISE
• Increase exercise tolerance
• Increase quality of life
• Improve co-ordination and efficiency of
movement
• Improve strength particularly respiratory
muscles
• Encourage relaxation
• Confidence in physical abilities
• Flexibility
What we want to do
• As we all know there is so much data on the
patients deposited in the
hospital,however,that is not well exploited
• So we want to use these data to make a
disease model to help doctors to make a
appropriate diagnostic and therapeutic
scheme for the patients with COPD
• We also can use this model to predict the
progress of the disease and the prognosis
mathematics, statistics,
cybernetics, system
theory, computer science
The
Theinformation
informationfrom
from
the
thedata
database
baseininthe
the
hospital
hospital
The knowledge of
medicine(Pathology
Physiology Pharmacology…)
COPD
Disease
Model
therapeutic
scheme
Disease
progress
prognosis
doctor
31