Chronic Obstructive Pulmonary Disease

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Chronic Obstructive Pulmonary Disease

• Hou-haifeng

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LUNG STRUCTURE
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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.

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COPD DISORDERS

• Chronic Bronchitis
• Emphysema
• Asthma (?)
• Although not strictly a COPD disorder ASTHMA is
  often
• linked with being a COPD disorder.

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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

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE
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Pathogenesis of COPD
NOXIOUS AGENT(tobacco smoke, pollutants,
occupational agent)
COPD
Genetic factors Respiratory infection Other
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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

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MECHANISMS II

• Increases in RBC, Blood viscosity, BP
• Ventilation / Perfusion imbalances
• Hypoxemia
• Carbon dioxide retention
• Bronchial hyperreactivity
• Hyperinflation

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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.

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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.

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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

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MUCUS PRODUCTION
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MUCUS PRODUCTION
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CHANGES IN LUNG VOLUMES
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VENTILATION COST

• In COPD work of breathing is greater for any
  given level of ventilation than normal.

SEVERE COPD
The cost of work at a given ventilation for
normal and COPD patients (ACSM, 1998)
WORK OF BREATHING
MODERATE COPD
NORMAL COPD
VENTILATION
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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

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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

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Diagnosis of COPD
EXPOSURE TO RISK FACTORS
SYMPTOMS
cough
tobacco
sputum
occupation
dyspnea
indoor/outdoor pollution
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SPIROMETRY
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Spirometry Normal and COPD
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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

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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)

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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

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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

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mathematics, statistics, cybernetics, system
theory, computer science
COPD Disease Model
The information from the data base in the hospital
The information from the data base in the hospital
Disease progress prognosis
The knowledge of medicine(Pathology Physiology
Pharmacology)
therapeutic scheme
doctor
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