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13 Cards in this Set

  • Front
  • Back
Etiology - Exposures
-Smoking/tobacco use
-Occupational dusts
-Air pollution
Etiology - Host Factors
-Hereditary a1-antitrypsin deficiency
-Airway hyperresponsiveness
-Infancy or childhood lung impairments
Smoking
-Promotes lung injury
-Stimulate inflammatory cells
-Increase oxidative stress
Inherited a1-antitrypsin deficiency
-Antiprotease enzyme that functions to protect the lung
-Deficiency leads to lung damage
-Inhibits neutrophil elastase
-1% of call COPD cases
-More common in younger emphysema patients
-Autosomal recessive disorder
-Smoking further decreases the enzyme
Pathological changes
-Inflammatory exudate
Increase goblet cells
increase mucus
decrease ciliary motility
-thickening of smooth muscle and connective tissue
-Scarring --> airway narrowing
Parenchymal changes
-Affect gas-exchanging units
Alveoli & pulmonary capillaries
-Smoking-related disease
Centrolobular emphysema
Affects the bonchioles
Initial preservation of alveoli
-AAT-related disease
Panlobular emphysema
Initial involvment of the peripheral alveoli
Later expansion into bronchioles
Vascular changes
-Thickening of pulmonary vessels
-Increase pulmonary pressure
Thoracic hyperinflation
-Air trapping
-Leads to flattening of diaphram
-Increases functional residual capacity
Air left in lung after exhalation
Symptoms
-Cough
-Sputum production
-Dyspnea
Physical exam
-Use of accessory muscles
-Increased resting respiratory rate
-Barrel chest
-Expiration through pursed lips
-Shallow breathing
Arterial blood gas
-Hypoxemia
-Hypercapnia
-Cyanosis
Pulmonary function tests (PFT)
-Airway obstruction --> Increase expiratory phase
-Forced Vital Capacity (FVC)
Normal = 4-6 seconds
Increased for COPD
-Forced Expiratory Volume in 1 second
Decreased in COPD
-Increased total lung capacity
FEV1.0/FVC
-<70% FEV1 - COPD
-Decreased in COPD
-<70% with
FEV1 of >80% Stage 1:mild
FEV1 50-80% Stage 2: moderate
FEV1 30-50% Stage 3: severe
FEV1 <30% or 50% with respiratory failure or right heart failure = Stage 4: severe disease