7. Emphysema & Chronic Bronchitis - Cox

Cards (41)

  • COPD subset - triad
    • emphysema
    • chronic bronchitis
    • asthma - transient
  • Chronic Obstructive pulmonary disease (COPD) - airway restriction causing respiratory issues
  • COPD - typical symptoms
    • cough
    • breathlessness
    • wheeze
  • Global initiative for chronic obstructive lung disease defines
    • airflow limitation that is not fully reversible
    • abnormal inflammatory response to inhaled noxious gases
    • usually progressive
  • COPD pathophysiology
    • airflow obstruction due to
    • inflammation, fibrosis -> airway narrowing
    • excess mucus production -> airway obstruction
    • disrupted airway structural support -> airway collapse
  • Emphysema - abnormal permanent air space enlargement distal to terminal bronchioles
  • Classical key concept of emphysema - irreversible acinar damage
  • Emphysematous process - alveolar septal destruction --> elastin degradation
    • alveolar wall destruction leading to
    • impaired expiratory airflow
    • progressive alveoli air trapping
    • impairs gas exchange
  • emphysema can lead to alveolar wall destruction that can cause alveoli air trapping
    • alveolar hyperinflation or ballooning
  • What is an established risk factor for emphysema?
    smoking
  • what gene can lead to emphysema?
    alpha-1 antitrypsin deficiency (AATD)
  • Emphysema pathophysiology - due to inflammatory reaction
    1. reactive oxygen species
    2. immune mediated tissue damage
    3. proteolytic matrix metalloproteinase
    4. elastase
    5. proteolytic elastin degradation
  • emphysema - immune mediated reaction will cause remodeling
    • leading to airway narrowing
    • due to smooth muscle hypertrophy
    • goblet cell hyperplasia --> mucus hypersecretion
  • Emphysema remodeling will cause small airway narrow in expiration
    • leading to outflow obstruction
    • decrease elastin - which normally maintain airway during expiration
    • increase mucous secretion - plug airway
  • Emphysema will cause poor expulsion of air during expiration
    • air trapped in alveoli
    • **hyperinflation
  • Emphysema - air trapping
    • diminished structural/tethering support --> impaired alveolar expiration
    • trapping worsen by mucus build up --> ** expiratory plugging
    • air becomes trapped in alveoli causing alveolar hyperinflation
  • Emphysema - gross - can be described as
    • alveolar wall destruction - thin and delicate walls without intervening fibrosis
    • honeycomb fibrosis subpleural lung parenchyma
  • Emphysema - honeycomb fibrosis subpleural lung parenchyma
    • abnormal air spaces due to alveolar wall destruction and dilation
    • small airways separated by fibrous bands tissue
  • Emphysema - histopathology
    • airspace enlargement
    • fragmented alveolar wall due to acinar destruction
  • Lung hyperinflation - decrease x-ray attenuation
    • radiolucent lungs
  • Highly specific sign for COPD - hyperinflated lung compression
  • Emphysema presentation - pink puffer
    • due to severe constant dyspnea or tachypnea ("puffing")
  • Emphysema - Pink puffer is due to
    • severe constant SOB
    • trapping/decrease recoiling --> poor air exchange
    • body will try to compensate bad ventilation by
    • accessory muscles
    • hyperventilation
    • pursed lip breathing
  • ** Emphysema - pink puffer will have pursed lips
    • to try to maintain positive end pressure
    • to preventing airway collapse
  • dyspnea in people with emphysema will cause respiratory muscle fatigue due to increase use
    • flat diaphragm also impair respiratory excursions
  • why are people with emphysema initially called pink puffer?
    • noncyanotic due to matched V/Q defect
    • no hypoxemia
    • but progressive capillary loss will lead to poor gas exchange leading to hypoxemia and tissue hypoxia
  • Emphysema will progress from pink puffer to hypoxia
    1. perfusion drops (↓V/↓↓↓Q)
    2. poor gas exchange
    3. arterial hypoxemia
  • Chronic hypoxia in emphysema will eventually lead to cor pulmonale
    1. chronic hypoxia
    2. vasoconstriction
    3. pulmonary HTN
    4. cor pulmonale
  • People with emphysema will have hyperinflation
    • diminished breath sounds
    • hyper-resonant percussion
  • People with emphysema will also be thin why?
    • inadequate oral intake
    • muscle and fat atrophy
    • high levels of inflammatory cytokines will worsen wasting
  • Chronic bronchitis is defined by
    • cough and sputum > 3 month/year period of 2 consecutive years
    • rule out other causes of chronic cough
    • common observed symptoms - productive cough
  • Chronic bronchitis - productive cough
    • associated with large airway mucus producing glands hypertrophy
    • sputum production
    • progressive airflow limitation or remodeling
  • The most common risk factor for chronic bronchitis is?
    smoking
  • Chronic bronchitis can cause hypoxia leading to pulmonary HTN
    • causing cor pulmonale
  • Chronic bronchitis histopathology
    • Early
    • mucus hypersecretion in large airways
    • hypertrophy of submucosal glands
    • Late
    • small airway epithelial goblet cell proliferation --> airway obstruction
    • reid index - increase percentage bronchial wall submucosal mucous glands
    • index directly correlates with sputum production
  • Chronic bronchitis - presentation - blue bloater
    • cyanotic (blue)
    • V/Q mismatch
    • inadequate blood oxygenation (hypoxemia)
    • most prominent lips and nail beds
  • Chronic bronchitis - Presentation
    • Volume overload
    1. pulmonary HTN
    2. RV hypertrophy
    3. RV failure
    4. poor LV filling with decrease CO
    5. induction of RAAS
    6. Na and H2O retention
  • Chronic bronchitis
    • lots of sputum production
    • produced by goblet cells
    • cough - mucus hypersecretion
    • wheeze - airway obstruction due to turbulent airflow
    • rhonchi - gurgling sound due to mucus hypersecretion in airway
  • What is used to diagnosis COPD?
    spirometry
  • COPD pulmonary function
    • increase resistance to expiratory airflow due to small airway obstruction
    • increase in lung compliance
    • decrease in lung elasticity