COPD Flashcards
chronic obstructive pulmonary disease
What is COPD?
- progressive development of airflow limitation.
- most irreversible with current medication
- airflow limitation: progressive and results from an abnormal response of the lungs to noxious particles or gases.
- blockages: anywhere from bronchi to respiratory
chronic obstructive bronchitis
due to fibrosis of small airways (< 2 mm internal diameter)
Emphysema
enlargement of alveoli and destruction of alveolar walls
COPD triggers
- triggered by cigarette smoke and environmental factors over many years
- cells trigger immune response
- macrophages have key roles
- chronic inflammation
- leads to irreparable tissue damage
- development of COPD
Oxidative Stress and COPD
cigarette smoke/ environmental triggers = increased oxidative stress and increased reactive oxygen species (ROS).
defective phagocytosis
COPD - macrophages are defective at phagocytosing bacteria, an impaired ability to carry out efferocytosis of apoptotic cells - results in failure to resolve inflammation.
Acute Bronchitis
= inflammation of the large bronchi (medium sized airways) in the lungs that is usually caused by viruses or bacteria and may last several days or weeks.
Chronic Bronchitis
= presence of chronic bronchial secretions, enough to cause expectoration, occurring on most days for a min of 3 months of the year for 2 years.
- increased secretion of mucus due to inflammation - can lead to further obstruction of the airways and an increased likelihood of bacterial infection.
COPD
- increased mucus production
- enlargement of mucus secreting glands
- increased goblet cell number
- inflammatory cell proliferation
COPD Pathophysiology
chronic bronchitis - inflammation of the airways
- reduced lumen diameter
- loss of ciliated epithelial function
Emphysema pathophysiology
- Alveoli can become distended and form large air filled spaces.
Emphysema characteristics
Loss of elasticity
- reduced alpha1 - anti-trypsin an ‘anti’ protease resulting in destruction of elastic fibres
- acquired- tobacco smoking
- intrinsic - A1 anti-trypsin deficiency (associated with liver dysfunction).
Collapse of alveoli
- loss of reticular structure
- loss of associated vasculature
Pathogenesis of Exacerbations
- episodes of symptoms worsening
- acute events
- increased airway inflammation and systemic inflammatory effects and can last from days to 12 weeks
- major cause of hospital admissions
- triggered by respiratory viral infections
- pollutants that reach airways may be associated with precipitating exacerbations
COPD Exacerbations
- worsening breathlessness
- increased sputum volume and purulence
- cough/wheeze
- fever without obvious source
- upper respiratory tract infection in the past 5 days
- increased respiratory rate or HR increase above 20% above baseline.
Treatment of COPD
symptom reduction
- pulmonary rehabilitation and physical exercise
- short acting inhaled bronchodilators
- one long acting inhaled bronchodilator (LABA / LAMA)
- LABA - LAMA combination
risk reduction
- one long acting bronchodilator
- ICS - LABA combo
- LABA - LAMA combo
- Roflumilast
