Pathophysiology Of COPD Flashcards
COPD Context (4)
o COPD = the 4th leading cause of death worldwide
o 35,000 deaths/year in UK (3 million worldwide)
o 380 million people estimated to have COPD worldwide
o Significant economic burden (working days lost, expense of treatments/care)
What is Chronic Obstructive Pulmonary Disease? (4)
COPD = term used for a mixture of chronic bronchitis, irreversible airway obstruction, and emphysema, that encompasses a long-term, progressive, and accelerated decline in respiratory function.
o >95% of COPD associated with long-term tobacco smoke exposure
o ≈20% of long-term smokers develop COPD (need vulnerability to actually get it)
o Other factors = genetic (e.g. Alpha-1 antitrypsin deficiency) and environmental hazards (e.g. pollution)
How does smoking reduce respiratory function and lead to COPD?
images EXPLAINING SMOKING AND COPD
vicious cycle of tissue damage from cig/tobac
= All results in decreased rep function
COPD severity is defined and quantified by airway obstruction (FEV1) (3)
– Mild FEV1 50-80% predicted
– Moderate FEV1 30-50% predicted
– Severe FEV1 <30% predicted
It can
Why do you think FEV1 (vs. predicted) is used in COPD rather than FEV1/FVC? (2)
Chronic Bronchitis: Signs, Symptoms and Diagnosis (5)
Symptoms:
o Chronic productive cough
o Consistent sputum production
o Dyspnoea (especially on exertion)
Signs:
o Airflow obstruction (↓FEV1 & wheeze) mostly affecting large/proximal airways
Diagnostic criteria:
o “A sputum-producing cough on most days for a 3 months period, for 2 consecutive years”
Pathological features of large airways in COPD (chronic bronchitis) (7)
Thickening of airway wall (smooth muscle hyperplasia, fibrosis)
Mucus hypersecretion (↑ goblet cells +↑ mucus gland activation)
Inflammation, immune cell infiltration
Loss of attachment providing radial traction
o Impaired mucociliary clearance = increased risk of infection = recurrent infection
o Irritation of sensory neurons = cough
o Decreased luminal area = increased airway resistance and airway obstruction
Emphysema: Symptoms, Signs and Diagnosis (5)
Symptoms:
o Progressive dyspnoea with minimal cough/sputum
o Hyperinflation of lungs
Signs:
o Hypoxemia
o Increased lung compliance
Diagnostic criteria:
o “Abnormal permanent enlargement of distal airspaces accompanied by destruction of their walls without obvious (mice study)
What pathological features are observed within the lungs of COPD patients? (2)
Decreased surface area + perfusion = ↓ gas exchange
Loss of elastin fibres = ↑compliance, ↓recoil
Measuring extent of Emphysema (3)
- CT scanning
- Pulmonary function testing:
– Increased residual volume
– Reduced gas transfer: (TLCO/KCO)
Small airway disease - additional (yr3) pathphys (3)
o Feature of COPD district from chronic bronchitis (large airways) and emphysema (alveoli/acini)
o Constitutes from pathology within “small” airways, i.e. airways <2mm diameter, between 4th and 13th generation of airway branching (1st generation = trachea, 23rd = alveoli)
o Further reduces airflow, increases gas trapping, and reduces ventilatory capacity of respiratory system
Path features of small airways disease (6)
- Thickening of airway wall (smooth muscle hyperplasia, fibrosis)
- Mucus hypersecretion (↑ goblet cells +↑ mucus gland activation)
- Inflammation, immune cell infiltration
- Loss of attachment providing radial traction
o Impaired mucociliary clearance = increased risk of infection = recurrent infection
o Decreased luminal area = increased airway resistance and airway obstruction
70 year old male (smoker; ≈50 pack years). Coughing for past 2 years. His
cough is productive of yellow sputum. He has noticed that he is getting more
easily breathless and fatigued; he now finds it hard to walk up stairs without
his breathing becoming extremely laboured.
On examination, he is:
o Barrel chested, breathing through ‘pursed lips’
o Oxygen Saturation: 90% on room air, PaCO2 = 7 kPa (normal = 4.9 - 6.0)
o Wheeze throughout chest, increased residual volume, FEV1 = 55% of
predicted value.
o Haematocrit = 59% (40-54% in males), Right ventricular hypertrophy
How can we explain these changes, symptoms, and signs by relating them to
the pathology we have discussed?
SMALL AIRWAYS DISEASE
Why do patients with COPD have “barrel” chests? (6)
The normal ratio of anteroposterior diameter to transverse diameter within the chest = 1:2(oval shape)
In patients with barrel chest, this ratio approaches 1:1(circle)
The transverse shape of the chest basically goes from oval to circular.
Small airways disease + emphysema = lungs with reduced recoil and airways that collapse during expiration.
This causes “air-trapping”, a greater volume of air than normal is left in the lungs at the end of expiration (increased residual volume).
Tidal volume then has to occur ‘on top of’ the increased residual volume.
Why do patients with COPD breathe through ‘pursed lips’? - mechanism (4)
Pursed lips generate increased resistance to the outflow of air
↓
This helps to prevent airway collapse by increasing airway pressure
↓
An increased volume and rate of air can be expired
↓
Patient able to breathe more normally
