COPD Flashcards
Define COPD
o Chronic condition
o Characterized by respiratory symptoms (cough, Exertional dyspnea) and airflow obstruction (reduced FEV1/FVC) that are incompletely reversible
Subdivided into:
• Chronic bronchitis
• Emphysema
Describe the epidemiology and natural history of COPD.
Epidemiology
o Majority cases = result from smoking
COPD Pathogenesis
• Leading cause = smoking
Evidence:
o Raises risk of death from COPD 20-30x
o COPD develops in 15% of smokers; only 2% of nonsmokers
o Autopsy evidence correlates with dose and duration
o Smokers at early age demonstrate respiratory bronchiolitis:
• Earliest pathologic abnormality in smokers
• Structural changes in bronchioles
• Inflammation
• Infiltrates of airway walls
• Goblet cell metaplasia
• Smooth muscle hypertrophy
• Fibrosis and narrowing
• Apparent site of obstruction in mild COPD
• Thought to be a precursor for emphysema
• Reverses with smoking cessation
Describe the epidemiology and pathogenesis of chronic bronchitis
Disease of airways (bronchi and bronchioles)
Hypersecretion of mucous → intralumenal blockage
Bronchi structural abnormalities:
• Inflammation
• Metaplasia of epithelium
• Expansion of submucosal glands
Clinically: chronic cough and sputum production
o Cough with sputum for at least 3 months per year for at least 2 consecutive years
Types:
Chronic simple bronchitis
• “Smoker’s cough”
• Meet above criteria but do not have airflow obstruction
Chronic obstructive bronchitis
• Have chronic productive cough associated with airflow obstruction
Describe the epidemiology and pathogenesis of emphysema.
Destructive process involving lung parenchyma
o Loss of alveolar attachments to bronchioles → can’t maintain airways → collapsible bronchioles
o Destruction of alveolar walls → airspace enlargement and loss of pulmonary capillaries
Defined anatomically
o Histology or CT scan
o Destruction of alveolar walls and loss of associated capillaries
o Enlargement of airspaces distal to terminal bronchioles (typically more affects upper lobe)
Universally present in advanced COPD
Clinical finding: dyspnea
Epidemiology
o Fourth leading cause of death in USA
o Second only to CAD as a Social Security compensated disability
Pathogenesis
o Smoke induces inflammation
o Activates macrophage = produce NCF (neutrophil chemotaxis factors = IL-8)
o Amplification by neutrophils
o Inflammation and protease (elastase) release → alveolar destruction
Genetic defect = alpha-1-antiprotease deficiency → early onset emphysema
Also: smoking decreases antiprotease activity
• Alpha-1-antiprotease is susceptible to oxidative inactivation
• With smoking = contains oxidants
• Get influx of neutrophils + mononuclear cells → release myeloperoxidase and ROS
• Result = reduces AAP activity
Explain the changes in PFT’s that occur in chronic bronchitis and emphysema.
- Invariable low FEV1/FVC and FEV1
- FVC may be normal (reduced in advanced cases)
- Absent or incomplete response to bronchodilators
Lung volumes
o Normal or increased TLC (hyperinflation)
o Normal or increased FRC
o Normal or increased RV (gas trapping)
Reduction in DLCO (diffusion capacity)
o Due to airspace enlargement = loss of surface area and capillaries
o Produces areas of high V/Q → increased dead space
o Result: minute ventilation (VE) must increase to maintain same alveolar ventilation (VA) and PaCO2
Blood gases:
o May have hypoxemia and hypercapnea
Explain the changes in lung volume that occur in chronic bronchitis and emphysema.
Decreased VC and FVC
o Slowing of expiratory airflow
o Premature airway closure at high lung volumes
o Result = increased RV
Hyperinflation
o Due to loss of elastic recoil → increased compliance
o Result = increased TLC and FRC
o Larger lung volume → reduces airway resistance → reduces frictional work
o BUT: diaphragm is shortened = mechanical disadvantage (length-tension relationship)
Explain the changes in oxygenation that occur in chronic bronchitis and emphysema.
Determinants of hypoxemia in COPD:
o V/Q mismatch (low V/Q units)
o Alveolar hypoventilation (CO2 retention)
o Low mixed O2 due to low CO in patients with RV failure secondary to PA hypertension
o Shunt typically NOT a major factor
PA hypertension Mostly result of alveolar hypoxia and resultant vasoconstricton o Other contributors: • Vascular bed obliteration (emphysema) • Increased blood viscosity (erythrocytosis) Compensatory RV hypertrophy RV failure (cor pumonale) • Peripheral edema • Jugular venous distention
Supplemental O2 corrects hypoxemia
Illustrate how to make a diagnosis of chronic bronchitis or emphysema.
COPD symptoms o Persistent and progressive dyspnea o Chronic productive cough o Transient periods of sputum discoloration o Wheezing o Lower extremity edema (cor pulmonale) o Orthopnea o Hemoptysis
Physical exam o May be normal o “Barrel chest” from hyperinflation o Hyperresonant percussion and low diaphragm o Diminished breath sounds o Prolonged expiratory phase o Rhonchi (coarse rattling), wheeze o Lower extremity edema, cyanosis, cachexia
Radiographic changes o May be minimal o Hyperlucency = decrease in peripheral vascular lung markings o Hyperinflation • Low flattened diaphragm • Increase in retrosternal airspace • Narrow, vertical cardiac silhouette o Bollous disease • Bulla = an airspace > 1 cm o Enlargement of pulmonary arteries (PA hypertension)
Pulmonary function tests
o Invariable low FEV1/FVC and FEV1
• Airflow obstruction that persists after inhaled bronchodilator
• FEV1/FVC < 0.70
o FVC may be normal (reduced in advanced cases)
o Absent or incomplete response to bronchodilators
o Lung volumes
• Normal or increased TLC (hyperinflation)
• Normal or increased FRC
• Normal or increased RV (gas trapping)
Reduction in DLCO (diffusion capacity)
• Due to airspace enlargement = loss of surface area and capillaries
• Produces areas of high V/Q → increased dead space
• Result: minute ventilation (VE) must increase to maintain same alveolar ventilation (VA) and PaCO2
Blood gases:
• May have hypoxemia and hypercapnea
• Low alveolar oxygen (PAO2) → pulmonary arteriolar constriction → increased pulmonary vascular resistance and pulmonary HT → right ventricular failure
• Treat with supplemental O2
Discuss the principles of management of chronic bronchitis or emphysema.
Prevention o Smoking cessation o Immunization against pneumococcus and influenza Bronchodilation o Anti-cholinergics o Beta-agonists o Theophylline Suppression of inflammation (corticosteroids) Treatment of hypoxemia (when PaO2 <55 mmHg) Exacerbation management o Associated with bacterial or viral lower respiratory tract infections o Treatment: • Systemic corticosteroids • Antibiotics • May need hospitalization • Ventilatory assistance Pulmonary rehabilitation
The Pink Puffer (Type A)
Clinical presentations of COPD o “Emphysematous” phenotype o Long history of Exertional dyspnea o Little sputum o Infrequent exacerbations o Hyperinflation o Use of accessory muscles o Pursed-lips breathing o Normal oxygenation o Thin; weight loss a problem
The Blue Bloater (Type B)
Clinical presentations of COPD o “Bronchitic” phenotype o Long history of cough and sputum production o Frequent exacerbations o Less dyspnea o Chronic hypoxemia o Pulmonary HT o Cor pulmonale o Right-sided HF o Normal habitus or obese
