| What is COPD? | Preventable and treatable disease with extrapulmonary effects, pulmonary airflow limitation not fully reversible, progressive and associated with inflammatory response of lung to noxious particles/gases. |
| How is the epidemiology of COPD? | 3rd cause of morbidity and mortality in world, 4-10% of people worldwide, among smokers:15% (in lebanon 9.7% of population, only 20% were diagnosed and treated) |
| What are risk factors of COPD? | Smoking is well known cause, others include : dust exposure, animal farming, crop farming, chemical exposure, diesel exhaust, road dust
80% of COPD is due to smoking, rest is exposure other than smoking
Host factors: genetics (AAT deficiency >90% homo ZZ)
gender (male more risk), socioeconomic (low), BHR (strong predictor), atopy and asthma, childhood illnesses
Pipe and cigars have lower risk than cigarettes. |
| How is pathophysiology of COPD? | Structural changes in both large and small airways and parenchyma, inflammation of submucosal glands and hyperplasia of goblet cells (chronic sputum production)
Airway remodeling and emphysema (poorly reversible airflow obstruction)
Smooth muscle contraction, airway inflammation, mucus accumulation and plasma exudate (reversible airflow limitation)
Most charcateristic COPD change is airway narrowing (inflammation by cigarette smoking repeated cycle of injury and repair of peripheral airways, thus emphysema , and loss of elastic recoil of lung, poor expiration and airflow obstruction)
(emphysema is broken alveolar walls attachements) |
| What are inflammatory cells seen in COPD? | Neutrophils (potent chemokines IL8 and LTB4 attract neutrophils, increased in sputum and BAL fluid not airway walls, correlate with COPD severity, secrete proteinases (elastase and proteinase-3-A cause of mucus hypersecretion)
Macrophages (activated by cigarette smoking, increased in sputum, BAL and lungs, release pro-inflammatory cytokines and proteinases)
T cells (increased in airway walls, shift in balance of CD4/CD8 towards CD8, found in large and small airways and parenchyma and arteries, correlated with airflow obstruction |
| What are proteinases responsible for in COPD? | They are involved in alveolar wall destruction.
Smokers have high neutrophil elastase (NE) and BAL fluid, higher with emphysema, degrades elastic tissues
Matrix metalloproteinases (MMPs) can degrade whole matrix.
Collagen breakdown results in emphysema |
| How does a1 antitrypsin deficiency cause COPD | imbalance between NE and antitrypsin causes elastin destruction.
Antitrypsin is elastase inhibitor and protects against proteolytic degradation of elastin |
| What is GOLD standard of COPD? | number of airways, as it decreases we go up in score, stage 0 (no obstruction), stage I (140 airways), stage II (less) stage III and IV even less |
| Describe the pathophysio of COPD in small, large airways and parenchyma? | Large airways (mucus hyper, neutrophils sputum, epithelia metaplasia, macrophage, CD8, smooth muscle hyperplasia)
Small airways (inflammatory exudate, emphysema, inflammatory wall thickening, fibrosis, lymphoid follicle (if severe))
Parenchyma (alveolar wall destruction, loss of elasticity, destruction of capillary bed, increased inflammatory cells) |
| What are symptoms of COPD? | Chronic progressive SoB (air hunger/ sensation of grasping air)
Variable sputum production and cough (chronic, usually first symptom), usually seen daytime symptoms (not night or early) |
| What are signs of COPD? | PE finding varies with severity, initially minor wheezing with prolonged expiration.
More progress: thin cachectic appearance Barrel-shaped chest
Severe cases: accessory muscle use, retraction of intercostal spaces, pursed-lip breathing and severe wheezes (expiratory) + Tripod position |
| What are tests in COPD? | FEV1/FVC -> <0.7 (obstructive airway disease)
This occurs since increased intrathoracic pressure during expiration can lead to collapse of airways during expiration, so amount of exhaled air is decreased in first second (FEV1) while FVC remains same |
| What happens to lung volumes in COPD? | Initially stable, more severe obstruction we get airtrapping and later hyperinflation
Manifested as increase in total lung capacity (TLC) (hyperinflation) and increased residual volume (air-trapping)
Diffusion capacity (DLCO) usually normal, but can decrease due to emphysema |
| What are image findings in COPD? | Barrel Chest (Lateral CXR), flat diaphragm bullae, lucency of lung)
CT shows emphysema |
| How is diagnosis of COPD? | Must be confirmed by spirometry to detect obstruction (FEV1/FVC <0.7)
ACP, GOLD and NICE guidelines dx made by hx and PE and confirmed by spirometry |
| How is classification of severity of COPD? | According to number of symptoms, exacerbation hx, and severity of obstruction.
4 categories (A: mild-mod obstruction, min symptoms and few exacerbations
B: mild-mod obstruction, severe symptoms and few exacerbations
C: severe obstruction, min symptoms and many exacerbations
D: severe severe severe all |
| How is management of pt with stable COPD? | Pharmacotherapy (bronchodilators, phosphodiesterase inhibitors, theophylline, chronic Abx, PPIs)
Reduction of risk factors (smoking)
Indication for home oxygen therapy
Non-invasive ventilation (NIV), lung volume reduction surgery, lung transplant
No long term drug, just symptom relief drugs |
| When do we indicate supplemental O2? | Arterial hypoxemia (PaO2 < 55 mmHg/ SaO2 <88%)/ PaO2 btw 55-60 with right heart failure/ erythrocytosis.
give supplemental O2 keep SaO2 >90% recheck in 60-90 days |
| Do smokers and non-smokers and smoker cessators have same risk? | Just when you smoke, you are at risk higher than non-smoker even if you stopped after 10 years, or 25 years
Still same decline, while non-smokers won't have this decline. |
| What is COPD exacerbation? | An acute event characterized by worsening of pt respiratory symptoms that is beyond normal day-to-day variation leads to change in medication
Cough increase frequency, sputum production increase, dyspnea increase. |
| What are factors associated with increased risk of exacerbations? | Increased age, airway obstruction severity, bronchial mucus hypersecretion, longer COPD duration, productive cough and wheeze, Abx/ Corticosteroid use in past year, bacterial colonization, poor healthy QoL |
| How is epidemiology of exacerbation? | Its frequency increases with the decline of FEV1, associated with more rapid decline in pulmonary function
50% caused by bacteria, 30% by viruses, 15% pollution, 5% atypical bacteria (C.pneumonia) |
| How is management of COPD exacerbation? | O2 if SaO2<89%, IV corticosteroids, bronchodilators, IV Abx, NIPPV (if hypercapnic with respiratory acidosis), fulminant failure need mechanical ventilator |
