COPD Flashcards
What are the major types of COPD?
Chronic Obstructive Pulmonary Disease (COPD) is a progressive, irreversible airway obstruction due to chronic bronchitis or emphysema.
What define the two major types of COPD?
- Chronic Bronchitis: Productive cough for at least 3 months over 2 consecutive years.
- Emphysema: Alveolar destruction due to excess protease activity.
What is the primary cause of COPD?
Cigarette smoking is the most common cause of COPD.
What are the major risk factors for COPD?
- Smoking
- Alpha-1 antitrypsin deficiency
- Environmental/occupational exposure
- Air pollution
- Secondhand smoke
- Chronic poorly controlled asthma
What is the most common cause of COPD?
Smoking.
What is the key pathophysiologic process in emphysema?
Destruction of alveolar walls due to excess protease activity, leading to air trapping and loss of elastic recoil.
What is the difference between centrilobular and panlobular emphysema?
Centrilobular: Seen in smokers, affects upper lobes.
Panlobular: Seen in alpha-1 antitrypsin deficiency, affects lower lobes.
What are the symptoms of COPD?
Dyspnea, chronic cough, sputum production, wheezing, and chest tightness.
What are the classic physical exam findings for chronic bronchitis?
Prolonged expiration, wheezing, coarse crackles, cyanosis (‘blue bloaters’).
What are the classic physical exam findings for emphysema?
Decreased breath sounds, hyperinflation, barrel chest, pursed lip breathing (‘pink puffers’).
What imaging findings are seen in COPD on chest X-ray?
Hyperinflation, increased lung translucency, flattened diaphragm, and subpleural blebs.
What is the gold standard for diagnosing COPD?
Pulmonary Function Tests (PFTs).
What is the hallmark of COPD on PFTs?
- FEV1/FVC ratio <0.7
- Decreased FEV1
- Increased total lung capacity (TLC)
- Increased residual volume (RV)
- Decreased DLCO in emphysema
What is the GOLD classification for COPD severity?
- Mild (FEV1 ≥80%)
- Moderate (FEV1 50-79%)
- Severe (FEV1 30-49%)
- Very severe (FEV1 <30%)
What is the stepwise treatment for COPD according to GOLD stages?
- Mild (FEV1 ≥80%): SABA (Albuterol)
- Moderate (50-79%): SAMA or LAMA (Ipratropium, Tiotropium)
- Severe (30-49%): Add Inhaled Corticosteroids (ICS)
- Very Severe (<30%): Add Home Oxygen Therapy
What is the mMRC dyspnea scale?
0: shortness of breath with strenuous activity
1: shortness of breath with heels or brisk walk
2: walk slower than others of the same age at a slower pace
3: takes a break after 100 yard walk
4: shortness of breath while dressing and can’t leave the house due to symptoms
0-1 with one exacerbation is class A so give LAMA with as needed SABA
2 or more with one exacerbation is class B so give LAMA+LABA with as needed SABA
2 or more exacerbations or 1 hospitalization is class E so give LAMA+LABA with as needed SABA with ICS
What is the role of SABAs and LABAs in COPD?
SABAs (Albuterol) for acute relief, LABAs (Salmeterol, Formoterol) for maintenance therapy.
What is the role of SAMAs and LAMAs in COPD?
SAMAs (Ipratropium) and LAMAs (Tiotropium, Aclidinium) provide long-term bronchodilation by blocking muscarinic receptors.
When should inhaled corticosteroids (ICS) be added in COPD treatment?
For patients with frequent exacerbations (GOLD Stage 3 or 4).
What is Roflumilast and when is it used?
A phosphodiesterase-4 inhibitor used in severe COPD with chronic bronchitis to reduce exacerbations.
When is home oxygen therapy indicated in COPD?
When FEV1 is less than 30% or If PaO2 <55 mmHg or SpO2 <88% (or <60 mmHg or SpO2 <92% if the patient also has polycythemia, CHF, or pulmonary hypertension).
What defines a COPD exacerbation?
An acute worsening of symptoms with increased cough, sputum production, or dyspnea.
What are common triggers of COPD exacerbation?
- Respiratory infections (most commonly Haemophilus influenzae)
- Environmental irritants
- Noncompliance with treatment
- Cardiac events
How is COPD exacerbation managed?
- Bronchodilators: SABA (Albuterol) + SAMA (Ipratropium)
- Systemic corticosteroids: Prednisone (5-7 days)
- Oxygen therapy: Maintain SpO2 88-92%
- Noninvasive positive pressure ventilation (NIPPV) if needed
When should noninvasive ventilation be used in COPD exacerbation?
If pH <7.35 or CO2 >45 mmHg with respiratory distress.
What is the role of magnesium sulfate in COPD exacerbation?
Used in severe exacerbations as a bronchodilator to reduce airway resistance.
When are antibiotics indicated in COPD exacerbation?
If 2 of 3 symptoms are present: increased dyspnea, sputum volume, or sputum purulence.
What antibiotics are used for uncomplicated COPD exacerbation?
Azithromycin or 2nd/3rd gen cephalosporins (Cefpodoxime, Cefuroxime).
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Complicated COPD exacerbation includes age greater than 65, and FEV1 less than 50%, or more than two exacerbations in a year.
What antibiotics are used for complicated COPD exacerbation (FEV1 <50%, >2 exacerbations/yr)?
Levofloxacin or Cefepime to cover Pseudomonas.
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Complicated COPD exacerbation includes age greater than 65, and FEV1 less than 50%, or more than two exacerbations in a year.
How does DLCO change in COPD?
DLCO is decreased in emphysema due to alveolar destruction but remains normal in chronic bronchitis.
How does DLCO differ in other lung diseases?
Decreased: Emphysema, pulmonary fibrosis, pulmonary hypertension.
Normal: Chronic bronchitis, asthma.
Increased: Polycythemia vera, pulmonary hemorrhage.
What is the most important intervention to improve COPD survival?
Smoking cessation. The other therapy that lowers mortality is home oxygen.
How does smoking cessation improve a patient’s FEV1?
In healthy persons who never smoke, lung function peaks at approximately age 30. Afterward, there is a gradual decline in forced expiratory volume in 1 second (FEV,) of approximately 25 mL/year. In the average person who smokes tobacco, the rate of lung function declines approximately 3 times faster.
Cigarette smoke contains numerous toxins (eg, formaldehyde, acrolein) that provoke inflammatory proteolytic damage to the airways and alveoli. These changes are responsible for airway inflammation and narrowing (chronic bronchitis: increase airway resistance) and alveolar septal destruction (emphysema: decrease elastic recoil pressure). Together these conditions lead to expiratory flow limitation, typically measured as a reduction in FEV1. Once lost, lung function is not recoverable. However, smoking cessation can markedly slow the decline in FEV1. Within a year of complete abstinence, a successful quitter’s rate of FEV, decline returns to that of normally aging nonsmokers. Therefore, after a patient quits smoking, the slope of the FEV1 decline curve will decrease, but no function will be regained.
What is the best initial treatment for mild COPD?
Short-acting bronchodilator (SABA or SAMA).
Which COPD phenotype has decreased DLCO?
Emphysema.
Which COPD phenotype has normal DLCO?
Chronic bronchitis.
