COPD Flashcards
COPD Definition
Characteristized by chronic airflow limitation which is not fully reversible
Includes:
- Emphysema: destruction and enlargement of alveoli
- Chronic bronchitis: chronic cough and phlegm production
- Small airway disease: narrowing of small bronchioles
Risk Factors
Cigarette smoking
Asthma (increased airway responsiveness)
Occupational exposures, air pollution (indoor and outdoor), and second hand smoke (less important than smoking)
α1 Antitrypsin Deficiency
GERD
Other associations: age, FHx of COPD, and low SES
Molecular Pathogenesis of COPD
Inflammation
- Smoking activates epithelial cells and alveolar macrophages, and destroys cilia
- Neutrophils and macrophages are recruited and accumulate in alveoli and respiratory bronchioles, leading to the accumulation of pus.
- Loss of cilia leads to decreased clearing of the inflammatory cells.
- Neutrophils and macrophages release free radicals, inhibiting antiproteases, and leading to the destruction of tissue (**ECM Degradation) **edema, and mucus hypersecretion.
Cell Death–Both cells and matrix disappear leading to airspace enlargement
Ineffective Repair– Limited ability to repair alveolar damage
Pathology of COPD (Large airways, small airways, parenchyma)
Large Airways
- Squamous metaplasia in bronchi (dec’d ciliary clearance of mucus)
- Hypertrophy of bronchial smooth muscle, therefore bronchial hyperreactivity and air flow obstruction
Small Airways
- Clara cells (surfactant) replaced by goblet cells (mucus)
- Airway narrowing secondary to fibrosis, edema, cellular inflammation, mucus
- Loss of patency secondary to loss of parenchyma
Parenchyma
- Destruction fo respiratory bronchioles, alveolar ducts, and alveoli (gas exchange surfaces)
- Loss of elastic recoil (affects the bellows function0
Bellows function
Impaired movement of air due to decreased elastic recoil and support for airways (inc’d resistance)
Obstructive pattern on spirometry
Changes in Lung Volumes in COPD and its Effects
Air trapping because decreased elastic recoil leads to incomplete expiration. This increases residual volume.
Therefore, hyperinflation occurs, increasing the work of breathing as diaphragm flattens
Because of the air trapping, VQ mismatches occur.
Pulmonary HTN occur, which may lead to cor pulmonale and RV failure
Type A vs. Type B
Type A:
- Dry emphysema: cough, dyspnea, barrel chest, CXR with hyperinflation.
- No fibrosis and decreased pulmonary vasculature
- Prognosis good
Type B:
- Wet emphysema: severe cough with copious sputum production; rales; wheezing; cyanosis.
- Moderate hyperinflation on CXR and dyspnea later
- Fibrosis in lower lobes, increase in central pulmonary vascularity
COPD Recap (Reference)
- airflow limitation (loss of elastic recoil and supporting tissue)
- airflow obstruction (mucus hypersecretion, mucus plugging, airway edema, bronchospasm)
- increased work of breathing (increased airway resistance, hyperinflation) may lead to alveolar hypoventilation, hypocapnia, and hypoxia
- also, hypoxia from V/Q mismatch
- hypoxemia → increase pulmonary vascular tone → pulmonary hypertension→ cor pulmonale
Diagnosis
**Dyspnea **
- Most significant presenting symptom. Described variably
- Modified Medical Research Council Questionnaire for Assessing the Severity of Breathlessness
Cough
- Chronic cough that is progressive (intermittent to throughout the day)
**Sputum Production **
- regular sputum production in three or more months in 2 consecutive years (chronic bronchitis definition)
- Often small amounts of tenacious sputum. Purulent sputum suggests inflammation
- Large volumes of sputum may suggest bronchiectasis
Wheezing and Chest Tightness
- Non-specific, more commonly found in severe COPD
- Does not differentiate between COPD and asthma, or rule in or r/o either
Physical Exam
No specific findings, only suggestive
Hyperinflation of chest/barrel chest
Use of accessory muscles, paradoxical lower rib movement, reduced expansion
Pursed lip breathing, prolonged expiration
Distant breath sounds, hyperresonant chest
Signs of cor pulmonale: peripheral edema, elevated JVP, hepatomegaly
Signs of hypoxemia
Cachexia
Ancillary Examinations (tests)
Spirometry to measure airflow obstruction
CXR to r/o other pathologies
Hemoglobin (anemia or polycythemia)
CT if sxs > PFTs
EKG, echo
Oximetry
Differential Diagnosis
Asthma
Bronchiectasis
Obliterative bronchitis
CHF
Upper airway lesions, including LCA
Treatment Goals of COPD
Control sxs
Improve exercise tolerance
Decrease frequency and severity of exacerbations
Management of Stable COPD
Spirometry should be used to screen and diagnose airflow obstruction.
Avoid Risk Factors
Influenza vaccine annually
Pneumococcal polysaccharide vaccine (S. pneumo)
Treat complications
Pulmonary Rehab: improves survival, quality of life (inc’d exercise tolerance, reduces hospitalizations, psychosocial benefit, benefits extend beyond period of training)
Changes in quality of life
Depression due to changes in exercise tolerance, difficulty with “just trying to breathe,” etc.
Social isolation as activity becomes more difficult, oxygen apparatus limits movements, etc.
