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COPD Definition
- -persistent airflow limitation
- -usually progressive
- -usually associated with an enhanced chronic inflammatory response in the airways and lung to noxious particles or gases
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Pink Puffer
- -Type A COPD
- -Predominantly emphysema
- Sx and Signs:
- -severe dyspnea
- -thin, wasted
- -NOT cyanotic
- -low/normal PaO2
- -low/normal PaCO2
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Blue Bloater
- -Type B COPD
- -Predominantly Bronchitis
- Sx and Signs:
- -cough and sputum
- -obese
- -cyanotic
- -low PaO2
- -High/normal PaCO2
- -Polycythemia
- -Cor pulmonale
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Mechanisms of Airflow Limitation
- 1. Small Airways Disease
- -airway inflammation
- -airway fibrosis, luminal plugs
- -increased airway resistance
- 2. Parenchymal Destruction
- -loss of alveolar attachments
- -decreased elastic recoil
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Chronic Bronchitis
- -presence of chronic productive cough for 3 months within 2 successive years
- -exclude other causes
- Pathology:
- -airways narrowed by plugged and swollen mucous membranes
- -mucus and pus impede action of respiratory cilia
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Emphysema
-abnormal permanent enlargement of the air spaces distal to the terminal bronchioles -accompanied by destruction of bronchiole walls and without obvious fibrosis
- Pathology:
- -destruction of the alveolar wall damages pulmonary capillaries by tearing, fibrosis or thrombosis
- -walls of individual sacs torn (not repairable)
- -enlarged air sacs due to destruction of alveolar walls (Bullae)
- -inelastic collapsible bronchioles
- Gross Pathology:
- -large holes in parenchyma
- -hyperinflated (larger)
- -black deposits
- (vs. bronchitis)
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Features that distinguish COPD from asthma
Cell: NPs, CD8 T cells
Mediators: LTB4, IL8, TNFa
- Consequences:
- -squamous metaplasia of epithelium
- -parenchymal destruction
- -mucus metaplasia
- -glandular enlargement
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Alpha1- Antitrypsin Deficiency
-1-2% of patients with emphysema
- S variant:
- -28% of southern europeans
- -AAT levels = 60%
- -NO PULMONARY EFFECTS
- Z Variant:
- -severe ATT deficiency (10%)
- -accumulation of ATT in RER of liver
- -predisposed to: juvenile hepatitis, cirrhosis and HCC
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COPD Pathophysiological Features
- 1. Airflow Limitation
- -bronchoconstriction
- -mucus hypersecretion
- -loss of elastic recoil
- -airway narrowing
- 2. Inflammation
- -increased neutrophils
- -increased macrophages
- -increased CD8 T cells
- -increased IL8 and TNFa
- -protease/antiprotease imbalance
- 3. Structural Changes
- -alveolar destruction
- -gladular hypertrophy
- -airway fibrosis
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COPD Epidemiology
-COPD deaths have increased steadily since the 1940s, preceded by a parallel increase in cigarette smoking 40 years earlier
- -prevalence: 10-20% >55 years
- -3rd leading cause of death in the US
- -COPD mortality is increasing (vs. accidents, heart disease)
- -not an "old man's disease" anymore
-Subclinical COPD is more common than clinical COPD
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Risk Factors for COPD
- -Genes
- -Infections
- -Socioeconomic status
- -Aging populations
- -CIGARETTE SMOKE
- -occupational dust and chemicals
- -indoor/outdoor air pollution
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Increasing burden of COPD
- -increase in tobacco use (esp in women and developing countries)
- -more ppl are living into the COPD age range
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COPD Risk and Smoking Cessation
Quitting smoking can decrease the rate of progressive decline in FEV1
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COPD Spirometry
Decreased FEV1 and FVC (reflects severity of COPD)
FEV1/FVC < 0.70
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Classification of COPD
- Mild: FEV1 > 80% predicted
- Moderate: 50% < FEV1 < 80% predicted
- Severe: 30% < FEV1 < 50%
- Very Severe: FEV1 < 30% predicted
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COPD Therapy by Stages
- Mild:
- -reduction of risk factors
- -short acting bronchodilator
- Moderate:
- -add regular tx with 1+ long acting bronchodilator
- -add rehabilitation
- Very Severe:
- -add long term O2
- -consider surgery
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Goals of Treatment
- 1. Prevention
- -slow progression
- -maintain function
- -minimize complications
2. Reduce sx
3. Improve fxn
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Treatment of COPD
- 1. Stop smoking
- 2. Meds (BDs, Steroids)
- 3. O2
- 4. Vaccination
- 5. Rehabilitation
- 6. Surgery: LVRS, Transplant
- 7. Disease Modification?
* None of existing meds has been shown to modify long term decline of lung fxn
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Bronchodilators
-Rx as needed or on a regular basis
-principally: Beta2-agonists, anticholinergics, theophylline, combo therapy
-can combine classes
-long acting bronchodilators are convenient and more effective for sx relief than short acting bronchodilators
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Corticosteroids
-regular tx (improves sx, lung fxn, QOL, reduces exacerbation)
-in pts with FEV1 < 60%
-increased risk of pneumonia
-chronic treatment should be avoided
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Pulmonary Rehabilitation
- -exercise training programs
- -improve exercise tolerance
- -improve sx of dyspnea and fatigue
-individually tailored
-GOAL: restore pt to highest level of independent function
-improve disability not necessarily change disease process
- CONTENT:
- -education
- -chest physiotherapy
- -psychosocial support
- -exercise
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O2 Therapy
-longer term in pts with chronic resp failure
-can increase survival in pts with resting hypoxemia (PaO2 < 55)
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COPD Comorbidities
- CV disease
- Osteoporosis
- Respiratory infections
- Anxiety and Depression
- Diabetes
- Lung Cancer
- Weight Loss/Gain
- Nutritional Abnormalities
- SKM dysnfunction
- Sleep Apnea
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