L6 COPD

• -persistent airflow limitation
• -usually progressive
• -usually associated with an enhanced chronic inflammatory response in the airways and lung to noxious particles or gases

• -Type A COPD
• -Predominantly emphysema

• Sx and Signs:
• -severe dyspnea
• -thin, wasted
• -NOT cyanotic
• -low/normal PaO2
• -low/normal PaCO2

• -Type B COPD
• -Predominantly Bronchitis

• Sx and Signs:
• -cough and sputum
• -obese
• -cyanotic
• -low PaO2
• -High/normal PaCO2
• -Polycythemia
• -Cor pulmonale

• 1. Small Airways Disease
•      -airway inflammation
•      -airway fibrosis, luminal plugs
•      -increased airway resistance

• 2. Parenchymal Destruction
•      -loss of alveolar attachments
•      -decreased elastic recoil

• -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
• 

-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)

Cell: NPs, CD8 T cells

Mediators: LTB4, IL8, TNFa

• Consequences:
• -squamous metaplasia of epithelium
• -parenchymal destruction
• -mucus metaplasia
• -glandular enlargement

-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

• 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

-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

• -Genes
• -Infections
• -Socioeconomic status
• -Aging populations

• -CIGARETTE SMOKE
• -occupational dust and chemicals
• -indoor/outdoor air pollution

• -increase in tobacco use (esp in women and developing countries)
• -more ppl are living into the COPD age range

Quitting smoking can decrease the rate of progressive decline in FEV1

Decreased FEV1 and FVC (reflects severity of COPD)

FEV1/FVC < 0.70

• Mild: FEV1 > 80% predicted
• Moderate: 50% < FEV1 < 80% predicted
• Severe: 30% < FEV1 < 50%
• Very Severe: FEV1 < 30% predicted

• Mild:
• -reduction of risk factors
• -short acting bronchodilator

• Moderate:
• -add regular tx with 1+ long acting bronchodilator
• -add rehabilitation

• Severe:
• -add inhaled GCs

• Very Severe:
• -add long term O2
• -consider surgery

• 1. Prevention
•      -slow progression
•      -maintain function
•      -minimize complications

2. Reduce sx

3. Improve fxn

• 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

-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

-regular tx (improves sx, lung fxn, QOL, reduces exacerbation)

-in pts with FEV1 < 60%

-increased risk of pneumonia

-chronic treatment should be avoided

• -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

-longer term in pts with chronic resp failure

-can increase survival in pts with resting hypoxemia (PaO2 < 55)

• CV disease
• Osteoporosis
• Respiratory infections
• Anxiety and Depression
• Diabetes
• Lung Cancer

• Weight Loss/Gain
• Nutritional Abnormalities
• SKM dysnfunction
• Sleep Apnea