COPD in smoker

- Clinically:
- Symptoms: cough, sputum production, dyspnea during exertion and eventually at rest. morning is usually worse. decreased
breath sounds, prolonged expiration, end expiratory wheezes, inspiratory crackles. tachycardia, tachypnea, cyanosis, accessory
muscle use, hyperresonance. expiration through pursed lips, leaning forward weight supported on palms or elbows. severe
hypercapnia, enlarged tender liver from right heart failure. JVD
- History: smoking, family history of COPD/asthma/heart disease, occupation of industrial dust/fumes, respiratory infections.
- Diagnosis:
- FEV1/FVC < 0.75-0.80, FEV1 decrease, VC decrease, TLC increased, RV increased, FRC increased.
- CXR: low sensitivity, hyperinflated, flattened diaphragm, vascular markings diminished, rule out PNA or pneunomothorax.
- ABG: CO2 retention, decreased O2. metabolic alkalosis respiratory acidosis.
- CT lung: for airway, parenchyma, pulmonary vasculature
- DLCO: decreases in proportion to the severity of emphysema; cannot detect mild emphysema
- Classifications:
- chronic bronchitis: 3 months in each successive two years, chronic cough
- emphysema: permanent enlargement of airspaces distal to terminal bronchioles, destruction of airspace walls
- asthma: chronic inflammation airway responsiveness, reversible. bronchial inflammation, CD4+ T cells, eosinophils.
- Comorbid diseases: lung cancer, CAD, osteoporosis, skeletal muscle weakness, depression, cognitive dysfunction
- Pathogenesis: excess mucus that narrows airways, productive cough. inflammation scars airways, enlarged globlet cells and
submucosal glands, smooth muscle hyperplasia, firbosis. PMN or macrophages excess elastase, radical production, increased
oxidative stress. airflow limitation. narrowing of small airways, collapse. CD8+, neutrophils, macrophages. frequent clinician office
visits. Usually progressive. Lung parenchyma and pulmonary vasculature (intimal hyperplasia and smooth muscle hypertrophy/
hyperplasia. hypoxic vasoconstriction of small arteries, damage to capillary beds) changes.
- Treatment:
- smoking cessation: rate of decline slows to someone of same age who never smoked, but never reversed. prolongs survival rate
- oxygen therapy: improved survival & quality of life for long standing hypoxemia <88% saturation, paO2 <55mmHg; vaccination
against flu/strep pneumonia; antibiotics: acute exacerbation
- inhaled beta2 agonist: bronchodilator symptomatic relief, long-term improvements, exercise capacity, airflow
- inhaled anticholinergic: bronchodilator that lasts longer
- inhaled corticosteroid: with long acting bronchodilator, significant symptoms, repeated exacerbation, decrease inflammation
- triple therapy: severe COPD long-acting beta agonist + inhaled glucocorticoid + long-acting anticholinergic

- mild-moderate: anticholinergic and/or beta2 agonist. with glucocorticoids

- severe disease: add O2 & long acting inhaler (triple therapy)
- acute: increase in dyspnea, increased sputum, increased cough. beta-2 agonist with anticholingergics, systemic corticosteroids IV,
antibiotics, BIPAP/CPAP

Asthma
- Clinically:
- Symptoms: Chest tightness, episodic cough, SOB, inspiratory and expiratory wheezing, worsen at night. Can also have sputum
production or chest pain. hyperventilation, low PaCO2, increased respiratory effort. high incidence in children but affects all ages.
Effects of genetics and environment (allergens pets, cockroaches pollen, cigarette smoke, pollution). Th2 response, IgE
production.
- Pathogenesis: Airway infiltration with eosinophils, mast cells, macrophages, T cells producing cytokines, leukotrienes, bradykinins.
Inhaled allergen in sensitized, hyper-responsive patient => crosslinking of IgE on mast cells causing degranulation => release of
mediators causing acute bronchoconstriction, increased airway resistance and wheezing, mucus hypersecretion. Hyperplasia and
hypertrophy of smooth muscle cells, edema, inflammatory infiltrate, angiogenesis, increased deposition of connective tissues
causing airway wall remodeling. airway inflammation, airway hyperresponsiveness, Reversible airway obstruction.
- Diagnosis:
- Spirometry: (Obstructive) low FEV1, low FVC. FEV1/FVC <0.75. Improves with bronchodilator, increase FEV1 or FVC by
>12%. Diffusion capacity is typically normal (normal DLCO)
- Bronchoprovocation testing (cold air, exercise, histamine, or methacholine to produce 20% decline in FEV1 from baseline). if
PFTs nondiagnostic.
- Blood tests could show eosinophilia and increased IgE
- possible skin tests to identify potential allergens
- ABG: hypocarbia, hypoxemia, hyperventilation.
- Treatment:
- expiratory peak flow meters that can be used at home
- SABA for exacerbations. Maintenance therapy with inhaled corticosteroids. LABAs for additional control, not monotherapy,
exercise induced or nighttime use. IV steroids for severe acute exacerbation.
- Leukotriene inhibitors as adjuncts, but not first line. Theophylline, but this is an older drug not used commonly.

mild-intermittent: symptoms <2x/week. Short acting beta-2 agonist.

mild-persistent: symptoms >2x/week. short acting beta-2 agonist & low dose inhaled steroid
moderate-persistent: daily symptoms. SABA + daily lower dose inhaled corticosteroid
severe-persistent: continued symptoms, limited activity. SABA + daily high dose inhaled corticosteroid + LABA
acute: inhaled beta-2 agonist, IV or oral corticosteroids.