Obstructive lung disease Flashcards
Define COPD in general
• progressive, and irreversible condition of the lung characterized by chronic obstruction to
airflow with many patients having periodic exacerbations, gas trapping, lung hyperinflation and
weight loss
• 2 subtypes (chronic bronchitis or emphysema): usually coexist to variable degrees
• gradual decrease in FEV1 over time with episodes of acute exacerbations
How is Chronic Bronchitis defined?
Defined clinically:
Productive cough on most days for at least
3 consecutive months in 2 successive years
Obstruction is due to narrowing of the airway lumen by mucosal thickening and excess mucus
How is emphysema defined?
Defined pathologically:
Dilation and destruction of air spaces distal to the terminal bronchiole
without obvious fibrosis
Decreased elastic recoil of lung parenchyma causes decreased
expiratory driving pressure, airway collapse, and air trapping
What are the (2) pathological types of emphysema?
1) Centriacinar - most common (respiratory bronchioles predominantly affected)
• Typical form seen in smokers, primarily affects upper lung zones
2) Panacinar (respiratory bronchioles, alveolar ducts, and alveolar sacs affected)
• Accounts for about 1% of emphysema cases
α1-antitrypsin deficiency, primarily affects lower lobes
What is the risk factor for COPD?
• SMOKING (#1)
• environmental: air pollution, occupational exposure, exposure to wood smoke or other
biomass fuel for cooking
• treatable factors: α1-antitrypsin deficiency, bronchial hyperactivity
• demographic factors: age, family history, male sex, history of childhood respiratory infections, low socioeconomic status
What are blue bloater and pink puffer?
Bronchitis - Blue Bloater
Emphysema - Pink Puffer
Px of Chronic bronchitis?
Chronic productive cough
Purulent sputum
Hemoptysis
Mild dyspnea initially
Cyanosis (2º to hypoxemia and hypercapnia)
Peripheral edema from RVF (cor pulmonale)
Crackles, wheezes
Prolonged expiration if obstructive
Frequently obese!! (c.f. emphysema)
Px of emphysema
Dyspnea (± exertion) Minimal cough Tachypnea Decreased exercise tolerance
Pink skin Pursed-lip breathing Accessory muscle use Cachectic!! appearance due to anorexia and increased work of breathing Hyperinflation/barrel chest, hyperresonant percussion Decreased breath sounds Decreased diaphragmatic excursion
Pulmonary function test of Chronic bronchitis vs. Emphysema
Chronic bronchitis:
low FEV1, low FEV1/FVC
N TLC, low or N DLCO
Emphysema: low FEV1, low FEV1/FVC high TLC (hyperinflation) high RV (gas trapping) low DLCO
CXR of chronic bronchitis vs. emphysema
Chronic bronchitis:
- AP diameter normal
- High bronchovascular markings
- Enlarged heart with cor pulmonale
Emphysema:
- high AP diameter
- Flat hemidiaphragm (on lateral CXR)
- low heart shadow
- high retrosternal space
- Bullae
- low peripheral vascular markings
Ideal O2 sat for chronic CO2 retainers
88-92%
to prevent Haldane effect and decreased
respiratory drive.
retainers have chronically elevated CO2 levels with a normal pH.
What is alpha-1-antitrypsin deficiency
Inherited disorder of defective production of a1-antitrypsin, a protein
produced by hepatocytes.
Acts in the alveolar tissue by INHIBITING the action
of PROTEASES from destroying alveolar
tissue.
Hence when low/deficient -> proteases win -> destroy lung alveoli -> emphysema
How do you Rx stable COPD? List (3) for prolonging survival and (2) for symptomatic relief with no mortality benefit
Prolonging survival:
1. Smoking cessation
2 Vaccination (influenza, pneumococcal)
3. Home oxygen (prevents cor pulmonale)
Symptomatic relief
1. Bronchodilators (Inhaled corticosteroids + LABA combination, SABA)
2. Corticosteroids (as combination with LABA)
Others: lung volume reduction surgery, lung transplant, pt education, rehab
Define acute exacerbation of COPD
sustained (>24-48 h) worsening of dyspnea, cough, or sputum production leading to an
increased use of medications
What causes acute exacerbation of COPD?
viral URTI, bacteria, air pollution, CHF, PE, MI must be considered
Rx of acute exacerbation of COPD
· ABCs, consider assisted ventilation if decreasing LOC or poor ABGs
· O2: target 88-92% SaO2 for CO2 retainers
· bronchodilators by MDI with spacer or nebulizer
○ SABA + anticholinergic, e.g. salbutamol and ipratropium bromide via nebulizers x 3 back-to-back
· systemic corticosteroids: IV solumedrol or oral prednisone
· antibiotics if purulent sputum
○ simple exacerbation (no risk factors): amoxicillin, 2nd or 3rd generation cephalosporin, macrolide, or TMP/SMX
○ complicated exacerbation (one of: FEV1 ≤50% predicted, ≥4 exacerbations per year, ischemic heart disease, home O2 use, chronic oral steroid use): fluoroquinolone or β-lactam + β-lactamase inhibitor (Augmentin: amoxicillin/clavulanate)
· post exacerbation: rehabilitation with general conditioning to improve exercise tolerance
What is BODE index?
Index used to predict risk of death in COPD
10 point system consisting of 4 factors:
- Body index
- Obstruction
- Dyspnoea
- Exercise capacity
- greater score = higher probability the patient will die from COPD; score can also be used to predict hospitalization
What are the common (4) conditions that cause airway obstruction (decreased FEV1)?
- Asthma
- COPD
- Bronchiectasis
- Cystic fibrosis
What are the red flags of asthma?
- severe tachypnoea, tachycardia
- respiratory muscle fatigue
- reduced expiratory effort
- cyanosis
- silent chest!!!
- decreased LOC
Define asthma
- chronic inflammatory disorder of the airways resulting in episodes of reversible bronchospasm causing airflow obstruction
- associated with REVERSIBLE airflow limitation and airway hyper-responsiveness to endogenous or exogenous stimuli
Who gets asthma?
- common, 7-10% of adults, 10-15% of children
- most children with asthma significantly improve in adolescence
- often family history of ATOPY (asthma, allergic rhinitis, eczema)
- occupational asthma (organic allergies, isocyanates, animals, etc.)
What are the triggers of asthma?
• URTIs, allergens (pet dander, house dust, moulds), irritants (cigarette smoke, air pollution), drugs (NSAIDs, β-blockers), preservatives (sulphites, MSG), other (emotion/anxiety, cold air, exercise, GERD)
Pathophysiology of asthma
airway obstruction -> V/Q mismatch -> hypoxemia (type 1 RF) -> ↑ ventilation -> ↓ PaCO2 -> ↑ pH and
muscle fatigue -> ↓ ventilation, ↑ PaCO2/↓ pH (type 2 RF)
Px of asthma
- dyspnea, wheezing, chest tightness, cough (especially nocturnal), sputum
- symptoms can be paroxysmal or persistent
- signs of respiratory distress (see sidebar R3)
- pulsus paradoxus
Ix of asthma (make a comment about how CO2 levels can tell us how severe the asthma is)
• O2 saturation
• ABGs decreased PaO2 during attack (V/Q mismatch)
- decreased PaCO2 in mild asthma (hyperventilation)
- normal or increased PaCO2 is a dangerous sign: patient is no longer able to hyperventilate (worsened airway obstruction or respiratory muscle fatigue)
• PFTs (do when stable)
Rx of asthma (in emergency & less severe cases)
- inhaled β2-agonist first line (MDI route and spacer device recommended)
- systemic steroids (PO or IV, if severe)
- add anticholinergic therapy ± magnesium sulphate
- rapid sequence intubation in life-threatening cases (plus 100% O2, monitors, IV access)
- SC/IV adrenaline, IV salbutamol if unresponsive
- corticosteroid therapy at discharge
Less severe:
- symptomatic relief in acute episodes: short-acting β2-agonist, anticholinergic bronchodilators, oral steroids, addition of a long acting β2-agonist - long-term prevention: inhaled/oral corticosteroids, anti-allergic agents, long-acting β2-agonists, methylxanthine, LTRA, anti-IgE antibodies (e.g. Xolair®)
patient education: features of the disease, goals of treatment, self-monitoring
Define bronchiectasis
- IRREVERSIBLE dilatation of airways due to inflammatory destruction of airway walls resulting from persistently infected MUCUS
- usually affects medium sized airways
What are the risk factors of bronchiectasis & what is the most common pathogen?
- Obstruction (E.g. tumour, foreign body, thick mucus)
- Post-infectious (pneumonia, TB, ABPA)
- Impaired defenses (CF, hypogammaglobulinemia)
Pseudomonas aeruginosa = the most common pathogen
S. aureus, H. influenzae and nontuberculous mycobacteria also common
Px of bronchiectasis
- chronic cough, purulent sputum (but 10-20% have dry cough), hemoptysis (can be massive), recurrent pneumonia, local crackles (inspiratory and expiratory), wheezes
- clubbing
- may be difficult to differentiate from chronic bronchitis
Ix of bronchiectasis
• CXR
- nonspecific: increased markings, linear atelectasis, loss of volume in affected areas
- specific: “tram tracking” – parallel narrow lines radiating from hilum, cystic spaces, honeycomb like structures
• high-resolution thoracic CT (diagnostic, gold standard):
- 87-97% sensitivity, 93-100% specificity
- “signet ring”: dilated bronchi with thickened walls where diameter bronchus > diameter of accompanying artery
• sputum cultures (routine + AFB)
• serum Ig levels
• sweat chloride if cystic fibrosis suspected (upper zone predominant)
Rx of bronchiectasis
- vaccination: influenza and Pneumovax®
- antibiotics: macrolides may be used chronically for an anti-inflammatory effect
- inhaled corticosteroids: decrease inflammation and improve FEV1
- oral corticosteroids for acute, major exacerbations
- chest physiotherapy, breathing exercises, physical exercise
- pulmonary resection: in selected cases with focal bronchiectasis
How does cystic fibrosis present?
Usually presents in childhood as recurrent lung infections that become persistent and chronic.
- results in severe lung disease, pancreatic insufficiency, diabetes and azoospermia
- other manifestations: meconium ileus in infancy, distal ileal obstruction in adults, sinusitis, liver disease
What organisms commonly cause chronic lung infections in CF?
- S. aureus: early
- P. aeruginosa: most common
- B. cepacia: worse prognosis but less common
- Aspergillus fumigatus
Ix for CF
• sweat chloride test
- increased concentrations of NaCl and K+ ([Cl-] >60 mmol/L is diagnostic in children)
- heterozygotes have normal sweat tests (and no symptoms)
• PFTs
- early: airflow limitation in small airways
- late: severe airflow hyperinflation, gas trapping, decreased DLCO (very late)
• ABGs
- hypoxemia, hypercapnia later in disease with eventual respiratory failure and cor pulmonale
• CXR
- hyperinflation, increased pulmonary markings (especially upper lobes)
Rx of CF
- chest physiotherapy and postural drainage
- bronchodilators (salbutamol ± ipratropium bromide)
- inhaled mucolytic (reduces mucus viscosity), hypertonic saline DNase
- inhaled tobramycin
- antibiotics (e.g. ciprofloxacin)
- lung transplant
- pancreatic enzyme replacements
What is pathophysiology of CF?
chloride transport dysfunction: thick secretions from exocrine glands (lung, pancreas, skin, reproductive organs) and blockage of secretory ducts
Hence increased Cl-
