Obstructive Lung Disease Flashcards
Obstructive lung diseases
Characterized by airway narrowing, obstructive lung diseases restrict air movement and often cause air trapping.
Etiologies of OLDs are seen in mnemonic ABCT (Asthma, bronchiectasis, cystic fibrosis/COPD, Tracheal or bronchial obstruction
Asthma
Defined as reversible airway obstruction secondary to bronchial hyperreactivity, airway inflammation, mucous plugging and smooth muscle hypertrophy
BEWARE - all that wheezes is not asthma.
Suspect in kids with multiple episodes of croup and URIs associated with dyspnea
history and physical for Asthma
1) Presents with cough, episodic wheezing, dyspnea, and/or chest tightness. Symptoms often worsen at night or early in morning
2) Exam reveals wheezing, prolonged expiratory duration (lower I/E), accessory muscle use, tachypnea, tachycardia, hyperresonance, and possible pulsus paradoxus
3) Reduced breath sounds and low O2 sat are late signs
Dx of asthma
1) ABGs: Mild hypoxia and respiratory alkalosis. Normalizing PCO2, respiratory acidosis, and more severe hypoxia may indicate fatigue and impending respiratory failure
2) Spirometry/PFTs: Low FEV1/FVC. Peak flow is diminished acutely. Increased RV and TLC. PFTs are often normal between exacerbations.
3) CBC. Possible eosinophilia
4) CXR: Hyperinflation
5) Methacholine challenge: Tests for bronchial hyperresponsiveness. Useful when PFTs are normal but asthma is still suspected.
Treatment of asthma
In general, avoid allergens or any potential triggers. Management is as follows
Acute:
1) O2, bronchodilating agents (short acting B agonists are first line), ipratropium (never use alone for asthma), systemic steroids, magnesium (for severe exacerbations)
2) Maintain a low threshold for intubation in severe cases or acutely in patients with a PCO2 over 50 or PO2 below 50.
Chronic:
1) Administer long acting inhaled bronchodilators and/or inhaled corticosteroids, systemic steroids, cromolyn or rarely theophylline
2) Montelukast and other leukotriene antagonists are oral adjuncts to inhalant therapy
Meds for asthma exacerbation = ASTHMA
Albuterol Steroids Theophylline (rare) Humidified O2 Magnesium (severe exacerbations) Anticholinergics
B2 agonists mechanism
Albuterol: Short acting. Relaxes bronchial smooth muscle
Salmeterol: Long acting for ppx
Corticosteroids mechanism
Inhaled: First line for long term control of asthma
Beclomethasons, prednisone: Inhibit the synthesis of virtually all cytokines
Muscarinic antagonists mechanism
Ipratropium: Competitively blocks muscarinic receptors, preventing bronchoconstriction
Methylxanthines mechanism
Theophylline: Likely causes bronchodilation by inhibiting phosphodiesterase, thereby decreasing cAMP hydrolysis and increasing cAMP. Usage is limited bc of its narrow therapeutic-toxic index (cardiotoxic, neurotoxic)
Cromolyn mechanism
Prevents the release of vasoactive mediators from mast cells. Useful for exercise-induced bronchospasm. EFFECTIVE ONLY FOR PPX of asthma. Not effective during an acute attack. Toxicity is rare.
Antileukotrienes mechanism
Zileuton: A 5-lipoxygenase pathway inhibitor. Blocks conversion of arachidonic acid to leukotrienes
Montelukast, zafirlukast: Block leukotriene receptors
Mild intermittent asthma
2 days/w or less
2 nights/m or less
FEV1 is 80% or more
No daily meds. PRN short acting bronchodilator.
Mild persistent asthma
More than 2/w but less than 1/d
More than 2 nights/m
FEV1 is 80% or more
Daily low dose inhaled steroids. PRN short acting dilator
Moderate persistent asthma
Daily symptoms
More than 1 night/w
FEV1 60-80
Low to medium dose inhaled steroids plus long acting inhaled B agonists. PRN short acting dilator
Severe persistent asthma
Continual or frequent symptoms
FEV1 less than 60
High dose inhaled steroids plus long acting inhaled B agonists. Possible PO steroids. PRN short acting dilators
Bronchiectasis
A disease caused by cycles of infection and inflammation in the bronchi/bronchioles that lead to fibrosis, remodeling, and permanent dilation of bronchi
History and physical of bronchiectasis
1) Presents with chronic cough accompanied by frequent bouts of yellow or green sputum production, dyspnea, and possible hemoptysis and halitosis
2) Associated with a history of pulmonary infections, hypersensitivity, cystic fibrosis, immunodeficiency, localized airway obstruction, aspiration, autoimmune disease, or IBD
3) Exam reveals rales, wheezes, rhonchi, purulent mucus and occasional hemoptysis
Dx of bronchiectasis
1) CXR: shows increased bronchovascular markings and TRAM LINES (parellel lines outlining dilated bronchi as a result of peribronchial inflammation and fibrosis)
2) High resolution CT: dilated airways and ballooned cysts are seen at the end of the bronchus (mostly lower lobes)
3) Spirometry shows a reduced FEV1/FVC ratio consistent with obstruction
Tx of bronchiectasis
1) Antibiotics for bacterial infections. Consider inhaled steroids
2) Maintain bronchopulmonary hygiene (cough control, postural drainage, chest PT)
3) Consider lobectomy for localized disease or lung transplant for severe disease
Asthma triggers
Allergens, URIs, cold air, exercise, drugs, stress
Normal PFTs
1) FEV1 (percent of FVC): More than 75
2) RV (percent of predicted): 80-120
3) FVC (percent of predicted): More than 80
Obstructive PFTs
1) Mild: FEV1 60-75, RV 120-150.
2) Moderate: FEV1 40-60, RV 150-175
3) Severe: FEV1 less than 40, RV above 200
Restrictive PFTs
1) Mild: FVC 60-80, FEV1 Above 75, RV 80-120
2) Moderate: FVC 50-60, FEV1 above 75, RV 70-80
3) Severe: FVC less than 50, FEV1 above 75, RV 70
Inhaled Corticosteroids side effect
Corticosteroids are inhaled in a RUSH and can lead to THRUSH
COPD
A disease with lower lung function associated with airflow obstruction. Generally secondary to chronic bronchitis or emphysema, which are distinguished as follows:
1) Chronic bronchitis: productive cough for more than 3 months per year for 2 consecutive years
2) Emphysema: terminal airway destruction and dilation that may be secondary to smoking (centrilobular) or to alpha 1 antitrypsin deficiency (panlobular)
History and physical for COPD
1) Symptoms are minimal or nonspecific until the disease is advanced
2) The clinical spectrum includes the following (most patients are a combination of the 2 phenotypes
Emphysema (pink puffer): Dyspnea, pursed lips, minimal cough, reduced breath sounds, late hypercarbia/hypoxia. Patients often have a thin, wasted appearance. Pure emphysematous patients tend to have few reactive episodes between exacerbations
Chronic bronchitis (blue bloater): Cyanosis with mild dyspnea, productive cough. Patients are often overweight with peripheral edema, rhonci, and early signs of hypercarbia/hypoxia
3) Look for the classic barrel chest, use of accessory muscles, JVD, end expiratory wheezing, and muffled breath sounds
Dx of COPD
1) CXR: Hyperinflated lungs, reduced lung markings with flat diaphragms, and a thin-appearing heart and mediastinum are seen. Parenchymal bullae or subpleural blebs (pathognomonic of emphysema) are also seen
2) PFTs: Low FEV1/FVC. Normal or low FVC. Normal or high TLC (emphysema, asthma). Low DL of CO (emphysema)
3) ABG: Hypoxemia with acute or chronic respiratory acidosis (high PCO2)
4) Consider a gram stain and sputum culture in setting of fever or productive cough, especially if infiltrate is seen on CXR
Tx of COPD - acute exacerbation
1) O2, inhaled B agonists and anticholinergics. IV plus or minus inhaled steroids, antibiotics. Severe cases benefit from BiPAP
2) Consider intubation in the setting of severe hypoxemia or hypercapnia, impending respiratory fatigue or AMS
Tx of COPD - chronic
1) Smoking cessation, inhaled B agonsts, anticholinergics, systemic or inhaled steroids
2) Supplemental O2 if resting PaO2 is less than 55 or SaO2 is 89% or less, or in the setting of cor pulmonale, pulmonary HTN, a Hct above 55% or nocturnal hypoxia
3) Give pneumococcal and flu vaccines
COPD oxygen goals
In COPD patients with chronic hypercapnia, high concentrations of O2 may suppress patients’ hypoxic respiratory drive
Supplemental O2 titrated above 90% for more than 15h a day and smoking cessation are the only interventions proven to improve survival in patients with COPD
