Obstructive Lung Diseases Flashcards
What patients are at the greatest risk of asthma?
Lower SES, blacks, women, born prematurely to a young mother who smoked
What is the function of the of the parasympathetic nervous system with regards to the airway?
Maintains bronchial smooth muscle tone -> narrows the airway
This is blocked by ipratropium and tiotropium
What are examples of nonadrenergic noncholinergic neural pathways and how are they controlled?
Nitric oxide and VIP will relax airway smooth muscle
Substance P and neurokinins A and B will contract airway smooth muscle -> released in response to nerve injury secondary to inflammation
-> activation can be prevented via steroids
What is the pattern of decline in lung function in asthma and how is this prevented?
Biphasic decline in FEV1
Early - within 2 hours, a small decline due to initial release of histamine and production of leukotrienes (blocked by antihistamines / leukotriene antagonists)
Late - Peaking in 6-8 hours, remaining inflammatory cells lead to bronchial hyperreactivity -> prevented by leukotriene antagonists and corticosteroids
What lung volumes increase during an asthmatic attack? How will these values be between attacks?
RV and FRC -> due to air trapping and resulting lung hyperinflation
All spirometry values will be normal or near normal between attacks (acute and reversible obstructive disease)
Give three reasons why there is increased work of breathing in asthma.
- Increased airway resistance due to bronchoconstriction
- Hyperinflation of lung flattens diaphragm, which cannot optimally stretch prior to contraction -> more work
- Hyperinflated lungs sit higher on lung compliance curve, where lung is less compliant
What happens to gas exchange during asthma?
It is poorer, with increased deadspace due to loss of adequate ventilation to certain areas, dropping the V/Q ratio (ventilation perfusion mismatch)
What are the symptoms of an asthma attack and what is a really important thing to diagnose it?
Sudden onset dyspnea, wheezing, chest tightness, and feeling of suffocation
To diagnose it -> patient often has a family history of atopy or asthma
-> may be able to identify triggers
What clinical test is commonly used as a confirmatory test for bronchial hyperreactivity?
Methacholine (or histamine)
-> nonspecific, also positive in many other individuals such as atopics or COPD
Who is of greater concern:
- A known asthmatic who appears in distress, wheezes, is tachypneic / tachycardic, and using accessory respiratory muscles
or
- A known asthmatic patient with a quiet chest, with fatigue / somnolence, and cyanosis
The latter patient -> this is a severe asthma attack, where the chest is quiet so it is not moving any are
The former patient has a moderate asthma attack
Least severe attacks involve wheezing and prolonged expiratory time
What do arterial blood gases show in mild, moderate, and severe asthma (keep in mind, we talked about how asthma can go BOTH ways!)
Mild - respiratory alkalosis (decreased PaCO2) due to hyperventilation
Moderate - mild hypoxemia, PaCO2 will be decreased or normal (worse sign)
Severe - Severe hypoxemia, and respiratory acidosis (increased PaCO2)
What is the dichotomy which is most important to make when diagnosing asthma, and how is this done?
Intermittent vs Persistent (mild, moderate, or severe)
Intermittent asthma defined by rule of 2’s
Symptoms <= 2 days a week
Awakenings <= 2x a month
Use of SABAs <= 2 days a week
<2 a year having exacerbations requiring systemic corticosteroids
No interference in normal activity
What is treatment of asthma directed towards?
The inflammation
Treating the inflammation will treat the bronchospasm, but treating the bronchospasm will not treat the inflammation
What general measures can be taken to improve asthma symptoms in patients, outside of medication?
patient education
Self-monitoring with peak expiratory flow monitors
Environmental control with avoidance of triggers
Treatment of GERD and nasal sinus congestion / post-nasal drip syndrome
What is the treatment paradigm for intermittent vs persistent asthma?
Intermittent - give rescue inhaler PRN (SABA)
Persistent - give SABA, low dose inhaled corticosteroid (fluticasone, budesonide), and oral / IV prednisone during exacerbations
Step up ICS as needed / use LABA to control symptoms
What therapy is used as an adjunct for mild asthmatics and is also effective in the treatment of allergic rhinitis?
Leukotriene antagonists such as montelukast and zafirlukast
Give two biologics which are used to control asthma and their role in therapy?
Omalizumab -> binds IgE
Mepolizumab -> anti IL-5
Role: poorly controlled asthmatics, who require high-dose inhaled corticosteroids and have frequent hospitalizations
What are the first and second line bronchodilators in asthmatics?
First-line:
Beta-2 agonists - albuterol (SABA) or salmeterol / formoterol (LABAs)
Second line:
Anticholinergics - ipratropium (short-acting) or tiotropium (long-acting)
What are the two components of asthma which measure its severity and control?
- Impairment - frequency and intensity of symptoms / functional impairment
- Risk - likelihood of exacerbations or progressive decline in lung function
What is the primary difference between chronic bronchitis and asthma apart from asthma being acutely reversible?
Asthma affects the large airways, chronic bronchitis affects the small airways.
What are the major risk factors for COPD and what is this the umbrella term for?
Umbrella term for spectrum of chronic bronchitis and emphysema
Risk factors:
Smoking, male gender, low SES, asthma, occuptational hazards, and biomass fuel inhalation in developing nations
How does lung function in smokers vs nonsmokers change with age? What if you quit? How will this manifest?
Both groups will deteriorate with age, smokers about 5x faster. If you quit, deterioration will happen slower, but still faster than smokers.
Manifests as a drop in FEV1
What factors can lead to a lower FEV1 to begin with?
Factors which lead to decreased lung development in childhood / adolescence
Includes genetics, maternal smoking, childhood infections, air pollution, asthma, and SMOKING during adolescence
What are the primary inflammatory cell types found in COPD? How does this relate to its overall severity compared to asthma?
Macrophages, T lymphocytes (CD8+), and neutrophils
These cell types are less responsive to steroids -> ICS not as good for preventing exacerbations of COPD
(mast cells in asthma respond to ICS well)
How is lung compliance and airway resistance altered in COPD?
Emphysema - increased lung compliance
Chronic bronchitis - increased airway resistance
How is V/Q ratio altered in COPD?
Areas of low and high ratios
Low - hypoxemia
high - increased deadspace and hypercapnia
What three things can tip you off that a COPD exacerbation is occurring and what usually causes it?
- Change in sputum quality
- Increase in shortness of breath
- New or increased cough
Usually due to a bacterial or viral infection
How do exacerbations of COPD relate to prognosis?
Patients who require hospitalization -> clear increase in mortality due to rapid decline in lung function
What are the systemic changes which occur in COPD?
- Weight loss -> due to increased work of breathing and circulating TNF -> cachexia (being fat increases survival)
- Skeletal muscle dysfunction
- Osteoporosis
- Cardiovascular morbidity / mortality
Why does skeletal muscle dysfunction occur in COPD? How can this be slowed?
Due to immobility from decreased activity, as well as hypoxia and muscle wasting from cachexia
-> make sure that COPD patients at least ATTEMPT physical activity
What are the chest X-ray findings with severe emphysema?
Increased anteroposterior diameter of chest
Hyperinflation with small cardiac silhouette and heart displaced towards center (from hyperinflated lungs)
Large retrosternal airspace
How will PCO2 be in COPD? What is the important thing to compare it to in exacerbation?
Can be low, normal, high
Important to compare to their baseline values. Some people are “chronic CO2 retainers” and have a compensated respiratory acidosis at all times.
What are the two measures used to assess COPD severity?
- Degree of flow limitation - FEV1
2. Severity of symptoms / exacerbations
What are the four GOLD category cutoffs?
GOLD 1: FEV > 80% predicted
GOLD 2: 50 < FEV < 80
GOLD 3: 30 < FEV < 50
GOLD 4: FEV < 30% predicted
What is the overall treatment for COPD?
Primarily supportive, as lung function cannot be restored.
QUIT SMOKING
Oxygen if PaO2 < 55mmHg
Nutritional support if losing weight at normal BMI or underweight
What preventative treatment must all COPD patients make sure to get?
yearly influenza and pneumococcal vaccinations
How is dyspnea managed in COPD?
Long-acting beta agonists or Long-acting anticholinergics are drugs of choice, despite no significant benefits to lung function via spirometry.
Ipratropium or albuterol can be used for rapid relief
Theophylline!! is seeing a comeback in patients with severe disease
When are steroids used in COPD?
Systemically during exacerbations only
Inhaled steroids work in only SEVERE COPD
