Obstructive Lung Diseases

Question 1

What patients are at the greatest risk of asthma?

Answer 1

Lower SES, blacks, women, born prematurely to a young mother who smoked

Question 2

What is the function of the of the parasympathetic nervous system with regards to the airway?

Answer 2

Maintains bronchial smooth muscle tone -> narrows the airway

This is blocked by ipratropium and tiotropium

Question 3

What are examples of nonadrenergic noncholinergic neural pathways and how are they controlled?

Answer 3

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

Question 4

What is the pattern of decline in lung function in asthma and how is this prevented?

Answer 4

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

Question 5

What lung volumes increase during an asthmatic attack? How will these values be between attacks?

Answer 5

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)

Question 6

Give three reasons why there is increased work of breathing in asthma.

Answer 6

1. Increased airway resistance due to bronchoconstriction
2. Hyperinflation of lung flattens diaphragm, which cannot optimally stretch prior to contraction -> more work
3. Hyperinflated lungs sit higher on lung compliance curve, where lung is less compliant

Question 7

What happens to gas exchange during asthma?

Answer 7

It is poorer, with increased deadspace due to loss of adequate ventilation to certain areas, dropping the V/Q ratio (ventilation perfusion mismatch)

Question 8

What are the symptoms of an asthma attack and what is a really important thing to diagnose it?

Answer 8

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

Question 9

What clinical test is commonly used as a confirmatory test for bronchial hyperreactivity?

Answer 9

Methacholine (or histamine)

-> nonspecific, also positive in many other individuals such as atopics or COPD

Question 10

Who is of greater concern:

1. A known asthmatic who appears in distress, wheezes, is tachypneic / tachycardic, and using accessory respiratory muscles

or

2. A known asthmatic patient with a quiet chest, with fatigue / somnolence, and cyanosis

Answer 10

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

Question 11

What do arterial blood gases show in mild, moderate, and severe asthma (keep in mind, we talked about how asthma can go BOTH ways!)

Answer 11

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)

Question 12

What is the dichotomy which is most important to make when diagnosing asthma, and how is this done?

Answer 12

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

Question 13

What is treatment of asthma directed towards?

Answer 13

The inflammation

Treating the inflammation will treat the bronchospasm, but treating the bronchospasm will not treat the inflammation

Question 14

What general measures can be taken to improve asthma symptoms in patients, outside of medication?

Answer 14

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

Question 15

What is the treatment paradigm for intermittent vs persistent asthma?

Answer 15

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

Question 16

What therapy is used as an adjunct for mild asthmatics and is also effective in the treatment of allergic rhinitis?

Answer 16

Leukotriene antagonists such as montelukast and zafirlukast

Question 17

Give two biologics which are used to control asthma and their role in therapy?

Answer 17

Omalizumab -> binds IgE

Mepolizumab -> anti IL-5

Role: poorly controlled asthmatics, who require high-dose inhaled corticosteroids and have frequent hospitalizations

Question 18

What are the first and second line bronchodilators in asthmatics?

Answer 18

First-line:
Beta-2 agonists - albuterol (SABA) or salmeterol / formoterol (LABAs)

Second line:
Anticholinergics - ipratropium (short-acting) or tiotropium (long-acting)

Question 19

What are the two components of asthma which measure its severity and control?

Answer 19

1. Impairment - frequency and intensity of symptoms / functional impairment
2. Risk - likelihood of exacerbations or progressive decline in lung function

Question 20

What is the primary difference between chronic bronchitis and asthma apart from asthma being acutely reversible?

Answer 20

Asthma affects the large airways, chronic bronchitis affects the small airways.

Question 21

What are the major risk factors for COPD and what is this the umbrella term for?

Answer 21

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

Question 22

How does lung function in smokers vs nonsmokers change with age? What if you quit? How will this manifest?

Answer 22

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

Question 23

What factors can lead to a lower FEV1 to begin with?

Answer 23

Factors which lead to decreased lung development in childhood / adolescence

Includes genetics, maternal smoking, childhood infections, air pollution, asthma, and SMOKING during adolescence

Question 24

What are the primary inflammatory cell types found in COPD? How does this relate to its overall severity compared to asthma?

Answer 24

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)

Question 25

How is lung compliance and airway resistance altered in COPD?

Answer 25

Emphysema - increased lung compliance

Chronic bronchitis - increased airway resistance

Question 26

How is V/Q ratio altered in COPD?

Answer 26

Areas of low and high ratios

Low - hypoxemia

high - increased deadspace and hypercapnia

Question 27

What three things can tip you off that a COPD exacerbation is occurring and what usually causes it?

Answer 27

1. Change in sputum quality
2. Increase in shortness of breath
3. New or increased cough

Usually due to a bacterial or viral infection

Question 28

How do exacerbations of COPD relate to prognosis?

Answer 28

Patients who require hospitalization -> clear increase in mortality due to rapid decline in lung function

Question 29

What are the systemic changes which occur in COPD?

Answer 29

1. Weight loss -> due to increased work of breathing and circulating TNF -> cachexia (being fat increases survival)
2. Skeletal muscle dysfunction
3. Osteoporosis
4. Cardiovascular morbidity / mortality

Question 30

Why does skeletal muscle dysfunction occur in COPD? How can this be slowed?

Answer 30

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

Question 31

What are the chest X-ray findings with severe emphysema?

Answer 31

Increased anteroposterior diameter of chest
Hyperinflation with small cardiac silhouette and heart displaced towards center (from hyperinflated lungs)
Large retrosternal airspace

Question 32

How will PCO2 be in COPD? What is the important thing to compare it to in exacerbation?

Answer 32

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.

Question 33

What are the two measures used to assess COPD severity?

Answer 33

1. Degree of flow limitation - FEV1

2. Severity of symptoms / exacerbations

Question 34

What are the four GOLD category cutoffs?

Answer 34

GOLD 1: FEV > 80% predicted
GOLD 2: 50 < FEV < 80
GOLD 3: 30 < FEV < 50
GOLD 4: FEV < 30% predicted

Question 35

What is the overall treatment for COPD?

Answer 35

Primarily supportive, as lung function cannot be restored.

QUIT SMOKING

Oxygen if PaO2 < 55mmHg

Nutritional support if losing weight at normal BMI or underweight

Question 36

What preventative treatment must all COPD patients make sure to get?

Answer 36

yearly influenza and pneumococcal vaccinations

Question 37

How is dyspnea managed in COPD?

Answer 37

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

Question 38

When are steroids used in COPD?

Answer 38

Systemically during exacerbations only

Inhaled steroids work in only SEVERE COPD