STEPUP Diseases of the Pulmonary System: Obstructive Lung Diseases Flashcards
1
Q
What are two classic types of chronic obstructive pulmonary disease (COPD)?
A
1) Chronic bronchitis
2) Emphysema
2
Q
How is the diagnosis of chronic bronchitis made?
A
Chronic bronchitis is a clinical diagnosis: chronic cough productive of sputum for at least 3 months per year for at least 2 consecutive years
3
Q
How is the diagnosis of emphysema made?
A
Emphysema is a pathologic diagnosis: permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls
4
Q
Can a person have both chronic bronchitis and emphysema?
A
Yes. The two often coexist. Pure emphysema or pure chronic bronchitis is rare
5
Q
How common of a cause of death is COPD?
A
It is the fourth leading cause of death in the United States
6
Q
What are some risk factors and causes of COPD?
A
1) Tobacco smoke (indicated in almost 90% of COPD cases)
2) alpha1-Antitrypsin deficiency - risk is even worse in combination with smoking
3) Environmental factors (e.g., second-hand smoke)
4) Chronic asthma - speculated by some to be an independent risk factor
7
Q
What is the pathogenesis of chronic bronchitis?
A
1) Excess mucus production narrows the airways; patients often have a productive cough
2) Inflammation and scarring in airways, enlargement in mucous glands, and smooth muscle hyperplasia lead to obstruction
8
Q
What is the pathogenesis of emphysema?
A
1) Destruction of alveolar walls is due to relative excess in protease (elastase) activity, or relative deficiency of antiprotease (alpha1-antitrypsin) activity in the lung
2) Tobacco smoke increases the number of activated PMNs and macrophages, inhibits alpha1-antitrypsin, and increases oxidative stress on the lung by free radical production
9
Q
What are some common symptoms in COPD?
A
1) Any combination of cough, sputum production, and dyspnea (on exertion or at rest, depending on severity) may be present
2) Dyspnea is initially during exertion but eventually becomes progressively worse with less exertion and even at rest
10
Q
How do patients avoid the most common early symptom of COPD?
A
1) Some patients have very sedentary lifestyles but few complaints
2) They may avoid exertional dyspnea, which is the most common early symptom of COPD by limiting their activity
11
Q
In which patients is centrilobular emphysema seen in? What part of the lung is destroyed?
A
1) Most common type, seen in smokers (rarely in nonsmokers)
2) Destruction limited to respiratory bronchioles (proximal acini) with little change in distal acini
3) Predilection for upper lung zones
12
Q
In which patients is panlobular emphysema seen in? What part of the lung is destroyed?
A
1) Seen in patients with alpha1-antitrypsin deficiency
2) Destruction involves both proximal and distal acini
3) Predilection for lung bases
13
Q
In COPD, what is the FEV1/FVC ratio? What happens to FEV1? What happens to TLC? What happens to residual volume?
A
1) The FEV1/FVC ratio is
14
Q
What is the weight of a patient with predominant emphysema (“Pink Puffer”)? What do patients tend to do while seated? What does their chest look like?
A
1) Patients tend to be thin due to increased energy expenditure during breathing
2) When sitting, patients tend to lean forward
3) Patients have a barrel chest (increased AP diameter of chest)
15
Q
What is the breathing rate and pattern seen in emphysema? Is a patient with emphysema in respiratory distress?
A
1) Tachypnea with prolonged expiration through pursed lips is present
2) Patient is distressed and uses accessory muscles (especially strap muscles in neck)
16
Q
What is the weight of a patient with predominant chronic bronchitis (“Blue Bloater”)? What are typical symptoms? What may be present in severe or long-standing disease?
A
1) Patients tend to be overweight and cyanotic (secondary to chronic hypercapnia and hypoxemia)
2) Chronic cough and sputum production are characteristic
3) Signs of cor pulmonale may be present in severe or long-standing disease
17
Q
What is the respiratory rate in a patient with chronic bronchitis? Is the patient in respiratory distress?
A
1) Respiratory rate is normal or slightly increased
2) Patient is in no apparent distress, and there is no apparent use of accessory muscles
18
Q
What are signs to look for in COPD?
A
1) Prolonged expiratory time
2) During auscultation, end-expiratory wheezes on forced expiration, decreased breath sounds, and/or inspiratory crackles
3) Tachypnea, tachycardia
4) Cyanosis
5) Use of accessory respiratory muscles
6) Hyperresonance on percussion
7) Signs of cor pulmonale
19
Q
What is FEV1? What does a lower FEV1 cause?
A
1) FEV1 is the amount of air that can be forced out of the lungs in 1 second
2) The lower the FEV1, the more difficulty one has breathing
20
Q
What is necessary to diagnose diagnose airway obstruction?
A
To diagnose airway obstruction, one must have a normal or increased TLC with a decreased FEV1
21
Q
What is the definitive diagnostic test of COPD? What happens to FEV1 and FEV1/FVC ratio in COPD? What is the GOLD staging based on? What three values are increased in COPD? What happens to vital capacity?
A
1) Pulmonary function testing (spirometry)
2) Obstruction is evident based on the following:
a) Decreased FEV1 and decreased FEV1/FVC ratio - GOLD staging is based on FEV1. FEV1 >=80% of predicted value is mild disease, 50% to 80% is moderate disease, 30% to 50% is severe disease, and <30% is very severe disease
b) Increased total lung capacity (TLC), residual volume, and functional reserve capacity (FRC) (indicating air trapping). Although COPD increases TLC, the air in the lung is not useful because it all becomes residual volume and does not participate in gas exchange
c) Decreased vital capacity
22
Q
What are key points in taking history of COPD patients in general? What about pulmonary symptoms?
A
1) a) History of cardiopulmonary diseases
b) Smoking history (duration, intensity, current smoker)
c) Family history - COPD, heart disease, asthma
d) Occupation - industrial dusts, fumes
e) Overall health
f) History of respiratory infections - frequency, severity
g) Pulmonary medications
2) a) Dyspnea - quantitate severity
b) Cough
c) Sputum production - quantity, quality, duration, hemoptysis
d) Wheezing
23
Q
What is a good screening test for COPD?
A
One can measure the peak expiratory flow rate using a peak flow meter. If <350 L/min, one should perform pulmonary function testing, because this is a good screening test for obstruction
24
Q
What kind of acid/base disorder does COPD lead to?
A
COPD leads to chronic respiratory acidosis with metabolic alkalosis as compensation
25
What does clinical monitoring of COPD patients entail?
1) Serial FEV1 measurements - this has the highest predictive value
2) Pulse oximetry
3) Exercise tolerance
26
What tests are used to diagnose COPD?
1) Pulmonary function testing (Spirometry)
2) Chest radiograph (CXR)
3) Measure alpha1-antitrypsin levels in patients with a personal or family history of premature emphysema (<=50 years old)
4) Arterial blood gas (ABG) - chronic PCO2 retention, decreased PO2
27
Is a CXR a good test for diagnosing COPD? When is a CXR useful for COPD?
1) Low sensitivity for diagnosing COPD; only severe, advanced emphysema will show the typical changes, which include: Hyperinflation, flattened diaphragm, enlarged retrosternal space, diminished vascular markings
2) Useful in acute exacerbation to rule out complications such as pneumonia or pneumothorax
28
Are the following values low, normal, or high in obstructive lung disease? restrictive lung disease? FEV1, FEV1/FVC, peak expiratory flow rate, residual volume, total lung capacity, and vital capacity
1) Obstructive: Low, low, low, high, high, low
| 2) Restrictive: Normal or slightly low; normal or high; normal; low, normal, or high; low; low
29
What can be used for treatment of COPD?
1) Smoking cessation - the most important intervention
2) Inhaled anticholinergic drugs (e.g., ipratropium bromide): bronchodilators
3) Inhaled beta2-agonists (e.g., albuterol): bronchodilators
4) Combination of beta-agonist albuterol with ipratropium bromide
5) Inhaled corticosteroids (e.g., budesonide, fluticasone): anti-inflammatory
6) Theophylline (oral) - role is controversial
7) Oxygen therapy
8) Pulmonary rehabilitation
9) Vaccination
10) Antibiotics are given for acute exacerbations
11) Surgery - may be beneficial in selected patients
30
Why does smoking cessation help in treatment of COPD? What happens to the rate of FEV1 decrease around age 35? How does quitting smoking help? Does smoking cessation return your survival rate to normal? When do respiratory symptoms improve after quitting?
1) Disease progression is accelerated by continued smoking and can be greatly slowed by its cessation
2) At around age 35, FEV1 decreases approximately 25 to 30 mL/yr
3) In smokers, the rate of decline is faster (threefold to fourfold). If a smoker quits, the rate of decline of FEV1 slows to that of someone of the same age who has never smoked. However, quitting does not result in complete reversal
4) Smoking cessation prolongs the survival rate but does not reduce it to the level of someone who has never smoked
5) Respiratory symptoms improve within 1 year of quitting
31
What is total lung capacity (TLC)? What is functional residual capacity (FRC)? What is residual volume (RV)? What is tidal volume (TV)? What is vital capacity (VC)?
1) Volume of air in the lungs after maximum inspiration
2) Volume of air in the lungs after a normal expiration
3) Volume of air in the lungs at maximal expiration
4) Volume of air breathed in and out of the lungs during quiet breathing
5) Volume of air expelled from the lungs during a maximum expiration
32
What are the only interventions shown to lower mortality in COPD patients?
1) Smoking cessation
| 2) Home oxygen therapy
33
How do inhaled anticholinergic drugs differ from beta-agonists?
Slower onset of action than the beta-agonists, but last longer
34
How do inhaled beta2-agonists help in COPD? When should you use a long-acting beta2-agonist in COPD patients?
1) Provide symptomatic relief
| 2) Use long-acting (e.g., salmeterol) for patients requiring frequent use
35
What are two advantages of the combination of beta-agonist albuterol with ipratroprium bromide inhaler?
1) More efficacious than either agent alone in bronchodilation
2) Also helps with adherence to therapy (both medications in one inhaler)
36
How may inhaled corticosteroids help in COPD? Do they have any benefit in pulmonary function? What are they typically used in combination with and for which patients?
1) May minimally slow down the decrease in FEV1 over time
2) However, many studies have failed to show any benefit in pulmonary function
3) Typically used in combination with a long-acting bronchodilator for patients with significant symptoms or repeated exacerbations
37
How should you treat COPD? What about for acute exacerbations?
1) Treat COPD with bronchodilators (anticholinergics, beta2-agonists, or both)
2) Give steroids and antibiotics for acute exacerbations
38
What drug class is generally contraindicated in acute COPD or asthma exacerbations?
Beta-blockers
39
How may theophylline help in COPD? What is important to monitor with theophylline use? How effective is it and when can it be used?
1) May improve mucociliary clearance and central respiratory drive
2) Narrow therapeutic index, so serum levels must be monitored
3) Only modestly effective and has more side effects than other bronchodilators. Occasionally used for patients with refractory COPD
40
What has oxygen therapy in COPD been shown to improve? How do you determine the need for oxygen? What may long-standing hypoxemia lead to? How do you reduce mortality from this complication?
1) Shown to improve survival and quality of life in patients with COPD and chronic hypoxemia
2) Some patients need continuous oxygen, whereas others only require it during exertion or sleep. Get an ABG to determine need for oxygen
3) Long-standing hypoxemia may lead to pulmonary HTN and ultimately cor pulmonale. Continuous oxygen therapy for >=18 hr/day has been shown to reduce mortality in patients with these complications by controlling pulmonary HTN
41
What is pulmonary rehabilitation and how does it help in COPD?
1) Education, exercise, and physiotherapy
2) A major goal is to improve exercise tolerance
3) Pulmonary rehabilitation improves functional status and quality of life
42
What vaccinations should be given to patients with COPD?
1) Influenza vaccination annually for all patients
2) Vaccination against Streptococcus pneumoniae every 5 to 6 years - should be offered to patients with COPD over 65 years old, or under 65 who have severe disease
43
When are antibiotics given to patients with COPD?
Antibiotics are given for acute exacerbations - increased sputum production in volume or change in character or worsening shortness of breath
44
When is surgery beneficial for COPD? What are two options?
1) Surgery may be beneficial in selected patients; carefully weight potential benefits with risks
2) Options include lung resection and lung transplantation
45
For mild to moderate COPD, what treatment should you begin with? What other medication can be used? What else can considered if these medications do not adequately control the symptoms?
1) Begin with a bronchodilator in a metered-dose inhaler (MDI) formulation (with spacer to improve deliver). Antichoinergic drugs and/or beta-agonists are first-line agents
2) Inhaled glucocorticoids may be used as well. Use the lowest dose possible
3) Theophylline may be considered if the above do not adequately control symptoms
46
For severe COPD, what treatment should you begin with?
1) Begin with a bronchodilator in a metered-dose inhaler (MDI) formulation (with spacer to improve deliver). Antichoinergic drugs and/or beta-agonists are first-line agents
2) Inhaled glucocorticoids may be used as well. Use the lowest dose possible
3) Theophylline may be considered if the above do not adequately control symptoms
4) Continuous oxygen therapy (if patient is hypoxemic)
5) Pulmonary rehabilitation
6) Triple inhaler therapy (long-acting beta-agonst plus a long-acting anticholinergic plus an inhaled glucocorticoid) is an option for severe disease
47
What is an acute COPD exacerbation? What can acute COPD exacerbation lead to?
1) Definition: Increased dyspnea, sputum production, and/or cough
2) Acute COPD exacerbation can lead to acute respiratory failure requiring hospitalization, and possibly mechanical ventilation; potentially fatal
48
What treatments are used for COPD exacerbation?
1) Bronchodilators
2) Systemic corticosteroids
3) Antibiotics
4) Supplemental oxygen
5) Noninvasive positive pressure ventilation (NPPV)
6) Intubation and mechanical ventilation may be required
49
What is the first-line therapy for an acute COPD exacerbation? What treatment is used for patients requiring hospitalization?
1) Bronchodilators (beta2-agonist) alone or in combination with anticholinergics are first-line therapy
2) Systemic corticosteroids are used for patients requiring hospitalization (IV methylprednisolone is a common choice). Taper with oral prednisone on clinical improvement. Do not use inhaled corticosteroids in acute exacerbations
50
Which antibiotics are used in acute COPD exacerbation? What have studies shown for which antibiotics to use?
1) Azithromycin, levofloxacin, doxycycline, etc.; no antibiotic superior to another
2) Studies have shown that patients who receive broad-spectrum antibiotics do slightly better than a placebo group
51
Supplemental oxygen is used in acute COPD exacerbation to keep O2 sat at what level? How should the oxygen be given? What if the SaO2 is above 93%?
1) Supplemental oxygen is used to keep O2 saturation 90% to 93%
2) Start with a nasal cannula; a face mask may need to be used
3) If SaO2 is >93%, the patient is at risk of CO2 retention from worsening V/Q mismatch, loss of hypoxemic respiratory drive, and the Haldane effect
52
What type of ventilation is used in acute COPD exacerbation? How may it help these patients?
1) Noninvasive positive pressure ventilation (NPPV) (bilevel positive airway pressure [BIPAP] or CPAP): Studies have shown a benefit in acute exacerbations
2) It may decrease the likelihood of respiratory failure requiring invasive mechanical ventilation
53
When are intubation and mechanical ventilation necessary in acute COPD exacerbation?
1) May be required if the above treatment do not stabilize the patient
2) Intubate if increasing RR, increasing PaCO2, and worsening acidosis
54
What is one of the main treatment goals for COPD patients?
To reduce the number and severity of exacerbations they experience each year
55
What is one of the main precipitants of a COPD exacerbation?
Pulmonary infection
56
What are the most common organisms in pulmonary infections that precipitate a COPD exacerbation?
S. pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Moraxella catarrhalis, and viruses
57
If a patient presents with COPD exacerbation, what steps should you take to diagnosing them and treating them?
1) CXR
2) Beta2-agonist and anticholinergic inhalers
3) Systemic corticosteroids
4) Antibiotics
5) Supplemental oxygen
6) NPPV if needed
58
What are three complications of COPD?
1) Acute exacerbations - most common causes are infection, noncompliance with therapy, and cardiac disease
2) Secondary polycythemia (Hct > 55% in men or >47% in women) - compensatory response to chronic hypoxemia
3) Pulmonary HTN and cor pulmonale - may occur in patients with severe, long-standing COPD who have chronic hypoxemia
59
What triad is asthma characteristically defined by?
1) Airway inflammation
2) Airway hyperresponsiveness
3) Reversible airflow obstruction
60
At what age can asthma being?
At any age
61
What is extrinsic asthma? At what age do patients develop extrinsic asthma? What is intrinsic asthma related to?
1) Patients are atopic, that is, produce immunoglobulin E (IgE) to environmental antigens. May be associated with eczema and hay fever
2) Patients become asthmatic at a young age
3) Intrinsic asthma - not related to atopy or environmental triggers
62
What are triggers of asthma?
Pollens, house dust, molds, cockroaches, cats, dogs, cold air, viral infections, tobacco smoke, medications (beta-blockers, aspirin), and exercise
63
What are signs of acute severe asthma attacks? What is a sign of impending respiratory failure in an acute severe asthma attack?
1) Tachypnea, diaphoresis, wheezing, speaking in incomplete sentences, and use of accessory muscles of respiration
2) Paradoxic movement of the abdomen and diaphragm on inspiration is a sign of impending respiratory failure
64
What are clinical features of asthma? How severe are the symptoms and are they present simultaneously? When do symptoms usually occur?
1) Intermittent symptoms of SOB, wheezing, chest tightness, and cough
2) Symptoms have variable severity and may not be present simultaneously
3) Usually occur within 30 minutes of exposure to triggers
65
At what time of the day are asthma symptoms typically worse?
At night
66
When should systemic glucocorticoids be used for COPD?
Only for acute exacerbations and should not be used for long-term treatment, even for patients with severe COPD
67
What are criteria for continuous or intermittent long-term oxygen therapy in COPD?
1) PaO2 55 mm Hg OR
2) O2 saturation <=88% (pulse oximetry) either at rest or during exercise OR
3) PaO2 55 to 59 mm Hg plus polycythemia or evidence of cor pulmonale
Note that the above must be consistent findings despite optimal medical therapy
68
What is the most common cause of wheezing? Can other conditions cause wheezing? Which ones and how?
1) Asthma
2) Any condition that mimics large-airway bronchospasm can cause wheezing
3) a) CHF - due to edema of airways and congestion of bronchial mucosa
b) COPD - inflamed airways may be narrowed, or bronchospasm may be present
c) Cardiomyopathies, pericardial diseases can lead to edema around the bronchi
d) Lung cancer - due to obstruction of airways (central tumor or mediastinal invasion)
69
What is the most common finding on physical examination in a patient with asthma and when does it occur in respiration?
Wheezing (during both inspiration and expiration)
70
What test is required for diagnosis of asthma? What do these tests show?
1) Pulmonary function tests (PFTs) are required for diagnosis
2) They show an obstructive pattern: decrease in expiratory flow rates, decreased FEV1, and decreased FEV1/FVC ratio (<0.70)
71
When should spirometry be done to confirm the diagnosis of asthma?
1) Spirometry before and after bronchodilators can confirm diagnosis by proving reversible airway obstruction
2) If inhalation of a bronchodilator (beta2-agonist) results in an increase in FEV1 or FVC by at least 12%, airflow obstruction is considered reversible
72
When should patients use peak flow? When should peak flow be used for mild persistent asthma and what should the patient do if peak flow decreases? When should peak flow be used for moderate persistent asthma and what should the patient do if peak flow decreases? When should peak flow be used for severe persistent asthma and what should the patient do if peak flow decreases?
1) Peak flow (peak expiratory flow rate) is a useful measure of airflow obstruction. Patients should self-monitor their peak flow
2) Periodic monitoring is sufficient. Increase the dose of inhaled steroid if the peak flow decreases
3) Moderate persistent asthma: Daily monitoring is required. Increase the dose of inhaled steroid if the peak flow decreases
4) Severe persistent asthma: Daily monitoring is required. Initiate prednisone if the peak flow decreases
73
When may the bronchoprovocation test be useful? What does it measure? How does it work?
1) May be useful when asthma is suspected but PFTs are nondiagnostic
2) Measures ease with which airways narrow in response to stimuli
3) Measures lung function before and after inhalation of increasing doses of methacholine (muscarinic agonist); hyperresponsive airways develop obstruction at lower doses
74
What does a Chest X-ray show in asthma patients? When is it necessary to do a CXR and why?
1) Normal in mild cases; severe asthma reveals hyperinflation
2) Only necessary in severe asthma to exclude other conditions (e.g., pneumonia, pneumothorax, pneumomediastinum, foreign body)
75
When should ABGs be considered for asthma? What may happen if the PaCO2 is normal or increased? Why is this so? What should you do for this patient?
1) ABGs should be considered if the patient is in significant respiratory distress. Hypocarbia is common. Hypoxemia may be present
2) If the PaCO2 is normal or increased, respiratory failure may ensure
3) Remember that patients with an asthma attack have an increased respiratory rate, which should cause the PaCO2 to decrease. Increased PaCO2 is a sign of respiratory muscle fatigue or severe airway obstruction
4) The patient should be hospitalized and mechanical ventilation considered
76
What happens to the PFTs FEV1, FVC, and FEV1/FEC ratio in asthma? What happens to the FEV1 if albuterol is given to an asthmatic patient? What happens to the FEV1 with methacholine or histamine?
1) Decreased for all three
2) Increase in FEV1 > 12% with albuterol
3) Decrease in FEV1 > 20% with methacholine or histamine
77
What is the quickest method of diagnosis of asthma when patient is SOB?
Although asthma can be diagnosed with PFTs and spirometry, in an acute setting (ED) when patient is SOB, peak flow measurement is quickest method of diagnosis
78
During asthma exacerbations, what happens to the patient's respiratory rate and what does this lead to? If the patient is no longer doing this, what could this be a sign of?
1) During asthma exacerbations, the patient hyperventilates, leading to low PaCO2 levels
2) If the patient is no longer hyperventilating (CO2 level is normal or high), this could be a sign that the patient is decompensating (due to fatigue) and that intubation may be required
79
What medication should you avoid in asthmatics?
Beta-blockers
80
What are treatment options for asthmatics?
1) Inhaled beta2-agonists
2) Inhaled corticosteroids for moderate to severe asthma
3) Montelukast - leukotriene modifiers
4) Cromolyn sodium/nedocromil sodium
81
When are short-acting beta2-agonists (e.g., albuterol) used? How long does it take to work and how long does it last for? What are long-acting versions (e.g., salmeterol) especially useful for?
1) For acute attacks (rescue)
2) Onset is 2 to 5 minutes, duration is 4 to 6 hours
3) Nighttime asthma and exercise-induced asthma
82
Why are inhaled corticosteroids preferred over oral steroids for moderate to severe asthma? What happens if you use inhaled corticosteroids on a regular basis?
1) Fewer systemic side effects (oral steroids are reserved for severe, persistent asthma)
2) Airway hyperresponsiveness decreases, and the number of asthma exacerbations decreases
83
What long-term control medications are used for mild intermittent (symptoms two or fewer times per week) asthma? Mild persistent (symptoms two or more times per week but not everyday)? Moderate persistent (daily symptoms; frequent exacerbations)? Severe persistent (continual symptoms, frequent exacerbations, limited physical activity)?
1) None
2) Low dose inhaled corticosteroids
3) Daily inhaled corticosteroid (low dose) with long-acting inhaled beta-agonist, or daily inhaled corticosteroid (medium dose). Alternatives include adding a leukotriene modifier to theophylline to the daily inhaled corticosteroid (low dose)
4) Daily inhaled corticosteroid (medium or high dose) and long-acting inhaled beta2-agonists. Omalizumab (anti-IgE) may be considered additionally. If poor control, systemic corticosteroids should be considered
84
When is montelukast useful? How can they help the dose of steroids and bronchodilators?
1) It is less efficacious than inhaled steroids but useful for prophylaxis of mild exercise-induced asthma and for control of mild to moderate persistent disease
2) They may allow reductions in steroid and bronchodilator requirements
85
When is cromolyn sodium used? Is it used in adults?
1) Only for prophylaxis (e.g., before exercise)
| 2) Rarely used in adults
86
What are side effects of inhaled corticosteroids due to and what are they? What should you do to reduce side effects?
1) Due to oropharyngeal deposition and include sore throat, oral candidiasis (thrush), and hoarseness
2) Using a spacer with MDIs and rinsing the mouth after use helps minimize these side effects
87
What tests should be ordered in acute asthma exacerbation?
1) PEF - decreased
2) ABG - increased A-a gradient
3) Chest x-ray - rule out pneumonia, pneumothorax
88
What treatments are used for acute severe asthma exacerbation (hospital admission)?
1) Inhaled beta2-agonist (first-line therapy)
2) Corticosteroids
3) Third-line agent includes IV magnesium
4) Supplemental oxygen (keep oxygen saturation >90%)
5) Antibiotics if severe exacerbation or suspicion of infection
6) Intubation for patients in respiratory failure or impending respiratory failure
89
How are inhaled beta2-agonists given? What is their onset of action? What should you do after giving a bronchodilator?
1) Via nebulizer or MDI
2) Mainstays of emergency treatment - have an onset of action of minutes
3) Assess patient response to bronchodilators (clinically and with peak flows)
90
How are corticosteroids administered in an acute severe asthma attack? When should you taper corticosteroids in this setting? What do you initiate when you begin the taper?
1) Traditionally given intravenously initially, but may also be given orally if given in equivalent doses
2) Taper IV or oral corticosteroids, but only when clinical improvement is seen
3) Initiate inhaled corticosteroids at the beginning of the tapering schedule
91
What does IV magnesium help with in an acute asthma attack?
Not as effective as beta-agonists, magnesium helps with bronchospasm but only used in acute severe exacerbation that has not responded to above medications (albuterol, steroids, oxygen)
92
What are complications of asthma?
1) Status asthmaticus - does not respond to standard medications
2) Acute respiratory failure (due to respiratory muscle fatigue)
3) Pneumothorax, atelectasis, pneumomediastinum
93
When should aspirin-sensitive asthma be considered in a patient? What should be avoided in these patients?
1) Patient with asthma and nasal polyps
2) Avoid aspirin or any nonsteroidal anti-inflammatory drugs in these patients because they may cause a severe systemic reaction
94
Is an MDI with a spacer as effective as a nebulizer? What is a spacer? What does spacer use lead to?
1) An MDI with a spacer is just as effective as a nebulizer
2) A spacer is a holding chamber that obviates the need to coordinate inhalation and depression of the canister, and thus makes the use of an MDI easier
3) Its use leads to a greater bronchodilator effect because more of the drug is deposited in smaller airways and less accumulates in the oropharynx
95
Is a nebulizer more effective than an MDI? When may it be preferred?
1) A nebulizer is no more effective than an MDI, but patients may report greater relief of symptoms simply because it provides more medication
2) It may be preferred by patients with very severe asthma unresponsive to MDIs
96
What is bronchiectasis? Is it common?
1) There is permanent, abnormal dilation and destruction of bronchial walls with chronic inflammation, airway collapse, and ciliary loss/dysfunction leading to impaired clearance of secretions
2) Less common today because modern antibiotics are used for respiratory infections
97
What are causes of bronchiectasis?
1) Recurrent infections (airway obstruction, immunodeficiency, allergic bronchopulmonary aspergillosis, mycobacterium)
2) Cystic fibrosis (CF) is most common cause of bronchiectasis (accounts for half of all cases)
3) Primary ciliary dyskinesia (e.g., Kartagener syndrome)
4) Autoimmune disease (rheumatoid arthritis, systemic lupus erythematosus, Crohn disease, etc.)
5) Humoral immunodeficiency (abnormal lung defense), airway obstruction
98
What are clinical features of bronchiectasis?
1) Chronic cough with large amounts of mucopurulent, foul-smelling sputum
2) Dyspnea
3) Hemoptysis - due to rupture of blood vessels near bronchial wall surfaces; usually mild and self-limited, but sometimes can be brisk and present as an emergency
4) Recurrent or persistent pneumonia
99
How do you diagnose bronchiectasis? What do PFTs show? CXR? Do you use bronchoscopy for diagnosis?
1) High-resolution CT scan is the diagnostic study of choice
2) PFTs reveal an obstructive pattern
3) CXR is abnormal in most cases, but findings are nonspecific
4) Bronchoscopy applies in certain cases
100
What is the treatment of bronchiectasis?
1) Antibiotics for acute exacerbations - superimposed infections are signaled by change in quality/quantity of sputum, fever, chest pain, etc.
2) Bronchial hygiene is very important
a) Hydration
b) Chest physiotherapy (postural drainage, chest percussion) to help remove the mucus
c) Inhaled bronchodilators
101
What is cystic fibrosis caused by genetically? What is the pathophysiology of cystic fibrosis? What type of lung disease does it result in and what other complications occur?
1) Autosomal recessive condition predominantly affecting Caucasians
2) Defect in chloride channel protein causes impaired chloride and water transport, which leads to excessively thick, viscous secretions in the respiratory tract, exocrine pancreas, sweat glands, intestines, and genitourinary tract
3) Typically results in obstructive lung disease pattern with chronic pulmonary infections (frequently Pseudomonas), pancreatic insufficiency, and other GI complications
102
What is the treatment for cystic fibrosis?
Pancreatic enzyme replacement, fat-soluble vitamin supplements, chest physical therapy, vaccinations (influenza and pneumococcal), treatment of infections with antibiotics, inhaled recombinant human deoxyribonuclease (rhDNase), which breaks down the DNA in respiratory mucus that clogs the airways
103
Why is cystic fibrosis a concern in adults?
Traditionally considered a pediatric topic; however, the prognosis has improved significantly, with the median age of death now over 30 years of age
104
How do infections usually cause bronchiectasis?
A variety of infections can cause bronchiectasis by destroying and damaging the bronchial walls and interfering with ciliary action
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What is the main goal in treating bronchiectasis?
To prevent complications of pneumonia and hemoptysis
