Unit 4 - Obstructive Lung Disease Flashcards
https://txwes-my.sharepoint.com/personal/deschneider_txwes_edu/Documents/Obstructive%20Lung%20Disease%20%2724%201.pdf?login_hint=deschneider%40txwes.edu (145 cards)
1
Q
4 groups of obstructive respirtory disease?
A
- Acute Upper Respiratory Tract Infection (URI)
- Asthma
- Chronic obstructive pulmonary disease (COPD)
- Miscellaneous respiratory disorders
slide 2
2
Q
URI
What rate do ages 25-44 experience the “common cold”? Ages 45-65?
A
25-44yo: 19% per year
45-65yo: 16% per year
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3
Q
URI
What accounts for about 95% of all URIs?
A
Infectious nasopharyngitis
slide 3
4
Q
URI
What are the most common associated viral pathogens for URIs?
A
- rhinovirus
- coronavirus
- influenza
- parainfluenza
- respiratory syncytial virus (RSV)
slide 3
5
Q
URI
What are the two causes on noninfectious nasopharyngitis?
A
allergic and vasomotor
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6
Q
URI
What perioperative resp. events are children with URIs at higher risk for?
A
- transient hypoxemia
- laryngospasm
- breath holding
- coughing
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7
Q
URI
Adverse respiratory events in pts with URI?
All pts. Not just kids.
A
- bronchospasm
- laryngospasm
- airway obstruction
- postintubation croup
- desaturation
- atelectasis
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8
Q
URI
When is is safe to proceed with surgery on a patient with an URI? If you had to reschedule surgery, how far out should you reschedule?
A
A patient that has had their URI for weeks and is stable can proceed with surgery.
Reschedule for 6 weeks out to avoid airway hyperreactivity period.
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9
Q
URI
COLDS scoring system:
What does it determine and what does it stand for?
A
Determines risk of proceeding with surgery.
C: current symptoms
O: onset of symptoms (higher risk within 2 weeks)
L: lung disease (comorbidities)
D: device for airway (ETT = higher risk)
S: surgery (major airway surgery = higher risk)
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10
Q
URI
Anesthesia mgmt for pts with URI?
A
- adequate hydration
- reducing secretions
- limiting airway manipulation
- neb or topical LA on vocal cords to dec. sensitivity
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11
Q
URI
What airway considerations would we do for URIs?
A
LMA over ETT to reduce laryngospasm. Deep extubation (if no contraindication) to allow for smoother emergence.
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12
Q
Asthma
Asthma definition:
A
chonic inflammation of the mucosa of the lower airways
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13
Q
Asthma
Inflammatory process:
A
inflammatory cascade leads to infiltration of the airway mucosa with eosinophils, neutrophils, mast cells, T cells, B cells, and leukotrienes.
Results in airway edema (esp. in the bronchi) and airway remodeling causing thickening to basement membrane and smooth muscle mass.
slide 7
14
Q
Asthma
3 main inflammatory mediators implicated in asthma?
A
- histamine
- prostaglandin D2
- leukotrienes
Release of these are caused by:
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15
Q
Asthma
Symptoms of exacerbations?
A
- expiratory wheezing
- productive or nonproductive cough
- dyspnea
- chest tightness that may lead to air hunger
- eosinophilia
most attacks are short lived (minutes to hours) and m
16
Q
Asthma
What is status asthmaticus?
A
dangerous, life threatening cronchospasm that persists despite treatment
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17
Q
Asthma
What should pre-op history questions be focused on?
A
- previous intubations
- ICU admissions
- 2+ hospitalizations for asthma within the past year
- presence of coexisting disease
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18
Q
Asthma
What symptoms lead to a **diagnosis **of asthma?
A
- wheezing
- chest tightness
- SOB
**AND ** a demonstrated airflow obstruction on PFT that is at least partially reversible with bronchodilators
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19
Q
Asthma
Table of most clinically useful Spirometric Tests of lung function:
A
slide 10
20
Q
Asthma
What is the FEV1 of the typical asthmatic patient that comes to the hospital?
A
< 35%
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21
Q
Asthma
Which three PFTs are direct measurements of the severity of expiratory obstruction?
A
FEV1, FEF, and midexpiratory phase flow
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22
Q
Asthma
What changes to FRC and TLC might we see during moderate or severe asthma attacks?
A
FRC: increase substantially
TLC: usually remains normal
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23
Q
Asthma
What causes tachypnea and hyperventilation during asthma attacks?
A
neural reflexes
NOT hypoxemia
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24
Q
Asthma
What are the two most common findings of asthma on an ABG?
A
hypocarbia
respiratory alkalosis
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25
# Asthma
When do we see a decrease in PaO2?
When the severity of expiratory obstruction increases and we have worsening of ventilation/perfusion mismatching leading to a PaO2 < 60 mmHg
## Footnote
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26
# Asthma
At what point do we see an increase in PaCO2 during an asthma attack?
When the FEV1 is < 25% of predicted
## Footnote
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27
# Asthma
What does an EKG tell us during an asthma attack?
Might show signs of right ventricular strain or ventricular irritability
## Footnote
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28
# Asthma
What chest xray findings would we see with an asthma attack?
hyperinflationa and hilar vascular congestion due to mucus plugging and pulmonary hypertension
## Footnote
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29
# Asthma
What is 1st line treatment for mild asthmatics?
PRN short acting inhaled B2 agonist
| only recommended for patients with < 2 exacerbations per month
## Footnote
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30
# Asthma
What other type of inhaler can we use to reduce exacerbations and decrease risk of hospitalizations? What do we give if symptoms persist?
daily inhaled corticosteroids
If symptoms persist, we can do a daily inhaled B2 agonist.
## Footnote
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31
# Asthma
What are last ditch effort treatment for severe asthma that is uncontrolled with inhalation medications?
systemic corticosteroids
## Footnote
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33
# Asthma
What other therapies can we try besides SABA and inhaled corticosteroids?
* inhaled muscarinic antagonists
* leukotriene modifiers
* mast cell stabilizers
## Footnote
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34
# Asthma
What is bronchial thermoplasty (BT)?
Uses bronchoscopy to deliver radiofrequency ablation of airway smooth muscles to all lung fields except the right middle lobe
Procedure is performed in 3 sessions and uses intense heat and the loss of airway smooth muscle mass is thought to reduce bronchoconstriction.
| Only non-pharmacologic treatment for refractory asthma.
## Footnote
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35
# Asthma
What are the two most common IV corticosteroids used in acute severe asthma?
When should we admnister them?
hydrocortisone and methylprednisone
Administer early because onset takes several hours.
## Footnote
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36
# Asthma
How often can we administer inhaled B2 agonists? What adverse effects might we see from them?
Q15-30 min
minimal adverse hemodynamic effects, but pts may have unpleasant sensations from adrenergic overstimulation.
## Footnote
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37
# Asthma
Table: Treatment for acute severe asthma.
## Footnote
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38
# Asthma
What types of surgeries increase risk of bronchospasm?
upper abdominal surgeries and oncologic surgeries
## Footnote
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39
# Asthma
What GA mechanisms increase airway resistance?
* depression of cough reflex
* impairment of mucociliary function
* increased fluid in the airway wall
* airway stimulation by intubation
* PNS activation
* release of neurotransmitters such as Substance P and neurokinins
## Footnote
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40
# Asthma
What lab value often mirrors the degree of airway inflammation?
eosinophil count
## Footnote
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41
# Asthma
When do we give a stress dose of hydrocortisone or methylprednisone prior to surgery?
If the patient has been taking systemic corticosteroids within the past 6 months.
## Footnote
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42
# Asthma
What are two requirements for pts to go to surgery?
1. free of wheezing
2. PEFR > 80% of predicted or the pt's personal best
## Footnote
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43
# COPD
What are the symptoms of COPD?
* emphysema characterized by lung parynchemal destruction
* chronic bronchitis
* productive cough
* small airway disease
* dyspnea at rest or exertion
* chronic sputum production
* decreased breath sounds
* expiratory wheezes
## Footnote
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44
# COPD
Risk factors for COPD?
* cigarette smoking
* occupational exposure to dust and chemicals, asbestos, gold mining, biomass fuel, air pollution
* genetic factors
* age
* female gender
* poor lung development during gestation
* low birth weight
* recurrent childhood respiratory infections
* low socioeconomic class
* asthma
## Footnote
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45
# COPD
COPD leads to:
1. deterioration in elastic recoil
2. decrease bronchial wall structure allowing collapse during expiration
3. inc. velocity through the narrowed bronchioli which lowers intrabronchial pressure
4. active bronchospasm and obstruction from inc. secretions
5. destruction of lung parynchema enlarged air sacs, and development of emphysema
## Footnote
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46
# COPD
What is a COPD exacerbation?
acute worsening in airflow
as expiratory obstruction increases, tachypnea and prolonged expiratory times become evident
## Footnote
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47
# COPD
What PFT changes are associated with COPD?
* decrease in FEV1:FVC ratio (<70%)
* FEF between 25% and 75% of vital capacity
* increased RV, FRC, and TLC (think higher lung volumes with loss of reserve)
* decreased DLCO (diffusing lung capacity for carbon monoxide)
## Footnote
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48
# COPD stages
Mild COPD
FEV1 ≥ 80% predicted
## Footnote
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49
# COPD stages
Moderate COPD
50% ≤ FEV1 < 80%
## Footnote
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50
# COPD stages
Severe COPD
30% ≤ FEV1 < 50% predicted
## Footnote
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51
# COPD stages
Very severe COPD
FEV1 < 30% predicted
## Footnote
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52
# COPD
Lung volume changes in COPD?
| VC, TLC, RV and FRC, RV:TLC ratio - increased or decreased?
VC: normal to decreased
TLC: normal to increased
RV and FRC: increased
RV:TLC ratio: increased
## Footnote
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53
# COPD
What CXR finding suggests and confirms emphysema?
suggests: hyperlucency
confirms: bullae
| only small % of pts have bullae
## Footnote
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54
# COPD
What is MOLT?
multi-organ loss of tissue
a phenotype of COPD associated with airspace enlargement, alcveolar destruction, loss of bone, muscle, and fat tissues, and carries higher rates of lung cancer
## Footnote
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55
# COPD
What is Bronchitic?
phenotype of COPD associated with bronchilar narrowing and wall thickening and is usually accompanied by metabolic syndrome and cardiac disease
## Footnote
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56
# COPD
What is the BODE index? What does a higher BODE mean?
Grading system that looks at BMI, degree of obstruction, level of dyspnea, and exercise tolerance to assess prognosis.
Higher BODE indicates greater risk of exacerbations, hospitalizations, and pulmonary death
## Footnote
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57
# COPD
What is a1-antitrypsin deficiency?
An inherited disorder associated with COPD. Low levels require lifelong replacement therapy.
## Footnote
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58
# COPD
When do we measure eosinophils in COPD pts and what does that measurement tell us?
measured with uncontrolled disease despite bronchodilators
High: indicate need for inhaled glucocorticoids
Low: associated with increased risk of pneumonia
## Footnote
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59
# COPD
When does PaO2 decrease in COPD patients? When does PaCO2 increase?
PaO2: decreases when FEV1 is < 50% of predicted (severe and very severe stages)
PaCO2: increases when FEV1 is even lower (think very severe stage)
## Footnote
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60
# COPD
What is the 1st step in treatment for COPD?
reduce exacerbations!! reduce exposure to smoke and environmental pollutants
*smoking cessation can decrease disease progression and lower mortality rates by up to 18%
## Footnote
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61
# COPD
In what order are inhaled medications prescribed to COPD patients?
1. long-acting inhaled muscarinic antagonists
2. long-acting B2 agonists
3. inhaled glucocorticoids
## Footnote
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62
# COPD
When are inhaled glucocorticoids most effective in COPD patients?
When they have associated asthma, rhinitis, elevated eosinophils, and history of exacerbations
## Footnote
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63
# COPD
When do we give COPD patients diuretics?
If right heart failure or congestive heart failure has developed
## Footnote
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64
# COPD
When is long-term home O2 recommended for COPD patients?
When PaO2 is < 55 mmHg, the HCT >55% or if there is evidence of cor pulmonale
## Footnote
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65
# COPD
What is the goal for supplemental O2 and how much O2 is usually required to reach this goal?
goal is PaO2 > 60mmHg
2 L NC
## Footnote
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66
# COPD
Table:
Treatment of Patients with COPD
Treatments of Patients with COPD exacerbations
## Footnote
Slide 35
67
# COPD
Who is a candidate for lung volume reduction surgery?
pts with severe refractory COPD and overdistended lung tissue
## Footnote
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68
# COPD
What is lung volume reduction surgery?
removal of overdistended areas allowing more areas of normal lung to expand and improve lung function
*Most commonly performed via a median sternotomy or VATS
## Footnote
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69
# COPD
3 things for anesthesia management for lung-volume reduction surgery?
1. double lumen ETT
2. avoidance of N2O
3. minimizing excessive airway pressure
## Footnote
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70
# COPD
Why might CVP be an unreliable guide for fluid management in lung-volume reduction surgery patients?
because surgical alterations affect intrathoracic pressures
## Footnote
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71
# COPD
Indications for pre-op pulmonary evaluation:
## Footnote
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72
# COPD
Table:
Major Risk Factors for Development of Postoperative Pulmonary Complications
## Footnote
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73
# COPD
Table:
Strategies to reduce post-op complications
74
# COPD
What percentage of smokers undergo general anesthesia annually?
5-10%
*This is an opportunity for us to teach about smoking cessation. *
## Footnote
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75
# COPD
What is the single most important risk factor for developing COPD and death caused by lung disease?
smoking
## Footnote
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76
# COPD
The maximum benefit of smoking cessation is not usually seen unless smoking is stopped at least ------- prior to surgery.
8 weeks
## Footnote
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77
# COPD
How long do the sympathomimetic effects of nicotine last on the heart?
20-30 minutes
## Footnote
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78
# COPD
What is the elimination half-life of carbon monoxide?
4-6 hours
## Footnote
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79
# COPD
Within 12 hours of quitting smoking, what changes will you see in P50 value and plasma levels of carboxyhemoglobin?
P50 increases from 22.9 to 26.4 mmHg
HbCO decreases from 6.5% to 1%
| Remember P50 is the PaO2 required to saturate 50% of Hb with oxygen.
## Footnote
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80
# COPD
How long after quitting smoking until we see return of normal immune function?
6 weeks
## Footnote
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81
# COPD
How long after quitting smoking until hepatic enzyme function returns to normal?
6 weeks or longer
82
# COPD
What are the disadvantages to stopping smoking in the immediate pre-op period?
* increase in sputum production
* inability to handle stress
* nicotine withdrawal
* irritability
* restlesness
* sleep disturbances
* depression
## Footnote
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83
# COPD
What interventions can we provide to assist with smoking cessation?
Behavioral support and pharmacotherapy:
* nicotine replacement (patches, inhalers, nasal sprays, lozenges, gum
* sustained release bupropion (Wellbutrin)
## Footnote
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84
# Bronchiectasis
What is bronchiectasis?
irreversible airway dilaiton, inflammation and chronic bacterial infection
## Footnote
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85
# Bronchiectasis
Symptoms of bronchiectasis?
* chronic productive cough
* purlent sputum
* hemoptysis
* clubbing
* poor mucocilliary activity (leading to recurrent infections)
## Footnote
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86
# Bronchiectasis
What is seen on CT that is the gold standard diagnosis for bronchiectasis?
dilated bronchi
## Footnote
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87
# Bronchiectasis
What are the key treatments?
* antibiotics based on sputum culture
* bronchodilators
* systemic corticosteroids
* O2 therapy
* surgery (rare)
## Footnote
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88
# Cystic FIbrosis
What is CF?
autosomal recessive disorder of the chloride channels leading to abnormal production and clearance of secretions
## Footnote
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89
# CF
What gene mutation causes CF?
mutation on chromosome 7
| encodes the cystic fibrosis transmembrane conductance regulator (CFTR)
## Footnote
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90
# CF
What does CFTR do?
produces a protein that aids in salt and water movement in and out of cells.
In CF, the mutated gene results in the production of abnormally thick mucus outside of epithelial cells.
## Footnote
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91
# CF
What is the primary cause of morbidity and mortality in CF patients?
chronic pulmonary infection
## Footnote
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92
# CF
How does chloride transport disrupt lung function?
decreased chloride transport is accompanied by decreased transport of sodium and water, which leads to:
* dehydrated viscous secretions
* luminal obstruction
* destruction and scarring of various glands and tissues
## Footnote
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93
# CF
What is the diagnostic criteria?
sweat chloride conc. > 60mEq/L **AND** clinical symptoms such as:
* cough
* purulent sputum
* exertional dyspnea
* family history of CF
## Footnote
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94
# CF
What is evidence of pancreatic exocrine insufficiency associated with CF?
malabsorption with a response to pancreatic enzyme treatment
## Footnote
slide 50
95
# CF
What reproductive test is an indicator of CF?
obstructive azoospermia confirmed by testicular biopsy
## Footnote
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96
# CF
What comorbidity is present in virtually all adult CF patients?
COPD
## Footnote
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97
# CF
What is the treatment for CF?
* symptom management
* pancreatic enzyme replacement
* O2 therapy
* nutrition
* prevention of intestinal obstruction
* gene therapy currently being investigated
## Footnote
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98
# CF
What is the main non-pharmacologic approach to enhancing clearance of secretions?
chest physiotherapy with postural drainage
high-frequency chest compression with an inflatable vest and airway oscillation devices are also good for this
## Footnote
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99
# CF
When are bronchodilators used for CF patients?
When they are "beneficial" lol duh.
Beneficial response = an increase of 10% or more in FEV1 after administration of bronchodilator
## Footnote
slide 51
100
# CF
What is present in secretions that makes it super viscous?
neutrophils and degredation products (DNA released from neutrophils that form long fibrils)
## Footnote
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101
# CF
What treatment can cleave the DNA fibrils and increase the clearance of sputum?
recombinant human deoxyribonuclease
## Footnote
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102
103
# CF
When do we give antibiotics to CF patients?
Only if they have a confirmed infection from bacteria isolated from sputum.
## Footnote
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104
# CF
What do we do if the sputum culture shows no pathogens?
Bronchoscopy to remove lower airway secretions
## Footnote
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105
# CF
When do we give Vitamin K?
if hepatic function is poor or exocrine pancreatic function is impaired
## Footnote
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106
# CF
What are ways we can maintain less-viscous secretions?
* humidification of gases
* hydration
* avoidance of anticholinergic drugs
## Footnote
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107
# CF
What are requirements prior to extubation?
| aside from the normal shizzz
* regain full airway reflexes
* and obvi have adequate TV and RR
## Footnote
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108
# CF
Why is post-op pain control important for CF patients?
Bc they gotsta be able to cough, deep breathe, and ambulate to prevent pulmonary complications.
## Footnote
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109
# Primary Ciliary Dyskinesia (PCD)
What is PCD?
congenital impairment of ciliary activity in respiratory tract, epithelial celss, and sperm tails/ciliated ovary ducts.
this leads to chronic sinusitis, recurrent respiratory infections, bronchiectasis, and infertility
## Footnote
slide 54
110
# PCD
What is Kartagener Syndrome?
triad of
1. chronic sinusitis
2. bronchiectasis
3. situs inversus (chest organ position is inversed)
## Footnote
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111
# PCD
What percentage of patient with congenitally nonfunctioning cilia exhibit situs inversus?
about half
## Footnote
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112
# PCD
Isolated dextrocardia is almost always associated with what?
congenital heart disease
*This is when the heart is located on the opposite side of the body but there are no other thoracic abnormalities. *
## Footnote
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113
# PCD
Do we prefer RA or GA for these patients?
RA to help decrease postop pulmonary complications
## Footnote
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114
# PCD
What does dextrocardia mean for our monitors?
EKG equipment should be reversed for accurate interpretation
## Footnote
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115
# PCD
What vein is preferred for CVC placement?
L IJ since the great vessels are inverted
| Normally we do RIJ since it goes straight to SVC.
## Footnote
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116
# PCD
Which way do we displace the uterus in pregnant women with PCD to prevent vena cava syndrome
right.
Normal mommas get displaced to the left.
## Footnote
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117
# Bronchiolitis Obliterans (BO)
What causes BO?
results from epithelial and subepithelial inflammation leading to bronchiolar destruction and narrowing
## Footnote
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118
# BO
Risk factors?
* viral respiratory infections
* environmental exposures
* lung transplant
* stem cell transplant
## Footnote
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119
# BO
PFT results with BO?
usually show obstructive lung disease
* reduced FEV1
* reduced FEV1:FVC ratio
## Footnote
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120
# BO
What do we see on CT for these pts?
air trapping and bronchiectasis in severe cases
## Footnote
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121
# Central Airway Obstruction (CAO)
What percentage of lung cancer patient can be affected by airflow obstruction?
20-30%
## Footnote
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122
# CAO
Which airways are included in CAO?
obstruction of airflow in the trachea and mainstem bronchi
## Footnote
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123
# CAO
What causes obstruction?
| think disease processes, not foreign body
* tumors
* granulation from chronic infection
* airway thinning from cartilage destruction
## Footnote
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124
# CAO
How can we cause tracheal stenosis?
with prolonged intubation either with an ETT or a tracheostomy tube
125
# CAO
How do we prevent tracheal stenosis from artificial airways?
high volume low pressure cuffs
## Footnote
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126
# CAO
What does tracheal mucosal ischemia progression cause?
* destruction of cartilaginous rings
* subsequent circumferential scar formation
## Footnote
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127
# CAO
At what point does tracheal stenosis become symptomatic?
When the lumen is decreased to < 5 mm in diameter
## Footnote
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128
# CAO
Tracheal stenosis symptoms?
* dyspnea (even at rest)
* accessory muscle use though all phase of respiratory cycle
* audible stridor
* tracheal narrowing on CT
* flattened flow volume loops characteristic of fixed obstruction
| may not develop for several weeks after extubation
## Footnote
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129
# CAO
What procedure can temporarily fix tracheal stenosis?
tracheal dilation via bronchoscopy with balloon dilators, surgical dilators, or laser resection of the tissue
## Footnote
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130
# CAO
Is tracheobronchial stent short or long term solution for tracheal stenosis?
trick question bitches, it can be both.
## Footnote
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131
# CAO
What is the most successful surgical treatment for tracheal stenosis and what kind of airway does it require?
surgical resection and reconstruction with primary re-anastomosis.
Requires a translaryngeal intubation
## Footnote
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132
# CAO
What anesthetic considerations are there for tracheal resection and reconstruction?
* use volatiles to ensure maximal FiO2
* may use high frequency ventilation
* may add helium gas to facilitate anesthetics
## Footnote
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133
# CAO
How does helium gas facilitate anesthetic gasses?
Helium decreases the density of the gas mixture and may improve flow through the area of tracheal narrowing
## Footnote
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134
# Kahoot:
What pathology is responsible for themajority of URIs?
A. Infectious laryngitis
B. Infectious brinchitis
C. Infectious nasopharyngitis
D. Infectious cystic fibrosis
C. Infectious Nasopharyngitis
135
# Kahoot:
Which interventions can minimize the risk of laryngospasm in URI patient?
A. LMA
B. Nebulized local anesthetics
C. bronchodilators
D. oropharyngeal suctioning
A, B, and D
LMA, neb locals, and oropharyngeal suctioning
136
# Kahoot:
The main inflammaotry mediators in asthma?
A. Histamine
B. Leukotrienes
C. Free radicals
D. Prostaglandin D2
A, B, and D
histamine
leukotrienes
prostaglandin d2
137
# Kahoot:
Which spirometric value refers to the volume of air exhaled with mex effort after deep inhalation?
A. FEV1
B. FRC
C. FVC
D. TLC
C. FVC
138
# Kahoot:
Which spirometric valure remains unchanged during an asthma attack?
A. DLCO
B. FEV1
C. FVC
D. FEF
A. DLCO
139
# Kahoot:
What is the mechanism stimulated tachypnea and hyperventilation during an asthma attack?
A. hypoxemia
B. hypercarbia
C. pulmonary neural reflexes
D. metabolic acidosis
C. pulmonary neural reflexes
140
# Kahoot:
At what level of FEV1 does the PaCO2 increase?
A. < 30%
B. < 25%
C. < 40%
D. < 50%
B. < 25%
141
# Kahoot
Select two types of surgery that are associated with a higher risk of bronchospasm.
A. oncologic surgery
B. laparoscopic surgery
C. upper abdominal surgery
D. neurosurgery
A and C
oncologic surgery
upper abdominal surgery
142
# Kahoot
Which lung volume may be decreased in COPD?
A. TLC
B. VC
C. FRC
D. RV
B. vital capacity
143
# Kahoot
Which radiologic finding confirms a diagnosis of COPD?
A. bullae
B. hyperlucency
C. kerly lines
D. blebs
A. Bullae
144
# Kahoot
Which disorder is associated with irreversible airway dilation, inflammation, and chronic bacterial infection?
A. cystic fibrosis
B. bronchiectasis
C. primary ciliary dyskinesia
D. bronchiolitis obliterans
B. Bronchiectasis
145
# Kahoot
Which respiratory disorder is commonly associated with situs inversus?
A. cystic fibrosis
B. bronchiectasis
C. primary ciliary dyskinesia
D. bronchiolitis obliterans
C. Primary ciliary dyskinesia
