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Pulmonary Review > Obstructive Lung Disease > Flashcards

Obstructive Lung Disease Flashcards

1
Q

This is a state of having IgE antibodies to specific allergens

A

Atopy

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2
Q

True or False: Higher IgE levels is correlated with higher asthma severity

A

True

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3
Q

Which WBCs are associated with the major pathophysiology behind the inflammatory reaction of asthma?

A

Th2 cells

Initial exposure with APCs to an allergen in the airway leads to the actiation of CD4 lymphocytes –> developp into Th2 cells –> secretion of IL-4, IL-5, and IL-13 –> B cell stimulation to synthesize IgE

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4
Q

Which medications stabilize mast cell membranes, so that they dont release inflammatory mediators (histamine, tryptase, PGD2, leukotrienes, cytokines) when exposed to an allergen?

A

ß-receptor agonists

Cromones (sodium cromoglycate)

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5
Q

Which cells are attracted to the bronchial walls by IL-3, IL5, and GM-CSF by Th2 cells that bind and release a large number of proinflammatory mediators like leukotrienes and basic proteins?

A

Eosinophils

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6
Q

Which class of medications decrease the number of eosinophils in circulation, decrease penetration in the bronchial walls, and prevent eosinophil activation that have entered the bronchial walls?

A

Corticosteroids

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7
Q

Which interleukins do basophils secrete in asthma?

A

IL-4 and IL-13

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8
Q

Which cells in asthma cause tissue inflammation and remodeling through release of INFg and TNF?

A

Th1 cells

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9
Q

Which cells in asthma secrete IL-17 which is associated with neutrophilic inflammaiton during acute exacerbation and with tissue remodeling?

A

Th17 cells

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10
Q

Which IL directs B lymphocytes to synthesize IgE?

A

IL-4

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11
Q

Which IL regulates eosinophil production and maturation?

A

IL-5

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12
Q

Which IL leads to airwya eosinophiolia, mucus gland hyperplasia, airway fibrosis, and remodeling?

A

IL-13

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13
Q

This is a non-immune asthma where a single exposure to an irritant renders the patient sensitive to subsequent exposures to similar compounds

A

Reactive airway dysfunction syndrome (RADS)

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14
Q

Prolonged asthma can lead to airway remodeling. The changes below lead to what consequences?

Smooth muscle mass increase -->
Mucus gland increase --> 
Inflammatory cell persistence -->
Fibrogenic growth factor release -->
Elastolysis -->
A

Smooth muscle mass increase –> severe bronchospasm during exacerbation

Mucus gland increase –> important mucous secretion during exacerbation

Inflammatory cell persistence –> ongoing inflammation

Fibrogenic growth factor release –> collagen deposition on RBM and ECM

Elastolysis –> reduced elasticity of airway wall

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15
Q 
22-year-old male is seen
for evaluation of his
asthma. He was born at a
gestational age of 42
weeks by planned
cesarean section to a 19-
year-old mother. During
pregnancy his mother took
herbal pills containing
vitamin K. Which of these
perinatal factors is
associated with the
development of childhood
asthma?
A 
Delivery by cesarean
section. Prematurity (birth
between 23-27 weeks
gestational age), neonatal
jaundice, and prenatal
exposure to maternal
smoking are other risk
factors. Maternal age and
vitamin K use have not
been shown to be risk
factors
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16
Q

True or False: a positive bronchodilator response is sufficient in the diagnosis of ashtma.

A

FALSE

Positive BD response can be seen in other conditions such as COPD, bronchiectasis, bronchiolitis, and CF

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17
Q

What can lead to a false negative bronchodilator response in asthma?

A

Inadequate dose of bronchodilator

Used inhaler before PFTs done

Presence of minimal airflow obstruction during testing

Concomitant presence of irreversible airway obstruction due to airway remodeling or fibrosis

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18
Q

This test is used to confirm asthma if there is a high clinical suspicion and normal spirometry

A

Bronchoprovocation testing

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19
Q

What are absolute contrainidications to bronchopovocation testing?

Think SMUK

A

Severe airflow limitation (FEV1<50% or <1L)

MI or CVA in last 3 months

Uncontrolled hypertension (SBP>200 or DBP>100)

Known aortic aneurysm

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20
Q

Which things can cause false positive bronchoprovocation testing?

Think ABCs

A 
Allergic rhinitis
Bronchitis
Congestive heart failure
COPD
CF
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21
Q

This test is used to evaluate for eosinophilic airway inflammation

A

Exhaled NO

Those with asthma have higher NO in their airways than those without asthma

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22
Q

What blood tests are recommended to be obtained for patients with a suspicion of asthma?

A

CBC with diff
RAST
IgE

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23
Q

True or False: chest imaging is recommended in the initial exam for asthma

A

TRUE

used to r/o other conditions that can mimic asthma

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24
Q

This is the asthma mimicker that has the following properties:

Exertional dyspnea, peripheral edema, elevated BNP

A

CHF

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25
Q

This is the asthma mimicker that has the following properties:

Symptoms with identifiable trigger, PFTs showing an obstructive/restrictive/mixed pattern with reduced DLCO, GGO’s on imaging

A

Hypersensitivity pneumonitis

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26
Q

This is the asthma mimicker that has the following properties:

Travel history, elevated IgE and eosinophilia

A

Parasitic lung infection

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27
Q

This is the asthma mimicker that has the following properties:

Peripheral blood eosinophilia, chronic rhinosinusitis, possible reduced DLCO on PFTs

A

Asthmatic granulomatosis

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28
Q

This is the asthma mimicker that has the following properties:

Imaging studies showing hilar adenopathy with or without reticular or nodular opacities

A

Endobronchial sarcoidosis

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29
Q

This condition shows obstruction on spirometry and has the following features:

Significant smoking history, family history of A1AT deficiency, reduced DLCO

A

COPD

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30
Q

This condition shows obstruction on spirometry and has the following features:

Excessive chronic sputum production, history of recurrent infections, HRCT showing mucus plugging + tram tracking + dilated airways

A

Bronchiectasis

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31
Q

This condition shows obstruction on spirometry and has the following features:

History of viral illness, inhlalation injury, lung transplant, rheumatoid lung disease, or IBD. PFTs show worsening obstruction with reduced DLCO.

A

Constrictive bronciolitis

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32
Q

This condition shows obstruction on spirometry and has the following features:

Stridor and monomorphic or localized wheezing, no bronchodilator response, flattening of flow-volume loop

A

Central airway obstruction

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33
Q

This condition shows obstruction on spirometry and has the following features:

Stridor, wheezing, typically symptomatic in response to an irritant, history of intubation or trauma to laryngeal nerve

A

Laryngeal dysfunction

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34
Q

This condition shows obstruction on spirometry and has the following features:

Recent URI, transient and usually resolves in weeks

A

Reactive airways viral syndrome

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35
Q

What type of imaging is recommended in severe asthma due to possible component of allergic rhinosinusititis?

A

Sinus CT

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36
Q

In patients without reflux symptoms and moderate-severe asthma, what studies is recommended?

A

pH probe for GERD

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37
Q

What body habitus is associated with worsened asthma severity?

A

Obesity

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38
Q

What study is recommended for patients with asthma in those with nocturnal symptoms, daytime sleepiness, and difficult to control asthma?

A

Polysomnography

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39
Q 
A 55-year-old patient with
asthma had three episodes
of fever with worsening
dyspnea as well as sputum
production with brownish
mucus plugs in the last 2
months. Chest radiographs
show fleeting infiltrates and
an HRCT shows central
bronchiectasis. Serum IgE
levels are elevated (1200
ng/mL) with peripheral
blood eosinophilia
(700/mL).
What is the most likely
diagnosis? Which test
should be done next?
A 
Allergic bronchopulmonary
aspergillosis.
A skin-prick test checking
reactivity to Aspergillus
fumigatus should be
performed.
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40
Q

Treatment of ABPA?

A

Glucocorticoids slowly tapered over 3-6 months.

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41
Q

Pathophysiology behind exercise induced asthma?

A

For the first 6-8 minutes of exercuse there is bronchodilation –> bronchoconstriction at 10-15 mins

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42
Q

Diagnostic testing modality behind exercise induced asthma?

A

Exercise challenge test with spirometric measurements before and after exercise

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43
Q

What medications are used for the treatment of exercise induced asthma?

A

SABA 10 mins before exercise

Cromoglycates 15-20 mins before exercise

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44
Q

Select from the list of work-related asthma based on the following clinical scenario

List: reactive airways dysfunction syndrome (RADS), occupational nonasthmatic eosinophilic bronchitis, irritant induced asthma, occupational asthma, work-exacerbated asthma

Scenario: adult onset, triggered by stimuli found only in the workplace

A

Occupational asthma

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45
Q

Select from the list of work-related asthma based on the following clinical scenario

List: reactive airways dysfunction syndrome (RADS), occupational nonasthmatic eosinophilic bronchitis, irritant induced asthma, occupational asthma, work-exacerbated asthma

Scenario: presence of pre-existing asthma, subjective worsening at the workplace

A

Work-exacerbated asthma

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46
Q

Select from the list of work-related asthma based on the following clinical scenario

List: reactive airways dysfunction syndrome (RADS), occupational nonasthmatic eosinophilic bronchitis, irritant induced asthma, occupational asthma, work-exacerbated asthma

Scenario: onset in adulthood, induced by irritant exposure, nonimmunologic response

A

Irritant induced asthma

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47
Q

Select from the list of work-related asthma based on the following clinical scenario

List: reactive airways dysfunction syndrome (RADS), occupational nonasthmatic eosinophilic bronchitis, irritant induced asthma, occupational asthma, work-exacerbated asthma

Scenario: acute single high-intensity exposure to a non-immunologic stimulus at a high level of intensity, followed by bronchial hyperresponsiveness and ongoing asthma symptoms for a long time

A

RADS

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48
Q

Select from the list of work-related asthma based on the following clinical scenario

List: reactive airways dysfunction syndrome (RADS), occupational nonasthmatic eosinophilic bronchitis, irritant induced asthma, occupational asthma, work-exacerbated asthma

Scenario: adult onset, asthma mimicker, develops at workplace, absence of bronchial hyperresponsiveness but high sputum eosinophils

A

Occupational nonasthmatic eosinophilic bronchitis

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49
Q

A 45 year old woman presents that every time she is at work she develops a sensation of fullness and tension in the throat and neck, dysphonia, and has a chronic cough. Diagnosis?

A

Work-related irritable larynx syndrome

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50
Q

What measurement can you do to confirm occupational asthma, where the patient can obtain these numbers 4x/day for 2 weeks and similar rates when not at work?

A

Peak expiratory flow rates

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51
Q

After exposure to an a irritant substance, how long can RADS last?

A

at least 3 months

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52
Q

What is the FEV1 threshold in order to use systemic steroid therapy for RADS?

A

<70%

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53
Q

What inhalers can you use with someone with RADS and has FEV1 >70%?

A

ICS and/or ß-agonist

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54
Q

Differential for patients with nocturnal asthma?

A

OSA
GERD
CHF

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55
Q

True/False: patients with aspirin exacerbated respiratory disease (AERD) with anosmia or peresistent nasal blockage should get a 15 day course of oral prednisone

A

TRUE

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56
Q

If patients with AERD fail to respond to oral steroids, what is the next management consideration?

A

Sinus surgery

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57
Q

Which antibiotic can reduce the size of nsal polyps and amount of secretions in those with AERD with nasal polyps?

A

Doxycycline

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58
Q

Mainstay of treatment for those with AERD and nasal polyps in patients without anosmia or persistent nasal blockage?

A

Topical corticosteroids

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59
Q

This is the protocol to inducing tolerance to ASA/NSAIDs in patients who experience pseudoallergic reactions

A

Desensitization

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60
Q

Indications for aspirin desensitization?

A
  1. Worsening nasal polyposis despite maximal therapy
  2. Treatment of other conditions that require daily or intermittent use of NSAIDs
  3. CAD or other vascular processes that require ASA
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61
Q

Which medication class reduces the pulmonary manifestations after exposure to ASA/NSAIDs but do not impact the nasal or ocular manifestations in AERD?

A

Leukotriene-modifying agents

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62
Q

Aspirin dose after the patient tolerates the full aspirin desensitization protocol?

A

650 bid for 3 months, then decrease to 325mg daily.

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63
Q

How many days of ASA can you miss before you need re-desensitized?

A

> 5 days

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64
Q

How to avoid the following allergen, that might exacerbate asthma?

Animal allergens

A

Five point palm exploding heart technique

Also, HEPA filters might work.

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65
Q

How to avoid the following allergen, that might exacerbate asthma?

Dust mites

A

Pillow covers
HEPA filters
Insecticide

Do for 3-6 months before seeing if it helps

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66
Q

How to avoid the following allergen, that might exacerbate asthma?

Cockroaches

A

Pest control. Air filters dont work.

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67
Q

How to avoid the following allergen, that might exacerbate asthma?

Indoor fungi

A

Decrease humidity and increase ventilation

Scrub off visible mold

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68
Q

How to avoid the following allergen, that might exacerbate asthma?

Outdoor plant allergens

A

Become a hermit

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69
Q

True/False: topical opthalmic nonselective ß blockers can trigger asthma

A

TRUE

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70
Q

Side effects of SABAs?

A

Tachycardia, tremors, palpitations, hypokalemia, lactic acidosis

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71
Q

Side effects of ICS?

A

Basically all the systemic side effects:

Thin skin
Adrenal supression
Cataracts
Osteoporosis
Thrush
Hoarse voice
Easy bruising
Hyperglycemia
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72
Q

Why can’t you use LABAs as monotherapy in asthma?

A

Increased risk of asthma-related death

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73
Q

So why do we use LABAs in asthma?

with an ICS, obviously

A

Steroid-sparing effect
Improved pulmonary function
Increase symptom-free days
Decrease need for rescue therapy

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74
Q

Classify the severity of asthma given the following clinical scenario:

Symptoms 3x/week but not daily
Night time symptoms 4/month
SABA use 3x/week but not every day
Minor life interference

A

Mild persistent

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75
Q

Classify the severity of asthma given the following clinical scenario:

Symptoms 2x/week
Night time symptoms 1/month
SABA use 1x/week
No life interference

A

Intermittent

76
Q

Classify the severity of asthma given the following clinical scenario:

Symptoms throughout the day
Night time symptoms 7x/week
SABA use 3x/day
Life sucks

A

Severe persistent

77
Q

Classify the severity of asthma given the following clinical scenario:

Symptoms daily
Night time symptoms 2x/week
SABA use daily
Some activity interference

A

Moderate persistent

78
Q

Intermittent asthma only needs “step 1” therapy. What medication(s) are included in this therapy?

A

SABA PRN

79
Q

Mild persistent asthma needs “step 2” therapy. What medication(s) are included in this therapy?

A

Low dose ICS

80
Q

Moderate persistent asthma needs “step 3” therapy. What medication(s) are included in this therapy?

A

Low dose ICS + LABA

OR

Medium dose ICS

81
Q

Severe persistent asthma needs “step 4” therapy. What medication(s) are included in this therapy?

A

Medium dose ICS + LABA

82
Q

Severe persistent asthma needs “step 5” therapy. What medication(s) are included in this therapy?

A

High dose ICS + LABA + biologic (if appropriate)

83
Q

Severe persistent asthma needs “step 6” therapy. What medication(s) are included in this therapy?

A

High dose ICS + LABA + oral steroids + biologic

84
Q

The following criteria might make one eligible for what therapy for asthma?

Dependency of oral steroids
FEV1 ≥ 50% predicted
No Hx of life-threatening exacerbations
Understanding that asthma might flare after treatment

A

Bronchial thermoplasty

85
Q

What peak flow % from the baseline is an indicator of asthma attack?

A

<20% of baseline

<50% means a severe attack

86
Q

Additive therapies in addition to the standard treatment (nebs, Mg, steroids) in treatment for status asthmaticus?

A

Anesthetic agents (ketamine, halothane)

HeliOx (low evidence data)

87
Q

Dose of methylpred for asthma exacerbation?

A

60-80mg IV Q6-12

88
Q

Say high or low for the following vent settings in asthma exacerbation:

Inspiratory flow rate
VT
RR

A

High inspiratory flow (80-100L/min)

Low VT (6-8mL/kg)

Low RR (10-14/min)

89
Q

True/False: all medications/inhalers for asthma are generally considered safe in pregnancy.

A

TRUE

biologics havent been studied though

90
Q

This condition is when there is alveolar wall destruction with irreversible enlargement of the air spaces distal to the terminal bronchioles and without evidence of fibrosis.

A

Emphysema

91
Q

How much coughing do you need to cough to be diagnosed with chronic bronchitis?

A

At least 3 months in 2 consecutive years

92
Q

Fill in the blanks for the pathophysiology behind COPD

Tobacco smoke/irritants –> activation of ___ –> release of cytokines like CXC chemokine ligant (CXCL) and CC chemokine ligand (CCL) –> recruitment of ___ ___ and ___ –> release of inflammatory mediators and ___ –> destrucction of lung production and mucus production.

A

Macrophages

CD8 Cytotoxic T cells, Th1 cells, neutrophils

Proteases

93
Q

What do epithelial cells secrete, which stimulates fibroblast production and thus fibrosis in small airways in COPD?

A

TGF

94
Q

These molecules belong to what class of enzymes that is behind the main pathophysiology of COPD?

Serine enzymes, elastases, and matrix metalloproteases (MMP-8, MMP-9, MMP-12)

A

Proteases

95
Q

What is the main antiprotease in the lung?

A

α1-antitrypsin

96
Q

Cigarette smokes also leads to further inflammation and protease-antiprotease imbalance by release of what substances that contributes to oxidative stress?

A

Reactive oxygen species

97
Q

What are the primary
lymphocytes involved in
pathogenesis of COPD?

A

CD8+ cytotoxic T cells

98
Q

In patients with α1-antitrypsin deficiency, what enzyme is over-run?

A

Neutrophil elastase

It then breaks down elastin in the lung.

99
Q

Tell me if this fits more with asthma or COPD based on the following:

Inciting factor: allergen or irritant

A

Asthma

100
Q

Tell me if this fits more with asthma or COPD based on the following:

Major cell types are epithelial cells, Th2 Cells, mast cells, and eosinophils

A

Asthma

101
Q

Tell me if this fits more with asthma or COPD based on the following:

Mediators: LTB4, TNFa, IL-8

A

COPD

102
Q

Tell me if this fits more with asthma or COPD based on the following:

Mediators: IL-4, IL-5, IL-13

A

Asthma

103
Q

Tell me if this fits more with asthma or COPD based on the following:

Involvement: mainly small airway fibrosis, parenchymal destruction

A

COPD

104
Q

Tell me if this fits more with asthma or COPD based on the following:

Changes: subepithelial fibrosis, smooth muscle hyperplasia, mucus hyperplasia, basement membrane thickening

A

Asthma

105
Q

If you smoke 1 pack per day, what is your chance of getting COPD?

If you smoke 2 ppd?

A

1 ppd = 15-20% chance

2 ppd = 25% chance

106
Q

True/False: you can get COPD from irritant exposure from your job. For instance, concrete workers from minteral dust, gold miner from silica, or rubber worker from industrial chemicals

A

TRUE

107
Q

In alpha-1 antitripsin (AAT) deficiency, what is the % chance of getting COPD in the following phenotype:

MM

A

0%

108
Q

In alpha-1 antitripsin (AAT) deficiency, what is the % chance of getting COPD in the following phenotype:

MZ

A

Very small (controversial)

109
Q

In alpha-1 antitripsin (AAT) deficiency, what is the % chance of getting COPD in the following phenotype:

SS

A

0%

110
Q

In alpha-1 antitripsin (AAT) deficiency, what is the % chance of getting COPD in the following phenotype:

SZ

A

20-50% if you smoke, rare if you dont smoke

111
Q

In alpha-1 antitripsin (AAT) deficiency, what is the % chance of getting COPD in the following phenotype:

ZZ

A

80-100%, accelerated in smokers

112
Q

In alpha-1 antitripsin (AAT) deficiency, what is the % chance of getting COPD in the following phenotype:

null

A

100% by age 30

113
Q

Mean age of onset for AAT deficiency?

A

~46 years

114
Q

What is the AAT level in order to qualify for AAT therapy (augmentation)?

A

<11 µmol/L

115
Q

Does AAT augmentation improve lung function?

A

No, it just slows the decline.

116
Q

What is the rate of decline in FEV1 every year at the age of 35 in nonsmokers?

Smokers?

A

Non smokers: 30ml/yr

Smokers: 60 ml/yr

117
Q

True/False: Digital clubbing is common in COPD

A

FALSE

it reflects another disease process such as lung cancer or ILD

118
Q

This PFT marker is a independent predictor of mortality in COPD

Hint: not FEV1, TLC, RV

Hint hint: it’s a ratio

A

IC:TLC ≤ 25%

119
Q

What are the mMRC and CAT cutoffs for being diagnosed with B or D COPD?

A

mMRC ≥ 2

CAT ≥ 10

120
Q

What are the components of BODE?

A

BMI
Obstruction (FEV1)
Dyspnea (mMRC)
Exercise (6MWT)

121
Q

This is a COPD mimicker of non-smokers of Japanese descent where they have chronic sinusitis, CT shows diffuse small centrilobular nodular opacities and hyperinflation, and positive response to macrolides?

A

Diffuse panbronchiolitis

122
Q 
56-year-old female with
COPD describes dyspnea
when hurrying on level
ground. Postbronchodilator FEV1 is 45%
predicted with no history of
exacerbations within the
past year. What is the
GOLD combined
assessment of this patient?
A

C.

She is GOLD III based
on her FEV1 and scores 1
on the mMRC without a
history of exacerbations.

123
Q

What type of pharmacotherapy am I talking about based on the following description?

Use for 2-3 months, comes in different routes, safe even in cardiovascular disease, can cause insomnia and vivid dreams if used at night

A

Nicotine replacement therapy

124
Q

What type of pharmacotherapy am I talking about based on the following description?

Not FDA-approved, side effects of dry cough, irritation of oropharynx

A

E-cigarettes

125
Q

What type of pharmacotherapy am I talking about based on the following description?

Doubles likleihood of smoking cessation compared to placebo, use for 7-12 weeks, can reduce seizure threshold

A

Bupropion

126
Q

What type of pharmacotherapy am I talking about based on the following description?

Monotherapy triples the odds of smoking cessation, superior to bupropion, use for 12 weeks, can increase suicidal events, cardiovascular events, and rates of accidental injuries

A

Varenicline

127
Q

What type of pharmacotherapy am I talking about based on the following description?

Tricyclic antidepressant, modest benefit compared to placebo, can cause dry mouth and sedation

A

Nortriptyline

128
Q

Hit me with some SABAs (5 total)

A 
Albuterol
Fenoterol
Levalbuterol
Salbutamol
Terbutaline
129
Q

Hit me with some LABAs (5 total)

A 
Formoterol
Salmeterol
Indacaterol
Aformoterol
Tulobuterol
130
Q

All LABAs improve FEV1, lung volumes, dyspnea, QOL, and exacerbation rates, but which one reduces the risk of hospitalizations?

A

Salmeterol

131
Q

Which LABA is once daily and has a similar bronchodilator effect as tiotropium?

A

Indacaterol

132
Q

What are the 2 SAMAs?

A

Ipratropium

Oxitropium

133
Q

Side effects of SAMAs?

A

Bitter metallic taste

Acute glaucoma when used via facemask

134
Q

What are the 3 LAMAs?

A

Tiotropium
Aclidinium bromide
Glucopyrronium

135
Q

By blocking the M3 receptors, what key factor does tiotropium prevent in COPD patients?

A

Reduces risk of exacerbations

136
Q

Which trial revealed that salmeterol reduced exacerebations, salmeterol-fluticasone reduced exacerbations, and pneumonia was more likely in paitents taking flutiasone?

A

TORCH trial

2007 NEJM. No reduction in mortality with ICS/LABA!

137
Q 
The UPLIFT trial revealed
that tiotropium was
associated with all the
following outcomes except:
A. Reduction in
exacerbations
B. Reduction in the rate
of FEV1 decline
C. Reduction in
hospitalizations related to
exacerbations
D. Improved quality of life
A

B; reduction in the rate of

FEV1 decline

138
Q

This medication reduced exacerbations in patients with chronic bronchitis, FEV1 50%, and a history of exacerbations

A

Roflumilast

139
Q 
What therapy has been
shown to slow the rate of
FEV1 decline?
A. LABA
B. LAMA
C. Smoking cessation
D. LAMA + LABA/ICS
E. LAMA + LABA
A

C; smoking cessation

140
Q 
Pulmonary rehabilitation
improves all of the
following except:
A. Dyspnea,
B. Quality of life,
C. FEV1
D. 6-minute walk distance
A

C. FEV1

141
Q

What are the qualifications for oxygen therapy in COPD?

A

PaO2 ≤ 55 (SaO2 ≤ 88%)

or

PaO2 56-59 (SaO2 ≤ 89%) with evidence of pulmonary hypertension or erythrocytosis

142
Q

Benefits of NIPPV in COPD if you have daytime hypercapnia or COPD with OSA (overlap syndrome)?

A

Improves hypercapnia

In overlap syndrome, improves survival and decreases hospitalizations

143
Q

Benefits of LVRS in COPD?

A

Improves survival, exercise, and QOL

144
Q

Contraindications to LVRS?

Think FEV1 and DLCO cutoffs and CT findings

A

FEV1 ≤ 20%
DLCO ≤ 20%
Diffuse emphysema on CT (ideally would be focal)

145
Q

What are the FEV1, CT findings, and TLC/RV cutoffs for inclusion for BLVRS?

A

FEV1 15-45%
Heterogenous emphysema
Hyperinflation with air trapping (TLC >100%, RV > 150%)

146
Q

How big does the bullae have to be in order to consider bullectomy?

A

A bulla that occupies 30-50% of hemothorax

147
Q

What is the BODE cutoff in order to be referred for transplant?

A

BODE > 5

148
Q 
A 55-year-old woman with
severe emphysema
presents for consultation.
FEV1 is 38% predicted,
DLCO is 38% predicted,
and she is on optimal
medical therapy. She has
completed pulmonary
rehabilitation but still has
poor exercise capacity. CT
of the chest reveals upper
lobe-predominant
emphysema. What is the
recommended treatment?
A. Bullectomy
B. Lung transplantation
C. Hospice care
D. Lung volume reduction
surgery (LVRS)
A

D; lung volume reduction

surgery (LVRS)

149
Q 
A 55-year-old women, a
25-pack-year ex-smoker,
presents with dyspnea
when walking on level
ground after a few minutes.
Her post-bronchodilator
FEV1/FVC is 0.62. FEV1 is
59% predicted. She has
never been treated for a
COPD exacerbation. What
should be the initial
management of her
COPD?
A. ICS + LABA
B. LAMA + LABA
C. LAMA or LABA +
pulmonary
rehabilitation
D. LAMA only
A

C; LAMA or LABA +

pulmonary rehabilitation

150
Q 
A 67-year-old male sees
you for breathlessness
when walking at his own
pace on level ground. His
post-bronchodilator FEV1
percent predicted is 55%.
He has been treated for a
COPD exacerbation twice
within the last year. What
GOLD classification is he
and what is the
recommended initial
therapy?
A

GOLD D; ICS + LABA

and/or LAMA

151
Q

First and second choice for GOLD A COPD?

A

First: SAMA or SABA PRN

Second: LAMA or LABA< or SAMA+SABA

152
Q

First and second choice for GOLD B COPD?

A

First: LAMA or LABA

Second: LAMA+LABA

153
Q

First and second choice for GOLD C COPD?

A

First: ICS+LABA

Second: LAMA+LABA, LAMA+PDE4i, LABA+PDE4i

154
Q

First and second choice for GOLD D COPD?

A

First: ICS+LABA and/or LAMA

Second: ICS+LAMA, or ICS+LABA+LAMA

155
Q

What % of COPD exacerbations do not have an identifiable source?

A

~33%

156
Q

Target SpO2 in AECOPD?

A

88-92%

157
Q

What are the benefits for using steroids in AECOPD?

A

Reduces early relapse, treatment failure, and hospital stay

158
Q

Prednisone dose in AECOPD?

A

30-40mg/day

159
Q

What are the benefits for NIPPV in AECOPD?

A

decreases mortality, hospital stay, and intubation rate

Also improves dyspnea, respiratory acidosis, and respiratory rate

160
Q

Give me the 3 possible infectious causes of bronchiectasis.

A

Bacterial - Staph, pseudomona,s mycoplasma
Mycobacteria - TB, MAC
Viral

161
Q

Give me the 3 possible immune deficiency causes of bronchiectasis.

A

Hypogammaglobulinemia
HIV
IgG subclass deficiency

162
Q

Give me the 3 possible mucociliary clearance defects that can cause bronchiectasis.

A

CF
Primary ciliary diskinesia (PCD)
Youngs syndrome (bronchiectasis, sinusitis, obstructive azoospermia)

163
Q

Give me the 4 possible bronchial obstructive causes of bronchiectasis.

A

Endobronchial tumor
Lymph node compression
Foreign body
Broncholith

164
Q

Give me the 5 possible autoimmune causes of bronchiectasis.

A 
Sjogrens
Rheumatoid arthritis
IBD
Relapsing polychrondirits
SLE
165
Q

Give me the 6 possible congenital causes of bronchiectasis.

A

Bronchial atresia
AAT deficiency
Williams-Campbell syndrome (congenital deficiency of the bronchial cartilage)
Mounier-Kuhn syndrome (tracheobronchomegaly)
Tracheal-esophageal fistula
Yellow nail syndrome

166
Q

Give me any other bonus causes of bronchiectasis.

A 
ABPA
Post-radiation
Post-transplant
Traction bronchiectasis
GVHD
167
Q

Fill in the blanks for the vicious cycle for the pathogenesis of bronchiectasis:

Neutrophil inflammation (release of __) –> airway destruction and destortion (bronchiectasis) –> abnormal __ clearance –> ___ colonization –> repeat

A

proteases

mucus

bacterial

168
Q

Classic symptoms and findings for bronchiectasis?

A 
Chronic productive cough
Hemoptysis
Dyspnea
Wweight loss
Recurrent lung infections
Wheezing (ABPA, asthma)
Clubbing
Obstructive pattern on PFTs
169
Q

What is the bronchoarterial ratio on CT scan to diagnose bronchiectasis?

A

> 1-1.5

170
Q

Which type of bronchiectasis is characterized by having mild diffuse dilatation of bronchi with thickened wall, leading to “tram track” and “signet ring” appearance on CT?

A

Cylindrical/tubular bronchiectasis

171
Q

What form of bronchiectasis is characterized by the beaded appearance of dilated bronchi with interspersed sites of relative narrowing?

A

Varicose bronchiectasis

Looks like a string of pearls on CT

172
Q

What form of bronchiectasis is the most severe with cyst-like bronchi that extend to the pleural surface?

A

Cystic/saccular bronchiectasis

173
Q

What antibiotic therapy is indicated in bronchiectasis for patients with frequent exacerbations?

A

Macrolides

174
Q

Describe what happens to the CFTR in class I mutation for CF

A

Nonsense mutation causing no CFTR synthesis

175
Q

Describe what happens to the CFTR in class II mutation for CF

A

Missense causing block in CFTR processing

This is delF508 mutation

176
Q

Describe what happens to the CFTR in class III mutation for CF

A

Missense causing dysregulation of CFTR

This is G551D (ivacaftor responsive)

177
Q

Describe what happens to the CFTR in class IV mutation for CF

A

Missense causing defective conductance across CFTR

178
Q

Describe what happens to the CFTR in class V mutation for CF

A

Missense causing reduced CFTR synthesis

179
Q

Describe what happens to the CFTR in class IV mutation for CF

A

Decreased stability of CFTR

180
Q

Say a newborn tests positive for IRT/DNA for CF. The sweat chloride is 79 mmol/L and 75 mmol/L. Is CF confirmed?

A

Yes, it’s >60mmol/L

181
Q

Say a 5 month old tests positive for IRT/DNA for CF. The sweat chloride is 45 mmol/L. Is CF confirmed?

A

No, it’s still possible though. Will need repeat sweat chloride and expanded DNA analysis

182
Q

Say a newborn tests positive for IRT/DNA for CF. The sweat chloride is 24 mmol/L. Is CF confirmed?

A

No, CF is unlikely

183
Q

This medication used in CF decreases the viscosity of sputum by cleaving denatured DNA released by degenerating neutrophils

A

DNAs I (dornase alpha)

184
Q

How often should you measure sputum cultures in CF?

A

every 3 months

185
Q

Place the following treatments in the appropriate order to do airway clearance regimen in CF:

Hypertonic saline
Dornase alpha
Bronchodilator
Aersolized antibiotic
Airway clearance
A

Bronchodilator –> hypertonic saline –> dornase alpha –> airway clearance –> aerosolized antibiotic

186
Q

Use of what oral antibiotic can be used long term in patients with chronic P. aeruginosa in their airways?

A

Azithromycin

Inhibits neutrophil migration and elastase production
Improves lung function and reduction in exacerbations
Screen for NTM before initiating azithomycin

187
Q

Done with obstructive lung disease!!!

Animal fact: which animal lays eggs, has electroreceptors in its snout for locating prey, eyes with double cones, no stomach, a single duct for their urinary, defecatory, and reproductive system, 10 chromosomes, and has venemous barbs on their hind legs?

A

Platypus

Pulmonary Review (14 decks)

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