Obstructive Lung Disease Flashcards by Daniel Guck

This is a state of having IgE antibodies to specific allergens

Atopy

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

True

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

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

ß-receptor agonists

Cromones (sodium cromoglycate)

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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?

Eosinophils

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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?

Corticosteroids

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Which interleukins do basophils secrete in asthma?

IL-4 and IL-13

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

Th1 cells

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

Th17 cells

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Which IL directs B lymphocytes to synthesize IgE?

IL-4

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Which IL regulates eosinophil production and maturation?

IL-5

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

IL-13

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

Reactive airway dysfunction syndrome (RADS)

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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 -->

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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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?

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

FALSE

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

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

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

Bronchoprovocation testing

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What are absolute contrainidications to bronchopovocation testing?

Think SMUK

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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Which things can cause false positive bronchoprovocation testing?

Think ABCs

Allergic rhinitis
Bronchitis
Congestive heart failure
COPD
CF

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This test is used to evaluate for eosinophilic airway inflammation

Exhaled NO

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

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

CBC with diff
RAST
IgE

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

TRUE

used to r/o other conditions that can mimic asthma

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This is the asthma mimicker that has the following properties:

Exertional dyspnea, peripheral edema, elevated BNP

CHF

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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

Hypersensitivity pneumonitis

This is the asthma mimicker that has the following properties: Travel history, elevated IgE and eosinophilia

Parasitic lung infection

This is the asthma mimicker that has the following properties: Peripheral blood eosinophilia, chronic rhinosinusitis, possible reduced DLCO on PFTs

Asthmatic granulomatosis

This is the asthma mimicker that has the following properties: Imaging studies showing hilar adenopathy with or without reticular or nodular opacities

Endobronchial sarcoidosis

This condition shows obstruction on spirometry and has the following features: Significant smoking history, family history of A1AT deficiency, reduced DLCO

COPD

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

Bronchiectasis

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.

Constrictive bronciolitis

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

Central airway obstruction

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

Laryngeal dysfunction

This condition shows obstruction on spirometry and has the following features: Recent URI, transient and usually resolves in weeks

Reactive airways viral syndrome

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

Sinus CT

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

pH probe for GERD

What body habitus is associated with worsened asthma severity?

Obesity

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

Polysomnography

``` 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? ```

``` Allergic bronchopulmonary aspergillosis. A skin-prick test checking reactivity to Aspergillus fumigatus should be performed. ```

Treatment of ABPA?

Glucocorticoids slowly tapered over 3-6 months.

Pathophysiology behind exercise induced asthma?

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

Diagnostic testing modality behind exercise induced asthma?

Exercise challenge test with spirometric measurements before and after exercise

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

SABA 10 mins before exercise Cromoglycates 15-20 mins before exercise

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

Occupational asthma

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

Work-exacerbated asthma

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

Irritant induced asthma

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

RADS

Occupational nonasthmatic eosinophilic bronchitis

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?

Work-related irritable larynx syndrome

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?

Peak expiratory flow rates

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

at least 3 months

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

<70%

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

ICS and/or ß-agonist

Differential for patients with nocturnal asthma?

OSA GERD CHF

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

TRUE

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

Sinus surgery

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

Doxycycline

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

Topical corticosteroids

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

Desensitization

Indications for aspirin desensitization?

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

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

Leukotriene-modifying agents

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

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

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

>5 days

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

Five point palm exploding heart technique Also, HEPA filters might work.

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

Pillow covers HEPA filters Insecticide Do for 3-6 months before seeing if it helps

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

Pest control. Air filters dont work.

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

Decrease humidity and increase ventilation | Scrub off visible mold

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

Become a hermit

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

TRUE

Side effects of SABAs?

Tachycardia, tremors, palpitations, hypokalemia, lactic acidosis

Side effects of ICS?

Basically all the systemic side effects: ``` Thin skin Adrenal supression Cataracts Osteoporosis Thrush Hoarse voice Easy bruising Hyperglycemia ```

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

Increased risk of asthma-related death

So why do we use LABAs in asthma? | with an ICS, obviously

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

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

Mild persistent

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

Intermittent

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

Severe persistent

Classify the severity of asthma given the following clinical scenario: Symptoms daily Night time symptoms 2x/week SABA use daily Some activity interference

Moderate persistent

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

SABA PRN

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

Low dose ICS

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

Low dose ICS + LABA OR Medium dose ICS

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

Medium dose ICS + LABA

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

High dose ICS + LABA + biologic (if appropriate)

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

High dose ICS + LABA + oral steroids + biologic

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

Bronchial thermoplasty

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

<20% of baseline <50% means a severe attack

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

Anesthetic agents (ketamine, halothane) HeliOx (low evidence data)

Dose of methylpred for asthma exacerbation?

60-80mg IV Q6-12

Say high or low for the following vent settings in asthma exacerbation: Inspiratory flow rate VT RR

High inspiratory flow (80-100L/min) Low VT (6-8mL/kg) Low RR (10-14/min)

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

TRUE | biologics havent been studied though

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.

Emphysema

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

At least 3 months in 2 consecutive years

# 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.

Macrophages CD8 Cytotoxic T cells, Th1 cells, neutrophils Proteases

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

TGF

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)

Proteases

What is the main antiprotease in the lung?

α1-antitrypsin

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

Reactive oxygen species

What are the primary lymphocytes involved in pathogenesis of COPD?

CD8+ cytotoxic T cells

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

Neutrophil elastase It then breaks down elastin in the lung.

Tell me if this fits more with asthma or COPD based on the following: Inciting factor: allergen or irritant

Asthma

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

Asthma

Tell me if this fits more with asthma or COPD based on the following: Mediators: LTB4, TNFa, IL-8

COPD

Tell me if this fits more with asthma or COPD based on the following: Mediators: IL-4, IL-5, IL-13

Asthma

Tell me if this fits more with asthma or COPD based on the following: Involvement: mainly small airway fibrosis, parenchymal destruction

COPD

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

Asthma

If you smoke 1 pack per day, what is your chance of getting COPD? If you smoke 2 ppd?

1 ppd = 15-20% chance 2 ppd = 25% chance

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

TRUE

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

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

Very small (controversial)

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

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

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

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

80-100%, accelerated in smokers

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

100% by age 30

Mean age of onset for AAT deficiency?

~46 years

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

<11 µmol/L

Does AAT augmentation improve lung function?

No, it just slows the decline.

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

Non smokers: 30ml/yr Smokers: 60 ml/yr

True/False: Digital clubbing is common in COPD

FALSE it reflects another disease process such as lung cancer or ILD

This PFT marker is a independent predictor of mortality in COPD Hint: not FEV1, TLC, RV Hint hint: it's a ratio

IC:TLC ≤ 25%

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

mMRC ≥ 2 | CAT ≥ 10

What are the components of BODE?

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

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?

Diffuse panbronchiolitis

``` 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? ```

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

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

Nicotine replacement therapy

What type of pharmacotherapy am I talking about based on the following description? Not FDA-approved, side effects of dry cough, irritation of oropharynx

E-cigarettes

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

Bupropion

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

Varenicline

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

Nortriptyline

Hit me with some SABAs (5 total)

``` Albuterol Fenoterol Levalbuterol Salbutamol Terbutaline ```

Hit me with some LABAs (5 total)

``` Formoterol Salmeterol Indacaterol Aformoterol Tulobuterol ```

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

Salmeterol

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

Indacaterol

What are the 2 SAMAs?

Ipratropium | Oxitropium

Side effects of SAMAs?

Bitter metallic taste Acute glaucoma when used via facemask

What are the 3 LAMAs?

Tiotropium Aclidinium bromide Glucopyrronium

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

Reduces risk of exacerbations

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

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

``` 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 ```

B; reduction in the rate of | FEV1 decline

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

Roflumilast

``` 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 ```

C; smoking cessation

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

C. FEV1

What are the qualifications for oxygen therapy in COPD?

PaO2 ≤ 55 (SaO2 ≤ 88%) or PaO2 56-59 (SaO2 ≤ 89%) with evidence of pulmonary hypertension or erythrocytosis

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

Improves hypercapnia | In overlap syndrome, improves survival and decreases hospitalizations

Benefits of LVRS in COPD?

Improves survival, exercise, and QOL

Contraindications to LVRS? Think FEV1 and DLCO cutoffs and CT findings

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

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

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

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

A bulla that occupies 30-50% of hemothorax

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

BODE > 5

``` 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) ```

D; lung volume reduction | surgery (LVRS)

``` 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 ```

C; LAMA or LABA + | pulmonary rehabilitation

``` 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? ```

GOLD D; ICS + LABA | and/or LAMA

First and second choice for GOLD A COPD?

First: SAMA or SABA PRN Second: LAMA or LABA< or SAMA+SABA

First and second choice for GOLD B COPD?

First: LAMA or LABA Second: LAMA+LABA

First and second choice for GOLD C COPD?

First: ICS+LABA Second: LAMA+LABA, LAMA+PDE4i, LABA+PDE4i

First and second choice for GOLD D COPD?

First: ICS+LABA and/or LAMA Second: ICS+LAMA, or ICS+LABA+LAMA

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

~33%

Target SpO2 in AECOPD?

88-92%

What are the benefits for using steroids in AECOPD?

Reduces early relapse, treatment failure, and hospital stay

Prednisone dose in AECOPD?

30-40mg/day

What are the benefits for NIPPV in AECOPD?

decreases mortality, hospital stay, and intubation rate Also improves dyspnea, respiratory acidosis, and respiratory rate

Give me the 3 possible infectious causes of bronchiectasis.

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

Give me the 3 possible immune deficiency causes of bronchiectasis.

Hypogammaglobulinemia HIV IgG subclass deficiency

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

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

Give me the 4 possible bronchial obstructive causes of bronchiectasis.

Endobronchial tumor Lymph node compression Foreign body Broncholith

Give me the 5 possible autoimmune causes of bronchiectasis.

``` Sjogrens Rheumatoid arthritis IBD Relapsing polychrondirits SLE ```

Give me the 6 possible congenital causes of bronchiectasis.

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

Give me any other bonus causes of bronchiectasis.

``` ABPA Post-radiation Post-transplant Traction bronchiectasis GVHD ```

# 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

proteases mucus bacterial

Classic symptoms and findings for bronchiectasis?

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

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

>1-1.5

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?

Cylindrical/tubular bronchiectasis

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

Varicose bronchiectasis Looks like a string of pearls on CT

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

Cystic/saccular bronchiectasis

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

Macrolides

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

Nonsense mutation causing no CFTR synthesis

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

Missense causing block in CFTR processing This is delF508 mutation

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

Missense causing dysregulation of CFTR This is G551D (ivacaftor responsive)

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

Missense causing defective conductance across CFTR

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

Missense causing reduced CFTR synthesis

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

Decreased stability of CFTR

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

Yes, it's >60mmol/L

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

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

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

No, CF is unlikely

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

DNAs I (dornase alpha)

How often should you measure sputum cultures in CF?

every 3 months

Place the following treatments in the appropriate order to do airway clearance regimen in CF: ``` Hypertonic saline Dornase alpha Bronchodilator Aersolized antibiotic Airway clearance ```

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

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

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

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?

Platypus