Exam Review Course Leslie Zimmerman, MD Professor of Clinical - - PDF document

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Pulmonary ¡ ABIM ¡Cer1fica1on ¡ Exam ¡Review ¡Course ¡

Leslie Zimmerman, MD Professor of Clinical Medicine, UCSF ICU Director, SFVAMC

Conflict ¡of ¡Interest/Disclosures ¡

n None

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Rela1ve ¡Value? ¡

n Medical Content

• CV

14%

• Pulmonary

10%

• ID

9%

• GI

9%

n Cross Content

• Critical Care

10%

• Geriatrics

10%

• Prevention

6%

• Women’s Health 6%

Rela1ve ¡Value? ¡

n Pulmonary:

• Obstructive disease:

20%

• Pulmonary vascular disease: 12%
• Pneumonia:

10%

• Pleural Disease:

10%

• Restrictive & Interstitial:

10%

• 0-2 questions on: ARDS, Sleep, lung

cancer, bronchiectasis…

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Lecture ¡Outline ¡

n Sleep n COPD/Asthma n ILDs n PVD n Solitary Pulmonary Nodule n Etc.

Ques1on ¡1 ¡

A 65 year-old man with daytime sleepiness is evaluated for sleep apnea. His Epworth sleepiness scale is 11/24. The polysomnogram reveals an overall apnea-hyponea index (AHI) of 24 (12 events/hour when on his side and 55 events/hour when supine). Lowest oxygen saturation was 86%. He had occasional leg jerks with sleep stage transition; he has no leg symptoms during day.

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Ques1on ¡1 ¡

65 yom with overall AHI of 24 (12 on side & 55 when supine). Nadir O2 sat’n = 86%. Occasional leg jerks with sleep stage transition; no leg symptoms during day. He should be offered:

• A. Screening for iron deficiency
• B. Modafinil
• C. Nighttime oxygen
• D. APAP
• E. BPAP-ST

Sleep ¡Disorders: ¡Office ¡Visits ¡

www.nhlbi.nih.gov/about/factbook-05/chapter4.htm

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Classic ¡pa1ent ¡with ¡OSA ¡

Obesity = #1 risk factor

Genetics Upper airway/facial abnormalities (nasal congestion) Tonsils! Post-menopause Hypothyroidism/ Acromegaly

Deeper stages of sleep, neural input to upper airway declines, decreased airway tone, tongue falls back.

en.wikipedia.org

Not ¡Obese? ¡

http://tonsillectomyrecovery.com/swollen-tonsils/ http://www.sublimis.com

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OSA ¡

Disruption in sleep causes daytime sleepiness Epworth Scale can estimate “sleepiness” 10 = Sleepy 18 = Very sleepy

http//:epworthsleepinessscale.com

OSA ¡

Air ir flo low

Apneas + Hyponeas/hour = AHI

10 seconds

“Hyponea” requires 4% desaturation

(Respiratory Disturbance Index) RDI = AHI + milder hyponeas that don’t meet criteria but disrupt sleep

10 seconds

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OSA ¡and ¡Death ¡

Untreated severe OSA (AHI > 30/hour) 3-6 fold increased risk of all-cause mortality compared to individuals without OSA. IN CONTRAST: Patients with untreated mild OSA may not be at increased risk for mortality compared to individuals without OSA.

Marin JM et al. Lancet 2005;365(9464):1046.

OSA ¡

Severity Mild: AHI 5-15 Moderate: AHI 15-30 Severe: > 30

If AHI of 5-15 and

• Asymptomatic
• Low Epworth
• No HTN/CAD/CVA
• Not “mission critical”

Many would not treat

Medicare reimbursement

TREAT AHI > 5 if symptoms (sleepiness, fatigue), signs of disturbed sleep (snoring, restless sleep, respiratory pauses), or HTN/CAD/CVA, or job requires Rx AHI > 15 in everyone

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Mandibular ¡Advance ¡Device ¡

If ¡AHI ¡< ¡15, ¡sleepy ¡& ¡can’t ¡tolerate ¡mask ¡à à ¡MAD

¡ ¡

We use them for symptomatic patients with mild disease who can’t tolerate PAP Repeat sleep study with device to check for efficacy

• Q. Severe OSA? (AHI > 30)

Wrong answer is MAD

Our ¡pa1ent ¡

AHI of 24 = moderate sleep apnea Nadir O2 sat’n = 86%. Occasional leg jerks with sleep stage transition; no leg symptoms during day. He should be offered:

• A. Screening for iron deficiency
• B. Modafinil
• C. Nighttime oxygen
• D. APAP
• E. BPAP-ST

Treatment for narcolepsy

He just has myoclonic jerks with falling asleep, no RLS or PLMD

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Our ¡pa1ent ¡

AHI of 24 = moderate sleep apnea Nadir O2 sat’n = 86%. He should be offered:

• C. Nighttime oxygen
• D. APAP
• E. BPAP-ST

Improves desaturation but not AHI, not daytime sleepiness, & not BP in HTN patients*

* N Engl J Med 2014; 370:2276-2285

WON’T ASK: CPAP vs. APAP vs. BPAP for the average person with OSA à No study shown superiority

Posi1ve ¡Airway ¡Pressure ¡Machines ¡

• Simplest
• Set pressure to bring AHI < 5/hr

CPAP

• Set mid point @ level to bring AHI < 5/

hr +/- 3 or 4 above and below

• Can check average pressure needed

at next visit (can be used to do “titration”)

APAP

• Set EPAP to bring Apneas < 5/hr;

IPAP until AHI/RDI < 5/hr

• USE:
• Comfort if required pressure high
• Supports Tidal Volume à essentially

“pressure support ventilation”

BPAP

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BPAP ¡

BPAP-S* (Regular)

• OSA needing

high pressures (comfort)

*S= Spontaneous

• No effort, no breath

BPAP-ST**

• Central Sleep Apnea
• Obesity Hypoventilation
• NM disease
• Chronic respiratory failure

**ST = Spontaneous + Timed delivery if no effort Basically a Non-invasive Ventilator

Our ¡pa1ent ¡

AHI of 24 = moderate sleep apnea Nadir O2 sat’n = 86%. He should be offered:

• D. APAP
• E. BPAP-ST

No report of:

• Obesity Hypoventilation
• Central Sleep Apnea
• NM disease
• Chronic respiratory failure

Given his big difference between side and supine, compliance may be better with APAP (but CPAP would be correct answer as well)

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What ¡were ¡those ¡OSA ¡numbers? ¡

n AHI 5-15 & symptoms or HTN/CAD/CVA

à PAP (MAD if can’t comply with f/u sleep study to prove efficacy). If “mission critical” job à PAP because only way to monitor compliance!

n AHI 15-30à PAP n AHI > 30 and esp. if < 70 years old, clearly

at increased CV mortality if not treated (so we really encourage use!)

Ques1on ¡2 ¡

A 59 year old man comes to the ED with a COPD exacerbation triggered by nearby forest fires. There is no increase in cough or purulence. He is on home tiotropium, formoterol, ICS and as needed albuterol. He is wheezy but responds to albuterol/ipatropium neb and you anticipate that he will be able to go home. O2 saturation is 91%. You add:

• A. Home O2 by NC at 2 LPM
• B. Azithromycin 250 mg daily
• C. Roflumilast daily
• D. Theophylline daily
• E. Prednisone 40 mg x 5 days
• F. Doxycycline x 7 days

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http://www.who.int/mediacentre/factsheets/fs310_2008.pdf

2004: ¡Worldwide ¡Leading ¡Causes ¡of ¡Death ¡

Millions

Affects 9% of World Population By 2020, will move to 3rd leading cause of death

In US, only common disease with RISING mortality

In US, h in COPD deaths is driven by very large h in women. In 2000, for 1st time, more women died of COPD than men in US.

Percent Change in Age-Adjusted Death Rates, US, 1965-1998 (proportion of 1965)

3.0 2.5 2.0 1.5 1.0 0.5 CAD CVA Other COPD All CVD Other

• 59%
• 64%
• 35%
• 7%

+163% http://www.goldcopd.org

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COPD ¡Pathogenesis: ¡Aging ¡+ ¡Genes ¡ ¡ ¡+ ¡Noxious ¡S1muli ¡

Chest 2009;135:173.

In US, 15-20% of COPD caused in part by occupational exposures (esp. dusts)

Lung Mature 18-25 years Total dysfunction 130-140 years

Lung Aging

Healthy COPD

Lung function (FEV1; alveoli)

In ¡non-­‑smokers, ¡environmental ¡ exposure ¡is ¡primary ¡risk ¡factor ¡

Indoor smoke from biomass solid fuels à Contribute up to 35% of COPD in above countries

World Health Organization

http://www.who.int/heli/risks/indoorair/en/webiapmap.jpg

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Diagnosis: ¡PFTs ¡

n Low FEV1/FVC = diagnosis of obstructive

disease (Asthma, chronic bronchitis, emphysema)

n FEV1 = severity of obstruction n TLC n DLCO: low in “airsac” disease and PVD, not

asthma

Especially emphysema Also long-standing poorly controlled asthma

↑TLC supports obstructive

disease

↓TLC diagnoses restrictive

disease

CT: ¡ ¡Map ¡of ¡the ¡lungs? ¡

Can diagnose emphysema (not asthma or chronic bronchitis). Not (yet) able to predict FEV1, but More emphysema on CT à higher mortality

Ann Intern Med 2014;161:863

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Ques1on ¡2 ¡

A 59 year old man comes to the ED with a COPD exacerbation triggered by nearby forest fires. There is no increase in cough or purulence. He is on home tiotropium, formoterol, ICS and as needed albuterol. He is wheezy but responds to albuterol/ipatropium neb and you anticipate that he will be able to go home. O2 saturation is 91%. You add:

• A. Home O2 by NC at 2 LPM
• B. Azithromycin 250 mg daily
• C. Roflumilast daily
• D. Theophylline daily
• E. Prednisone 40 mg x 5 days
• F. Doxycycline x 7 days

< 88% or PaO2 < 55

• r < 59 if ↑ Hct or RHF

Ques1on ¡2 ¡

A 59 yom with a COPD exacerbation triggered by nearby forest fires. No increase in cough or purulence. On home tiotropium, formoterol, ICS prn albuterol. Wheezy but responds to albuterol and you anticipate that he will be able to go home. O2 saturation is 91%. You add:

• E. Prednisone 40 mg x 5 days
• JAMA. 2013;309:2223-2231.

40 mg x 5 days 40 mg x 14 days

Just as good for average COPDer

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COPD: ¡Acute ¡Exacerba1on ¡Rx ¡

Not much new

n Short-acting albuterol = mainstay n Alternative or add short-acting ipratropium n Prednisone n Antibiotics:

• Early rx à better outcome in hospitalized patients
• JAMA. 2010;303(20):2035
• Decrease risk of next exacerbation Eur Respir J. 2009;33(2):282
• MILD exacerbation (no hospitalization needed & only

0-1 of increased dyspnea, sputum purulence, or sputum production): Recommendation àno antibiotic

COPD: ¡Maintenance ¡Rx ¡

Tiotropium:

n Improves function & decreases

exacerbations (UPLIFT trial: Lancet 2009; 374:1171.)

n UPLIFT trial: No increase in CV events n TIOSPIR trial: mist vs dry powder no diff in

CV events, but they excluded active CAD (recent MI, Vtach, and CHF patients) (NEJM

2013;369:1491) (vs. smaller BMJ. 2011;342:d3215.) n Overall CV risk seems small n Increase in urinary retention in some

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COPD: ¡Maintenance ¡Rx ¡

LABA + Inhaled corticosteroids: improved lung function & decreased exacerbations

(TORCH trial NEJM 2007;356:775).

Inhaled corticosteroids: decrease exacerbations but may increase risk of CAP

Arch Intern Med. 2009;169:219 Compare to asthma, in which

ICS are mainstay.

Statins, Vit D: Duds Sildenifil for P HTN and COPD: BAD! Worse

• xygenation (AJRCCM. 2010;181: 270.)

Our order: prn Albuterol or Combivent, add LAMA (change Combivent to albuterol), add LABA, if asthma component or still having exacerbations add combo LABA/ICS

Ques1on ¡2 ¡

A 59 yom with a COPD exacerbation triggered by nearby forest fires. No increase in cough or purulence. On home tiotropium, formoterol, ICS prn albuterol. Wheezy but responds to albuterol and you anticipate that he will be able to go home. O2 saturation is 91%. You add:

• B. Azithromycin 250 mg daily
• C. Roflumilast daily
• D. Theophylline daily
• E. Prednisone 40 mg x 5 days

Beyond “triple therapy”…Can other chronic therapies reduce recurrent exacerbations?

You need help with recovery for this exacerbation

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COPD ¡Exacerba1ons ¡

Recurrent exacerbations are bad

Lung function over lifetime with COPD

Lung Function

More exacerbations à Faster decline in FEV1

Can ¡Azithromycin ¡Help? ¡

Albert RK et al. “Azithromycin for Prevention of Exacerbations of COPD” NEJM 2011; 365:689.

n Azithromycin (250 mg daily) vs. placebo x 1 year.

Proportion free of Exacerbations days

Macrolides have immunomodulatory, anti-inflammatory, and anti-bacterial effects Fewer exacerbations (modest)

5% hearing loss (NNH =20)

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Azithromycin ¡Saga…. ¡

Wayne RA, et al. NEJM 2012; 366:1881

n Prescriptions for azithromycin in Tennessee Medicaid

registry & sudden death within 10 days – slight increase in sudden death (compared to amoxicillin prescriptions)

Vs.

Svanström H, et al. NEJM 2013; 368:1704-1712.

n Mostly young/middle aged adults à no increased risk.

Original article: Albert RK et al. NEJM 2011; 365:689.

n Excluded if Long QTc, other meds that can prolong QT or

associated with torsades.

Azithromycin ¡Saga…. ¡

RESERVE for: “Carefully selected patients, such as those who continue to have frequent exacerbations in spite of optimal therapy for their COPD with bronchodilators and anti-inflammatory agents.” After: LAMA, LABA, ICS Check baseline ECG and repeat ECG after starting!

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Roflumilast ¡

Phosphodiesterase-4 (PDE-4) inhibition

n Smooth muscle relaxation n Anti-inflammatory? n Targeted to those with > 2 hospitalized

exacerbations/year

n No head to head comparison with Azithromycin n Diarrhea/ wt loss problems

Theophylline? ¡

LOW (half) DOSE @ 100 -200 mg twice/day for levels 6-8 mcg/mL (half traditional target)

n Benefit as anti-inflammatory medication (not

as smooth muscle relaxer – that you likely need full dose)

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Ques1on ¡2 ¡

A 59 yom with a COPD exacerbation triggered by nearby forest fires. No increase in cough or purulence. On home tiotropium, formoterol, ICS prn albuterol. Wheezy but responds to albuterol and you anticipate that he will be able to go home. O2 saturation is 91%. You add:

• B. Azithromycin 250 mg daily
• C. Roflumilast daily
• D. Theophylline daily

Save for severe COPD

• Check for asthma

component (trigger control)

• Still smoking?

Ques1on ¡3 ¡

All of the following are risk factors for COPD exacerbations EXCEPT?

• A. Prior exacerbations
• B. Lower FEV1
• C. Male sex
• D. History of asthma

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COPD: ¡Lots ¡of ¡variability ¡in ¡course ¡

Exacerbations are bad – more inflammation, more airway remodeling à more rapid decline in FEV1 But who gets exacerbations?

v Prior exacerbations v Lower FEV1 (worse you are, the worse you are…) v Women v History of asthma

NEJM 2010;363:1128.

Phenotypes of frequent and infrequent “exacebators”

COPD ¡& ¡Asthma ¡

COPD

• Older, esp. smokers
• Slowly progressive
• Neutrophils
• Partially reversible
• Airway remodeling &

Lung destruction

ASTHMA

• Any age, esp. children
• Episodic
• Eosinophils
• May be fully reversible
• Airway remodeling

10% overlap Manage similar to asthma (ck for allergic triggers, ICS mainstay)

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Ques1on ¡4 ¡

A 45 year-old ex-smoker with 5 years of progressive DOE has the following CXR

And CT scan of Lung Bases

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Ques1on ¡4 ¡

Testing reveals that he has very low levels of alpha-1-antitrypsin (PiZZ variant). Treatment with replacement therapy has been shown to:

• A. Decrease risk of lung cancer
• B. Decrease number of exacerbations/year
• C. Improve oxygenation

D. Prevent liver disease

• E. Slow decline of FEV1

Alpha ¡1 ¡An1-­‑trypsin ¡Deficiency ¡

n Normal: PiMM n Heterozygotes make enough to be

protective

n Homozygous PiZZ, PiZnull, PiNullNull

elastase unchecked àearly emphysema in smokers, though RARE that lifetime non- smokers get emphysema

A1AT

Neutrophil Elastase

Panacinar

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Liver ¡Disease? ¡

n A1AT made in the liver à ZZ variant, it is

made but can’t get out of the ER of the hepatocyte à liver damage à cirrhosis

n PiNullNull – makes NO A1AT – they do

not get the liver disease

n IV Augmentation doesn’t help liver

Augmenta1on ¡with ¡A1AT ¡

n Cost: $60,000 to $150,000/ year n Approved by the FDA if level below the

protective level (PiZZ, PiZnull) & COPD

n Not in heterozygotes n Not if still smoking n Not if asymptomatic n NIH registry: augmentation decreases rate

• f decline of lung function & mortality (NOT

A RANDOMIZED TRIAL)

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Ques1on ¡4 ¡

Testing reveals that he has very low levels of alpha-1-antitrypsin (PiZZ variant). Treatment with replacement therapy has been shown to:

• A. Decrease risk of lung cancer
• B. Decrease number of exacerbations/year
• C. Improve oxygenation

D. Prevent liver disease

• E. Slow decline of FEV1

Increased risk in A1AT deficiency, but no decrease with Rx Adding normal A1AT won’t hurt; but won’t help

Ques1on ¡4 ¡

Testing reveals that he has very low levels of alpha-1-antitrypsin (PiZZ variant). Treatment with replacement therapy has been shown to:

• B. Decrease number of exacerbations/year
• C. Improve oxygenation
• E. Slow decline of FEV1

“Air sac” disease, not airway disease

No therapy will improve function, hope to just limit continued damage

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Ques1on ¡5 ¡

Volume

Flow

Normal

Exhalation Inhalation

A 34-year-old woman has periodic shortness of breath despite albuterol, formoterol, high dose inhaled steroids. Spirometry during an episode is

• shown. O2 sat’n during episode

is 96%. The next best step is:

• A. Check ABPA serology
• B. ENT evaluation
• C. HRCT
• D. Start Montelukast
• E. Start Pantoprazole

Flow-­‑volume ¡Loops ¡

Normal Restriction Obstruction Severe Obstruction

Volume Flow Volume Flow Normal Volume Flow Normal Volume Flow Normal

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Flow-­‑volume ¡Loops ¡ Upper ¡Airway ¡Obstruc1on ¡

Variable Extrathoracic Fixed Large Airway

+

• Variable

Intrathoracic

+

• Volume

Flow

Volume Flow

Volume Flow

Flow-­‑volume ¡Loops ¡ ¡Variable ¡Extrathoracic ¡Obstruc1on ¡ from ¡Vocal ¡Cord ¡Dysfunc1on ¡

• Psychogenic
• Most commonly in women, ages

20 - 40

• May present with respiratory distress

and dramatic inspiratory stridor

• Loudest noise at throat
• Normal ABGs and A-a gradient
• Resolves when asleep
• Minimal response to aggressive

asthma treatment

• Really hard when co-exists with

asthma

• Diagnosis by endoscopy

Volume Flow Normal

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Ques1on ¡5 ¡

FV loop

The next best step is:

• A. Check ABPA serology
• B. ENT evaluation
• C. HRCT
• D. Start Montelukast
• E. Start Pantoprazole
• Vs. Difficult to control asthma:
• Compliance
• Allergy trigger review
• Smoking cessation
• Weight loss if obese
• Treat allergic rhinitis
• Check for GERD (PPI)
• Consider: Tiotropium,

Leukotriene blocker

• ABPA serology (steroids &

itra or voriconazole)

• IgE levels (Anti-IgE rx?)
• Future: Anti IL5, IL13, IL17

Ques1on ¡6 ¡

A 23 year-old woman has increasingly use of prn albuterol for her asthma. Spirometry supports

• diagnosis. She has asthma symptoms approximately

3x a week and is awakened at night about 3x a month. Afebrile, BP 120/75, RR 16/min. Lungs: no wheezes. Her peak flow is 400 liters per minute (her best value is 450 LPM).

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Ques1on ¡6 ¡

Which of the following asthma medications would be the most appropriate addition to the treatment regimen at this time? A. Oral proton pump inhibitor B. Oral theophylline C. Low-dose inhaled corticosteroid D. Long-acting beta 2-agonist E. Leukotriene modifier

STEP 3 Moderate Persistent STEP 2 Mild Persistent STEP 1 Mild Intermittent STEP 4 Severe Persistent

STEPS 5 & 6

Management ¡of ¡Asthma ¡

Ini1al ¡Assessment ¡

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Management ¡of ¡Asthma ¡

A ¡Step-­‑Wise ¡Approach ¡

Symptoms Nocturnal STEP 4, 5, 6 Continual symptoms Frequent Severe persistent Limited physical activity Frequent exacerbations STEP 3 Daily symptoms > one/wk Moderate persistent Daily use of inhaler Exacerbations affect activity Exacerbations ≥ 2 times/wk STEP 2 Symptoms >2 times/wk,<1/day >2/mo Mild persistent Exacerbations may affect activity STEP 1 Symptoms ≤ 2 times/wk ≤2/mo Mild intermittent Asymptomatic between exacerbations Exacerbations brief

Management ¡of ¡Asthma ¡

Ini1al ¡Assessment ¡

STEP 3 Moderate Persistent STEP 2 Mild Persistent STEP 1 Mild Intermittent STEP 4 Severe Persist. Long-term Quick-relief Short-acting prn beta-2 agonist Low-dose* inhaled steroids Long-acting beta-2 agonist Low-med dose* inhaled steroids Med-dose inhaled steroids Consider Anti -IgE

* Alternatives: leukotriene modifiers, cromolyn, nedocromil, theophylline

High-dose Inhaled steroids STEP 5 & 6

Patient education & environmental control at each step

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Management ¡of ¡Asthma ¡

Ini1al ¡Assessment ¡

STEP 3 Moderate Persistent STEP 2 Mild Persistent STEP 1 Mild Intermittent STEP 4 Severe Persist. Long-term Quick-relief Short-acting prn beta-2 agonist Low-dose* inhaled steroids Long-acting beta-2 agonist Low-med dose* inhaled steroids Med-dose inhaled steroids Consider Anti -IgE

* Alternatives: leukotriene modifiers, cromolyn, nedocromil, theophylline

High-dose Inhaled steroids STEP 5 & 6

Patient education & environmental control at each step

Tiotropium

Asthma-­‑ ¡Tiotropium ¡ in ¡moderate ¡to ¡severe ¡asthma ¡

NEJM 2012;367:1198

In asthma patients poorly controlled with standard

• therapy. Tiotropium vs. placebo
• Improved lung function
• Decreased time to exacerbation
• Decreased # of severe exacerbations
• No increase in adverse events

N

• t

a s u b , b u t a n “ a d d

• n

”

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Take ¡home ¡points ¡

n If patient moves from intermittent à mild

persistent, add controller medication (best for most = inhaled corticosteroid)

n If poor control on ICS: increase ICS or add

long acting b-agonist (deals with concerns about safety of LABA)

n Long acting b-agonist without a controller

medication is always the wrong answer

n For emergency rescue, short acting b-agonist

always the right answer

LABA-­‑ ¡Safety? ¡

n Lots of large studies with mixed

results of the potential for increased mortality with LABA in a small number of patients

n Related to LABA or non-compliance with

ICS? Studies are so far insufficient to tell

THIS IS NOT AN ISSUE WITH COPD

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Ques1on ¡6 ¡

Which of the following asthma medications would be the most appropriate addition to regimen at this time (only on short acting b-agonists)? A. Oral proton pump inhibitor B. Oral theophylline C. Low-dose inhaled corticosteroid D. Long-acting beta 2-agonist E. Leukotriene modifier Not in asymptomatic pts All acceptable by guidelines, in practiceà like ICS; Caveat: some young people w/ exercise induced asthma do well on LT agents. Smokers have blunted response to ICS.

Ques1on ¡7 ¡

A 32 year old patient has poorly controlled asthma despite inhaled steroids, LABA, LTR-Blocker. Which of the following would predict a good response to Anti-IgE therapy? A. Eosinophilia B. Extremely high IgE levels (>2000 IU) C. Latex allergy D. Sensitization to dust mites

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An1-­‑IgE ¡(Omalizumab) ¡

n Consider for Steps 5 & 6 (difficult to

control asthma)

n Binds IgE à complex cleared n Rx: fewer exacerbations & less steroid

needed; no change in baseline FEV1

An1-­‑IgE ¡(Omalizumab) ¡

n Need to get IgE to extremely low levels for

it to work (very low levels trigger mast cell degranulation)

n Baseline serum IgE should be

between 30 - 700 IU/mL

n + Skin test or RAST to a perennial

aeroallergen (e.g., dust mite, animal danders, cockroach, molds)

n Sq each 2-4 weeks n Anaphylaxis 1:1,000 n Minimum dose $12,000/year

High, but not TOO HIGH

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Ques1on ¡7 ¡

A 32 year old patient has poorly controlled asthma despite inhaled steroids, LABA, LTR-Blocker. Which of the following would predict a good response to Anti-IgE therapy? A. Eosinophilia B. Extremely high IgE levels (>2000 IU) C. Latex allergy D. Sensitization to dust mites

Though usually a partner

TOO high

Best with aeroallergen

Ques1on ¡8 ¡

30 year-old woman was exposed to chlorine gas 2 months ago at work & now has a persistent cough & mild SOB. At exposure, she noted irritation of her eyes and mucus

• membranes. Immediately after the exposure, she developed

a cough. A chest x-ray was normal. No treatment was given. The patient has no history of asthma, but since this, has been wheezing at night. Exam is unremarkable with clear lungs. Spirometry: FVC of 89% of predicted FEV1 of 84% of predicted FEV1/FVC 73% Methacholine challenge + for bronchial hyperresponsiveness

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Ques1on ¡8 ¡

Which of the following is the most likely diagnosis?

• A. Cryptogenic organizing

pneumonitis (COP)

• B. Hypersensitivity pneumonitis

C. Diffuse panbronchiolitis D. Reactive airways dysfunction syndrome

Occupa1onal ¡Asthma ¡

Occupational asthma

Irritant-induced asthma

Reactive airways dysfunction

Acquired sensitization in the workplace Multiple exposures to irritant Single big exposure to irritant Non-immunologic

20-30% of new onset adult asthma = occupational!

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Reac1ve ¡Airways ¡Dysfunc1on ¡

Diagnos1c ¡Criteria ¡

n Exposure to irritant in high concentration n Onset of symptoms after single exposure

within 24 hrs; persist for at least 3 months and sometimes years!

n Symptoms of asthma n PFTs +/- airflow obstruction, but

Methacholine test positive

Brooks SM et al. Chest 1985;88:376

RADS ¡

Take home points

n “Big Bang” à big exposure,

symptoms right away

n + methacholine challenge n Rx like asthma, though typically harder to

control

n CHLORINE! (Including mixing household

cleaners)

n Gulf War à sulfur mustard gas

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Ques1on ¡8 ¡

Which of the following is the most likely diagnosis?

• A. COP
• B. Hypersensitivity pneumonitis
• C. Diffuse panbronchiolitis
• D. Reactive airways dysfunction

syndrome

Typically slower onset; HRCT scan + Japanese (Specific HLA), chronic sinusitis, productive cough, diffuse lung nodules à Rx Erythromycin x 6-24 months

Crytogenic ¡Organizing ¡ Pneumoni1s ¡

n Former Bronchiolitis Obliternans

Organizing Pneumonitis “BOOP”

n Like the flu that keeps coming back n Fevers, infiltrates that come and go n Biopsy n Treat with steroids

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Ques1on ¡9 ¡

77 year old man has progressive dyspnea x 2

• years. No sputum, hemoptysis, weight loss,
• r sweats. He previously smoked 1 ppd for

40 years, quit 15 years ago. PMH: HTN and peptic ulcer disease. Meds: lisinopril and omeprazole Exam: afebrile, RR 16, SaO2 92% RA Crackles bilaterally at bases + Clubbing Labs: negative serology for rheumatologic dz

Chest ¡X-­‑ray ¡

41

HRCT ¡ PFTS ¡

FVC 67% predicted FEV1 72% predicted TLC 74% predicted DLCO 55% predicted Oxygen saturation is 92% at rest and 87% after ambulation

42

Ques1on ¡9 ¡

77 yom former smoker with progressive dyspnea and restriction on PFTs. In addition to oxygen, which of the following is most appropriate at this time?

• A. VATS lung biopsy
• B. Listing for single lung transplant
• C. Prednisone
• D. Pirfenidone
• E. Sildenafil

IPF ¡– ¡What ¡DOESN’T ¡work ¡

“Prednisone, azathioprine, and N-acetylcysteine for pulmonary fibrosis” NEJM 2012;366:1968.

n Stopped early because of INCREASED death in

steroid patients! PREDNISONE SHOULD NOT BE USED FOR IPF “Randomized Trial of Acetylcysteine in Idiopathic Pulmonary Fibrosis” NEJM 2014; 370:2093

n No benefit

43

Nintedanib ¡and ¡Pirfenidone ¡ Won’t ¡ask ¡you ¡to ¡choose ¡

Nintedanib

NEJM 2014; 370:2071

Pirfenidone

NEJM 2014; 370:2083

$$$ $$$ Receptor blocker of multiple tyrosine kinases Antifibrotic agent that inhibits TGF-b-stimulated collagen synthesis Follow LFTs Follow LFTs Rumbly gut Rumbly gut MDC Conference MDC Conference Slows decline Slows decline

Ques1on ¡9 ¡

77 yom former smoker with progressive dyspnea and restriction on PFTs. In addition to oxygen, which of the following is most appropriate at this time?

• A. VATS lung biopsy
• B. Listing for SLT
• C. Prednisone
• D. Pirfenidone
• E. Sildenafil

Biopsy for confusing cases, not classic IPF by CT, symptoms,

• demographics. IPF

flare can be triggered by lung & non lung surgery Definite NO

44

HRCT: ¡Classic ¡for ¡IPF ¡

Bilateral, lower lobe predominant Traction bronchiectasis Subpleural honeycombing Consider other dx:

• Age < 55
• Productive cough
• Extensive GGOs

IPF ¡

End stage Honeycombing No drug will ever fix this part

45

Ques1on ¡9 ¡

77 yom former smoker with progressive dyspnea and restriction on PFTs. In addition to oxygen, which of the following is most appropriate at this time?

• B. Listing for SLT
• D. Pirfenidone
• E. Sildenafil

Age doesn’t rule out (but old), but DLT better outcomes, & track decline to see if might benefit Echo if DLCO < 35% to check for pulmonary HTN

IPF ¡– ¡Exacerba1on ¡

IPF exacerbation:

n Think about CHF n Think about PE n HRCT to look for classic GGO n BAL (if you can) to look for infection n Antibiotics unless confident no infection n Prednisone 1 mg/kg per day orally or

methylprednisolone 1 to 2 g per day intravenously

75% mortality

46

IPF-­‑Summary ¡

Some bad options à Steroids only for exacerbations, otherwise NO STEROIDS Symptomatic but not end stage, consider referral for Nintedanib or Pirfenidone N or P WILL NOT IMPROVE, only slows decline (not useful for severely debilitated) No data to chose between the 2 Sildenafil if Pulmonary HTN Exacerbation? Call for help

Ques1on ¡10 ¡

¡

34 year old man has DOE x 6 months and cough productive of yellow sputum. No fever, chills, or

• hemoptysis. HIV negative. Exam is normal.

Sputum smears are negative for AFB. He has had a pet pigeon for the past 2 years. Pulmonary function tests: FEV1/FVC 83% predicted ABG 7.49/30/60 TLC 68% predicted DLCO 50% predicted

47

Chest ¡X-­‑ray ¡ Chest ¡CT ¡Scan ¡

48

Lung ¡Biopsy ¡

Ques1on ¡10

¡

Which of the following is the most likely diagnosis?

• A. Idiopathic pulmonary fibrosis
• B. Lymphangioleiomyomatosis
• C. Mycobacterium Avium Complex

(MAC) infection

• D. Hypersensitivity pneumonitis

49

Inters11al ¡Lung ¡Diseases ¡

n Characterized by restriction (low TLC) on

PFTs with low diffusion capacity and desaturation with exercise (or if bad à hypoxemia at rest)

n High resolution Chest CT scan is almost

always the right answer to “what to do next” if hasn’t been ordered

• Some ILDs have classic findings
• Shows where to biopsy

“Mosiac” ¡Pakern ¡on ¡HRCT ¡

Could be “perfusion” issue:

• PE
• CHF

Or not a perfusion problem à just patchy alveolar infiltrates Inspiration Expiration

Vs.

If small airways inflamed, air can’t exit with exhalation. On CT scan, involved lung areas remain

• black. Mosaic suggests of small

airway (bronchiolar) disease: HP, Sarcoidosis, RB-ILD… BUT SOMETHING WRONG!

50

Ground ¡Glass ¡= ¡ac1ve ¡alveoli1s ¡

HRCT ¡What ¡to ¡order? ¡ ¡

Get inspiratory and expiratory views (small airway disease) Plus prone & supine images. Can open up atelectasis that can be confused with an ILD

51

Hypersensi1vity ¡Pneumoni1s ¡

Chronic granulomatous inflammation after repeated inhalation of environmental antigens

n Can present as acute, subacute or chronic dz n No single test is diagnostic: + serology just tells

exposure

n Suspect when there is a

• History of recurrent “pneumonias”
• Symptoms develop after moving to a new job or home
• r birds or water damage/visible mold in work/home
• Improvement in symptoms when away from work/home
• No eosinophilia

ILD: ¡HP ¡

Hypersensitivity pneumonitis: centrilobular nodules, ground glass opacities, and air trapping (mosiac pattern) on expiratory views

52

Lung ¡Biopsy ¡

Granulomas a bit less well formed than sarcoid But will not ask for diagnosis based just on biopsy

How ¡many ¡of ¡these ¡ILDs ¡do ¡you ¡ need ¡to ¡know? ¡ ¡My ¡Picks ¡are: ¡

n Hypersensitivity Pneumonitis

• Because non-drug intervention can cure (i.e.,

removing the antigen)

n Sarcoid

• Common and distinguishing HRCT

n IPF

• Common and distinguishing HRCT, new Rx

53

Sarcoid ¡ Sarcoid ¡on ¡HRCT ¡

Sarcoid: adenopathy and nodular thickening

• f bronchovascular bundles (lumpy-

bumpy), centrilobular nodules.

54

ILD: ¡Sarcoid ¡

Disease @ bronchovascular bundles

MAC ¡infec1on ¡

“Tree-in-bud” = infection Clear increase in prevalence in past few decades

55

MAC ¡Infec1on ¡Spectrum ¡

n HIV n COPD – older men, upper lobe, cavitary n In prior bronchiectasis (CF patients) n Healthy women in 50s: diffuse infiltrates à

cause bronchiectasis

• This subgroup à some have hypersensitivity

reaction to MAC; removal from exposure may help.

Biofilm in Hot Tubs and shower heads. Want hot water > 130oF

Mycobacterium ¡avium ¡Lung ¡ Disease ¡

Diagnostic criteria:

Symptoms + x-ray (nodules, cavities, or bronchiectasis) with:

n Positive cultures from at least 2 separate

sputum samples OR

n Positive culture from at least 1 bronchial wash

OR

n Transbronchial or other lung biopsy with

characteristic histology and positive culture on either biopsy or sputum

Am J Resp Crit Care Med 2007;175:367

If smear + or 3-4 + cultures àmore likely to progress

56

Treatment ¡of ¡Mycobacterium ¡ avium ¡Lung ¡Disease ¡ ¡

n For nodular/bronchiectasis: macrolide (clari or

azithro), ethambutol, & rifamycin (rifampin or rifabutin) 3 times weekly

n For cavitary disease : same drugs given daily +/-

streptomycin or amikacin

n Goal: 12 months of negative sputum cultures while

• n therapy--total duration is often 14-18 months

Am J Resp Crit Care Med 2007;175:367

Check for macrolide resistance: at start, and if fails to respond at 6 months, or if relapse post Rx

LAM ¡

Proliferation of atypical pulmonary interstitial smooth muscle with cyst formation

Classic LAM story: 35 year old woman with dyspnea and pneumothorax or chylothorax

57

Ques1on ¡10

¡

34 yo man with a bird. Which of the following is the most likely diagnosis?

• A. Idiopathic pulmonary fibrosis
• B. Lymphangioleiomyomatosis
• C. Mycobacterium Avium Complex (MAC)

infection

• D. Hypersensitivity pneumonitis

Too young Young women;

• bstruction not

restriction on PFTs Should have tree-in bud on CT scan; productive cough Typical HRCT, bird exposure favor HP Diagnosis important – need to remove antigen (bird)!

Ques1on ¡11 ¡

33 year-old woman presents with intermittent fever, night sweats, migratory joint pain, and red, painful nodules on her

• shins. She has no

pulmonary symptoms. Chest x-ray:

58

Ques1on ¡11 ¡

Bronchoscopy with transbronchial biopsy: non- caseating granulomas. Stains and cultures for fungi and mycobacteria were negative.

Which best describes the status of her lung disease in 2 years?

• A. Progression to advanced obstructive

lung disease

• B. Progression to advanced interstitial lung

disease with fibrosis

• C. Progression to pulmonary hypertension
• D. Normal lung function

Ques1on ¡11 ¡

59

Overview ¡of ¡Sarcoidosis ¡

n Multisystem granulomatous disorder of unknown

etiology characterized by non-caseating granulomas in involved organs

n Incidence varies geographically; much more

common in African-Americans (lifetime risk of 2.4%)

n Usually presents ages 10 - 40, half detected by

CXR without symptoms

n Any organ can be involved, lungs most frequent

(90%)

Should you bx asymptomatic pts with hilar adenopathy?

Won’t ask

Sarcoidosis-­‑Staging ¡

n Stage I

Bilateral hilar adenopathy

n Stage II

Above + interstitial infiltrates (upper>lower lung zones)

n Stage III

Interstitial disease with shrinking hilar nodes

n Stage IV Advanced fibrosis

Extra-pulmonary disease-skin (E. nodosum, lupus pernio), eyes, liver, lymph nodes most frequent

60

Sarcoidosis: ¡Dx ¡& ¡Rx ¡

n Histology = granulomas, must exclude infection! n Usual indications for treatment are: worsening

pulmonary symptoms, lung function, progressive radiographic changes, cardiac, eye, neuro, disfiguring skin lesions, high calcium

n Therapy is NOT indicated in

• Asymptomatic stage I disease patients
• Asymptomatic patients with stage II and mildly

abnormal lung function

n Follow first for 3-6 months (some say 6-12, even

with mild-moderate) and document impairment of lung function

Love to ask! Won’t ask

Sarcoidosis ¡

n No drug has been shown to change the course n Steroids treat granulomatous disease which can

cause symptoms but won’t change fibrotic disease

• EXAMPLE: hypercalcemia very responsive!

n Inhaled corticosteroids ? Most experts don’t give n Lupus pernio skin changes= rare

to have remission, but seems to be better with infliximab

n If severe lung disease by PFTs or need for

Oxygen à get Echo to check for pulm HTN

61

Her lung disease in 2 years? She has Stage I CXR, but lots of symptoms. She had Lofgren's syndrome: “Acute” sarcoid with abrupt onset with erythema nodosum, hilar adenopathy, migratory polyarthralgias, and fever seen primarily in women.

• Strongly associated with HLA-DQB1*0201
• Good prognosis and spontaneous remission

in 85-95%. Rx only if painful arthritis.

Ques1on ¡11 ¡ Ques1on ¡12 ¡

46 year old woman has 4 weeks of fever, night sweats, cough, and 10 lb weight loss. She also has arthralgias, epistaxis, nasal congestion. 2 weeks of clarithromycin did not relieve her

• symptoms. Now has hemoptysis.

Exam: 99.7, RR 24/min, crackles right chest, 1+ edema WBC 6800/mm3 Hgb 10.3 Platelets 568,000/mm3 Creatinine 1.3 mg/dL Urinalysis: 2+ protein, 0 WBCs, rare RBC casts

62

X-­‑ray ¡

American Journal of Roentgenology. 2009;192:676-682

Ques1on ¡12 ¡

Which of the following is the best diagnostic step?

• A. Serum angiotensin-converting enzyme
• B. Rheumatoid factor
• C. Antineutrophil cytoplasmic antibodies
• D. Culture of bronchoalveolar lavage fluid
• E. Percutaneous needle biopsy of the

lung

63

Pulmonary-­‑Renal ¡Syndromes ¡

Systemic vasculitis Wegener’s granulomatosis Microscopic polyangiitis Pauci-immune GN Churg-Strauss (allergic angiitis and granulomatosis) Goodpastures syndrome Systemic lupus erythematosus Henoch-Schonlein purpura Infection Post-streptococcal glomerulonephritis, endocarditis ANCA? C-ANCA 80% P-ANCA 10% P-ANCA 70% Most P-ANCA ½ ANCA P-ANCA 10-40% Some + Any + ANCA= bad news. You may not know which vasculitis it is…., but always abnormal.

Approach ¡to ¡Pulmonary-­‑Renal ¡ Syndromes ¡

n Serologic tests: ORDER

• Anti-GBM Abs, anti-neutrophil cytoplasmic Abs

(ANCA), ANA

n ANCAs are positive in 90% of those with

generalized Wegener’s (PR3-ANCA or “C- ANCA”)

n Tissue should be obtained to provide evidence

• f vasculitis
• Skin (easy), Kidney, or lung (surgical biopsy)
• If Anti-GBM possible, kidney better to bx than lung

64

Ques1on ¡12 ¡

Which of the following is the best diagnostic step?

• A. Serum angiotensin-converting enzyme
• B. Measure rheumatoid factor
• C. Antineutrophil cytoplasmic antibodies
• D. Culture of bronchoalveolar lavage fluid
• E. Percutaneous needle biopsy of the lung

Sarcoid is not pulm-renal syndrome Reasonable, but fungi, TB can not explain GN Not enough tissue to see vessel Lupus not RA

Ques1on ¡13 ¡

30 year old man has increasing dyspnea with exercise and chronic daily productive cough since adolescence. He also reports frequent bronchial and sinus infections, treated with multiple courses of antibiotics. Twice he was admitted for pneumonia. He has a 20-pack year history of smoking. No other medical problems or prior surgeries. He works in an

• ffice.

Exam: SaO2 86%, diffuse crackles, and digital clubbing.

65

Chest ¡X-­‑ray ¡ Chest ¡CT ¡Scan ¡

66

Ques1on ¡13 ¡

Which of the following should be ordered to establish the most likely diagnosis?

• A. Serum IgG and IgE for Aspergillus
• B. Serum IgA and IgG levels
• C. Sweat chloride measurement
• D. Nasal brushing for EM analysis
• E. Serum α1-antitrypsin level

Bronchiectasis: ¡Causes ¡

• Bronchopulmonary infections

– Bacterial, fungal, mycobacterial

• Bronchial obstruction

– Foreign-body, tumors, lymph nodes

• Immunodeficiency states

– IgA, IgG deficiency

• Hereditary abnormalities

– Cystic fibrosis, ciliary dyskinesia, α-1 antitrypsin deficiency

• Miscellaneous: Rheumatoid, Sjogren’s

67

Bronchiectasis ¡work-­‑up ¡in ¡adults ¡

Blood Imaging Other CBC HRCT Spirometry IgA, IgE, RF Sinus CT Sputum

• Aspergillus
• MAC

IgG Sweat chloride subclasses Nasal brush for EM Bronchoscopy

Primary ¡Ciliary ¡Dyskinesia ¡

n Chronic cough, rhinitis, and sinusitis n Cilia do not beat normally n Triad of situs inversus, chronic sinusitis,

and bronchiectasis = Kartagener’s syndrome

n Situs inversus is present in 50% of

patients with primary ciliary dyskinesia

68

Ques1on ¡13 ¡

Which of the following should be ordered to establish the most likely diagnosis?

• A. Serum IgG and IgE for Aspergillus
• B. Serum IgA and IgG levels
• C. Sweat chloride measurement
• D. Nasal mucosal biopsy
• E. Serum α1-antitrypsin level

ABPA All can cause bronchiectasis with purulent sputum and all part of an adult work-up, but with situs inversus, start with evaluation of cilia

Ques1on ¡14 ¡

65 year old man with a history of TB has intermittent hemoptysis but no fevers/chills/ weight loss. Recent spirometry: FEV1 1.0L (40%), FVC 1.5L. Today he coughs up 200 mL of bright red blood. Exam: afebrile, BP 145/82, pulse 104, RR 18, SaO2 93% on air. Bronchoscopy: blood coming from the left upper lobe bronchus.

69

Chest ¡X-­‑ray ¡ Chest ¡CT ¡Scan ¡

70

Ques1on ¡14 ¡

What is the best management option for this patient at the present time?

• A. Bronchial arteriography with embolization
• B. Four first-line drugs for tuberculosis
• C. Intravenous Amphotericin B
• D. Left upper lobe resection

Causes ¡and ¡Management ¡of ¡ ¡ Massive ¡Hemoptysis ¡

Massive usually means > 200 mL in 24hrs Most common causes include: 1) TB (active or inactive disease) 2) Bronchiectasis 3) Lung cancer 4) Mycetoma 5) Immunologic diseases (ANCA- associated vasculitis, Goodpasture’s, SLE)

More commonly à chronic mild hemoptysis

71

Management ¡of ¡ ¡ Massive ¡Hemoptysis ¡

n First, protect the airway n Bronchoscopy can localize; make some diagnoses n Majority of massive bleeds have bronchial

circulation à Bronchial arteriography with embolization next step. 85% successful especially with bronchiectasis and mycetomas. Less so with cancer

n Surgery is definitive, but high M&M if done urgently

Our patient has a mycetoma, and actively bleeding→ arteriography and embolization successful

Ques1on ¡14 ¡

What is the best management option for this patient at the present time?

• A. Bronchial arteriography with embolization
• B. Four first-line drugs for tuberculosis
• C. Intravenous Amphotericin B
• D. Left upper lobe resection

Old cavity; looks like a classic fungal mycetoma Doesn’t penetrate fungus ball well; Itraconazole may

72

Ques1on ¡15 ¡

Which of the following are used in the routine treatment of patients with idiopathic pulmonary arterial hypertension?

• A. Calcium channel blocker
• B. Digoxin
• C. Epoprostenol
• D. Nitric oxide
• E. Warfarin

Pulmonary ¡Hypertension ¡

Smooth Muscle Cell Endothelial Cell

NO Prostacyclin Endothelin Smooth muscle relaxation Smooth muscle contraction ET-R

Endothelin is also smooth muscle mitogen

73

Pulmonary ¡Hypertension-­‑ ¡RX ¡

Prostanoids: Prostacyclin =Epoprostenol (Flolan) continuous IV Endothelin receptor-blockers Bosentan (Oral) Ambrisentan

• Hepatotoxicity

Smooth muscle relaxation Calcium Channel Blockers Only 5-10% respond Iloprost (Inhaled) Treprostinil (IV or sq) Phosphodiesterase inhibitors: Prolong NO action: Sildenafil & Vardenifil

Pulmonary ¡Hypertension-­‑ ¡RX ¡

General recommendations:

n Treat primary cause if there is one n Oxygen if desaturates n Anticoagulation in chronic PE (mainstay)

and in IPAH

n Diuretics if needed n Advanced therapy guided by PA catheter

Love to ask

74

Ques1on ¡15 ¡

Which of the following are used in the routine treatment of patients with IPAH?

• A. Calcium channel blocker

B. Digoxin C. Epoprostenol D. Nitric oxide E. Warfarin Only 5% with sustained benefit, never do without R heart cath to prove efficacy No portable system yet Endothelial disruption: in-situ clotting, even small clots can tip a patient over Better outcomes: Circ 2014; 129(1): 57-65. BUT ONLY IN IDIOPATHIC PAH. OK if LV failure If severe

Ques1on ¡16 ¡

A 62 year old patient with COPD complains of SOB and has a negative CTA for PE, but the CT scan shows Nodule is not visible on Chest x-ray and there are no prior CT scans. PFTs with FEV1 of 65%. 5 mm

75

Ques1on ¡16 ¡

You recommend:

• A. Bronchoscopy
• B. PET scan
• C. Repeat Chest CT in 6 months
• D. Transthoracic needle aspirate
• E. Surgical resection

Solitary ¡Pulmonary ¡Nodule ¡

FLEISCHNER SOCIETY 2005 Recommendations F/U & Management of Incidental Nodules Detected at Nonscreening CT

Nodule Size Low-Risk Patient High-risk Patient (Smoker, radon (mm) asbestos, uranium, 1st degree relative or spiculated nodules) < or = 4 mm No f/u needed F/u CT 12 mo; if (risk < 1 %) unchanged, no further f/u >4-6 mm F/u CT 12 mo; F/u CT 6-12 mo then if unchanged, no f/u 18-24 mo if no change >6-8 mm F/u CT 6-12 mo, then F/u CT 3-6 mos, then 9-12 18-24 mo if no change and 24 mo if no change >8 mm F/u CT 3, 9, and 24 mo F/u CT 3, 9, and 24 mo if NOT changing if NOT changing

• vs. PET, FNA, resection vs. PET, FNA, resection

76

Solitary ¡Pulmonary ¡Nodule ¡

FLEISCHNER SOCIETY 2005 Recommendations F/U & Management of Incidental Nodules Detected at Nonscreening CT

Nodule Size Low-Risk Patient High-risk Patient (mm)

Translation: ü Bigger nodules more worrisome ü F/u CT at “3, 9, 24 months” means from the 1st CT (not 9 months after the 3 month CT) ü > 8 mm, we tend to work up now rather than watch CT scans unless other significant morbidities ü 2 year stability works for most solid nodules ü For “ground glass” nodules, don’t know – we use 3 years of stability

Ques1on ¡16 ¡

You recommend:

• A. Bronchoscopy
• B. PET scan
• C. Repeat Chest CT in 6 months
• D. Transthoracic needle aspirate
• E. Surgical resection

Unless central mass – yield

• f bronch low.

Yield of FNA high (80% but with 20% risk of PTX); harder if close to diaphragm!

Too small (1 cm is quoted size cut-off, we see + at 8mm), though if < 1 cm and neg, more false neg, still need to follow

77

Solitary ¡persistent ¡GGO ¡“Sub-­‑Solid ¡Nodules ¡ is ¡omen ¡BAC ¡(“adenocarcinoma ¡in ¡situ”) ¡ ¡

Naidich DP et al. Recommendations for the Mangement of Subsolid Pulmonary Nodules Detected at CT: A Statement from the Fleischner Society”. Radiology 2013;266:304.

PURE GGO § < 5 mm no f/u § > 5 mm, CT scan at 3 months (many disappear), then if no change CT scan q 1 year x 3 years MIXED GGO & solid § CT scan 3 months, if persistent à esp. if solid component is > 5 mm: think cancer!

Smoking history less important

Screening ¡for ¡Lung ¡Cancer ¡

n Know criteria from National Lung Screening

Trial:

• Age: 55-74
• Smoking: 30 pk years
• Quit < 15 years

n Positive LDCT = > 4 mm nodule n 20% decrease in lung cancer deaths

78

The ¡End! ¡

Extra ¡Ques1ons ¡for ¡fun ¡at ¡ home… ¡ ¡Ques1on ¡A. ¡

50 year old man presents for evaluation of a nonproductive cough and chest pain increasing for the past 3 months. He denies weight loss but notes weakness. Exam reveals a mild bilateral ptosis and is

• therwise normal. Labs: mild normocytic

anemia.

79

Chest ¡X-­‑ray ¡ Lateral ¡Chest ¡X-­‑ray ¡

80

Chest ¡CT ¡Scan ¡

Ques1on ¡A ¡

What is the most likely diagnosis?

• A. Bronchogenic cyst
• B. Intrathoracic thyroid
• C. Lymphoma
• D. Teratoma
• E. Thymoma

81

Ques1on ¡A ¡

What is the most likely diagnosis?

• A. Bronchogenic cyst
• B. Intrathoracic thyroid
• C. Lymphoma
• D. Teratoma
• E. Thymoma

Medias1nal ¡Masses ¡ Differen1al ¡Diagnosis ¡

First, localize to anterior, middle, or posterior mediastinum Anterior Mediastinum Middle Posterior “The 4 Ts” Bronchogenic cyst Neurogenic cyst Thymoma Pericardial cyst Esophagus Thyroid Lymph nodes Teratoma “Terrible” lymphoma

82

Thymomas ¡

Pearl: Disease of “35s” #1 anterior mediastinal mass in those > 35 35% are malignant 35% are associated with myasthenia 35% have a paraneoplastic syndrome

• Pure red blood cell aplasia
• Hypogammaglobulinemia
• Cushing’s syndrome

Ques1on ¡A ¡

What is the most likely diagnosis?

• A. Bronchogenic cyst
• B. Intrathoracic thyroid
• C. Lymphoma
• D. Teratoma
• E. Thymoma

Asymptomatic until infected All anterior mediastinal, but most have CT scan characteristics; clue here was anemia, myasthenia symptoms

83

Ques1on ¡B ¡

52 year old man with alcoholic cirrhosis with prior variceal bleeding has new onset of dyspnea x 3 days. Denies chest pain, fever,

• r sputum production. Has gained 5 pounds
• ver the past month.

Meds: propranolol.

Chest ¡X-­‑ray ¡

84

Lateral ¡Decubitus ¡

Right side

Ques1on ¡B ¡

Thoracentesis reveals a transudate. What is the optimal management in this case? A. Large volume thoracentesis B. Chest tube insertion C. Pleurx catheter insertion D. Pleurodesis E. Diuretics

85

Ques1on ¡B ¡

Thoracentesis reveals a transudate. What is the optimal management in this case? A. Large volume thoracentesis B. Chest tube insertion C. Pleurx catheter insertion D. Pleurodesis E. Diuretics

Pleural ¡Effusions ¡in ¡Pa1ents ¡ with ¡Liver ¡Disease ¡

n Hepatohydrothorax: Effusions usually

when ascitic fluid is present, but not always

n Fluid passes from peritoneum to pleural

space via diaphragmatic pores & possibly lymphatic channels. Negative pleural pressure draws fluid up.

n Fluid is transudative with very low protein n Typically free-flowing

86

Pleural ¡Effusions ¡in ¡Pa1ents ¡ with ¡Liver ¡Disease ¡

n Management: decrease ascites

formation

• Low salt diet
• Diuretics
• TIPS if refractory

Ques1on ¡B ¡

What is the optimal management in this case?

• A. Large volume thoracentesis
• B. Chest tube insertion
• C. Pleurx catheter
• D. Pleurodesis
• E. Diuretics

Just keeps draining; reserve large volume thoracentesis for acute dyspnea relief Can’t get pleural surfaces to meet

87

Ques1on ¡B ¡cont’d ¡

What is preferred management for malignant pleural effusions? Pleurx catheter vs. Pleurodesis

Institution dependent, tend to favor Pleurx for shorter length of stay, comfort