Pulmonary ABIM Certification Exam Review Course Leslie Zimmerman, MD - - PDF document

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Pulmonary ABIM Certification Exam Review Course

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

Relative Value?

 Medical Content

• CV

14%

• Pulmonary

10%

• ID

9%

• GI

9%

 Cross Content

• Critical Care

10%

• Geriatrics

10%

• Prevention

6%

• Women’s Health 6%

Relative Value?

 Pulmonary:

• Obstructive disease:

24%

• Pleural Disease:

13%

• Restrictive & Interstitial:

11%

• Pulmonary vascular disease:

11%

• All the other stuff….

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Lecture Outline

 Sleep  COPD/Asthma  ILDs  PVD  TB  Solitary Pulmonary Nodule  Etc.

Question 1

A 65 year-old man with daytime sleepiness is evaluated for sleep apnea with

• polysomnography. His Epworth sleepiness

scale is 11/24. The polysomnogram reveals obstructive sleep apnea with an apnea-hyponea index (AHI) of 12 events/hour. Lowest oxygen saturation was 86%. Treatment with continuous positive airway pressure (CPAP):

Question 1

65 year-old man with 11/24 Epworth & AHI

• 12. O2 sat’n nadir 86%. CPAP treatment:
• A. Will be reimbursed by Medicare
• B. Will decrease cardiovascular mortality
• C. Will likely need to be supplemented

with oxygen

• D. Should be offered only if “mission

critical job” (airline pilot, bus and truck drivers)

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Sleep Disorders: Office Visits

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

Classic patient with OSA

Obesity = #1 risk factor

Genetics Upper airway/facial abnormalities Post-menopause Hypothyroidism/ Acromegaly

Deeper stages of sleep, neural input to upper airway declines, decreased airway tone, tongue falls back. The vibrations from snoring may actually cause a myopathy!

en.wikipedia.org

OSA

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

http//:epworthsleepinessscale.com

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OSA

Air flow

Apneas + Hyponeas = AHI

10 seconds 10 seconds “Hyponea” has 4% desaturation

OSA

Severity Mild: AHI 5-15 Moderate: AHI 15-30 Severe: > 30 AHI > 15 in everyone or AHI > 5 if symptoms (sleepiness, fatigue, inattention) or signs of disturbed sleep (snoring, restless sleep, respiratory pauses), or HTN/CAD/CVA

So can have AHI of 6-15 and if asymptomatic, low Epworth, no HTN/CAD/CVA, not “mission critical” many would not treat.

Medicare reimbursement

OSA and Death

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

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

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Punjabi et al. PLoS Med. 2009 August; 6(8): e1000132

OSA and Mortality

6,441 people with untreated OSA Higher CV mortality in:

• Men with severe OSA (AHI > 30)

who were < 70 years old

• Not enough women enrolled to

estimate risk

Martinez-Garcia MA et a;. AJRCCM 2012;186:909

Observational, smaller (939 people) mean age 71. Even in older, untreated OSA 2x CV death if severe (AHI > 30)

Question 1

65 year-old man with 11/24 Epworth & AHI

• 12. O2 sat’n nadir 86%. CPAP therapy:
• A. Will be reimbursed by Medicare
• B. Will decrease cardiovascular mortality
• C. Likely need to be supplemented with
• xygen
• D. Should be offered only if “mission

critical job” (airline pilot, bus and truck drivers)

If AHI > 30

O2 alone can worsen OSA; with mild–moderate OSA & no sign’t heart/lung disease, CPAP alone typically enough AHI > 5 & symptoms  treat

Sleep Apnea – Cutting Edge

Sharma SK et al. “CPAP for the metabolic syndrome in patients with obstructive sleep apnea” NEJM 2011; 365:2277-86.

• Cross-over of sham CPAP vs. CPAP in obese

patients (80% with Metabolic syndrome) with mod to severe OSA

• CPAP decreased:
• Systolic BP
• Diastolic BP
• LDL
• Hgb A1c

3 mmHg 2.8 mmHg 5 mg/dL .03%

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Sleep Apnea – Cutting Edge

Karkow B,et al. “Prospective Assessment of Nocturnal Awakenings in a Case series of Treatment Seeking Chronic Insomnia patients: A Pilot Study of Subjective and Objective Causes” Sleep 2012; 35:1685-92.

• Small study of insomnia patients
• Most night awakenings actually caused by

sleep disordered breathing

What were those OSA numbers?

 AHI > 5 & symptoms or HTN/CAD/CVA or

“mission critical” job  CPAP

 AHI > 15  CPAP  AHI > 30 and if < 70 years old, clearly at

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

Question 2

A 60 year-old smoker complains of an insidious onset

• f dyspnea on exertion. PFTS reveal COPD. The

severity of the disease is determined by the: A. Air-trapping B. Diffusion capacity for carbon monoxide C. FEV1 D. FEV1/FVC E. Lack of response to bronchodilators

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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,  in COPD deaths is driven by very large  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

COPD Pathogenesis: Aging + Genes + Noxious Stimuli

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)

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In non‐smokers, environmental exposure is primary risk factor

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

World Health Organization

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

Spirometry

TLC

RV Time

Obstructive disease Restrictive disease

FVC

FEV1

TLC – elevated reflecting hyperinflation

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Diffusion Capacity for CO

DCO: integrity of the alveolar– capillary membrane

CO CO CO

Destroy alveoli or capillaries  Low DCO DCO: integrity of the alveolar– capillary membrane

CO CO CO

Just narrow airways  Normal DCO

Diffusion Capacity for CO Diffusion Capacity for CO

Normal

 Asthma

Low

 Emphysema  Fibrosis  Pneumocystis

jiroveci pneumonia

 PE

ELEVATED?

• Diffuse alveolar

hemorrhage Falling Hct Elevated DCO

CO

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Sample PFTs in emphysema

FVC (L) 2.4 (52%) FEV1 (L) 1.02 (38%) FEV1/FVC 41% TLC (L) 6.2 (103%) RV (L) 3.8 (150%) DCO 12 (48%)

< 70% diagnoses

• bstruction

Severity

Suggests emphysema more likely than asthma

• r chronic

bronchitis

Air trapping

Question 2

A 60 year-old smoker complains of an insidious onset

• f dyspnea on exertion. PFTS reveal COPD. The

severity of the disease is determined by the: A. Air-trapping B. Diffusion capacity for carbon monoxide C. FEV1 D. FEV1/FVC E. Lack of response to bronchodilators Consistent with emphysema; don’t stop BDs. BIG reversibility  Asthma component ?

COPD‐ a different GOLD severity scale?

GOLD = Global Initiative for Chronic Obstructive Lung Disease 2013

 Spirometry  Breathlessness  Exacerbation number

A = Few symptoms, OK numbers B = Lots of symptoms, OK numbers C = Few symptoms, Bad numbers D = Lots of symptoms, Bad numbers Why? Why?

Search for biomarkers

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Question 3

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

And CT scan of Lung Bases

Question 3

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

• A. Prevent liver disease
• B. Decrease risk of lung cancer
• C. Slow decline of FEV1
• D. Decrease number of exacerbations/year

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Alpha 1 Anti‐trypsin Deficiency

 Normal: PiMM  Heterozygotes make enough to be

protective

 Homozygous PiZZ, PiZnull, PiNullNull

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

A1AT

Neutrophil Elastase

Panacinar

Liver Disease?

 A1AT made in the liver  ZZ variant, it is

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

 PiNullNull – makes NO A1AT – they do

not get the liver disease

 IV Augmentation doesn’t help liver

Augmentation with A1AT

 Cost is $60,000 to $150,000/ year  Approved by the FDA if level below the

protective level (PiZZ, PiZnull) & COPD

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

• f decline of lung function & mortality (NOT

A RANDOMIZED TRIAL)

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Question 3

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

• A. Prevent liver disease
• B. Decrease risk of lung cancer
• C. Slow decline of FEV1
• D. Decrease number of exacerbations/year

Adding normal A1AT won’t hurt; but won’t help

“Air sac” disease, not airway disease

Increased risk, but no improvement with Rx

Other COPD stuff

Recurrent exacerbations are bad

Lung function over lifetime with COPD

Lung Function

Question 4

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  more rapid decline in FEV1 But who gets exacerbations?

 Prior exacerbations  Lower FEV1 ( or ?)  Women  History of asthma

NEJM 2010;363:1128.

Phenotypes of frequent and infrequent “exacebators”

Decrease exacerbations?

Tiotropium (UPLIFT trial: Lancet 2009:374:1171.) But patients not allowed Atrovent or Combivent Inhaled corticosteroids + LABA (TORCH trial

NEJM 2007;356:775).

Roflumilast: phosphodiesterase-4 inhbitor (Lancet

2009 374(9691):685.) But patients not allowed

inhaled corticosteroids. Will effect be additive? Inhaled corticosteroids decrease exacerbations but may increase risk of CAP (Arch Intern Med.

2009;169:219)

Can Azithromycin Help?

Albert RK et al. “Azithromycin for Prevention of Exacerbations

• f COPD” NEJM 2011; 365:689.

 570: azithromycin (250 mg daily) vs. 572: placebo x 1 year.

Proportion free of Exacerbations days

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

5% more hearing decrement

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COPD Azithro Saga….

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

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

associated with torsades. NNH for hearing loss = 20

Vs.

Wayne RA, et al “Azithromycin and the Risk of Cardiovascular Death” NEJM 2012; 366:1881

 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. Use of azithromycin and death from cardiovascular causes. N Engl J Med 2013; 368:1704-1712.

 Mostly young/middle aged adults  no increased risk

COPD Azithro Saga….

RESERVE for: “Carefully selected patients, such as those who continue to have frequent exacerbations in spite

• f optimal therapy for their COPD with

bronchodilators and anti-inflammatory agents.”

COPD and Pulmonary HTN

Sildenafil?  a dud!

 Worsens exercise oxygenation  Worsens 6 minute walk distance

PLoS One. 2012;7(12):e52248

• COPD. 2012 Jun;9(3):268-75

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Question 5

Which of the following BEST distinguishes asthma from COPD?

• A. Reversibility after bronchodilators
• B. Exhaled NO (nitric oxide)
• C. Methacholine testing
• D. Sputum eosinophilia

Exhaled NO

Arginine ----- NO NOS NO causes bronchodilation and vasodilation Inducible form of NOS (iNOS) up regulated with inflammation  so exhaled NO is a marker of airway inflammation. Studies good but not great that increasing levels can help tailor asthma management and control Approved by FDA Vs. Peak flow meter

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

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Question 5

Which of the following BEST distinguishes asthma from COPD?

• A. Reversibility after bronchodilators
• B. Exhaled NO (nitric oxide)
• C. Methacholine testing
• D. Sputum eosinophilia

Lots of overlap

Question 6

A 27 year-old woman has intermittent SOB &

• wheezing. She has a history of asthma & is on beta-

agonists, high dose ICS, and leukotriene modifiers. 2 prior hospitalizations; 1 prior intubation for respiratory

• distress. On exam, she is comfortable but anxious.

O2 saturation on room air is 99%. Her lungs have a faint inspiratory wheeze throughout. You send her for pulmonary function testing with flow volume loop and a chest x-ray. The chest x-ray is normal.

Question 6

Volume

Flow

Normal

Exhalation Inhalation

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Question 6

The clinical picture most likely represents:

• A. Allergic pulmonary aspergillosis
• B. Poor adherence to medications
• C. Tracheal stenosis
• D. Worsening of her underlying asthma
• E. Vocal cord dysfunction

Volume Flow Normal

Flow‐volume Loops

Normal Restriction Obstruction Severe Obstruction

Volume Flow Volume Flow Normal Volume Flow Normal Volume Flow Normal

Flow‐volume Loops Upper Airway Obstruction

Variable Extrathoracic Fixed Large Airway

+

• Variable

Intrathoracic

+

• Volume

Flow

Volume Flow

Volume Flow

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Flow‐volume Loops Variable Extrathoracic Obstruction from Vocal Cord Dysfunction

• 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

Question 6

The clinical picture most likely represents:

• A. Allergic pulmonary aspergillosis
• B. Poor adherence to medications
• C. Tracheal stenosis
• D. Worsening of her underlying asthma
• E. Vocal cord dysfunction

FV loop FV loop

Question 7

A 23 year-old woman is seen for increasingly frequent asthma exacerbations. She has asthma symptoms approximately 3x a week and is awakened at night about 3x a month. The patient is taking a short-acting inhaled beta 2-agonist for symptomatic relief. 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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Question 7

Which of the following asthma medications would be the most appropriate addition to the treatment regimen at this time? A. Oral corticosteroids 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

Initial Assessment

Management of Asthma

A Step‐Wise Approach

Sym ptom s 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 Sym ptom s > 2 tim es/ w k,< 1 / day > 2 / m o Mild persistent Exacerbations m ay affect activity STEP 1 Symptoms ≤ 2 times/wk ≤2/mo Mild intermittent Asymptomatic between exacerbations Exacerbations brief

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Management of Asthma

Initial Assessment

STEP 3 Moderate Persistent STEP 2 Mild Persistent STEP 1 Mild Intermittent STEP 4 Severe Persist. Long-term Quick-relief Short-acting 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 & environm ental control at each step

Management of Asthma

Initial Assessment

STEP 3 Moderate Persistent STEP 2 Mild Persistent STEP 1 Mild Intermittent STEP 4 Severe Persist. Long-term Quick-relief Short-acting 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 & environm ental 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

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Take home points

 If patient moves from intermittent  mild

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

 If poor control on ICS: increase ICS or add

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

 Long acting b-agonist without a controller

medication is always the wrong answer

 For emergency rescue, b-agonist always the

right answer

LABA

 Pharmacokinetics

• Salmeterol & Formoterol
• Effect lasts 12 hours
• Formoterol – quick onset
• Combo of ICS + Formoterol used for

exacerbations (plus action plan!)

 Concerns @ safety of LABAs?

• Genetic polymorphisms of beta-receptor

LABA

 “SMART Trial” Chest. 2006;129:15-26.

• Usual care +/- Salmeterol
• Asthma related deaths 4.4 x more likely in

salmeterol group  Black Box warning by FDA

• Related to LABA, subset with genetic

polymorphisms of beta receptor, or non- compliance with ICS? THIS IS NOT AN ISSUE WITH COPD

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Question 7

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 corticosteroids B. Oral theophylline C. Low-dose inhaled corticosteroid D. Long-acting beta 2-agonist E. Leukotriene modifier Works, but too big a gun All acceptable by guidelines, in practice like ICS; Caveat: some young people w/ exercise induced asthma do well on LT agents. Smokers have blunted response to ICS.

Question 8

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

Anti‐IgE (Omalizumab)

 Consider for Steps 5 & 6 (difficult to

control asthma)

 Binds IgE  complex cleared  Rx: fewer exacerbations & less steroid

needed; no change in baseline FEV1

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Anti‐IgE (Omalizumab)

 Need to get IgE to extremely low levels for

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

 Baseline serum IgE should be

between 30 - 700 IU/mL

 + Skin test or RAST to a perennial

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

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

High, but not TOO HIGH

Question 8

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

Question 9

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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Question 9

Which of the following is the most likely diagnosis?

• A. Bronchiolitis obliterans
• B. Hypersensitivity pneumonitis

C.Post nasal drip D.Reactive airways dysfunction syndrome

Occupational 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!

Reactive Airways Dysfunction

Diagnostic Criteria

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

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

 Symptoms of asthma  PFTs +/- airflow obstruction, but

Methacholine test positive

Brooks SM et al. Chest 1985;88:376

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RADS

Take home points

 “Big Bang”  big exposure, symptoms

right away

 + methacholine challenge  Rx like asthma, though typically harder to

control

 CHLORINE! (Including mixing household

cleaners)

 Gulf War  sulfur mustard gas

Question 9

Which of the following is the most likely diagnosis?

• A. Bronchiolitis obliterans
• B. Hypersensitivity pneumonitis
• C. Post nasal drip
• D. Reactive airways dysfunction

syndrome

Typically slower onset; HRCT scan + Can exacerbate asthma, but doesn’t CAUSE airway hypereactivity

Asthma – Cutting Edge

 High fat meal increases airway inflammation in

• bese and non-obese asthmatics. J Allergy Clin

Immunol 2011;127:1133  ICS non adherence predicts asthma

• exacerbation. Threshold of 75% adherence 

significantly fewer exacerbations. J Allergy Clin

Immunol 2011;1278:1185

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Asthma – Cutting Edge

 Lebrikizumab (binds IL-13) monthly, sq,

improved FEV1 (5.5%) but did not decrease exacerbation or overall control in Phase II trial.

NEJM 2011;365:1088.  Mepolizumab (binds IL-5) halved exacerbations

in asthma patients with high blood eosinophilia. No change FEV1. Lancet 2012;380:651.

 Azithromycin a dud overall (Some benefit in non-

eosinophilic asthma?). Thorax 2013;68:322.

Question 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

Chest X‐ray

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Chest CT Scan Lung Biopsy

Question 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

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Interstitial Lung Diseases

 Characterized by restriction on PFTs with

low diffusion capacity and desaturation with exercise (or if bad  hypoxemia at rest)

 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

ILD: HP

Hypersensitivity pneumonitis: centrilobular nodules, ground glass opacities, and air trapping on expiratory views

Ground Glass = active alveolitis

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Air‐trapping?

Inspiration Expiration

If small airways inflamed, air can’t exit well with

• exhalation. On CT scan, involved lung areas remain
• black. Splotchy pattern suggestive of small airway
• disease. Can be emphysema or any disease of small

airways: HP, sarcoidosis. BUT SOMETHING WRONG!

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

Hypersensitivity Pneumonitis

Chronic granulomatous inflammation after repeated inhalation of environmental antigens

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

exposure

 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

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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:

 Hypersensitivty pneumonitis

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

removing the antigen)

 Sarcoid

• Common and distinguishing HRCT

 IPF

• Common and distinguishing HRCT

Sarcoid

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Sarcoid on HRCT

Sarcoid: adenopathy and nodular thickening

• f bronchovascular bundles (lumpy-

bumpy), centrilobular nodules.

ILD: Sarcoid

Disease @ bronchovascular bundles

LAM

Proliferation of atypical pulmonary interstitial smooth muscle with cyst formation

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

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MAC infection

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

MAC Infection Spectrum

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

cause bronchiectasis

• This subgroup  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 + nodules, cavities, or bronchiectasis with:

 Positive cultures from at least 2 separate

sputum samples OR

 Positive culture from at least 1 bronchial wash

OR

 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 more likely to progress

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Treatment of Mycobacterium avium Lung Disease

 For nodular/bronchiectasis, therapy consists of

a macrolide (clari or azithro), ethambutol, and rifamycin (rifampin or rifabutin) 3 times weekly

 For cavitary disease, therapy consists of the

same drugs given daily +/- streptomycin or amikacin

 The goal of therapy is 12 months of negative

sputum cultures while on therapy--total duration is often 14-18 months

Am J Resp Crit Care Med 2007;175:367

IPF

Honeycombing Older man with gradual dyspnea

IPF

Traction bronchiectasis Bilateral, lower lobe “subpleural” honeycombing

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Question 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)!

Question 11

77 year old man has progressive dyspnea x 2 years. No sputum, hemoptysis, weight loss, or sweats. He previously smoked 1 ppd for 40 years, quit 15 years

• ago. PMH: HTN and peptic ulcer disease.

Meds: omeprazole and lisinopril Exam: afebrile, RR 16, SaO2 92% RA Crackles bilaterally at bases + Clubbing Labs: nl CBC, Chem-20, PFTs: low TLC & DCO ABG: 7.42/28/58

Chest X‐ray

36

HRCT Question 11

77 yo former smoker with dyspnea and restriction on PFTs. Which of the following is the most appropriate intervention at this time?

• A. Prednisone 1 mg/kg/day
• B. Sildenafil to lower pulmonary artery pressures
• C. Listing for single lung transplant
• D. Assessment for desaturation with exertion
• E. Schedule open lung biopsy

Go for the simplest

IPF – Cutting Edge

Noble PW et al. “Pirfenidone in patients with idiopathic pulmonary fibrosis (CAPACITY): two randomised trials.” Lancet 2011 May 21;377(9779):1760.

 Slowed rate of FVC decline a bit  FDA approval pending; they want another trial

“A Controlled Trial of Sildenafil in Advanced Idiopathic Pulmonary Fibrosis” NEJM 2010; 363: 620

 Slight improvement in QOL and dyspnea, not 1o

• utcome of 6 minute walk test

“A Placebo-Controlled Randomized Trial of Warfarin in Idiopathic Pulmonary Fibrosis” AJRCCM 2012;186:88.

 A dud

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IPF – Cutting Edge

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

 Stopped early because of INCREASED

death in steroid patients!

 NAC vs. placebo arm ongoing  2014

2012 Stable IPF: Enroll in trial vs. NAC vs. pirfenidone (if in Japan, Canada, Europe) vs. supportive care

IPF ‐Summary

No clear BEST option for therapy Some bad options  Move away from steroids!!! We enroll patients with new diagnosis of IPF in trials or offer NAC Common reason for Tx evaluation, but many age is an issue – but check with

• center. Strict age cut-off less

common….

IPF – Exacerbation

2013 IPF exacerbation:

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

methylprdnisolone 1 to 2 g per day intravenously

75% mortality

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Question 11

77 yo former smoker with dyspnea and restriction on PFTs. Which of the following is the most appropriate intervention at this time?

• A. Prednisone 1 mg/kg/day
• B. Sildenafil to lower pulmonary artery pressures
• C. Listing for single lung transplant
• D. Assessment for desaturation with exertion
• E. Schedule open lung biopsy

Biopsy for confusing cases, but IPF flare can be triggered by lung and non lung surgery

Question 12

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:

Question 12

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

39

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

Question 12

Overview of Sarcoidosis

 Multisystem granulomatous disorder of unknown

etiology characterized by non-caseating granulomas in involved organs

 Incidence varies geographically; much more

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

 Usually presents ages 10 - 40, half detected by

CXR without symptoms

 Any organ can be involved, lungs most frequent

(90%)

Should you bx asymptomatic pts with hilar adenopathy?

Won’t ask

Sarcoidosis‐Staging

 Stage I

Bilateral hilar adenopathy

 Stage II

Above + interstitial infiltrates (upper>lower lung zones)

 Stage III

Interstitial disease with shrinking hilar nodes

 Stage IV

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

40

Sarcoidosis: Dx & Rx

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

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

 Therapy is NOT indicated in

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

abnormal lung function

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

with mild-moderate) and document impairment of lung function

Sarcoidosis

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

cause symptoms but won’t change fibrotic disease

• EXAMPLE: hypercalcemia very responsive!

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

to have remission, but seems to be better with infliximab

 If severe lung disease by PFTs or need for

Oxygen  get Echo to check for pulm HTN

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.

Question 12

41

Question 13

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

X‐ray

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

Question 13

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

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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

 Serologic tests: ORDER

• Anti-GBM Abs, anti-neutrophil cytoplasmic Abs

(ANCA), ANA

 ANCAs are positive in 90% of those with

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

 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

Question 13

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

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Question 14

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.

Chest X‐ray Chest CT Scan

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Question 14

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 1-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, -1 antitrypsin deficiency

• Miscellaneous: Rheumatoid, Sjogren’s

Bronchiectasis work‐up in adults

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

• Aspergillus
• MAC

IgG Sweat chloride subclasses Nasal mucosal bx Bronchoscopy

45

Primary Ciliary Dyskinesia

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

and bronchiectasis = Kartagener’s syndrome

 Situs inversus is present in 50% of

patients with primary ciliary dyskinesia

Question 14

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 1-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

Question 15

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.

46

Chest X‐ray Chest CT Scan Question 15

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

47

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  chronic mild hemoptysis

Management of Massive Hemoptysis

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

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

 Surgery is definitive, but high M&M if done urgently

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

Question 15

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

48

Question 16

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

Pulmonary Hypertension‐ RX

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

• Hepatotoxicity

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

49

Pulmonary Hypertension‐ RX

Epoprostenol Bosentan Calcium Channel Blockers Only 5-10% respond Iloprost (Inhaled) Treprostinil (IV or sq) Cheap Even worth a trial? If severe, most start here Sildenafil Oral, well tolerated NOT if hepatopulmonary HTN Combos with other drug classes work

Question 16

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 OK if LV failure If severe

Don’t forget to correct Hypoxemia!

pH 7.38/ pCO2 44/ pO2 58/ sat’n 89% Prescribe oxygen!

50

Question 17

52 year old man with alcoholic cirrhosis with prior variceal bleeding has progressive dyspnea on exertion for 3 months. Denies chest pain, fever, or sputum production. Has gained 5 pounds over the past month. Meds: propranolol.

Chest X‐ray Lateral Decubitus

Right side

51

Question 17

What is the optimal management in this case?

• A. Large volume thoracentesis
• B. Chest tube insertion
• C. Pleurodesis
• D. Medical management with diuretics

Pleural Effusions in Patients with Liver Disease

 Hepatohydrothorax: Effusions usually

when ascitic fluid is present, but not always

 Fluid passes from peritoneum to pleural

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

 Fluid is transudative with very low protein  Typically free-flowing

Pleural Effusions in Patients with Liver Disease

 Management: decrease ascites

formation

• Low salt diet
• Diuretics
• TIPS if refractory

52

Question 17

What is the optimal management in this case?

• A. Large volume thoracentesis
• B. Chest tube insertion
• C. Pleurodesis
• D. Medical management

with diuretics

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

Question 18

32 year old woman from China with a known positive PPD has a chronic cough and night sweats for 2 months. Chest radiograph shows a right upper lobe

• cavity. Two of three smears are positive

for acid-fast organisms. She is currently 32 weeks pregnant.

Question 18

What is the most appropriate next step?

• A. Await final sputum culture results
• B. Begin treatment with isoniazid, rifampin,

ethambutol, and pyrazinamide

• C. Begin treatment with isoniazid, rifampin,

and ethambutol

• D. Begin treatment with isoniazid, rifampin,

and pyrazinamide

• E. Call the CDC and transfer her to

National Jewish Hospital

53

TB and Pregnancy

 Pregnancy per se does not increase the

risk of developing active TB

 This is different than simply a positive

tuberculin test during pregnancy, when treatment of latent TB infection can usually be deferred until after delivery

TB and Pregnancy

 Standard initial TB treatment is 4 drugs

(isoniazid/rifampin/ethambutol/ pyrazinamide)

 During pregnancy, it is recommended that

pyrazinamide be avoided although teratogenicity has not been proven

 Mnemonic: P = No PZA in pregnancy!  This means that treatment duration will be

prolonged to 9 months!

TB and Drug Resistance

Zhao Y et al. National Survey of Drug Resistant Tuberculosis in China. NEJM 2012;12:2161.

 34% some drug resistance  5.7% MDR  .5% XDR

54

Question 19

65-year-old man who has recently moved to the United States from Mexico has a tuberculin skin test placed. He denies previous exposure to tuberculosis. Four days later he returns to the clinic and his skin test is read as being 16 mm in induration. A chest radiograph shows apical pleural thickening but no evidence of parenchymal lung

• disease. He is HIV negative.

Question 19

What would be the most appropriate intervention?

• A. Repeat the tuberculin skin test
• B. Give 2 months of rifampin for treatment of

latent tuberculosis infection

• C. Give 9 months of isoniazid for treatment of

latent tuberculosis infection

• D. Collect three sputum specimens and start 4-

drug antituberculosis therapy

• E. Ignore +PPD if prior BCG vaccination

Who to test for Latent TB?

 Contacts to infectious cases  Health care workers  Other workers (prison guards, workers

in shelters) who are exposed to TB cases Risk for New Infection

ATS/CDC AJRCCM 2000;161:S221

55

Who to test for Latent TB?

 HIV infection (any stage)  Transplant, chemo, or other major

immunocompromise

 Lymphoma, leukemia, head & neck cancer  Abnormal chest x-ray with apical fibronodular

changes typical of healed TB (not granuloma)

 Silicosis  End stage renal disease (dialysis)  Treatment with TNF-alpha inhibitors

HIGHEST Risk of Reactivation

ATS/CDC AJRCCM 2000;161:S221

Rx of LTBI: Adult Drug Regimens

Regimen Duration Interval Comments (months)

Isoniazid 9 Daily Preferred

300 mg Isoniazid 9 2/wk DOT 900 mg Rifampin 4 Daily For patients 600 mg exposed to known INH-R, rifampin-S MTB

JAMA 2005; 293:2776.

Pyridoxine supplementation if on INH especially if predisposed to neuropathy (diabetes, uremia, alcohol, malnutrition & HIV infection) plus pregnancy & seizure disorders.

Question 19

What would be the most appropriate intervention?

• A. Repeat the tuberculin skin test
• B. Give 2 months of rifampin for treatment of

latent tuberculosis infection

• C. Give 9 months of isoniazid for treatment of

latent tuberculosis infection

• D. Collect three sputum specimens and start 4-

drug antituberculosis therapy

• E. Ignore +PPD if prior BCG vaccination

Too short, INH preferred Apical scarring or calcified granuloma = abnormal but stable In adults, ignore the BCG

56

Question 20

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.

Chest X‐ray Lateral Chest X‐ray

57

Chest CT Scan

Question 20

What is the most likely diagnosis?

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

Mediastinal Masses Differential 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

58

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

Question 20

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

Question 21

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

59

Question 21

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

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

60

Question 21

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)

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

Solitary persistent GGO “Sub‐Solid Nodules is often 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  esp. if solid component is > 5 mm: think cancer!

Smoking history less important

The End!