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PulmonaryABIM Certification Exam Review Course
Leslie Zimmerman, MDProfessor 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 1A 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 165 year-old man with 11/24 Epworth & AHI 12. O2 sat’n nadir 86%. CPAP treatment:
A. Will be reimbursed by MedicareB. Will decrease cardiovascular mortalityC. Will likely need to be supplemented
with oxygenD. 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
GeneticsUpper airway/facial abnormalitiesPost-menopauseHypothyroidism/ 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
OSADisruption in sleep
causes daytime sleepiness
Epworth Scale can estimate “sleepiness”
10 = Sleepy
18 = Very sleepyhttp//: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 OSAHigher 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 165 year-old man with 11/24 Epworth & AHI 12. O2 sat’n nadir 86%. CPAP therapy:
A. Will be reimbursed by MedicareB. Will decrease cardiovascular mortality
C. Likely need to be supplemented with oxygen
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 EdgeKarkow 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 2A 60 year-old smoker complains of an insidious onset
of dyspnea on exertion. PFTS reveal COPD. The severity of the disease is determined by the:
A. Air-trappingB. Diffusion capacity for carbon monoxide C. FEV1D. FEV1/FVCE. Lack of response to bronchodilators
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http://www.who.int/mediacentre/factsheets/fs310_2008.pdf
2004: Worldwide Leading Causes of Death
Mill
ions
Affects 9% of World
PopulationBy 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
0
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 dysfunction130-140 years
Lung Aging
Healthy
COPD
Lung
func
tion
(FE
V1;
alv
eoli)
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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 orcapillaries Low DCO
DCO: integrity of the alveolar–capillary membrane
CO
CO
CO
Just narrow airways Normal DCO
Diffusion Capacity for CO
Diffusion Capacity for CONormal
Asthma
Low
Emphysema
Fibrosis
Pneumocystis jiroveci pneumonia
PE
ELEVATED?
Diffuse alveolarhemorrhage
Falling HctElevated 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 obstruction
Severity
Suggests emphysema more likely than asthma or chronic bronchitis
Air trapping
Question 2A 60 year-old smoker complains of an insidious onset
of dyspnea on exertion. PFTS reveal COPD. The severity of the disease is determined by the:
A. Air-trappingB. Diffusion capacity for carbon monoxide C. FEV1D. FEV1/FVCE. 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 numbersB = Lots of symptoms, OK numbersC = Few symptoms, Bad numbersD = Lots of symptoms, Bad numbers
Why?
Why?
Search for biomarkers
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Question 3A 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 diseaseB. Decrease risk of lung cancerC. Slow decline of FEV1D. 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
A1ATNeutrophil 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 of 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 diseaseB. Decrease risk of lung cancerC. Slow decline of FEV1D. 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
Lu
ng
Fu
nct
ion
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 courseExacerbations 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 of COPD” NEJM 2011; 365:689.
570: azithromycin (250 mg daily) vs. 572: placebo x 1 year.
Pro
po
rtio
n f
ree
of
Ex
ac
erb
ati
on
s
da
ys
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 of 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
NOSNO 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 6A 27 year-old woman has intermittent SOB &wheezing. She has a history of asthma & is on beta-agonists, high dose ICS, and leukotriene modifiers. 2prior hospitalizations; 1 prior intubation for respiratorydistress. On exam, she is comfortable but anxious.O2 saturation on room air is 99%. Her lungs have afaint inspiratory wheeze throughout.
You send her for pulmonary function testing with flowvolume loop and a chest x-ray. The chest x-ray isnormal.
Question 6
Volume
Flo
w
Normal
Exh
alat
ion
Inha
latio
n
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Question 6
The clinical picture most likely represents:
A. Allergic pulmonary aspergillosisB. Poor adherence to medicationsC. Tracheal stenosisD. Worsening of her underlying asthmaE. Vocal cord dysfunction
Volume
Flo
w
Normal
Exh
ala
tion
Inh
ala
tion
Flow‐volume Loops
Normal
Restriction
Obstruction
Severe Obstruction
Volume
Flo
w
Volume
Flo
w
Normal
Volume
Flo
w
Normal
Volume
Flo
w
Normal
Exh
ala
tion
Inh
ala
tion
Flow‐volume LoopsUpper Airway Obstruction
VariableExtrathoracic
FixedLarge Airway
+ -
Variable Intrathoracic
+ -
Volume
Flo
wE
xha
latio
nIn
ha
latio
n
Volume
Flo
wE
xha
latio
nIn
ha
latio
n
Volume
Flo
wE
xha
latio
nIn
ha
latio
n
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Flow‐volume LoopsVariable 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
Flo
w
Normal
Exh
ala
tion
Inh
ala
tion
Question 6
The clinical picture most likely represents:
A. Allergic pulmonary aspergillosisB. Poor adherence to medicationsC. Tracheal stenosisD. Worsening of her underlying asthmaE. Vocal cord dysfunction
FV loopFV loop
Question 7A 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 7Which of the following asthma medications would be the most appropriate addition to the treatment regimen at this time?
A. Oral corticosteroidsB. Oral theophylline C. Low-dose inhaled corticosteroid D. Long-acting beta 2-agonistE. Leukotriene modifier
STEP 3Moderate Persistent
STEP 2Mild PersistentSTEP 1
Mild Intermittent
STEP 4Severe Persistent
STEPS 5 & 6
Management of AsthmaInitial Assessment
Management of AsthmaA Step‐Wise Approach
Symptoms NocturnalSTEP 4, 5, 6 Continual symptoms FrequentSevere persistent Limited physical activity
Frequent exacerbationsSTEP 3 Daily symptoms > one/wkModerate persistent Daily use of inhaler
Exacerbations affect activityExacerbations ≥ 2 times/wk
STEP 2 Symptoms >2 times/wk,<1/day >2/moMild persistent Exacerbations may affect activitySTEP 1 Symptoms ≤ 2 times/wk ≤2/moMild intermittent Asymptomatic between exacerbations
Exacerbations brief
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Management of AsthmaInitial Assessment
STEP 3Moderate Persistent
STEP 2Mild Persistent
STEP 1Mild Intermittent
STEP 4Severe Persist.
Long-termQuick-relief
Short-actingbeta-2 agonist
Low-dose*inhaled steroids
Long-actingbeta-2 agonist
Low-med dose*inhaled steroids
Med-doseinhaled steroids
ConsiderAnti -IgE
* Alternatives: leukotriene modifiers, cromolyn, nedocromil, theophylline
High-doseInhaled steroids
STEP 5 & 6
Patient education & environmental control at each step
Management of AsthmaInitial Assessment
STEP 3Moderate Persistent
STEP 2Mild Persistent
STEP 1Mild Intermittent
STEP 4Severe Persist.
Long-termQuick-relief
Short-actingbeta-2 agonist
Low-dose*inhaled steroids
Long-actingbeta-2 agonist
Low-med dose*inhaled steroids
Med-doseinhaled steroids
ConsiderAnti -IgE
* Alternatives: leukotriene modifiers, cromolyn, nedocromil, theophylline
High-doseInhaled steroids
STEP 5 & 6
Patient education & environmental control at each step
Tiotropium
Asthma‐ Tiotropiumin 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 controllermedication 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 +/- SalmeterolAsthma 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 7Which of the following asthma medications would be the most appropriate addition to regimen at this time (only on short acting b-agonists)?
A. Oral corticosteroidsB. Oral theophylline C. Low-dose inhaled corticosteroid D. Long-acting beta 2-agonistE. 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 8A 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 8A 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 930 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 obliteransB. Hypersensitivity pneumonitisC.Post nasal dripD.Reactive airways dysfunction
syndrome
Occupational Asthma
Occupational asthma
Irritant-inducedasthma
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 DysfunctionDiagnostic 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 obliteransB. Hypersensitivity pneumonitisC. Post nasal dripD. 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 obese 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 1034 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 10Which 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: HPHypersensitivity 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 or 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 sarcoidBut 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 HRCTSarcoid: adenopathy and nodular thickening
of bronchovascular bundles (lumpy-bumpy), centrilobular nodules.
ILD: SarcoidDisease @ bronchovascular bundles
LAMProliferation 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 samplesOR
Positive culture from at least 1 bronchial washOR
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
IPFTraction
bronchiectasis
Bilateral, lower lobe “subpleural” honeycombing
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Question 1034 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; obstruction not restriction on
PFTs
Should have Tree-in bud on CT scan; productive cough
Typical HRCT, bird exposure favor HPDiagnosis important – need to remove antigen (bird)!
Question 1177 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
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HRCT
Question 1177 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 EdgeNoble 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
outcome 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 – Exacerbation2013 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 1177 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 1233 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 12Bronchoscopy with transbronchial biopsy: non-
caseating granulomas. Stains and cultures for fungi and mycobacteria were negative.
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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 hilarnodes
Stage IV Advanced fibrosis
Extra-pulmonary disease-skin (E. nodosum, lupus pernio), eyes, liver, lymph nodes most frequent
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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
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Question 1346 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+ edemaWBC 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 13Which 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 vasculitisWegener’s granulomatosisMicroscopic polyangiitis Pauci-immune GNChurg-Strauss (allergic angiitis and granulomatosis)Goodpastures syndrome Systemic lupus erythematosus Henoch-Schonlein purpura
InfectionPost-streptococcal glomerulonephritis, endocarditis
ANCA?C-ANCA 80% P-ANCA 10%P-ANCA 70%Most P-ANCA½ 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 of vasculitis• Skin (easy), Kidney, or lung (surgical biopsy)
• If Anti-GBM possible, kidney better to bx than lung
Question 13Which 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 1430 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 office.
Exam: SaO2 86%, diffuse crackles, and digital clubbing.
Chest X‐ray
Chest CT Scan
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Question 14Which 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
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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 14Which 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.
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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
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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 cancer4) 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 bleedingarteriography 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
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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 CellNO
ProstacyclinEndothelin
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-blockersBosentan (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
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Pulmonary Hypertension‐ RX
Epoprostenol
Bosentan
Calcium Channel BlockersOnly 5-10% respond
Iloprost (Inhaled)Treprostinil (IV or sq)
CheapEven worth a trial?
If severe, most start here
Sildenafil Oral, well tolerated
NOT if hepatopulmonary HTN
Combos with otherdrug classes work
Question 16Which 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!
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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
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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
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Question 17What 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 18What is the most appropriate next step?A. Await final sputum culture resultsB. Begin treatment with isoniazid, rifampin,
ethambutol, and pyrazinamideC. Begin treatment with isoniazid, rifampin,
and ethambutolD. Begin treatment with isoniazid, rifampin,
and pyrazinamideE. Call the CDC and transfer her to
National Jewish Hospital
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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
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Question 1965-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 19What would be the most appropriate intervention? A. Repeat the tuberculin skin testB. Give 2 months of rifampin for treatment of
latent tuberculosis infectionC. Give 9 months of isoniazid for treatment of
latent tuberculosis infectionD. Collect three sputum specimens and start 4-
drug antituberculosis therapyE. 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
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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 Preferred300 mg
Isoniazid 9 2/wk DOT900 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 19What would be the most appropriate intervention? A. Repeat the tuberculin skin testB. Give 2 months of rifampin for treatment of
latent tuberculosis infectionC. Give 9 months of isoniazid for treatment of
latent tuberculosis infectionD. Collect three sputum specimens and start 4-
drug antituberculosis therapyE. Ignore +PPD if prior BCG vaccination
Too short, INH preferred
Apical scarring or calcified granuloma = abnormal but stable
In adults, ignore the BCG
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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 otherwise normal. Labs: mild normocytic anemia.
Chest X‐ray
Lateral Chest X‐ray
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Chest CT Scan
Question 20
What is the most likely diagnosis?
A. Bronchogenic cyst
B. Intrathoracic thyroid
C. Lymphoma
D. Teratoma
E. Thymoma
Mediastinal MassesDifferential 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
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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. ThymomaAsymptomatic until infected
All anterior mediastinal, but most have CT scan characteristics; clue here was anemia, myasthenia symptoms
Question 21A 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
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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 NoduleFLEISCHNER SOCIETY 2005 Recommendations F/U & Management of Incidental Nodules Detected at Nonscreening CTNodule 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 thenif 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 moif NOT changing if NOT changing vs. PET, FNA, resection vs. PET, FNA, resection
Solitary Pulmonary NoduleFLEISCHNER SOCIETY 2005 Recommendations F/U & Management of Incidental Nodules Detected at Nonscreening CTNodule Size Low-Risk Patient High-risk Patient
(mm)
Translation: Bigger nodules more worrisomeF/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 nodulesFor “ground glass” nodules, don’t know – we use 3 years of stability
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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 of 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 Nodulesis 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 yearsMIXED GGO & solid CT scan 3 months, if persistent esp. if solid component is > 5 mm: think cancer!
Smoking history less important
The End!