Neoplasm, CAP/VAP, Occupational, Atypical Infxn, CF/Bronchiectasis, Pulm Physio Flashcards
-neoplasm -biostats -CAP, VAP -occupational exposures -nocardia/actino -CF and non-CF bronchiectasis -Bronch intro
Types of lung cancer in descending order of frequency
35% adenocarcinoma (3% of which are BAC)
30% squamous cell carcinoma
20% small cell
10% large cell
10% unclassified/undifferentiated
Which lung CAs are generally
(a) peripheral vs. central?
(b) can cavitate
(c) Non-smokers
(a) adeno and large cell- peripheral, while squamous typically central (squamous cells line the airways => think larger airways like bronchus more central), small cell typically central too (can be endobronchial)
(b) squamous cavitates
(c) Non-smokers: adeno, smokers really small cell and squamous cell
Most common paraneoplastic syndrome associated with lung CA (and which lung CA)
SIADH from small cell
Paraneoplastic syndrome associated with
(a) squamous cell
(b) small cell
Paraneoplastic
(a) squamous- HPO (clubbing), hypercalcemia
(b) small cell- SIADH, myasthenia gravis, lambert eaton
Current USPSTF recs for lung CA screening
Ages 50-80, 20 pack year history, quit within 15 yrs
T staging based on size
Size of tumor
T1a: less than 1cm
T1b: 1-2cm
T1c: 2-3cm
T2: 3-5cm
T3: 5-7cm
T4: more than 7cm
What N-stage is an ipsilateral supraclavicular node?
Either ipsilateral or contralateral supraclavicular node = N3
N stages
Lymph node disease
N0- no involved nodes
N1- ipsilateral nodes hilar, peribronchial, or intrapulmonary (ipsilateral double digit like 10/11)
N2- mediastinal and subcarinal (single digit, 4/7s)
N3- contralateral double-digits or supraclavicular
What M-stage are the following
(a) malignant pleural effusion or pleural lesion
(b) single distant met
(c) nodule in contralateral lung
Metastasis
(a) Pleural involvement- M1a
(b) Single distant met- M1b
(vs multiple distant mets M1c)
(c) Contralateral lung- M1A
Solitary pulmonary nodules
(a) Percent benign vs. malignant
(b) Most common benign
(c) Most common malignant
Solitary pulmonary nodules
(a) 55% benign, 45% malignant
(b) Granulomatous, nonspecific. also hamartomas
(c) adenoCA, then squamous. very unlikely small cell
FEV1 and DLCO cutoffs for surgical management
If both are over 60% predicted- good to go, low risk.
Either under 30% predicted- high risk
Either in between, consider CPET or exercise tolerance testing (walking stairs)
How VO2 on CPET helps risk stratify lung CA patients for resection
VO2 (oxygen consumption): over 20- low risk
10-20: moderate risk
under 10 (ml/kg/min): high risk
Single lung nodules of what size do/don’t need follow-up?
- Low risk (non-smoker) under 6mm don’t need follow-up.
- high risk under 6mm continue annual screening
- 6-8mm: f/u CT scan in 6-12 months
- over 8mm: PET, repeat CT in 3 months, or tissue sampling
What qualifies as IA vs. IB lung cancer?
IA: T1 (under 3cm) with N0
IB: T2a (under 4cm) with N0
What qualifies as IIB lung cancer?
IIB- Any T1-T2 with N1 (so ipsilarateral nodes with tumor up to 5cm)
Treatment of stage I lung CA
Stage I: under 4cm with N0
Resection = lobectomy with mediastinal LN dissection
-no adjuvant chemo
Treatment of stage II lung CA
Stage II: either over 4cm and T0 or up to 5cm with N1 (hilar or peribronchial LN)
Resection with adjuvant chemo
Post-surgical management for lung CA patients- when to get screening CTs
Repeat CT chest q6 months x2 years, then annual for 5 years
Treatment for stage IIIa vs. IIIb lung CA
IIIa- chemoradiation with adjuvant immunotherapy x1 year
IIIb- chemo and XRT if good functional status, if poor functional status XRT alone
Timeline for immunotherapy-induced pneumonitis
Most commonly 30 days after initiation, but can happen anytime and even up to a year after stopping
How to grade severity of immunotherapy-induced pneumonitis and how that guides management
Symptoms and hypoxia
- Just imaging findings: hold drug, no steroids, can consider re-challenging
- Mild symptoms: stop drug, 1 mg/kg pred, don’t rechallenge
- Sever symptoms: stop drugs, 1-2 mg/kg pred
Which patients with lung cancer get prophylactic cranial radiation?
Small cell cancer in remission after initial treatment (chemo/XRT)
with good functional status
Differentiate treatment response for limited vs. extensive small cell lung CA
Both have decent response to initial chemo but then high recurrence rate
Limited disease- platinum based chemo + XRT with 80-90% response rate, 50-60% complete response
Extensive disease- platinum-based chemo alone
-60-80% response rate but only 15-20% complete response (high remission rate)
Difference in treatment for extensive and limited small cell (SCLC)
Limited small cell (30% at time of diagnosis, disease contained within one radiation port)- chemo and XRT
Extensive small cell- chemo alone, XRT only if for palliation
Small blue cells with prominent nucleoli, sparse cytoplasm, high N/C ratio
Terrible Ts
Anterior mediastinal masses
- thymoma- most common
- terrible ones- mets and lymphoma
- intrathoracic thyroid
- teratoma (germ cell tumors)
Mediastinal germ cell tumors
(a) triggers what further workup
(b) differentiate benign from aggressive
(c) Elevated tumor marker in most aggressive germ cell tumor
Mediastinal germ cell tumors
(a) gonadal ultrasound in young men
(b) Teratomas- heterogeneous, contain fat, cysts, calcification
Middle- seminomatous, normal AFB
Most aggressive- nonseminomatous
(c) AFP most specific, AFP and beta-HCG most likely to be elevated in nonseinomatous
Most common posterior mediastinal tumor
Neurogenic tumors
Typical location of pulmonary carcinoid/neuroendocrine
Well-differentiated neuroendocrine tumors = bronchial carcinoid
Endobronchial
-associated with nonsmokers
Imaging features of hamartoma
Contains calcium and fat
Pulmonary MALToma associated with what other disease?
Autoimmune disease most specifically Sjogren’s
Most common site of mets (of all CA)
(a) Second
Liver
(a) Second- lung
Differentiate Mallampati I and II
Mallampati I- can see hard palate, soft palate, uvula and tonsillar pillars
Mallampati II lose the tonsillar pillars
Differentiate Mallampati I and III
Mallampati I- can see hard palate, soft palate, uvula and tonsillar pillars
Mallampati III- lose tonsillar pillars, only see base of uvula
Mallampati IV- only see soft tissue and soft palate
When to be worried/cautious with bronchoscopy
(a) PA pressure
(b) Lab value
Relative contraindication to bronchoscopy b/c of increased risk of bleeding
(a) mean PA pressure over 40 dangerous for TBBx (ok for inspection)
(b) BUN over 30, Cr over 1.3- consider DDAVP 30 minutes before bronch
Who should and who shouldn’t get prophylactic beta-agonist before bronchoscopy?
Asthmatics should, COPDers shouldn’t
How long before bronchoscopy to stop
(a) DOACs
(b) Warfarin
(c) Lovenox
(d) Heparin gtt
Stop before bronch
(a) DOAC- 1-2 days, if reduced kidney function 2-3 days
(b) Warfarin- 5 days
(c) Lovenox- 24 hours
(d) Heparin gtt- 4-6 hours
Max dose of lidocaine to give topically during bronchoscopy
7 mg/kg lidocaine
Imaging features to differentiate thymoma from thymic carcinoma
Thymoma- homogeneous
Consider malignancy if heterogeneous, associated pleural/pericardial effusion, lymphadenopathy
Most common CAP pathogen
Strep pneumo
Which is 1st vs. 2nd generation macrolide?
1st gen- erythro
2nd gen- azithro, clarithro
Guidelines tx for CAP
CAP tx:
- Amoxicilin or doxy or azithro (if R rates low)
If comorbidities: combo augmentin or cefpo with macrolide or doxy
OR
respiratory fluoroquinolone
Most common VAP pathogens
Staph aureus (30%), then pseudomonas (24%), then other gram negatives (klebs, serratia, E. coli)
CURB-65 score- when can do outpatient
1 point for each
- confusion (AMS)
- uremia (BUN over 19)
- RR over 30
- BP: SBP under 90 or DBP under 30
- age over 65
0-1 points, less than 3% 30-day mortality => outpatient mgmt
Mechanism by which hospitalized CAP in pts over 50 worsens outcomes
Likely from increase in CV risk- elevated risk of ACS after pneumonia (possibly due to inflammatory mileu)
Which smoking cessation aid need to be careful for mental health side effects?
Chantix (varenicline)- partial nicotine receptor agonist => reduces rewarding aspects of cig smoking
had serious neuropsychiatric events (depression, SI) with comorbid psych conditions
Why higher risk of hypoxia at higher altitudes?
‘Thinner air’- at higher altitude, lower FiO2 => lower gradient for oxygen to diffuse into our capillaries
Best mgmt for acute altitude sickness symptoms?
Descend as rapidly as possible (not like the bends in divers where you want to go gradually)
Symptoms typically of CNS edema and pulmonary edema- best thing is to get down ASAP
When to start acetazolamide as ppx before an ascending hike
Start day before ascent, continue 1-2 days in
-remember it’s a diuretic so important to replace fluids (stay hydrated)
Explain decompression sickness, type I vs type II
Decompression sickness- N2 gas previously dissolved bubbles out of solution when moving from high to low pressure too quickly
type I- MSK effects (painful but not going to kill you)
type II- the bad stuff, CNS, respiratory
Typical presentation of asbestos
(a) Latency
(b) Radiology
(c) Cancer risk
Asbestos
(a) 20+ years
(b) Benign asbestos pleural effusions (exudative), pleural plaques
(c) Mesothelioma
Pt with mediastinal lymphadenopathy, clinical history of working in shipyeard or aerospace industry
Dx?
Think berylliosis for anything that seems like sarcoid plus environmental exposures
Berylliosis
(a) Path findings
(b) Imaging
(c) Mgmt
Berylliosis- hard metals, shipyard or aerospace industry
(a) Non-caseating granulomas (mimicks sarcoid)
(b) Mediastinal lymphadenopathy
(c) Steroids or immunosuppression, supportive
Special considerations when choosing smoking cessation aid
- history of poorly controlled mental health maybe stay away from chantix (varenicline)
- buproprion contraindicated in pts w/ seizure disorder (reduces seizure threshold)
Key air travel tip for divers
No flying within 24 hours of last dive- or else can re-develop the bends (when go from high to low pressure and nitrogen bubbles out of solution)
Key exposure to think of for
(a) UIP pattern developing over 20-30 years
(b) Rheumatoid nodules with layer of black dust
(a) Asbestosis- high latency period, while real UIP would develop rapidly (weeks/months)
(b) Caplan syndrome = pts with RA and pneumoconiosis related to occupational dust (coal, asbestos, silica)
Exposures to think of for silicosis
Anything that disrupts the earth’s core- especially with quartz (major component of granite, slate, and sandstone)
Tunnelers, miners, sandblasters, stone cutting, masonry
Differentiate chest imaging findings of
(a) acute silicosis
(b) simple silicosis
(c) progressive massive fibrosis
Chest imaging
(a) Acute silicosis (symptoms in weeks to a few years after high-level exposure)- bilateral diffuse GGOs with centrilobular nodules and lymph node calcification
Then chronic silicosis comes in two flavors- simple silicosis and PMF (both 10-30 yrs later)
(b) Simple silicosis- innumerable tiny nodules, upper lobe predominant
(c) PMF- nodules coalesce mainly in mid/upper lobes
What other disease mimics BAL findings of acute silicosis?
(a) Lab value to send off?
Acute silicosis- proteinaceous thick opaque effluent fluid similar to PAP
- and both can have crazy paving on imaging
- so use exposure history to differentiate
(a) Send of GM-CSF to rule out autoimmune PAP
Characteristic path for silicosis
Silicotic nodules- central hyaline with surrounding stuff (ew)
*Birefringent particles under polarized light
What level of CO-Hb on gas expected to develop symptoms of carbon monoxide poisoning
Normal CO-Hb in nonsmokers- 3%, 10-15% in smokers
Generally don’t expect symptoms under 10% in either
Which way to carbon monoxide shift the Hb-dissociation curve?
Hb dissociation curve- pO2 on x-axis, Hb saturation on y-axis. Shift to the left when the same pO2 causes a higher Hb saturation (b/c one CO binding increases affinity of more spots for O2) => less O2 dropped off into tissues
CO-Hb causes L-ward shift in Hb- dissociation curve
L-ward shift = less O2 in tissues
Compare CD4:CD8 ratio (BAL fluid) in sarcoid vs. chronic HP
Sarcoid- elevated CD4:CD8 ratio compared to all other ILDs (including HP)
So reduced CD4:CD8 (average 0.9) expected in chronic HP compared to sarcoid (ex: average 3-4)
Which way does exercise shift the Hb-dissociation curve?
Exercise- increase temperature and increase acid (lower pH) both shift Hb-dissociation curve (comparing pO2 to Hb saturation) to the right
Right-shift = more O2 drop off at tissues
How does higher altitude shift the Hb-dissociation curve?
Altitude increases 2,3-BPG which stabilizes the unbound form of Hb => offloading more O2 at tissues => shifts Hb-dissociation curve (comparing pO2 to Hb saturation) to the right
Occupational exposure buzzwords
(a) Black vs. white nodules in the lungs
(b) Giant cell interstitial pneumonia
Occupational exposure buzzwords
(a) Black nodules- coal-workers pneumoconiosis. vs. white nodules from silicosis
(b) giant cell interstitial pneumonia = hard metal (cobalt) lung disease
Occupational exposure buzzwords
(a) Egg-shell cacifications
(b) Bakers lung
(c) BAL with alveolar proteinosis
(d) Black nodules vs. white nodules in the lungs
(a) Egg-shell calcifications = calfcified mediastinal lymph nodes typically seen in chronic silicosis
(b) Baker’s lung = immunologic-induced work-exacerbated or occupational asthma, IgE mediated
(c) Acute silicosis typically BAL with alveolar proteinosis, also crazy paving on CT
(d)
Infection highly associated with chronic silicosis
Tuberculosis => workup for chronic silicosis has to include IGRA
Nitric oxide role in the respiratory tract
Disease with
(a) High FeNO
(b) Low FeNO
Nitric oxide- regulates vascular and bronchiole dilation
(a) Elevated in asthma, specifically eosinophilic inflammation. thought that eos stimulate NO production
(b) Low FeNO seen in ciliary dyskinesia and CF (hence why sometimes done for bronchiectasis workup)
Name two branching gram positive organisms
Branching/filamentous gram positive organisms
- Nocardia- weakly AFB positive
- Actinomycosis- not AFB positive
FeNO cutoffs for asthma in children and adults
FeNO- fraction of exhaled nitric oxide, marker of eosinophilic inflammation
>50 in adults, >35 in children associated with eosinophilic inflammation (asthma)
Nocardia vs. actinomycosis
(a) Which more typically in immunocompromsied
(b) First line treatment
(c) Clinical hallmark
(d) Surgical mgmt
(a) Nocardia more typically in immunocompromised, while actino in immunocompetent with EtOH or underlying lung disease
(b) First line tx:
nocardia- TMP-SMP (bactrim)
actino- high dose PCN (PCN G)
(c) Clinically
nocardia- pulmonary cavity with characteristic metastatic spread (typically CNS and skin)
actino- pulm less significant, chest wall/bony invasion, sinus tracts, craniofacial
(d) Surgical mgmt more needed in nocardia, typically actino responds to abx alone
Nocardia
(a) How to culture
(b) Clinical hallmark feature
Nocardia = branching filamentous gram pos bacilli, partially AFB stain
(a) Cx for weeks in aerobic bottle (doesn’t grow quickly)
(b) Clinically- pulmonary nodules or cavitation w/ CNS manifestations (brain parenchyma abscess) or skin (mycetoma)
Buzzwords histopath
(a) Sulfur granules
(b) Partially AFB staining bacteria
Histopath
(a) sulfur granules = actino
don’t actually contain sulfur but are entagled masses of the actino filaments
chronic granulomatous change in actino-infected tissues
(b) partially AFB positive gram positive bacilli = nocardia
Nocardia
(a) Most common sites of involvement
(b) First line treatment algorithm
Nocardia
(a) Most commonly involves lungs, then frequently spreads to
- CNS: parenchymal abscess
- Skin
(b) Bactrim alone if mild/moderate pulmonary disease.
- pulmonary w/ CNS involvement add imipenem
- severe pulmonary w/o CNS involvement add amikacin and consider surgical drainage!
Broad ddx for cavitary lung lesion
Cavitary lung disease
- Malignancy: typically squamous
- Infection: bacterial (klebs, staph), fungal (aspergillus), atypical bacterial (nocardia, actino), NTM, Tb, septic emboli
What is used for newborn screening for CF
Tyrptase- enzyme of pancreatic damage that is detectably elevated at birth
Sweat test for CF
(a) Explain what ion measuring and why
(b) Normal value
(c) Diagnostic cutoff
Sweat test = sweat chloride test
(a) CFTR transporter in lungs is used to move Na+ in and Cl- out, on the skin acts opposite and is supposed to bring in Chloride. When defective Cl cannot be taken into the skin => elevated skin chloride level
(b) Normal is Cl under 30
(c) Sweat chloride level over 60 on two occasions is diagnostic for CF
How sweat test cutoff is different for adult-diagnosed CF
Sweat chloride
-over 60 on two occasions diagnostic for anyone
Then in adults can be
-over 60 on one occasion with symptoms
-40-59 with a detectable mutation, family history
Most common infections in CF patients based on age
Childhood- staph aureus and H. influenza
Then around age 20 pseudomonas starts to dominate
Mechanism of dornase alpha in CF patients
Dornase alpha = enzyme that breaks down DNA in thick/dense mucus layer to thin secretions and reduce infection in CF
-due to defective CFTR protein respiratory tract epithelium cannot bring in Na+ so mucus layer is dense and thick with tons of DNA elements
FEV1 cutoff to refer CF patient for transplant
Refer for transplant when FEV1 starts dipping below 40%
Below 50% if also: rapidly declining, PASP over 50
Azithro TIW in bronchiectasis patients
(a) When to consider starting
(b) When contraindicated
Azithro for chronic inflammation in bronchiectasis
(a) Start when 3+ exacerbations in a year
(b) Contraindicated in pts with NTM
3 things to monitor for patients on long-term azithro
Long-term azithro (COPD, bronchiectasis, CF) monitor
- LFTs
- hearing
- QTc
Which NTM species to think of when see RML or lingular involvement
MAC loves the lingula and RML
Most common rapidly-growing NTM in the US
Most common rapid-growing (grows in culture in one week) in the US = Mycobacterium abscessus
vs. slow-growing = MAC (takes 4-8 weeks)
Factors that would trigger daily (vs TIW) tx for MAC
Consider daily (vs. TIW) MAC treatment when
- severe nodular disease
- cavitary disease
First line MAC treatment
3 drug regimen: azithro (not clarithro!!), ethambutol, rifamycin
- TIW for mild/moderate disease
- Daily for severe nodular or cavitary disease
+IV amikacin for severe disease
+Inhaled liposomal amikacin for recalcitrant (cultures pos beyond 6 months of disease)
+surgery for localized
Duration of MAC tx
MAC tx = 12 months from culture conversion (defined as 3 negative cultures)
When to add inhaled liposomal amikacin to MAC tx
Liposomal amikacin FDA-approved for refractory MAC = cultures not converted as 6 months
What sensitivities are important for different NTMs
(a) MAC
(b) M. abscessus
NTM sensitivities
(a) MAC- macrolides (azithro) and amikacin
2 RNA gene mutations that confer resistance
(b) M. abscessus- erm (erm41) gene causes inducible resistance to azithro- important b/c very poor prognosis if use azithro-backed regimen
Significant of erm gene mutation
Erm41 gene in rapidly-growing NTMs (M. abscessus) confer inducible macrolide resistance
-need to incubate sensitivities for 14 days
ex] M. abscessus susceptible to azithro at day 7, then R at day 14 (so important to ask how long lab incubated for)
Example M. abscessus tx regimen
M. abscessus treatment- consider surgery early if localized given poor response to abx alone
Typically start with azithro (if erm gene negative aka sensitive)
add 2 more (linezolid, clofazimine) + amikacin
IV for 3 months, then can consider PO regimen etc
Differentiate tracheobronchomalacia from EDAC
TBM- weakening of anterior tracheal cartilage
vs. EDAC = anterior bulging of the posterior membranous portion of trachea, while cartilaginous rings are intact
Definition of hyperdynamic airway collapse
Normal airway collapses up to 30% during exhalation, HDAC = collapse of more than 30% on exhalation
Type of tracheobronchomalacia typically seen in COPD
Saber-sheath TBM: tracheal rings much smaller, posterior wall working normally
- inward bowing of lateral walls typically worse on expiration
- AP elongation of tracheal diameter and lateral narrowing
Changes seen in TBM/EDAC (same for both)
(a) PFTs
(b) Dynamic CT
(c) Awake bronchoscopy
TBM/EDAC
(a) PFTs normal until very severe disease, would need at least 50% airway obstruction to see flattening of expiratory curve (flattening of airways during exhalation => obstructive pattern)
(b) Dynamic CT- see more than 50% narrowing on expiratory vs. inspiratory film
(c) Narrowing on awake bronchoscopy
Two cutoffs that make pts not a good surgical candidate for mgmt of tracheal stenosis
Tracheal stenosis, not a surgical candidate if
(a) Less than 2cm from the vocal cords b/c not enough room for healthy anastamosis
(b) If stenosed area more than 5-6cm b/c then surgically managing leads to significantly reduced neck obility
Type of emphysema most amenable to surgical lung volume reduction surgery
(a) Location of emphysema
(b) Exercise tolerance
Surgical LVRS
(a) Upper-lobe predominant
(b) Poor exercise tolerance
(b/c if they have good exercise tolerance there’s not much benefit just leave them alone)
Bronchoscopic lung volume reduction
(a) Explain theoretically how works
(b) Why want intact fissures
(c) Exclude transplant?
Bronchoscopic LVR
(a) Place a valve that doesn’t let air in but lets air out so diseased portion of lung collapses, allowing room for expansion of healthy lung
(b) If ventilation occurs across fissures (fissures not intact) then diseased lung won’t collapse so no more room made for healthy lung to expand (so pointless)
(c) Does not exclude transplant and can be done as bridge to transplant
Bronchoscopic lung volume reduction, can you do it if:
(a) FEV1 is 20%
(b) DLCO 20%
(c) Homogeneous emphysema
(d) PASP 35
Bronchoscopic lung volume reduction done in really sick patients in LIBERATE trial 2018
(a) Average FEV1 15-25%
(c) Average DLCO 20%
(c) Prefer heterogeneous emphysema but homogeneous not strict contraindication for valve
(d) Exclusion was PASP over 45 (so ok for valve if PASP 35)
Good candidates for bronchial thermoplasty
Bronchial thermoplasty- controlled heat to airway smooth muscle to reduce volume and therefore hopefully reactivity
- only for very refractory asthmatics who are not currently in exacerbation
- trials didn’t include ppl w/ frequent exacerbations or PO steroid requirement
Advanced directives are not portable/valid across state lines- true or false?
False- valid anywhere, highest ordered standard is known wishes (vs. substituted judgment or best-interests)
Physicians are obliged to continue mechanical ventilation after brain death if family wants- true or false?
FALSE- brain death = legal death everywhere in US, controversial but do not have to provide any further care
Informed consent is an example of which basic principle of medical ethics?
Autonomy
(not beneficience, nonmaleficience- do no harm)
(not justice- fair distribution of resources)
Which lung CA most likely:
(a) pancoast
(b) low activity on PET (false negative)
(c) Refractory/persistent infiltrate not resolving with abx
(a) Pancoast- most associated with squamous cell
(b) Low activity on PET- BAC (slow growing/lepidic subtype of adenoCA) and carcinoid = false negative on PET
(c) Refractory alveolar infiltrate- consider MALToma (lymphoid cells spread into and fill alveolar space)
Define large cell lung cancer (how differentiate from adenoCA?)
Large cell- undifferentiated (aka can’t classify it into adenoCA or squamous) that lack features of small cell, glandular (adeno), or squamous differentiation
General treatment for NSCLC
(a) Stage I
(b) Stage II
(c) Stage III
(d) Stage IV
Lung CA treatment
(a) Stage I- sublobar resection, can consider lymph node reseciton, no chemo/XRT
(b) Stage II- lobectomy, mediastinal lymph node dissection + adjuvant chemo
(c) Stage III
IIIA- chemo/XRT + immunotherapy
IIIB- chemo/XRT
(d) Stage IV- chemo alone, XRT only palliative
When to do radiation in stage I or II NSCLC?
Stage I tx = surgical resection. Stage II tx = surgical resection (lobectomy) with adjuvant chemo
Only XRT if poor surgical candidate or post-op if positive surgical margins
Which stage NSCLC gets immunotherapy?
Generally stage IIIa NSCLC gets immunotherapy
-pembrolizumab for stage III or IV NSCLC without EGFR or ALK mutation
Chemo of choice by mutation for metastatic NSCLC
(a) EGRF mutation
(b) ALK or ROS mutation
Chemo of choice for
(a) EGRF + metastatic NSCLC = erlotinib (TKI)
(b) ALK or ROS-1 positive metastatic NSCLC = crizotinib
Difference in treatment between Pancoast tumor and other NSCLC
Pancoast tumors (defined just by location in the apical pleuropulmonary groove)- neoadjuvant chemo/XRT then resection (not just straight to resection) even if localized disease
-chemo/XRT then resection instead of just resection even in localized disease
Size cutoffs differentiating stage I and stage II NSCLC
T1 0-3cm, T2 3-5cm, T3 5-7cm, T4 7cm
Stage I: 0-4cm with with NO (surgical resection)
Stage II: >5cm with N0, or 0-5cm with N1 (surgical resection + adjuvant chemo)
Difference in surgery for stage I vs. stage II NSCLC
Can do sublobar is tumor less than 3cm (stage I)
Stage II (technically over 4cm) do lobectomy
Treatment for lung neuroendocrine tumors
Well-differentiated neuroendocrine tumors = bronchial carcinoids- typically indolent/slow growing
-prognosis depends on path (# of mitosis): typical vs. atypical (more mitosis, more likely to metastasize)
Tx = surgical resection (w/ lymph node dissection), involvement of mediastinal lymph nodes does not preclude cure
-endobronchial resection not definitive (can recur)
Typically do not metastasize, if extensive can consider XRT
Anterior mediastinal masses
(a) appearance of thymoma vs. teratoma
(b) which lymphoma more likely, better or worse prognosis?
(c) which germ cell tumor has better prognosis?
Anterior mediastinal masses
(a) Thymoma- homogeneous, well-circumscribed and round
Teratoma- calcified with fat, cystic
(b) Hodgkins- which has better prognosis than NHL
(c) Seminoma (normal AFP) has better prognosis than nonseminoma (irregular appearance, elevated AFP
What mediastinal compartment would you find
(a) Bronchial cyst
(b) Extramedullary hematopoeisis of the spine
Mediastinal compartment
(b) Bronchial cyst- middle mediastinum- abnormal embryologic branching of tracheobronchial tree (so is lined by respiratory epithelium and cartilaginous plates)
Typically paratracheal or subcarinal
(b) Posterior mediastinum- can have extramedullary hematopoeisis adjacent to vertebrae or ribs, typically in myeloproliferative disorders or anemias
(a) Differentiate main clinical features of Lambert-Eaton and Myasthenia Gravis
(b) Differentiate EMG findings
(a) Lambert-Eaton (Ab against Ca2+ gated channels reducing neurotransmitter release at NMJ) can be paraneoplastic 2/2 NSCLC, clinically with slowly progressive proximal leg weakness and difficulty walking
while MG mainly oculobulbar dysfunction
(b) EMG for LE- post-activation facilitation where amplitude of action potential actually improves with repetitive stimulation
MG- fatigue, amplitude reduces with repeated stimulation
SIADH
(a) Typically due to which lung CA
(b) Expected UNa and Uosm
(a) Hyponatremia typically due to SIADH from SCLC (small cell)
(b) UNa under 40 (holding on to all sodium) and Uosm high over 500 (peeing out all the water)
2 other paraneoplastic syndromes associated with SCLC that aren’t SIADH
- Paraneoplastic neurologic syndrome due to autoantibodies- Lambert Eaton (Ab against voltage gated calcium channels), cerebellar ataxia (Anti-Yo Ab), limbic encephalitis (Anti-(Hu AB)
- Cushing- high cortisol and ACTH- moon facies, weight gain, striae (from ectopic cortisol production)
What does HPO stand for (paraneoplastic syndrome)
(a) Clinical features
(b) Managament
Hypertropic osteoarthropathy
(a) Digital clubbing and long bone arthralgias (bone pain) due to periosteal inflammation of long bones (ankles, knees, wrists, elbows)
(b) Typically resolves with treatment of underlying cancer
Mesothelioma
(a) Risk factor
(b) Not a risk factor
(c) How to make diagnosis
(d) Imaging findings
(e) Prognosis
Mesothelioma
(a) 85% with known asbestos exposure, but notably mesotheliomas do NOT arise from pleural plaques
(b) Smoking not associated/risk factor, asbestos not synergistic risk factor with smoking
(c) Can drain if pleural fluid present, sometimes can get away with closed pleural biopsy, often will need VATS for large enough tissue sample for immunostains
(d) Imaging- unilateral pleural thickening w/ pleural effusion
(e) Very poor prognosis, under 1 yr
Once cleared for surgery from cardiac perspective (cardiac risk acceptable), proceed to PFTs for pre-op evaluation
(a) What to do for PFT-based moderate risk patients
(b) What to do for PFT-based high risk patients
(a) PFT moderate risk, DLCO and FEV1 between 30-60% predicted- can do shuttle walk test or stair climb, if good than ok, if poor than proceed to CPET
(b) DLCO or FEV1 under 30% do CPET- high risk if VO2max is under 10 ml/kg/min (less than 35% predicted)
VO2 max cuttoffs for low, moderate, and high risk for surgical clearance
(a) absolute value
(b) percent predicted
VO2 max over 20 ml/kg/min, above 75% predicted- lower risk
VO2 max under 10 ml/kg/min, below 35% predicted- high high risk
Lung volumes
(a) Differentiate vital capacity from functional residual capacity
(a) Differentiate total lung capacity from inspiratory capacity
Lung volumes
(a) Vital capacity = TV + IRV + ERV, while FRC is ERV + residual volume
(b) TLC = everything, TV + IRV + ERV + FRC, while inspiratory capacity is TV IRV
Four respirtaory variables measured during CPET and what values they let us derive
TV, RR, EtCO2, EtO2
- TV and RR give us minute ventilation (VE)
- EtCO2 gives us VCO2, with VE/VCO2 gives us ventilatory equivalents
- EtO2 gives us VO2, with heart rate (from EKG) gives us O2 pulse
Describe change in cardiac output during exercise and how this is guided by change in SV and HR
Beginning of exercise SV increases then plateaus off (similar to tidal volume for minute ventilation). Then after SV plateaus (early) the remaining increase in cardiac output is due to increase in HR
How to tell if max effort is achieved on CPET?
3 ways:
- 80% of max work achieved (showed on time vs. work graph as red bar of panel 3)
- 80% of max HR achieved (time vs. HR goes within maroon box in panel 2)
- Respiratory exchange ratio (VCO2/VO2) exceeds 1.15
From which CPET graph is anaerobic threshold measured?
Anaerobic threshold = when amount of O2 needed exceeds supply of O2 given by cardiopulmonary system
=> muscles start to use anerobic metabolism (from no available O2), make lactate which uses bicarb to buffer, creating more CO2
so at anerobic threshold see an increase in CO2 produced per O2 used
Graph: VO2 vs. VCO2- when the slope of this changes (increases), the VO2 at this point is the anerobic threshold
In picture shown- AT occurs at 1.45 L/min
How to identify anerobic threshold on graph of ventilatory equivalents
At anerobic threshold- will start to increase minute ventilation more in proportion to Vo2 (VE/VCO2 rises) while VE/VCO2 remains the same
minute ventilation increases proportionally to VCO2, but disproportionately to VO2
-so on graph when see red dotted line start to increase (around minute 11ish)
General step-wise approach to CPET
- Max effort achieved (can we trust this VO2 max)- 80% of max work rate and 80% max HR
- Look at max VO2 (max O2 usage)
- Anerobic threshold
- If abnormal- look at O2 pulse and EKG for cardiac limitation, look at ventilatory reserve (reach max voluntary ventilation?) and ventilatory equivalents for respiratory limitation
Expected abnormality in CPET for patient with significant cardiac limitation
Low VO2 max (0.9 L/min in this chart, 14 ml/kg/min)
Low anerobic threshold (0.7 L/min, 10 ml/kg/min)
Normal ventilatory reserve (doesn’t reach max voluntary ventilation in panel 7) with significant abnormality in O2 pulse (stroke volume response)- see purple line in panel 2 doesn’t increase with exercise
How to calculate maximum voluntary ventilation and why this is important during CPET?
MVV = FEV1 x 40 (or 37 depending on the lab)
important b/c normally at end-exercise there is respiratory reserve (max VE does not exceed 80% of MVV)
if 80% or above of MVV achieved suggests respiratory limitation
Expected CPET abnormality in respiratory limitation
- See if max effort achieved (80% max work, 80% max HR, RER over 1.15
- VO2 max (panel 2 red dotted line)
- anerobic threshold (panel 5 where purple slopes diverge)
Both VO2 and AT reduced, then see if due to respiratory limitation (no ventilatory reserve seen in panel 7 as tidal volume exceeds 80% of max voluntary ventilation)
or if due to cardiac limitation (either abnormal rise in HR or O2 pulse, not seen here in panel 2)
Describe the breakpoint in minute ventilation where slope significant increases during exercise
During exercise- minute ventilation initially rises linearly as first TV then RR increases.
Once anerobic threshold met- increased CO2 production (anerobic metabolism) causes increase in slope of MV, acocunted for by increase in RR
Normal anerobic threshold is what percent of VO2 max?
Above 40%
So you should meet anerobic threshold (convert into anerobic metabolism due to less O2 supply than demand) anytime above 40% of VO2 max
ex: anerobic threshold in normal healthy patient achieved at 50% of peak VO2
How to identify ventilatory inefficiency on CPET
Increased ventilatory equivalents- meaning more minute ventilation needed to get rid of the same amount of gas (due to more dead space)
Generally expect ventilatory equivalents to drop below 35 at nadir
(example of abnormal where at nadir both are above 40)
Measuring anaerobic threshold
(a) Invasively
(b) Non-invasively
(a) Invasively- use A-line and see when lactate production starts to rise
(b) Noninvasively (obv way more used) is the V-slope method of comparing rate of exhaled CO2 (VCO2) with rate of oxygen used (VO2)
when slope of this curve changes (increases)- starting to exhale more CO2 for same amount of oxygen = anerobic threshold
Differentiate HR response likely demonstrating lung disease vs. heart disease
Dashed diagonal line = healthy individual
(A) Heart disease (ex: cardiomyopathy)- curved shifted left with increased slope- HR increases faster with same amount of work and max predicted HR achieved faster
(B) Lung disease- max HR not predicted b/c stopped by respiratory system first
Which respiratory response demonstrates normal/healthy vs. pt with lung disease
(a) Cutoff of max minute ventilation reached in a healthy patient
(a) Typically peak minute ventilation approaches ~70% of maximal value, leaving about 30% of ventilatory Reserve
(A)- normal patient; MVV (max voluntary ventilation) not reached during exercise
(B) Abnormal- c/w lung disease, MVV reached and even exceeded
What measurements will help differentiate deconditioning from lung disease on CPET
(a) Heart rate reserve
(b) Ventilatory equivalents and ventilatory reserve
Deconditioning:
(a) Heart rate reserve normal in deconditioning while reserve is increased in lung disease (b/c max HR not met given have to stop early from ventilatory limitation)
(b) Normal ventilatory equivalents (while elevated in COPD/ILD)
Normal ventilator reserve in deconditioning, elevated VE/MVV in lung disease (get to higher MV compared to max voluntary ventilation)
Normal CPET values for
(a) VO2max
(b) Anaerobic threshold
© Heart rate reserve (max expected HR - max achieved HR)
(d) Oxygen pulse
Normal CPET values
(a) VO2 max ~ 85% predicted based on height/weight
(b) AT normal if 40% or above of VO2max
© HRR normal under 15, basically should reach max HR (which would be a small HR reserve) unless heart disease and stopped early
(d) Oxygen pulse normal is over 80% predicted, indirect measure of stroke volume
Normal CPET values for
(a) Ventilatory reserve (VE/MVV)
(b) Ventilatory equivalent of CO2 (VE/VCO2)
Normal CPET value
(a) Ventilatory reserve (VE/MVV) under 85%, in lung disease as minute ventilation rises (numerator) pt using more minute ventilation, if approaches one then pt has no ventilatory reserve (abnormal given cardiovascular system is typically the limiting step
(b) VE/VCO2 under 34
- higher than 34 suggests needs more minute ventilation to get rid of CO2
Main CPET values to differentiate heart disease from lung disease
Both: reduced VO2 max and reduced anearobic thresohld
HR:
- heart rate reserve: normal in heart disease (max HR reached) while elevated in lung disease (don’t get to max HR b/c stopped first by ventilatory max)
- max HR achieved in heart disease, not achieved in lung disease
Ventilatory:
-VE/MVV (minute ventilation over maximum voluntary ventilation, normal under 85%): normal in heart disease, elevated in lung disease (get to higher MV)
Pre-op for transbronchial biopsy- what to do with antiplatelets?
Ok to TBBX on ASA, hold plavix 5-7 days
Point out two abnormal things about end-exercise spirometry and what this tells you about patient’s cardiopulmonary function
-expiratory flow limitation at all points (rest, during, and end-exercise)
- significant dynamic hyperinflation during exercise- end-expiratory lung volume is 600ml lower during exercise (EELV)
- near-absent inspiratory reserve volume at end exercise (only 160ml, should be way more)
Likely to also see absent breathing reserve on CPET and elevated ventilatory equivalents
If all lymph nodes negative (N0), list lung cancer size cutoffs for stages I, II, and III
N0
- Up to 4cm: stage I
- 4-5cm: IIA
- 5-7cm: IIB
- over 7cm: IIIA
Two categories of stage IIB lung cancer
IIB:
Over 5cm with N0, or
0-5cm with N1 (ipsilateral 10/11 hilar/peribronchial)
Differentiate stage IIA and stage IIB lung cancer
Stage IIA = 4-5cm with N0
Then once over 5cm with N0 or 0-5cm with N1 = stage IIB
3 categories of stage IIIA lung cancer
Stage IIIA:
- Over 7cm with N0
- Over 5cm with N1 (under 5cm with N1 = stage IIB)
- 0-5cm with N2 (4/7 mediastinal or subcarinal LN)
Differentiate stage IIB and IIIA lung cancer
Stage IIIA:
- Over 7cm with N0
- Over 5cm with N1 (under 5cm with N1 = stage IIB)
- 0-5cm with N2 (4/7 mediastinal or subcarinal LN)
vs.
Stage IIB
- 5-7cm with N0
- 0-5cm with N1
2 categories of stage IIIB lung cancer
Stage IIIB
- 5-7cm with N2
- 0-5cm N3
Which type of work-related asthma requires PPE vs. removal from job?
PPE can safely be used for irritant-induced asthma or RADS where thought to be non-immunologic response => exposure to lower-dose less likely to trigger symptoms
While removal from job required for immunologic/sensitizer-induced (IgE mediated) b/c repeated exposure can lead to progressive decline in lung function and potentially fatal event
What are some common etiologies of sensitizer-induced asthma?
Sensitizer-induced asthma (immunologic, IgE mediated):
high molecular weight compounds: paint, bakers lung (wheat/rye), latex, animal (rats, cockroach)
low molecular weight compounds (wood dust, cleaning agents)
Symptoms to differentiate sensitizer-induced asthma from irritant-induced asthma?
(a) Treatment implication
Sensitizer-induced (immunologic, IgE mediated) typically standard latency period between exposure and symptoms
vs.
Irritant-induced: no latency period
(a) PPE to reduce level of exposure b/c if not truly sensitized then lower level exposure
What type of work-related asthma is RADS?
Management of work-exacerbated asthma?
48M no PMH, works applying paint to agricultural instruments w/ several months of cough, chest tightness, and nocturnal wheezing
- peak flow persistently lower at work
- temporal relationship btwn job and symptoms
(a) Most likely diagnosis
(b) Best management
(a) Sensitizer-induced asthma = IgE mediated (immunologic) with latency btwn exposure and symptoms
- supported by no history of respiratory complaints
- classic painting compound isocyanate-based
(b) Mgmt = restrict from returning to work, speak to supervisor regarding accomodations (worker’s comp benefits)
- have to avoid b/c recurrent exposures => progressive deterioration
Describe features of work-related asthma that meets requirements for worker’s compensation benefits
Workers compensation applies to sensitizer-induced asthma, so
- no h/o asthma that is just made worse by exposure on job (so not work-aggravated and work-exacerbated)
- no acute exposure with abrupt onset symptoms thought to be non-immune related b/c that can be treated with PPE
Sensitizer-induced asthma = IgE/immunologic where repetitive exposure can lead to progressive decline in lung function and potentially fatal outcome
Treatment for the ‘bends’ (joint pain after ascending too quickly from scuba diving):
Oxygen to reduce partial pressure of nitrogen in blood and increase gradient to help the nitrogen dissolve
-so high flow nasal oxygen or hyperbaric
Nothing to do with fluid restriction b/c wouldn’t limit cerebral edema anyway silly goose
Diagnosis?
Arrows outlining a masson body = loose polypoid plugs of granulation tissue in terminal and respiratory bronchioles, alveolar ducts, and sacs characteristic of organizing PNA
Describe the histologic findings
Green circles = histiocytes (giant cells)
Yellow arrows = non-necrotizing granulomas
Particular picture of GPA = large areas of necrosis (black arrows) with irregular borders in inflammatory background with non-necrotizing granulomas
Active smoker not yet ready to attempt quitting- what to offer?
As of 2021 answer is pharmacologic options even before express ready b/c then are more likely to express readiness to quit
-so offer varenicline + nicotine patches
(even if have history of bipolar I offer varenicline and then just monitor closely for symptoms)
Characteristic pathology findings of hard metal (cobalt) lung disease
Giant cell interstitial pneumonitis = multinucleated giant cells filling the interstitium
Most common middle mediastinal masses
Middle mediastinum- A’s
- Adenopathy- malignant (lymphoma), infection
- aneurysm- aortic
- abnormality of development- bronchogenic (lower trachea or mainstem bronchi), pericardial cysts (R cardiophrenic angle)
Most common non-AIDS defining malignancy in HIV patients
Lung cancer
-same histologic types as non-HIV patients but much higher rate at lower age
Solitary fibrous tumor of the pleura
(a) Typical location/imaging finding
(b) Typical clinical presentation
~5% of pleural-based tumors = mesenchymal origin solitary fibrous tumors
(a) Visceral pleura based, well-circumscribed, and can be mobile if pedunculated (unique mobile feature in pic)
(b) Typically asymptomatic and found incidentally on imaging
Solitary fibrous tumor of the pleura pathologic findings
Solitary fibrous tumor on pathology:
- hypocellular
- dense collagen background with collagen bands
- atypical spindled cells, storiform configuration
- spindle cells
2 rare extrathoracic symptoms of solitary fibrous tumors of the pleura
Solitary fibrous tumors of the pleura = mesenchymal-origin pleural-based mass
Random extrathoracic symptoms
- Hypoglycemia
- HPO (hypertrophic osteoarthropathy) = digital clubbing, painful arthropathy
