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CM Pulmonary Boards > Neoplasm, CAP/VAP, Occupational, Atypical Infxn, CF/Bronchiectasis, Pulm Physio > Flashcards

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

1
Q

Types of lung cancer in descending order of frequency

A

35% adenocarcinoma (3% of which are BAC)
30% squamous cell carcinoma
20% small cell
10% large cell
10% unclassified/undifferentiated

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2
Q

Which lung CAs are generally

(a) peripheral vs. central?
(b) can cavitate
(c) Non-smokers

A

(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

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3
Q

Most common paraneoplastic syndrome associated with lung CA (and which lung CA)

A

SIADH from small cell

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4
Q

Paraneoplastic syndrome associated with

(a) squamous cell
(b) small cell

A

Paraneoplastic

(a) squamous- HPO (clubbing), hypercalcemia
(b) small cell- SIADH, myasthenia gravis, lambert eaton

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5
Q

Current USPSTF recs for lung CA screening

A

Ages 50-80, 20 pack year history, quit within 15 yrs

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6
Q

T staging based on size

A

Size of tumor

T1a: less than 1cm
T1b: 1-2cm
T1c: 2-3cm
T2: 3-5cm
T3: 5-7cm
T4: more than 7cm

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7
Q

What N-stage is an ipsilateral supraclavicular node?

A

Either ipsilateral or contralateral supraclavicular node = N3

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8
Q

N stages

A

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

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9
Q

What M-stage are the following

(a) malignant pleural effusion or pleural lesion
(b) single distant met
(c) nodule in contralateral lung

A

Metastasis
(a) Pleural involvement- M1a
(b) Single distant met- M1b
(vs multiple distant mets M1c)
(c) Contralateral lung- M1A

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10
Q

Solitary pulmonary nodules

(a) Percent benign vs. malignant
(b) Most common benign
(c) Most common malignant

A

Solitary pulmonary nodules

(a) 55% benign, 45% malignant
(b) Granulomatous, nonspecific. also hamartomas
(c) adenoCA, then squamous. very unlikely small cell

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11
Q

FEV1 and DLCO cutoffs for surgical management

A

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)

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12
Q

How VO2 on CPET helps risk stratify lung CA patients for resection

A

VO2 (oxygen consumption): over 20- low risk
10-20: moderate risk
under 10 (ml/kg/min): high risk

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13
Q

Single lung nodules of what size do/don’t need follow-up?

A
  • 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
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14
Q

What qualifies as IA vs. IB lung cancer?

A

IA: T1 (under 3cm) with N0
IB: T2a (under 4cm) with N0

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15
Q

What qualifies as IIB lung cancer?

A

IIB- Any T1-T2 with N1 (so ipsilarateral nodes with tumor up to 5cm)

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16
Q

Treatment of stage I lung CA

A

Stage I: under 4cm with N0

Resection = lobectomy with mediastinal LN dissection
-no adjuvant chemo

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17
Q

Treatment of stage II lung CA

A

Stage II: either over 4cm and T0 or up to 5cm with N1 (hilar or peribronchial LN)

Resection with adjuvant chemo

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18
Q

Post-surgical management for lung CA patients- when to get screening CTs

A

Repeat CT chest q6 months x2 years, then annual for 5 years

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19
Q

Treatment for stage IIIa vs. IIIb lung CA

A

IIIa- chemoradiation with adjuvant immunotherapy x1 year

IIIb- chemo and XRT if good functional status, if poor functional status XRT alone

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20
Q

Timeline for immunotherapy-induced pneumonitis

A

Most commonly 30 days after initiation, but can happen anytime and even up to a year after stopping

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21
Q

How to grade severity of immunotherapy-induced pneumonitis and how that guides management

A

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
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22
Q

Which patients with lung cancer get prophylactic cranial radiation?

A

Small cell cancer in remission after initial treatment (chemo/XRT)

with good functional status

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23
Q

Differentiate treatment response for limited vs. extensive small cell lung CA

A

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)

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24
Q

Difference in treatment for extensive and limited small cell (SCLC)

A

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

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25
Q

Terrible Ts

A

Anterior mediastinal masses

  1. thymoma- most common
  2. terrible ones- mets and lymphoma
  3. intrathoracic thyroid
  4. teratoma (germ cell tumors)
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26
Q

Mediastinal germ cell tumors

(a) triggers what further workup
(b) differentiate benign from aggressive
(c) Elevated tumor marker in most aggressive germ cell tumor

A

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

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27
Q

Most common posterior mediastinal tumor

A

Neurogenic tumors

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28
Q

Typical location of pulmonary carcinoid/neuroendocrine

A

Well-differentiated neuroendocrine tumors = bronchial carcinoid

Endobronchial
-associated with nonsmokers

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29
Q

Imaging features of hamartoma

A

Contains calcium and fat

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30
Q

Pulmonary MALToma associated with what other disease?

A

Autoimmune disease most specifically Sjogren’s

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31
Q

Most common site of mets (of all CA)

(a) Second

A

Liver

(a) Second- lung

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32
Q

Differentiate Mallampati I and II

A

Mallampati I- can see hard palate, soft palate, uvula and tonsillar pillars

Mallampati II lose the tonsillar pillars

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33
Q

Differentiate Mallampati I and III

A

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

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34
Q

When to be worried/cautious with bronchoscopy

(a) PA pressure
(b) Lab value

A

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

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35
Q

Who should and who shouldn’t get prophylactic beta-agonist before bronchoscopy?

A

Asthmatics should, COPDers shouldn’t

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36
Q

How long before bronchoscopy to stop

(a) DOACs
(b) Warfarin
(c) Lovenox
(d) Heparin gtt

A

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

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37
Q

Max dose of lidocaine to give topically during bronchoscopy

A

7 mg/kg lidocaine

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38
Q

Imaging features to differentiate thymoma from thymic carcinoma

A

Thymoma- homogeneous

Consider malignancy if heterogeneous, associated pleural/pericardial effusion, lymphadenopathy

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39
Q

Most common CAP pathogen

A

Strep pneumo

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40
Q

Which is 1st vs. 2nd generation macrolide?

A

1st gen- erythro
2nd gen- azithro, clarithro

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41
Q

Guidelines tx for CAP

A

CAP tx:
- Amoxicilin or doxy or azithro (if R rates low)

If comorbidities: combo augmentin or cefpo with macrolide or doxy
OR
respiratory fluoroquinolone

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42
Q

Most common VAP pathogens

A

Staph aureus (30%), then pseudomonas (24%), then other gram negatives (klebs, serratia, E. coli)

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43
Q

CURB-65 score- when can do outpatient

A

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

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44
Q

Mechanism by which hospitalized CAP in pts over 50 worsens outcomes

A

Likely from increase in CV risk- elevated risk of ACS after pneumonia (possibly due to inflammatory mileu)

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45
Q

Which smoking cessation aid need to be careful for mental health side effects?

A

Chantix (varenicline)- partial nicotine receptor agonist => reduces rewarding aspects of cig smoking

had serious neuropsychiatric events (depression, SI) with comorbid psych conditions

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46
Q

Why higher risk of hypoxia at higher altitudes?

A

‘Thinner air’- at higher altitude, lower FiO2 => lower gradient for oxygen to diffuse into our capillaries

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47
Q

Best mgmt for acute altitude sickness symptoms?

A

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

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48
Q

When to start acetazolamide as ppx before an ascending hike

A

Start day before ascent, continue 1-2 days in
-remember it’s a diuretic so important to replace fluids (stay hydrated)

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49
Q

Explain decompression sickness, type I vs type II

A

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

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50
Q

Typical presentation of asbestos

(a) Latency
(b) Radiology
(c) Cancer risk

A

Asbestos

(a) 20+ years
(b) Benign asbestos pleural effusions (exudative), pleural plaques
(c) Mesothelioma

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51
Q

Pt with mediastinal lymphadenopathy, clinical history of working in shipyeard or aerospace industry

Dx?

A

Think berylliosis for anything that seems like sarcoid plus environmental exposures

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52
Q

Berylliosis

(a) Path findings
(b) Imaging
(c) Mgmt

A

Berylliosis- hard metals, shipyard or aerospace industry

(a) Non-caseating granulomas (mimicks sarcoid)
(b) Mediastinal lymphadenopathy
(c) Steroids or immunosuppression, supportive

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53
Q

Special considerations when choosing smoking cessation aid

A
  • history of poorly controlled mental health maybe stay away from chantix (varenicline)
  • buproprion contraindicated in pts w/ seizure disorder (reduces seizure threshold)
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54
Q

Key air travel tip for divers

A

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)

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55
Q

Key exposure to think of for

(a) UIP pattern developing over 20-30 years
(b) Rheumatoid nodules with layer of black dust

A

(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)

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56
Q

Exposures to think of for silicosis

A

Anything that disrupts the earth’s core- especially with quartz (major component of granite, slate, and sandstone)

Tunnelers, miners, sandblasters, stone cutting, masonry

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57
Q

Differentiate chest imaging findings of

(a) acute silicosis
(b) simple silicosis
(c) progressive massive fibrosis

A

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

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58
Q

What other disease mimics BAL findings of acute silicosis?

(a) Lab value to send off?

A

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

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59
Q

Characteristic path for silicosis

A

Silicotic nodules- central hyaline with surrounding stuff (ew)

*Birefringent particles under polarized light

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60
Q

What level of CO-Hb on gas expected to develop symptoms of carbon monoxide poisoning

A

Normal CO-Hb in nonsmokers- 3%, 10-15% in smokers

Generally don’t expect symptoms under 10% in either

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61
Q

Which way to carbon monoxide shift the Hb-dissociation curve?

A

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

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62
Q

Compare CD4:CD8 ratio (BAL fluid) in sarcoid vs. chronic HP

A

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)

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63
Q

Which way does exercise shift the Hb-dissociation curve?

A

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

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64
Q

How does higher altitude shift the Hb-dissociation curve?

A

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

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65
Q

Occupational exposure buzzwords

(a) Black vs. white nodules in the lungs
(b) Giant cell interstitial pneumonia

A

Occupational exposure buzzwords

(a) Black nodules- coal-workers pneumoconiosis. vs. white nodules from silicosis
(b) giant cell interstitial pneumonia = hard metal (cobalt) lung disease

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66
Q

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

(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)

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67
Q

Infection highly associated with chronic silicosis

A

Tuberculosis => workup for chronic silicosis has to include IGRA

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68
Q

Nitric oxide role in the respiratory tract

Disease with

(a) High FeNO
(b) Low FeNO

A

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)

69
Q

Name two branching gram positive organisms

A

Branching/filamentous gram positive organisms

  1. Nocardia- weakly AFB positive
  2. Actinomycosis- not AFB positive
70
Q

FeNO cutoffs for asthma in children and adults

A

FeNO- fraction of exhaled nitric oxide, marker of eosinophilic inflammation

>50 in adults, >35 in children associated with eosinophilic inflammation (asthma)

71
Q

Nocardia vs. actinomycosis

(a) Which more typically in immunocompromsied
(b) First line treatment
(c) Clinical hallmark
(d) Surgical mgmt

A

(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

72
Q

Nocardia

(a) How to culture
(b) Clinical hallmark feature

A

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)

73
Q

Buzzwords histopath

(a) Sulfur granules
(b) Partially AFB staining bacteria

A

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

74
Q

Nocardia

(a) Most common sites of involvement
(b) First line treatment algorithm

A

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!

75
Q

Broad ddx for cavitary lung lesion

A

Cavitary lung disease

  • Malignancy: typically squamous
  • Infection: bacterial (klebs, staph), fungal (aspergillus), atypical bacterial (nocardia, actino), NTM, Tb, septic emboli
76
Q

What is used for newborn screening for CF

A

Tyrptase- enzyme of pancreatic damage that is detectably elevated at birth

77
Q

Sweat test for CF

(a) Explain what ion measuring and why
(b) Normal value
(c) Diagnostic cutoff

A

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

78
Q

How sweat test cutoff is different for adult-diagnosed CF

A

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

79
Q

Most common infections in CF patients based on age

A

Childhood- staph aureus and H. influenza

Then around age 20 pseudomonas starts to dominate

80
Q

Mechanism of dornase alpha in CF patients

A

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

81
Q

FEV1 cutoff to refer CF patient for transplant

A

Refer for transplant when FEV1 starts dipping below 40%

Below 50% if also: rapidly declining, PASP over 50

82
Q

Azithro TIW in bronchiectasis patients

(a) When to consider starting
(b) When contraindicated

A

Azithro for chronic inflammation in bronchiectasis

(a) Start when 3+ exacerbations in a year
(b) Contraindicated in pts with NTM

83
Q

3 things to monitor for patients on long-term azithro

A

Long-term azithro (COPD, bronchiectasis, CF) monitor

  • LFTs
  • hearing
  • QTc
84
Q

Which NTM species to think of when see RML or lingular involvement

A

MAC loves the lingula and RML

85
Q

Most common rapidly-growing NTM in the US

A

Most common rapid-growing (grows in culture in one week) in the US = Mycobacterium abscessus

vs. slow-growing = MAC (takes 4-8 weeks)

86
Q

Factors that would trigger daily (vs TIW) tx for MAC

A

Consider daily (vs. TIW) MAC treatment when

  • severe nodular disease
  • cavitary disease
87
Q

First line MAC treatment

A

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

88
Q

Duration of MAC tx

A

MAC tx = 12 months from culture conversion (defined as 3 negative cultures)

89
Q

When to add inhaled liposomal amikacin to MAC tx

A

Liposomal amikacin FDA-approved for refractory MAC = cultures not converted as 6 months

90
Q

What sensitivities are important for different NTMs

(a) MAC
(b) M. abscessus

A

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

91
Q

Significant of erm gene mutation

A

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)

92
Q

Example M. abscessus tx regimen

A

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

93
Q

Differentiate tracheobronchomalacia from EDAC

A

TBM- weakening of anterior tracheal cartilage

vs. EDAC = anterior bulging of the posterior membranous portion of trachea, while cartilaginous rings are intact

94
Q

Definition of hyperdynamic airway collapse

A

Normal airway collapses up to 30% during exhalation, HDAC = collapse of more than 30% on exhalation

95
Q

Type of tracheobronchomalacia typically seen in COPD

A

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
96
Q

Changes seen in TBM/EDAC (same for both)

(a) PFTs
(b) Dynamic CT
(c) Awake bronchoscopy

A

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

97
Q

Two cutoffs that make pts not a good surgical candidate for mgmt of tracheal stenosis

A

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

98
Q

Type of emphysema most amenable to surgical lung volume reduction surgery

(a) Location of emphysema
(b) Exercise tolerance

A

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)

99
Q

Bronchoscopic lung volume reduction

(a) Explain theoretically how works
(b) Why want intact fissures
(c) Exclude transplant?

A

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

100
Q

Bronchoscopic lung volume reduction, can you do it if:

(a) FEV1 is 20%
(b) DLCO 20%
(c) Homogeneous emphysema
(d) PASP 35

A

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)

101
Q

Good candidates for bronchial thermoplasty

A

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
102
Q

Advanced directives are not portable/valid across state lines- true or false?

A

False- valid anywhere, highest ordered standard is known wishes (vs. substituted judgment or best-interests)

103
Q

Physicians are obliged to continue mechanical ventilation after brain death if family wants- true or false?

A

FALSE- brain death = legal death everywhere in US, controversial but do not have to provide any further care

104
Q

Informed consent is an example of which basic principle of medical ethics?

A

Autonomy

(not beneficience, nonmaleficience- do no harm)
(not justice- fair distribution of resources)

105
Q

Which lung CA most likely:

(a) pancoast
(b) low activity on PET (false negative)
(c) Refractory/persistent infiltrate not resolving with abx

A

(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)

106
Q

Define large cell lung cancer (how differentiate from adenoCA?)

A

Large cell- undifferentiated (aka can’t classify it into adenoCA or squamous) that lack features of small cell, glandular (adeno), or squamous differentiation

107
Q

General treatment for NSCLC

(a) Stage I
(b) Stage II
(c) Stage III
(d) Stage IV

A

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

108
Q

When to do radiation in stage I or II NSCLC?

A

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

109
Q

Which stage NSCLC gets immunotherapy?

A

Generally stage IIIa NSCLC gets immunotherapy

-pembrolizumab for stage III or IV NSCLC without EGFR or ALK mutation

110
Q

Chemo of choice by mutation for metastatic NSCLC

(a) EGRF mutation
(b) ALK or ROS mutation

A

Chemo of choice for

(a) EGRF + metastatic NSCLC = erlotinib (TKI)
(b) ALK or ROS-1 positive metastatic NSCLC = crizotinib

111
Q

Difference in treatment between Pancoast tumor and other NSCLC

A

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

112
Q

Size cutoffs differentiating stage I and stage II NSCLC

A

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)

113
Q

Difference in surgery for stage I vs. stage II NSCLC

A

Can do sublobar is tumor less than 3cm (stage I)

Stage II (technically over 4cm) do lobectomy

114
Q

Treatment for lung neuroendocrine tumors

A

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

115
Q

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?

A

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

116
Q

What mediastinal compartment would you find

(a) Bronchial cyst
(b) Extramedullary hematopoeisis of the spine

A

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

117
Q

(a) Differentiate main clinical features of Lambert-Eaton and Myasthenia Gravis
(b) Differentiate EMG findings

A

(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

118
Q

SIADH

(a) Typically due to which lung CA
(b) Expected UNa and Uosm

A

(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)

119
Q

2 other paraneoplastic syndromes associated with SCLC that aren’t SIADH

A
  1. Paraneoplastic neurologic syndrome due to autoantibodies- Lambert Eaton (Ab against voltage gated calcium channels), cerebellar ataxia (Anti-Yo Ab), limbic encephalitis (Anti-(Hu AB)
  2. Cushing- high cortisol and ACTH- moon facies, weight gain, striae (from ectopic cortisol production)
120
Q

What does HPO stand for (paraneoplastic syndrome)

(a) Clinical features
(b) Managament

A

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

121
Q

Mesothelioma

(a) Risk factor
(b) Not a risk factor
(c) How to make diagnosis
(d) Imaging findings
(e) Prognosis

A

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

122
Q

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

(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)

123
Q

VO2 max cuttoffs for low, moderate, and high risk for surgical clearance

(a) absolute value
(b) percent predicted

A

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

124
Q

Lung volumes

(a) Differentiate vital capacity from functional residual capacity
(a) Differentiate total lung capacity from inspiratory capacity

A

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

125
Q

Four respirtaory variables measured during CPET and what values they let us derive

A

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
126
Q

Describe change in cardiac output during exercise and how this is guided by change in SV and HR

A

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

127
Q

How to tell if max effort is achieved on CPET?

A

3 ways:

  1. 80% of max work achieved (showed on time vs. work graph as red bar of panel 3)
  2. 80% of max HR achieved (time vs. HR goes within maroon box in panel 2)
  3. Respiratory exchange ratio (VCO2/VO2) exceeds 1.15
128
Q

From which CPET graph is anaerobic threshold measured?

A

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

129
Q

How to identify anerobic threshold on graph of ventilatory equivalents

A

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)

130
Q

General step-wise approach to CPET

A
  1. Max effort achieved (can we trust this VO2 max)- 80% of max work rate and 80% max HR
  2. Look at max VO2 (max O2 usage)
  3. Anerobic threshold
  4. 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
131
Q

Expected abnormality in CPET for patient with significant cardiac limitation

A

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

132
Q

How to calculate maximum voluntary ventilation and why this is important during CPET?

A

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

133
Q

Expected CPET abnormality in respiratory limitation

A
  1. See if max effort achieved (80% max work, 80% max HR, RER over 1.15
  2. VO2 max (panel 2 red dotted line)
  3. 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)

134
Q

Describe the breakpoint in minute ventilation where slope significant increases during exercise

A

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

135
Q

Normal anerobic threshold is what percent of VO2 max?

A

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

136
Q

How to identify ventilatory inefficiency on CPET

A

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)

137
Q

Measuring anaerobic threshold

(a) Invasively
(b) Non-invasively

A

(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

138
Q

Differentiate HR response likely demonstrating lung disease vs. heart disease

A

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

139
Q

Which respiratory response demonstrates normal/healthy vs. pt with lung disease

(a) Cutoff of max minute ventilation reached in a healthy patient

A

(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

140
Q

What measurements will help differentiate deconditioning from lung disease on CPET

(a) Heart rate reserve
(b) Ventilatory equivalents and ventilatory reserve

A

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)

141
Q

Normal CPET values for

(a) VO2max
(b) Anaerobic threshold

© Heart rate reserve (max expected HR - max achieved HR)
(d) Oxygen pulse

A

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

142
Q

Normal CPET values for

(a) Ventilatory reserve (VE/MVV)
(b) Ventilatory equivalent of CO2 (VE/VCO2)

A

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

143
Q

Main CPET values to differentiate heart disease from lung disease

A

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)

144
Q

Pre-op for transbronchial biopsy- what to do with antiplatelets?

A

Ok to TBBX on ASA, hold plavix 5-7 days

145
Q

Point out two abnormal things about end-exercise spirometry and what this tells you about patient’s cardiopulmonary function

A

-expiratory flow limitation at all points (rest, during, and end-exercise)

  1. significant dynamic hyperinflation during exercise- end-expiratory lung volume is 600ml lower during exercise (EELV)
    1. 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

146
Q

If all lymph nodes negative (N0), list lung cancer size cutoffs for stages I, II, and III

A

N0

  • Up to 4cm: stage I
  • 4-5cm: IIA
  • 5-7cm: IIB
  • over 7cm: IIIA
147
Q

Two categories of stage IIB lung cancer

A

IIB:

Over 5cm with N0, or

0-5cm with N1 (ipsilateral 10/11 hilar/peribronchial)

148
Q

Differentiate stage IIA and stage IIB lung cancer

A

Stage IIA = 4-5cm with N0

Then once over 5cm with N0 or 0-5cm with N1 = stage IIB

149
Q

3 categories of stage IIIA lung cancer

A

Stage IIIA:

  1. Over 7cm with N0
  2. Over 5cm with N1 (under 5cm with N1 = stage IIB)
  3. 0-5cm with N2 (4/7 mediastinal or subcarinal LN)
150
Q

Differentiate stage IIB and IIIA lung cancer

A

Stage IIIA:

  1. Over 7cm with N0
  2. Over 5cm with N1 (under 5cm with N1 = stage IIB)
  3. 0-5cm with N2 (4/7 mediastinal or subcarinal LN)

vs.

Stage IIB

  1. 5-7cm with N0
  2. 0-5cm with N1
151
Q

2 categories of stage IIIB lung cancer

A

Stage IIIB

  1. 5-7cm with N2
  2. 0-5cm N3
152
Q

Which type of work-related asthma requires PPE vs. removal from job?

A

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

153
Q

What are some common etiologies of sensitizer-induced asthma?

A

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)

154
Q

Symptoms to differentiate sensitizer-induced asthma from irritant-induced asthma?

(a) Treatment implication

A

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

155
Q

What type of work-related asthma is RADS?

A
156
Q

Management of work-exacerbated asthma?

A
157
Q

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

(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

158
Q

Describe features of work-related asthma that meets requirements for worker’s compensation benefits

A

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

159
Q

Treatment for the ‘bends’ (joint pain after ascending too quickly from scuba diving):

A

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

160
Q

Diagnosis?

A

Arrows outlining a masson body = loose polypoid plugs of granulation tissue in terminal and respiratory bronchioles, alveolar ducts, and sacs characteristic of organizing PNA

161
Q

Describe the histologic findings

A

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

162
Q

Active smoker not yet ready to attempt quitting- what to offer?

A

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)

163
Q

Characteristic pathology findings of hard metal (cobalt) lung disease

A

Giant cell interstitial pneumonitis = multinucleated giant cells filling the interstitium

164
Q

Most common middle mediastinal masses

A

Middle mediastinum- A’s

  1. Adenopathy- malignant (lymphoma), infection
  2. aneurysm- aortic
    1. abnormality of development- bronchogenic (lower trachea or mainstem bronchi), pericardial cysts (R cardiophrenic angle)
165
Q

Most common non-AIDS defining malignancy in HIV patients

A

Lung cancer

-same histologic types as non-HIV patients but much higher rate at lower age

166
Q

Solitary fibrous tumor of the pleura

(a) Typical location/imaging finding
(b) Typical clinical presentation

A

~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

167
Q

Solitary fibrous tumor of the pleura pathologic findings

A

Solitary fibrous tumor on pathology:

  • hypocellular
  • dense collagen background with collagen bands
  • atypical spindled cells, storiform configuration
  • spindle cells
168
Q

2 rare extrathoracic symptoms of solitary fibrous tumors of the pleura

A

Solitary fibrous tumors of the pleura = mesenchymal-origin pleural-based mass

Random extrathoracic symptoms

  • Hypoglycemia
  • HPO (hypertrophic osteoarthropathy) = digital clubbing, painful arthropathy

CM Pulmonary Boards (11 decks)

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