Old SEEK Qs/Misc Flashcards
Most common antibiotic-associated cause of acute eosinophilic PNA
(a) Risk more dose-dependent or duration dependent?
Daptomycin
(a) Duration dependent, mechanism unclear (even tho obv inactivated by surfactant
Big radiographic difference between acute and chronic eosinophilic PNA
AEP- 70% have bilateral pleural effusions, while uncommon to have pleural effusions in CEP
Match the gene with the cystic lung disease
(a) FLCN
(b) BRAF
(c) TSC-2
Cystic lung diseases
(a) Folliculin mutation seen in Birt-Hogg-Dube (aut recessive triad of skin lesions, renal masses, and cystic lung disease)
(b) BRAF in PLCH (association with smokers)
(c) TSC-2 (tuberous sclerosis gene) in spontaneous LAM
Match the immunostain to the cystic lung disease
(a) HMB45
(b) CD1a
Immunostains
(a) HMB45 = muscle stain seen in LAM (myomatosis)
(b) CD1a stain in biopsy or BAL stains for PLCH
Describe the mechanism of microliths in Pulmonary Alveolar Macrolithiasis
Aut recessive disorder of mutation in phosphate transporter- can’t get phosphate out of type II pneumocytes => CaPO4 precipitates (microliths) diffusely
Different imaging findings of pulmonary alveolar macrolithiasis and metastatic pulmonary calcification
Both with diffuse nodular calcification
PAM- lower lobe predominant (aut recessive mutation in phosphate transporter) => CaPO4 precipitated microliths deposit in type II pneumocytes
Metastatic pulmonary calcification- usually in ESRD or secondary hyperparathyroidism, upper lobe predominant
Lymphoid interstitial PNA vs. follicular bronchiolitis
(a) Imaging features
(b) Histo features
Spectrum of lymphoproliferative pulmonary disease
(a) LIP with cysts and septal thickening
While FB without cysts
(b) LIP- plasma cells, lymphocytes, and histiocytes
While FB with lymphoid follicles with *germinal centers
but no plasma cells
Difference in steroid duration for acute vs. chronic eosinophilic PNA
Acute- 2-4 weeks typically with rapid response and doesn’t recur
Chronic- longer steroids with steroid and recurs if taper too soon
First line treatment systemic-sclerosis-related ILD
Typically NSIP pattern
First line treatment- MMF (mycophenolate mofetil = cellcept) over cyclophosphamde b/c MMF just as efficacious as cyclophosphamide with fever side effects
No official guidelines for when to add anti-fibrotic, but generally once MMF added if fibrosis progresses will add nintedanib
What are the current guidelines for GERD treatment in IPF
Treat everyone, even if no clinical symptoms
-possible mechanism: microaspiraation and reflux causing repeat lung injury
-abnormal manometry seen in 90% of IPF patients with over 40% not having classic heartburn symptoms
-observational data of IPF pts treated with either PPI or H2 blocker having slower decline in FVC
CXR finding that can differentiate CF from primary ciliary dyskinesia
Situs inversus = primary ciliary dyskinesia
ex: heart on R side, liver on left
Most helpful bronchoscopic finding to support dx of HP
BAL cell diff over 30% lymphocytes
lymphocytosis
2 possible reasons survival for IPF has increased from 3 to 4 years
-not using steroids which are actually contraindicated in IPF
-use of antifibrotics
Differentiate risk factors of PBML and LIP
Both benign cystic lung disease, few cysts
PBML (pulmonary benign metastatizing leiomyoma)- history of uterine leiomyoma
LIP- history of immunodeficiency or autoimmune disease (most commonly Sjogrens)
Best potentiator(s) for CF patient with F508d and G542X mutations
Anyone with a F508D (either homozygous or heterozygous) qualifies for triple therapy = elexacaftor/tezacaftor/ivacaftor
Antibodies associated with good vs. poor prognosis in myositis-assocated ILDs
Myositis-associated ILDs
-worse prognosis seen in anti-MDA5 Abs
-better prognosis (and response to immunosuppression) in anti-tRNA synthetase Abs (anti-Jo, Ro, EJ, Anti-Ha)
55M with sickle cell- recommendation for pneumococcal vaccine?
PCV13 now then PPSV23 in 8 weeks
-PCV13 (15 pending approval) way better than PPSV23, give PCV13 first
-PCV13 indicated for everyone 65 and older and pts over age 19 with another immunocompromising disease (sickle cell- functionally asplenic)
Which two candida species causing candidemia would require initial tx w/ echinocandin (over azole)
C glabrata and C paraopsilosis- start with echinocandin due to growing resistance
While C. albicans candidemia will respond to azoles
(in general for candidemia use echinocandin, caspo or mica, until have speciation or sensitivity)
<p>Differentiate 4 benign pulmonary cystic lung diseases by CT scan alone</p>
<p>Top = (pulmonary benign metastasizing leiomyoma) PBML, specifically in pt with history of uterine leiomyoma, multiple nodules of smooth muscle cells met to the lungs</p>
<p>Second = PLCH- ill-defined centrilobular micronodules that eventually cavitate, so combo of bizarre-shaped cysts and nodules</p>
<p>LAM = extremely thin walled cysts and diffuse</p>
<p>LIP = few cystic airspaces, more GGOs, centrilobular nodules</p>
<p>TBBx of patient 9 months s/p lung transplant with new nodular infiltrates on chest imaging and fatigue, dry cough, and fevers</p>
<p>"sea of blue" = all lymphocytes</p>
<p>lymphoproliferation- post transplant think PTLD = post-transplant lymphoproliferative disorder</p>
<p>-nodular infiltrates of lymphoid proliferation</p>
<p>-assocaited with EBV seroconversion</p>
<p>Lung transplant 6 months post-op p/w SOB, following on TBBx</p>
<p>Owl's eye cells inclusion of CMV-infected cells</p>
<p>30M 15-days s/p autologous stem cell transplant for Hodgkin's lymphoma with progressive SOB requiring intubation. S/p vanc/zosyn, vori treatment still worsening</p>
<p>-ANC 700, Hb 7, PLt 74k, BNP 50, T 38.3</p>
<p>(a) Dx</p>
<p>(b) Diagnostic test</p>
<p>(a) DAH- typical after stem cell transplant with dyspnea/hypoxia</p>
<p>(b) BAL fluid gets progressively bloodiel aliquots and over 20% hemosiderin laiden macrophages</p>
<p></p>
<p>Post-transplant patient, febrile</p>
<p>CMV- basophilic intranuclear inclusion body separated from nuclear membrane by a halo</p>
<p>Formula for Aa gradient</p>
<p>(a) Normal value</p>
<p>Alveolar-arteriolar graident of the partial pressure of oxygen, Aa gradient = PAO2 - PaO2</p>
<p>(a) Normal Aa gradient under 15</p>
<p>-PaO2 taken straight from ABG</p>
<p>-PAO2 calculated from alveolar gas equation:</p>
<p>PAO2 = [FiO2 x 713] - (PaCO2 / RQ)</p>
<p>Name the fungus based on the following histology</p>
<p>61F with odynophagia, cough, and fevers</p>
<p>Prominent L neck swelling and pain but no crepitus</p>
<p>CT attached</p>
<p>(a) Dx</p>
<p>(b) Tx</p>
<p>Not immunocompromised with cervicofacial involvement spreading into the mediastinum with bronchial fistula- actinomyces!</p>
<p>Cavitating PNAs- think actino (immuoncompetent, chest wall invasion/fisutalization, cervicofacial involvement) vs. nocardia (immunosuppressed, skin and CNS dissemination)</p>
<p>(a) Actinomyces</p>
<p>(b) High-dose penG</p>
<p>Differentiate oblique and horizontal fissures of the R lung</p>
<p>Horizontal = minor fissure, separates RUL from RML</p>
<p></p>
<p>Oblique = major fissure, separates RML from RLL</p>
Differentiate typical appearance of 4 tracheal inflammatory diseases
Sparing posterior wall:
-relapsing polychondritis
-TPO (tracheobronchopathia osteochondroplastica) = calcifications protruding out of anterior and lateral walls into lumen
Involving posterior membrane
-amyloid: can have calcification
-GPA- nodular or smooth thickening
Safest place for thoracentesis by landmarks
Midaxillary line- b/c intercostal artery most likely to sit in the subcostal groove towards the midaxillary line
-as move more posterior (either posterior axillary line or midscapular line) there is an increased risk that the intercostal artery does not remain in the subcostal groove and actually shifts upwards
With the following abnormality on CT chest- think of what drug side effect?
Diffuse tracheobronchial calcification 2/2 long-term warfarin therapy
-also associated with advanced age and dialysis-dependent CKD
But key is that warfarin-associated airway calcification is a thing, no pathophysiologic consequence => don’t need to stop warfarin
Incidental finding on chest imaging
(a) Most likely diagnosis
(b) Mgmt
Well-circumscribed water-attenuated cystic lesion in middle mediastinum = (a) bronchogenic cyst
(b) Mgmt- removal, not monitoring b/c high risk of enlargmenet and association with future symptoms
-specifically VATS resection (over thoracotomy) b/c shorter recovery and fewer peri-op complications
ARDSNet protocol of LTV
Improves or worsens
(a) Lung compliance
(b) Oxygenation
ARDNET
Worsens both compliance (V/P) and oxygenation, however those compromises shown to be worth it to protect lungs from VILI/barotrauma
Illness script for familial Mediterranean fever
FMF- recurrent sporadic fevers and pain due to serositis (abd, chest, joint, or skin pain) from serosal inflammation (peritonitis, pleuritis, pericarditis, arthritis, erysipelas-like erythema)
-at times of inflammation have elevated inflammatory markers, maybe see a small pericardial effusion
-at risk genetics: family from Turkey, Greece, non-Ashkenazi Jews
-not necessary but supported by +MEFV mutation
27F recurrent episodes of disabling chest pain, two occasions found to have pericardial fluid, occasional fever. Egyptian, Turkey, and Greek ancestry, +MEFV gene
(a) Dx
(b) Tx
Recurrent fever and pain from serositis in at-risk genetic profile
(a) Familial mediterranean fever
(b) Tx- colchicine
Differentiate tracheal inflammatory diseases
(a) Two that involve the posterior membrane
(b) Two that involve the posterior wall
Tracheal inflammatory disease
(a) Involve the posterior wall: amyloidosis, GPA, tracheobronchomalacia
(b) Spare the posterior membrane: relapsing polychondritis, TPO (tracheobronchopathia osteochondrolplastica)
Differentiate tracheobronchopathia osteochondroplastica from
(a) relapsying polychronditis of the trachea
(b) amyloidosis of the trachea
TPO- benign disease of submucosal osteocartilaginous (calcified) nodules projecting into the lumen of the large airways, spares the posterior membranous wall of the trachea
(a) RP- also spares posterior wall but causes diffuse thickening (not nodular protrusions) and not calcified
(b) amyloidosis- involves posterior wall, diffuse thickening, can be calcified
Diagnosis? 57F with chronic cough and occasional trace hemoptysis
Dx = tracheobronchopathia osteochondroplastica (TPO) = benign disease of submucosal osteocartilaginous nodules projecting into the lumen of the large airways
-unknown etiology
-can dx w/o biopsy if imaging findings classic
Explain mechanism by which factor V leiden mutation causes thrombophilia
Heterozygous mutation in factor V leiden- factor V becomes resistance to anti-thrombotic effects of activated protein C = APC resistance
resistance to the anticoagulant effects of activated protein C => increased thrombin generation
Hard contraindications to tPA
-prior ICH (intracranial hemorrhage)
-ischemic stroke w/in 3 months
-known malignant intracranial neoplasm or structural cerebral vascular lesion
Differentiate positive vs. negative delta-delta gap
Delta-delta = (change in anion gap) - (change in bicarbonate)
Normal delta-delta gap is +/- 0-6
If dAG more than 6 over dHCO3 = concomitant metabolic alkalosis
If dHCO3 more than 6 over dAG = concomittant nonanion (hyperchloremic) gap metabolic acidosis
Sjogren’s vs systemic sclerosis
(a) Antibodies
(b) Symptoms
Sjogrens
(a) Anti-Ro/La
(b) Exocrinopathy of salivary and lacrimal glands => dry eyes, mouth, dry skin, interstitial nephritis
Systemic sclerosis/scleroderma
(a) Anti-SCl-70
(b) Normal tissue replaced by thick/dense connective tissue => sclerodactyly, Raynaud’s, telangiectasias, calcinosis, esophageal dysfunction
Tx of active tuberculosis (pan-sensitive, HIV negative) during pregnancy
Active Tb during pregnancy- need to treat
IRE are considered safe, PZA lacks data so is avoided
IRE x2 months, then IR x7 months for total 9 months
Tx of LTBI in pregnancy
(a) Who to treat
(b) First line tx
LTBI in pregnancy
(a) Generally can wait until 3 months post-partum, but if high risk of conversion (exposure to active or HIV with CD4 under 350) then same tx as non-pregnant
(b) Rifampin 10 mg/kg x4 mo
Diagnostic criteria for chylothorax
Chylothorax = presence of chyle in the pleural space
Detection of chylomicrons OR
TG over 110
Purpose of esophageal pressure manometry
(a) What would increase esophageal pressure
Esophageal pressure manometry tells you pressure contribution from the chest wall/abdomen (aka not from the parenchyma/airways)
(a) Elevated in obesity, ascites
Pt has aspiration event- Pplat increases, what happens to esophageal manometry pressure?
Esophageal manometry pressure (correlates to chest wall compliance) unchanged by aspiration event
55F from Japan p/w dyspnea x2 years. H/o recurrent sinusitis. PFTs w/ obstruction and wheezing not improved with ICS/LABA.
VATS with thickening of respiratory bronchioles and foamy macrophages in airway walls
(a) Dx?
(b) Tx
(a) Diffuse panbronchiolitis = rare entity of constrictive bronchiolitis in Japanese patients, thickening of respiratory bronchioles => obstructive defect and strong association with sinusitis/upper airway (so includes both upper and lower airway)
(b) Tx = macrolide abx for antiinflammatory properties (regardless of culture)
Illness script for diffuse panbronchiolitis
(a) First line tx
Diffuse panbronchiolitis- higher incidence in Japanese, upper and lower airway features (recurrent sinusitis, wheezing). Imaging with centrilobular nodules/tree-in-bud due to impaction/inflammation and bronchiole level
PFTs with obstructive defect
(a) Macrolide abx for antiinflammatory properties regardless of culture data
How does orgaphophosphate poisoning become fatal?
- Typically from respiratory failure from combo of CNS respiratory center depression + nicotinic receptor mediated diaphragmatic weakness, bronchospasm, copious secretions
-low threshold for intubation
- Cardiac- bradycardia, heart block, hypotension
Organophosphate poisoning
(a) Mechanism of action
(b) Sources of exposure
(a) Organophosphate binds and inhibits acetylcholinesterase (AChE) which breaks down ACh –> acetic acid
-so when AChE inhibited, too much ACh around
= sarin gas (nerve gas)
(b) Agricultural pesticides/ insecticides, roach and ant sprays
Mnemonic for cholinergic excess
Cholinergic excess (ex: organophosphate poisoning, overdose of anticholinesterase pyridostigmine)
DUMBELS
Defecation
Urination
Miosis (pinpoint pupils, think rest/digest not fight/flight)
B- bronchorrhea
Clinical features of organophosphate poisoning
Cholinergic excess- DUMBELS
Defecation
Urination
Miosis (pinpoint pupils)
Bronchorrhea, bronchospasm, bradycardia
Emesis
Lacrimation
Salivation
First line treatment for organophosphate poisoning
(a) Second agent
- Atropine = cholinergic receptor antagonist
titrate dose to secretions/bronchospasm - pralidoxime = reactivates AChE that has been inactivated by phosphorylation due to exposure to organophosphate pesticides and cholinesterase-inhibiting nerve agents (sarin gas)
2 clinical indications for pralidoxime (AChE reactivator)
Reactivates acetylcholinesterase enzyme that was inactivated by
- phosphorylation due to organophosphate (pesticide) poisoning or sarin gas
- overdose of anticholinesterase medications (neostigmine/pyridostigmine) used to treat myasthenia gravis
Differentiate clinical features of toxidrome with inhaled chlorine vs. inhaled phosgene
Inhaled chlorine = immediate/rapid onset respiratory distress with eye, nose, throat irritation
-high water solubility => affect upper airway and rapid onset pulm edema
vs.
Phosgene = more lipid-soluble => delayed pulmonary symptoms (12-24 hrs later)
ex: acute respiratory failure 24h after exposure to unknown chemical agent at agricultural pesticide factory
52M with asthma, recurrent sinusitis, nasal polyposis, and dysphonia/wheezing to prior aspirin use
(a) Dx
(b) First line tx for mild disease
(c) Tx for refractory disease
(a) Aspirin-exacerbated respiratory disease
(b) First line- avoid ASA/NSAIDs, montelukast (leukotriene inhibitor)
Second line- ASA desensitization, dupilumab (IL-4Ra blocker)
Aspirin exacerbated respiratory disease
(a) First line management of mild disease
(b) 2 options for refractory disease
Triad- aspirin sensitivity, asthma, nasal polyposis/sinusitis
(a) First line- avoid ASA/NSAID compounds, leukotriene inhibitors (montelukast)
(b) Refractory disease
-ASA desensitization then daily ASA
-Dupilumab = anti-IL4Ra MAb
59F with slowly enlarging solitary pulmonary nodule x 3 yrs
H/o Cushing syndrome
(a) Dx
(b) Mgmt
(a) Pulmonary carcinoid
-slow growing
-h/o carcinoid b/c tumor producing ACTH
(b) Surgical resection with lymph node dissection
Yield of navigational bronchoscopy for nodules under 2cm
~50% even if proximal
Tracheobronchial tumors
(a) Most common benign
(b) Most common malignant
Tracheobronchial tumors
(a) MC benign = hamartoma
(b) MC malignant = squamous cell
-carcinoid of course but not most common (b/c not as prevalent as squamous cell)
Are tracheobronchial tumors more likely to be benign or malignant?
90% tracheobronchial tumors are malignant
squamous cell, carcinoid, adenoid cystic carcinoma
Utility of delayed thallium/gallium scintigraphy in AIDs patients
AIDs patients- can use delayed thallium/gallium scintigraphy to differentiate AIDs pulmonary complications
-mainly to differentiate Kaposi’s sarcoma, lymphoma, and opportunistic infection
Ex: sequential thallium and gallium scintigraphy showing abnormal delayed thallium uptake and absence of gallium uptake = highly specific for pulmonary KS but sensitivity reduced in s/o opportunistic infections
28M with AIDs p/w DOE
-CT A/P with extensive lymphadenopathy and hypoattenuating liver lesions
-sequential thallium and gallium scintigraphy: abnormal delayed thallium uptake and absence of gallium uptake
Dx?
Sequential thallium and gallium scintigraphy can be used in AIDS-associated pulmonary complications to differentiate pulmonary KS, lymphoma, and opportunistic infections
+thallium and -gallium highly specific for
(a) Pulmonary KS
Differentiate stage IVA from IVB NSCLC
Stage IVA = M1A and M1B
M1A = pleural or pericardial lesion, separate tumor in contralateral lung
M1B = single extrathoracic met
vs. Stage IVB = M1C = multiple distal/extrathoracic mets
Differentiate M1a, b, c
(degrees of metastatic disease in NSCLC)
Mets
M1a = lesion in contralateral lung, pleural or pericardial lesion
M1b = single extrathoracic met
M1c = multiple extrathoracic met
M1a and M1b = stage IVA
M1c = stage IVB
Most common paraneoplastic presentation of 65M with this chest imaging
Anterior mediastinal mass, most likely thymoma
Most common paraneoplastic syndrome seen in thymoma = myasthenia gravis
Thymoma
(a) Most common paraneoplastic syndrome overall
(b) Most common hematologic paraneoplastic syndrome
(c) Good syndrome
Thymoma
(a) Most common overall- myasthenia gravis, seen in up to 50% of thymomas
(b) Most common hematologic paraneoplastic = pure red cell aplasia
(c) Good syndrome = thymoma + acquired hypogammaglobulinemia (immunodeficiency)
Differentiate Lung-RADS category 2 and 3
ACR (American College of Radiology) developed lung-RADS to standardize reporting and management of screening-detected pulmonary nodules
Category 1- no nodules
Cat 2- largest nodule under 6mm, less than 1% risk (very low risk) of malignancy
Cat 3- largest solid nodule 6-8mm, 1-2% (low risk) of malignancy
Cat 4- largest nodule has at least moderate (over 5%) risk of malignancy
Purpose of American College of Radiology’s Lung-RADS system?
Standardized way of reporting and managing screening-detected nodules and reduce unnecessary additional imaging
Differentiate lung-RADS category 1 and 2
ACR (American College of Radiology) developed lung-RADS to standardize reporting and management of screening-detected pulmonary nodules
Category 1- no nodules
Cat 2- largest nodule under 6mm, less than 1% risk (very low risk) of malignancy
Cat 3- largest solid nodule 6-8mm, 1-2% (low risk) of malignancy
Cat 4- largest nodule has at least moderate (over 5%) risk of malignancy
Differentiate lung-RADS category 3 and 4
ACR (American College of Radiology) developed lung-RADS to standardize reporting and management of screening-detected pulmonary nodules
Category 1- no nodules
Cat 2- largest nodule under 6mm, less than 1% risk (very low risk) of malignancy
Cat 3- largest solid nodule 6-8mm, 1-2% (low risk) of malignancy
Cat 4- largest nodule has at least moderate (over 5%) risk of malignancy
Cat 4A- 5-15% malignancy
Cat 4B- over 15% malignancy
Differentiate lung-RADS category 4A and 4B
Category 1- no nodules
Cat 2- largest nodule under 6mm, less than 1% risk (very low risk) of malignancy
Cat 3- largest solid nodule 6-8mm, 1-2% (low risk) of malignancy
Cat 4- largest nodule has at least moderate (over 5%) risk of malignancy
Cat 4A- 5-15% malignancy
- solid nodule 8-15mm
Cat 4B- over 15% malignancy
- solid nodule over 15mm
Recommended management for lung nodules lung-RADS categories 3 and 4
Cat 1- no nodules
Cat 2- nodule under 6mm
Category 3 = solid nodule 6-8mm, mgmt = 6 month LDCT
-or part solid with total diameter over 6mm but solid component under 6mm
Category 4 = solid nodule 8mm or above
-or part solid 6mm or above with solid component 6mm or above, mgmt- 3 month LDCT vs. PET/CT (if solid component 8mm or above) or sampling
Recommended management for lung nodules lung-RADS categories 1 and 2
Management based on lung-RADS
Category 1- no nodules, continue w/ annual screening
Cat 2- largest nodule under 6mm (solid or ground glass), continue with annual screening
60F lung CA screening revealed category 4B lung nodule PET avid with L adrenal gland uptake (no other uptake).
-adrenal biopsy with adenoCA of lung, no mets on brain MRI or other on PET
Next step?
Currently T1bN0M1b = stage IVA
-tempting to say chemo and immunotherapy BUT would first stage the mediastinum b/c if negative can try curative intent resection (for single met to brain or adrenal)
So next best step = invasive staging of mediastinum
-if negative: can do surgical resection of lung nodule and single met then adjuvant chemo
-if positive: chemo and immunotherapy based on molecular markers
Compare LDCT radiation dose to
(a) Diagnostic CT chest
(b) Standard AP/lateral CXR
Low-dose CT delivers about
(a) 1/5th (20%) radiation dose of diagnostic CT chest
(b) 10x dose of standard AP/lateral CXR
Suspecting malignant mesothelioma given imaging- initial thora with rare atypical cells on cytology.
Next best diagnostic step- repeat thora vs. VATS biopsy
VATS biopsy of pleura
-pleural fluid analysis from thora is not sensitive for dx of mesothelioma. malignant cells difficult to differentiate adenoCA from mesothelioma => definitive diagnosis almost always requires surgical biopsy of the pleura
Median survival of malignant mesothelioma
(a) Two prognostic indicators
6-18 months (yikes)
(a) Histology and stage correlate with prognosis
3 distinct histological patterns
-epitheliod = best prognosis
-biphasic
-sarcomatoid = worst prognosis
Stage:
I/II: local invasion to lung parenchyma
III: N2
IV: N3 or distant mets
Pre-op FEV1 2.12L (80% pred) and pre-op DLCO 15.7 (70%) predicted
Quantitative perfusion imaging shows 49% perfusion to R lung
Plan for R pneumonectomy
Calculated predicted-postop FEV1 and DLCO
.51 x 80% predicted = ppoFEV1 40%
.51 x 70% predicted = ppoDLCO 35%
Since both are above 30% don’t need to go straight to CPET, but since at least one is below 60% would do more testing = stair climb (cutoff 22m) or shuttle walk (cutoff 400m)
PpoFEV1 40% and ppoDLCO 35%
low, medium, or high risk of pulmonary complications of planned procedure?
Can’t tell- need more testing if ppoFEV1 or ppoDLCO are between 30-60% predicted
-if both are above 60% predicted: low risk
-if one is below 30%, do CPET
-if both are above 30% but one is below 60%- stair climb or shuttle walk
Pt with ppoFEV1 50%, ppDLCO 50% so do more testing- cutoff for stair climb and shuttle walk to be considered low risk
Stair climb over 22m OR
shuttle walk over 400m
= low risk
67F smoker on screening CT chest:
-1.5cm RUL PET-avid, transthoracic needle showed lung adenoCA
-second smaller nodule in RLL, wedge resection also showed adenoCA
-LN path all negative
-No distant spread on PET
Stage the CA?
Can’t stage without molecular and histologic characterization of the adenoCAs to see if they’re the same or two separate primaries
-tumors in this question were different histologic subtypes => managed as two separate primaries
If they were the same histo/staining- T4 b/c separate lobes
Same tumor histology/stains but two different nodules, what are the stage if second nodule is in
(a) same lobe
(b) separate lobe of ipsilateral lung
(c) contralateral lung
Two nodules with same driver mutations/histo (so don’t treat them as two separate lesions)
(a) Same lobe = T3
(b) Different lobe but ipsilateral lung = T4
(c) Contralateral lung = M1a
41M asymptomatic, abnormal CT chest, moderate FDG avidity, no B-symptoms and infectious workup negative
Attached- histology from lung resection after nondiagnostic EBUS and CT-guided biopsy
Dx?
Dx = unicentric Castleman’s: typically mediastinal or hilar rounded solitary mass in asymptomatic patients
-Expect lymphoma or squamous cell to be way more FDG avid
-histology with lymph follicles, concentric whorls of mantle lymphocytes giving ‘onion skin’ pattern
Recommended management for lung nodules lung-RADS categories 3 and 4
Cat 1- no nodules
Cat 2- nodule under 6mm
Category 3 = solid nodule 6-8mm, mgmt = 6 month LDCT
-or part solid with total diameter over 6mm but solid component under 6mm
Category 4 = solid nodule 8mm or above
-or part solid 6mm or above with solid component 6mm or above, mgmt- 3 month LDCT vs. PET/CT (if solid component 8mm or above) or sampling
Pt with severe asthma currently controlled on omalizumab wants to get pregnant- what to do with drug?
Continue omazliumab- anti-IgE MAb, safe in pregnancy, also much better than having uncontrolled asthma
-less robust evidence for newer asthma MAbs (omalizumab is the oldest => has the most data)
Diagnostic criteria for spontaneous bacterial empyema
(a) Most common bugs
SBE in cirrhotics with preexisting pleural effusion (hepatic hydrothorax) that gets infected
-pleural fluid neutrophils over 500 OR neutrophils over 250 with positive fluid culture
(a) Typically gram negative- E. coli and klebs
Reduces mortality after admission for COPD
After COPD admission
-initiation of pulmonary rehab within 90 days of discharge reduces mortality and readmission
-nocturnal noninvasive ventilation reduces hospital readmission and mortality only in hypercapnics
While roflumilast reduces readmission but not mortality
PTLD treatment
PTLD
1. Reduce immunosuppression
2. Rituximab
3. CHOP (chemo)
Which pts are good candidates for hypoglossal nerve stimulation?
Hypoglossal nerve stimulation for OSA treatment in pts with BMI under 32 with moderate-severe OSA with AP narrowing of the upper airway during sleep (pts with concentric narrowing do not respond)
Indications for inhaled treprostinil
- Group I PAH with NYHA class III symptoms to improve exercise ability
- PAH with ILD (not COPD!, not all group 3)
MSSA bacteremia treatment- cefazolin vs. dicloxacillin
MSSA bacteremia first line = nafcillin or cefazolin (keflex non-inferior)
Dicloxacillin is a good anti-MSSA agent but is only oral => not ideal for bacteremia
SV = (LVOT CSA) x (LVOT VTI)
CSA = cross sectional area = pie x r^2
So SV = (2.96) x (6.5) = 19.5 cc of stroke voume
45F with dyspnea and cough x4 months after viral URI
Dx?
Bronchial atresia
-congenital anomaly of focal obliteration of a segment (most commonly LUL apicoposterior) typically c/b mucoid impaction and air trapping distal to the lesion
ST elevation in which EKG leads correlate with blockage of which coronary?
Hypokinesis of which LV segments correlate with blockage of
RCA
LAD
LCx
Aside from squamous cell, what other pulmonary malignancy (hint: pleural based) is associated with hypertrophic osteoarthropathy
Solitary fibrous tumors- 5% of pleura-based tumors
-associated with HPO
-smooth bordered, pleural based, can be benign or malignant, typically easy to resect (separate from pleura)
Mechanism of humoral hypercalcemia of malignancy
(a) Which malignancy
PTHrP by
(a) Squamous cell carcinoma
What is the following histology of a lung biopsy showing?
(a) Associated diagnosis
Masson body = rounded ball of myxomatous (bluish) connective tissue loosely packed, forming intraluminal polyps within bronchioles and air spaces
(a) Organizing PNA
What history is associated with pulmonary benign metastasizing leiomyoma?
H/o uterine fibroids (leiomyoma)
Cephalosporines
(a) 1st generation not keflex (cefalexin)
(b) 3rd generation not ceftriaxone or cefpodoxime
(a) Cefazolin = 1st generation
(b) Ceftazidime = 3rd generation
Cefoxitin and cefuroxime = 2nd generation
2 things to improve CPAP compliance
- Eszopiclone (lunesta)
- heated (not cooled) humidification
Education, CBT
How does higher altitude impact DLCO?
ex] DLCO measured at Aspen is slightly reduced from when measured in LA- more concerned or less concerned?
Higher altitude will falsely elevate DLCO
Lower PaO2 => less O2 available to compete for CO at Hb binding sites => 0.5% elevation in DLCO for every 100m up elevation
Be more concerned by a small drop in DLCO at elevation b/c likely falsely elevated from true value
GPA initially treated with PLEX, methylpred, and cyclophosphamide- what is first line for maintenance?
Azathioprine
-superior to MMF for maintenance therapy for GPA
-noninferior to cyclophosphamide and cyclophos has much higher side effect effects (increase risk of secondary malignancy)
What is the FEV1 cutoff for a positive mannitol inhalation challenge?
15%
Mannitol = indirect stimulus, causes bronchoconstriction by increasing airway osmolarity => mast cell activation
-indirect stimulus test is positive if FEV1 drops by 15% or more
vs. direct stimulus (methacholine) requires 20% drop
Hantavirus
(a) Typical respiratory presentation
(b) Hematologic abnormalities
Hantavirus from wild rodents
(a) Rapid progressive viral PNA
(b) Hematologic- thrombocytopenia, presence of immunoblasts on CBC diff
What does an increase in prevalence do to
(a) PPV
(b) NPV
When disease more common in a population (increased prevalence):
(a) PPV increases (more likely true positive than false positive)
(b) NPV decreases
What does a decrease in prevalence do to the following attributes of a test
(a) PPV
(b) NPV
Decrease in prevalence
(a) Reduces PPV
(b) Improves (increases) NPV b/c less likely false negative
Following tumor markers correlate to what cancer
(a) CK20
(b) Napsin-A
(c) TTF-1
(d) Calretinin, WT-1
(a) CK20 = colon adenoCA
(b) Napsin-A = lung adenoCA
(c) TTF-1 = lung adenoCA
(d) Calretin, WT-1 = mesothelioma (differentiate mesothelioma from lung adenoCA)
LTOT- how many hours per day recommended?
At least 15 hrs per day (understanding 24hr likely not plausible)
Preferred management for recurrence of primary spontaneous PTX- chemical pleurodesis through chest tube of medical thoracoscopic pleurodesis (VATS)
VATS preferred over chemical pleurodesis (talc through chest tube) b/c lower rate of recurrence
Meds known to worsen or unmask myasthenia gravis
Antibiotics- aminoglycosides (amikacin), macrolides (azithro), and floroquinolones (ex: cipro)
also beta-blockers and magnesium
Pt in myasthenia crisis requiring NIV- why not increase home dose of pyridostigmine?
Pyridostigmine (anticholinesterase medication to reduce ACh breakdown)- hold during fulminant respiratory failure to reduce cholinergic features of increased salivation and respiratory secretions
-so just keep baseline dose or can downtitrate to secretions
Mechanism of icatibant for acute episodes of hereditary angioedema
Icatibant = bradykinin receptor antagonist (blocker)
-mechanism of vascular permeability in hereditary angioedema is excess bradykinin (causing potent vasodilation) due to dysfunctional or deficient C1 esterase
-excess bradykinin => excessive mucocutaneous swelling (swollen lips, face) and GI tract (severe abdominal pain)
Typical clinical features of hereditary angioedema
(a) Feared complication
Hereditary angioedema- increased vascular permeability due to excess bradykinin => episodic cutaneous angioedema (w/o hives) and severe abdominal pain
(a) Airway compromise- not in most events but since pts have so many events over lifespan it happens
Pathogenesis of angioedema in hereditary angioedema
Excess bradykinin (potent vasodilator) due to either deficiency or dysfunction of C1 inhibitor
-so low C1 esterase => excessive bradykinin
Describe mechanism of quant gold test (what does it detect?)
Quant gold measures a delayed hypersentivitiy (type IV) reaction
-measures ex-vivo release of IFN-gamma as blood is exposed to MTb-specific antigen
Pulmonary AVM
(a) Most common cause
(b) Size cutoff for embolization
Pulmonary AVMs
(a) 95% in pts with HHT (Hereditary hemorrhagic telangiectasia)
(b) If feeding artery bigger than 2-3mm, embolization preferred to observation
Most common clinical features of pulmonary AVMs
Pulmonary AVMs clinically:
-signs of shunted circulation = stroke (CVA) and cerebral/brain abscess
-dyspnea, platypnea/orthodeoxia
-uncommon but possible = hemothorax, hemoptysis
Best line landmark for thoracentesis and why
Midaxillary line
-as move posterior the posterior intercostal artery has more variable course (doesn’t as reliably sit below rib in costal groove)
What are the borders for the triangle of safety for thoracentesis
Superiorly- base of the axilla
Anteriorly- pectoralis major
posteriorly- latissimus dorsi
inferiorly- 5th intercostal space
What other clinical features are seen in the disease that is the most common cause of pulmonary AVMs?
95% of pujlmonary AVMs in patients with HHT (hereditary hemorrhagic telangiectasia)
other features of HHT = mucocutaneous telangiectasias (mouth, tongue), epistaxis, GI bleed
Pt with cerebral abscess found to have oral telangiectasias- suspect what dx?
HHT- heredtiary hemorrhagic telangiectasia
-mucocutaneous telangiectasias (mouth, lips)
-pulmonary AVMs = shunt = elevated risk for stroke and cerebral abscess
Why do pts with HHT require abx prior to surgery/nonsterile procedures?
And to be very careful of any air in venous lines, because shunt from venous to arterial circulation so risk of stroke and cerebral abscess
Differentiate two bug-borne infectious that cause hemolytic anemia
- Babesiosis- from tick
- Malaria- from mosquito
Differentiate treatment of babesiosis and malaria
First line tx for babesiosis (from tick bite, Maltese cross on peripheral smear) = atovaquone + azithro
Maltese cross buzzword
Peripheral smear finding of babesiosis (from tick)
-not malaria from mosquito
Buzzword for path finding of hard metal lung disease
Hard metal lung disease = dust of cobalt, tungsten
Giant cell interstitial pneumonitis = alveolar macrophages and multinucleated giant cells in alveolar spaces
Benefit of baloxavir over oseltamivir
Two antivirals- different mechanisms
Baloxavir benefit- reduces viral load within one day of initiation
-same time to reduction in symptoms, but not used as much b/c emergency of nucleic acid substitutions conferring resistance
Name two tracheal inflammatory diseases that
(a) Involve the posterior membrane
(b) Spare the posterior tracheal membrane
Tracheal inflammatory diseases
(a) Involving posterior membrane:
-amyloid
-GPA
(b) Spares posterior membrane
-TPO = tracheobronchopathia osteochondroplastica
-relapsing polychondritis
Differentiate the two tracheal inflammatory diseases that spare the posterior membrane
Spares posterior membrane
-TPO = tracheobronchopathia osteochondroplastica = calcified nodules protruding into the airway
-relapsing polychondritis = diffuse smooth thickening
First line tx for GBS (guillain-barre)
GBS first line tx = PLEX or IVIG
-get rid of the antibodies attacking myelinated peripheral nerves, mechanism is molecular mimicry of immune response to antecedent event (typically infection)
Use steroids in GBS or MG?
Steroids are not first line for either GBS or myasthenia crisis, first line = PLEX or IVIG (either, whatever is available)
-steroids NOT recommended in GBS at all
-can use steroids for maintenance in MG
Mechanism of peripheral nerve destruction in GBS
GBS mechanism- molecular mimicry- immune response to a preceding event (infection typically) cross-reacts with a share epitope on myelinated peripheral nerves
Describe the mechanism of bronchiectasis in Mounier-Kuhn syndrome
Mounier-Kuhn syndrome = tracheobronchomegaly, defined as trachea diameter over 3cm
-poor airway clearance due to dilation => chronic infection and bronchiectasis
-also can get impaction in airway diverticulum
