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
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
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 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
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
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
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
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
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
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
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
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
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)
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
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
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
