misc thoracic CA/tumors (meso, thymoma, chest wall, etc) Flashcards
NCCN guideline mesothelioma re-staging after induction chemo
CT chest with contrast ± PET-CT
NCCN: PET “for mediastinal assessment based on CT or other evidence of advanced disease”
NCCN guideline mgmt of residual [lung] nodule(s)/mass(es) in seminoma
with post-tx (1st-line chemo) CT C/A/P with contrast &
with αFP & β-hCG WNL
- ≤3cm ⇒ surveil
- >3cm ⇒ PET-CT (≥6w post-chemo) → bx/resxn if PET⊕ → 2nd-line chemo if ⊕viable seminoma → same mgmt cycle but this time resect if PET⊕
with progressive dz (↑ αFP & β-hCG OR nodule/mass growing)
- 2nd-line chemo
NCCN guideline mgmt of residual [lung] nodule(s)/mass(es) in non-seminomatous germ cell tumor after 1st-line chemo
with αFP & β-hCG levels:
- WNL ⇒ resect
- ↓ ⇒ resect
- ∅∆ (still ↑) ⇒ resect (UpToDate) v surveil (NCCN)
- ↑ ⇒ 2nd-line chemo (NCCN)
(normalized v decreased v stable elevated v increased)
NCCN guideline mgmt after resxn of residual [lung] nodule(s)/mass(es) in non-seminomatous germ cell tumor (after 1st-line chemo)
if resxn pathology shows:
- teratoma or necrosis ⇒ surveil
- residual GCT ⇒ more chemo
chemo = non-BEP 1st-line or 2nd-line (EP/TIP/VIP/VeIP)
NCCN Preferred Regimens
EP = Etoposide/cisplatin
TIP = Paclitaxel/ifosfamide/cisplatin
VIP = Etoposide/ifosfamide/cisplatin
VeIP = Vinblastine/ifosfamide/cisplatin
Do serum tumor markers have to normalize to consider resxn in seminoma?
YES
if not, give more chemo
Do serum tumor markers have to normalize to consider resxn in non-seminomatous germ cell tumor?
NO
Are mixed seminoma/non-seminoma germ cell tumors treated as seminoma or NSGCT?
treated as non-seminomatous germ cell tumor
NCCN guideline 1st-line systemic tx regimen for germ cell tumors (both seminoma & non-seminomatous)
- BEP (platinum-based triplet): bleomycin + etoposide + cisplatin (Platinol)
- EP: etoposide + cisplatin OR
VIP(/IEP) (platinum-based triplet): etoposide (VP16) + ifosfamide + cisplatin (Platinol)
NCCN guideline mgmt of unicentric Castleman dz
- resectable: surgery
- unresectable: rituximab ± chemo → resect
- incomplete resxn:
asx = observe v
sx = back to unresectable pathway
strongest predictor of metastatic potential of an pleuropulmonary SFT (solitary fibrous tumor)
>4 mitoses / 10 high-power fields
predictor(s) of risk of recurrence/metastasis of pleuropulmonary SFT (solitary fibrous tumor)
- high mitotic rate (SESATS: >4 mitoses / 10 HPF)
- +tumor necrosis
- T>10cm
- mets @ dx
indication(s) for adjuvant RT after resxn of pleuropulmonary SFT
NONE
if >R0: re-resect
if high-risk: surveil & re-resect
(UpToDate)
indication(s) for adjuvant systemic tx after resxn of pleuropulmonary SFT
NONE
indication(s) for neoadjuvant tx before resxn of pleuropulmonary SFT
maybe neoadj RT to aid resectability (prob not in chest)
surveillance after resxn of pleuropulmonary SFT
CT Q1Y xforever
required margin for resection of a pedunculated visceral pleura-based pleuropulmonary SFT
negative
(wedge of stalk base is adequate for small tumors)
UpToDate: “Pedunculated tumors can generally be resected with a wedge resection, but large sessile tumors and those with ipsilateral intrapleural metastases may occasionally require a lobectomy, pneumonectomy, or a chest wall or diaphragm resection to achieve negative (R0) margins.”
What proportion of pleuropulmonary SFTs occur on the parietal v visceral pleura?
1/3 parietal v 2/3 visceral
(usu pedunculated v sessile/broad-based respectively)
paraneoplastic syndromes a/w pleuropulmonary SFT
- IGF-2 secretion ⇒ refrx hypoGlc = Doege-Potter syndrome (<5%)
- clubbing + periostitis + synovial effusions = hypertrophic pulmonary osteoarthropathy (HPO) = Pierre-Marie-Bamberger syndrome
IGF-2 = insulin-like growth factor 2
[pleuropulmonary] SFT histopathology
spindle cell neoplasm
- characterized by dense collagenous background, often with hyalinized or thick collagen bands
- variably atypical spindled cells arrayed haphazardly within this stroma
in a storiform configuration or in randomly oriented fascicles characteristically referred to as “patternless pattern”
- less and more cellular areas alternate
- thin-walled, branching capillaries are always present but may not be prominent
Which are more common: bronchogenic or esophageal duplication cysts?
bronchogenic
indication(s) to resect bronchogenic or esophageal duplication cysts
infxn
ppx for cx like infxn (?)
sxs
Do bronchogenic duplication cysts typically communicate with the airway?
NO
(So if you see an air-fluid level, you should suspect infection.)
Do esophageal duplication cysts typically communicate with the GI tract?
NO
location predilection of esophageal duplication cysts
R mediastinum
common presenting sxs in bronchogenic duplication cyst
incidental
compression
infxn
common presenting sxs in esophageal duplication cyst
incidental
bleeding (2/2 ectopic gastric mucosa)
dysphagia (2/2 esophageal compression)
bx of a middle mediastinal mass shows pseudostratified columnar epithelium
esophageal duplication cyst
bx of a middle mediastinal mass shows normal respiratory epithelium
bronchogenic duplication cyst
rounded fluid or soft tissue density mass in middle mediastinum with layering milk of calcium
bronchogenic duplication cyst
Are posterior mediastinal tumors in adults usually benign or malignant?
most are BENIGN
(v most malignant e.g. neuroblastoma in <10yo)
most common etiology anterior mediastinal mass in ♀ <40yo
lymphoma
most common etiology anterior mediastinal mass in ♀ >40yo
thymoma
% of thymoma pts with MG
~50%
% of MG pts with thymoma
~15%
Do thymic cysts have solid components?
NOa
if mixed, ddx: thymoma, lymphoma, germ cell tumor
anterior mediastinal mass with mixed cystic & solid components with enhancing septae
germ cell tumor
Are internal calcs in a thymic mass a/w more or less aggressive behavior/etiology?
MORE aggressive
a/w thymic CA
thymic CA is MORE likely to have calcs than thymoma
- stippled calcs within the mass = thymic CA
- curvilear peripheral/capsular calcs = calcified thymomas
Which is more aggressive: mucoepidermoid carcinoma OR adenoid cystic carcinoma?
adenoid cystic CA = aggressive
mucoepidermoid CA = meek
ACC more likely to spread longitudinally(submucosal)/perineural/lymphatic AND more likely to invade mediastinum/outside trachea
most common 1° tracheal tumor
SCC (50-60%)
most common tracheobronchial sites of:
- SCC
- adenoid cystic CA
- mucoepidermoid CA
- SCC = distal 2/3 trachea + prox mainstem bronchi
- ACC = prox 1/3 trachea
- MEC = bronchi
posterior mediastinal mass ddx
- neurogenic tumor
- sarcoma
- SFT
- desmoid
(SESATS)
order of most common after neurogenic??? correct???
most common neurogenic tumor type
nerve sheath tumors (40-65%)
most common nerve sheath tumor type
Schwannoma
% of nerve sheath tumors that are malignant
5%
mgmt of neurogenic tumors
resxn
indication(s) for adjuvant tx for neurogenic tumors
NONE
indication(s) for RT for neurogenic tumors
NONE
(RT not effective)
frequency of neural foramen/spinal canal invasion by neurogenic tumors
10%
preop w/u for neurogenic tumors
CT scan
bx
MRI chest/spine
minimum relative tracheal luminal narrowing to cause obstructive sxs
50-74%
absolute tracheal luminal size threshold to cause exertional dyspnea as obstructive sx
8mm
absolute tracheal luminal size threshold to cause rest dyspnea as obstructive sx
5mm
tracheal tumor that most commonly causes or p/w hemoptysis
SCC
max resectable length of trachea
usu 4cm
absolute limit is 1/2 of trachea ≈ 6cm (normal trachea 11-12cm)
strongest prognostic factor for osteosarcoma OS
histologic grade
(like all sarcoma)
osteosarcoma (all malignant chest wall masses???) margins
2-4cm
incidence of delayed (several weeks postop) mesh infxn in chest wall reconstruction
10%
esp if +RT
Masaoka staging
-
I: encapsulated
“macroscopically & microscopically completely encapsulated” -
II: pericapsular (incl fat/pleura)
IIA = “microscopic transcapsular invasion”
IIB = “macroscopic invasion into surrounding fatty tissue or grossly adherent to but not through mediastinal pleura or pericardium” -
III: adjacent (mediastinal) structures
“macroscopic invasion into neighboring organs (ie, pericardium, great vessels, lung)”
IIIA = ⊖great vessels
IIIB = ⊕great vessels -
IVA: pleura/pericardium
“pleural or pericardial dissemination” (implants) -
IVB: distant mets
“lymphogenous or hematogenous metastasis”
Masaoka stage:
completely encapsulated without invasion
I
(encapsulated:
“macroscopically & microscopically completely encapsulated”)
Masaoka stage:
microscopic invasion through the capsule
IIA
(II: pericapsular (incl fat/pleura)
IIA = “microscopic transcapsular invasion”
IIB = “macroscopic invasion into surrounding fatty tissue or grossly adherent to but not through mediastinal pleura or pericardium”)
Masaoka stage:
invasion into surrounding fat
IIB
(II: pericapsular (incl fat/pleura)
IIA = “microscopic transcapsular invasion”
IIB = “macroscopic invasion into surrounding fatty tissue or grossly adherent to but not through mediastinal pleura or pericardium”)
Masaoka stage:
invasion into mediastinal pleura
IIB
(II: pericapsular (incl fat/pleura)
IIA = “microscopic transcapsular invasion”
IIB = “macroscopic invasion into surrounding fatty tissue or grossly adherent to but not through mediastinal pleura or pericardium”)
Masaoka stage:
invasion into pericardium
IIIA
(III: adjacent (mediastinal) structures
“macroscopic invasion into neighboring organs (ie, pericardium, great vessels, lung)”
IIIA = ⊖great vessels
IIIB = ⊕great vessels)
Masaoka stage:
invasion into SVC
IIIB
(III: adjacent (mediastinal) structures
“macroscopic invasion into neighboring organs (ie, pericardium, great vessels, lung)”
IIIA = ⊖great vessels
IIIB = ⊕great vessels)
Masaoka stage:
invasion into lung
IIIA
(III: adjacent (mediastinal) structures
“macroscopic invasion into neighboring organs (ie, pericardium, great vessels, lung)”
IIIA = ⊖great vessels
IIIB = ⊕great vessels)
Masaoka stage:
invasion into innominate artery
IIIA
(III: adjacent (mediastinal) structures
“macroscopic invasion into neighboring organs (ie, pericardium, great vessels, lung)”
IIIA = ⊖great vessels
IIIB = ⊕great vessels)
Masaoka stage:
invasion into Ao
IIIB
(III: adjacent (mediastinal) structures
“macroscopic invasion into neighboring organs (ie, pericardium, great vessels, lung)”
IIIA = ⊖great vessels
IIIB = ⊕great vessels)
Masaoka stage:
invasion into pulmonary pleura / pleural implants
IVA
(pleura/pericardium:
“pleural or pericardial dissemination”)
Masaoka stage:
pericardial implants
IVA
(pleura/pericardium:
“pleural or pericardial dissemination”)
Masaoka stage:
distant mets (outside pleura or pericardium)
IVB
(distant mets:
“lymphogenous or hematogenous metastasis”)
thymoma/thymic CA
cutoff criteria between I & II & III(A&B)
TNM
T-size:
T1 / T2 / T3 / T4
all N0 M0
thymoma/thymic CA
IIIA v IIIB
TNM
T3 v T4
i.e. resectable v potentially un-resectable structures
all N0 M0
basis of T-stage in thymoma/thymic CA
level of invasion
(NO SIZE critera)
thymoma/thymic CA
T1
within mediastinum:
encapsulated OR into mediastinal fat ± mediastinal pleura
thymoma/thymic CA
T1a
⊖mediastinal pleura invasion
(encapsulated OR into mediastinal fat)
thymoma/thymic CA
T1b
⊕mediastinal pleura invasion
thymoma/thymic CA
T2
⊕pericardium invasion
(either partial OR full-thickness)
thymoma/thymic CA
T3
⊕invasion of readily resectable structures:
- lung
- innominate vein
- SVC
- phrenic
- chest wall
- hilar/extrapericardial pulm vessels (PA or PV)
thymoma/thymic CA
T4
⊕invasion of potentially un-resectable structures:
- Ao (asc/arch/desc)
- arch vessels
- intrapericardial PA
- myocardium (heart)
- trachea
- esophagus
thymoma/thymic CA
N0
self-explanatory
thymoma/thymic CA
N1
anterior/perithymic LNs