Lung cancer Flashcards
average 5 year survival for lung cancer
15%
risk factors for lung cancer
tobacco smoking, occupational/environmental exposure (beryllium, radon, aresenic), asbestos, pulmonary fibrosis, pulmonary scarring (TB)
benign morphology of nodules
central, laminar, diffuse calcification; small <3mm, non-round shape, subpleural location
popcorn calcifications (pulmonary hamartoma)
intralesion fat (hamartoma, lipoid granuloma)
malignant morphology of nodules
large size: 0.8-3cm
irregular edge/spiculated
round shape
cavitary nodule, nodule containing cystic spaces
pulmonary nodule follow-up –NO
no follow up if small <4mm and no history of smoking; stability >2 years
pulmonary nodule follow-up
interval nodule growth
note that transient decrease may be due to collapsed alveoli or necrosis
Fleishner society: patient population
patients >35yo, no history of malignancy
high risk patients: smoker, other lung cancer risk factors
Follow up guidelines: Fleischner Society
Nodule ≤4 mm
Low-risk: No follow-up needed.
High-risk: At least one follow-up at 12 months. If unchanged, no further follow-up. Nodule >4 and ≤6 mm
Low-risk: At least one follow-up at 12 months. If unchanged, no further follow-up.
High-risk: At least two follow-ups at 6–12 months and 18–24 months if no change. Nodule >6 and ≤8 mm
Low-risk: At least two follow-ups at 6–12 months and 18–24 months if no change.
High-risk: At least three follow-ups at 3–6 months, 9–12, and 24 months if no change. Nodule >8 mm
Regardless of risk, either PET, biopsy, or at least three follow-ups at 3, 9, and 24 months.
Types of lung cancer
small cell
not small cell (adenocarcinoma, SCC)
adenocarcinoma: location, appearance, pathologic marker
most common ; related to smoking
peripheral lung
spiculated margin due to reactive fibrosis, may cavitate
TTF-1: thyroid transcription factor
squamous cell carcinoma
centrally from main/lobar/segmental bronchi > bronchial obstruction or hilar mass
lobar atelectasis, mucoid impaction, consolidation, bronchiectasis; cavitates
bronchioalveolar carcinoma
well differentiated adenocarcinoma which has lepidic growth–spread through alveolar walls
indolent, negative on PET
hillic growth
invasion and destruction of lung parenchyma
spectrum of BAC
adenomatous hyperplasia, adenocarcinoma in situ, minimally invasive adenocarcinoma, invasive mucinous adenocarcinoma, nonmucinous/adenocarcinoma predominantly invasive with some nonmucinous lepidic component
small cell carcinoma
3rd most common lung cancer cell type
strongly associated with smoking
occurs in central bronchi with invasion through bronchial wall; can cause SVC syndome»_space; disseminated disease
large cell carcinoma
smoking, poor prognosis
occurs in lung periphery as a large mass
carcinoid tumor
endobronchial mass distal to carina can cause obstructive atelectasis
diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH)
precursor lesion to typical carcinoid; multiple foci of neuroendocrin hyperplasia and bronchiolitis obliterans
pulmonary nodule vs mass
nodule <3 cm
mass >3cm
hilar mass cancer types
squamous cell and small cell carcinoma
tapered bronchus specific for lung cancer
superior sulcus tumor
lung cancer in apex
pancoast tumor
stage T3
pancoast tumor
superior sulcus tumor involving sympathetic ganglia»_space; Horner syndromer
Horner syndrome
ipsilateral ptosis, miosis, anhidrosis
lymphangitic carcinomatosis
diffuse neoplastic disease through pulmonary lymphatics
nodule interlobular thickening; asymmetric
pleural effusion in cancer
lymphatic obstruction/pleural mets
malignant effusion: M1a lesion; precludes curative resection
cytology evaluation necessary
lung cancer staging: TNM, treatment
T: tumor
N: nodules
M: mets
surgery: IIB/IIIA
unresectable: IIIB (N3 contralateral/supraclavicular nodes; T4/N2)
Stage IV not treated surgically
