Lung Cancer Flashcards

1
Q

What is the morbidity of lung cancer?

Including all stages and subtypes, what is the 5-year survival of lung cancer?

Smoking is thought to cause what percent of all lung cancers?

What occupational and environmental exposures are risk factors for lung cancer?

What are two other risk factors?

A
  • Lung cancer is the leading cause of cancer death in the USA.
  • Including all stages and subtypes, the 5-year survival is 15%.
  • Tobacco smoking is thought to cause 80-90% of lung cancers.
    • Almost all cases of squamous cell and small cell carcinoma are seen in smokers.
    • Adenocarcinoma is also associated with smoking, but primary bronchogenic carcinoma arising in a lifelong nonsmoker with no history of secondhand exposure is almost always adenocarcinoma.
  • Occupational and environmental exposures, including beryllium, radon, arsenic, etc., remain an important risk factor for lung cancer. Asbestos exposure increases the risk of lung cancer by a factor of five, synergistic with smoking.
  • Pulmonary fibrosis increases the risk of lung cancer by a factor of ten.
  • Pulmonary scarring, such as from prior TB, also increases the risk of lung cancer.
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2
Q

Are pulmonary nodules common?

Are they more likely to be benign or malignant? What do we do with them?

Does calcifcation portend benignity or malignancy?

Ground glass nodules are more or less likely to be malignant than a solid nodule?

A
  • Pulmonary nodules are very common and the vast majority are benign; however, nodules are often followed with serial CT scans to screen for development of lung cancer.
  • Calcified nodules are usually benign.
  • Although less commonly seen, ground glass nodules (or mixed attenuation nodules containing both solid and ground glass) are more likely to be malignant than a solid nodule.
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3
Q

What nodule morphology is essentially diangostic for a benign etiology?

A
  • Central, laminar, and diffuse calcification are almost always benign.
  • Popcorn calcification, suggestive of a pulmonary hamartoma, is benign.
  • Intra-lesional fat, suggestive of hamartoma or lipoid granuloma, is benign.
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4
Q

What nodule morphology is suggesting, but not diagnostic for, a benign etiology?

A
  • Small nodules are usually benign. A nodule <3 mm has a 0.2% chance of being cancer and a 4-7 mm nodule is malignant in 2.7% of cases.
  • Any calcification in a small nodule is usually benign.
  • Non-round shape, including oblong, polygonal, triangular, or geometric is probably benign.
  • Subpleural location is often benign.
  • Clustering of nodules suggests an infectious process.
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5
Q

What nodule morphology suggests malignancy? What is the single most important risk factor?

A
  • Large size is the single most important risk factor for malignancy, regardless of morphology: 0.8 to 3 cm nodules have 18% risk of being lung cancer and masses >3 cm have a very high chance of being malignant.
  • Irregular edge or spiculated margin is concerning.
  • Round shape (as opposed to oblong) is suggestive of malignancy.
  • A cavitary nodule or nodule containing small cystic spaces is suspicious for malignancy.
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6
Q

Follow-up of Pulmonary Nodule

In what setting is follow-up not necessary?

What increase in diameter is a doubling in volume?

Doubling time in cancers ranges?

What do you do with a nodule that hasn’t changed in size over two years?

Is a decrease in the size of a suspicious nodule sufficient to establish a benign etiology?

A
  • Follow-up is not recommended for a solitary pulmonary nodule if the nodule is small (<4 mm) and the patient doesn’t have a history of smoking or other risk factors.
  • Any interval nodule growth is suspicious. A 26% increase in diameter (for instance, from 1.0 to 1.26 cm) is a doubling in volume.
  • Doubling time for lung cancers ranges from 42 days in very aggressive tumors to over 4 years in indolent lesions such as preinvasive adenocarcinoma.
  • A nodule that has not changed in size over 2 years is very likely, but not definitely, benign. Follow-up of ground glass nodules, which are often preinvasive adenocarcinoma, may be appropriate beyond 2 years.
  • A decrease in the size of a suspicious nodule on a single follow-up study is not sufficient to establish a benign etiology. Transient decrease in size of a malignant lesion can occur with collapse of aerated alveoli or necrosis.
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7
Q

Lung Adenocarcinoma

Prevalence relative to other lung cancers? Increased risk with smoking?

Does it like to develope in a certain part of the lung?

Imaging appearance?

Can it cavitate?

What is a useful pathologic marker?

A
  • Adenocarcinoma is the most common subtype of lung cancer. It is related to smoking, but less strongly than squamous cell.
  • Adenocarcinoma tends to occur in the peripheral lung.
  • The typical radiographic appearance of adenocarcinoma is of a pulmonary nodule, which often has a spiculated margin due to reactive fibrosis.
  • Cavitation can occur but is less commonly seen compared to squamous cell.
  • A useful pathologic marker is TTF-1 (thyroid transcription factor), which is positive in primary lung adenocarcinoma and negative in pulmonary metastases from an extrathoracic adenocarcinoma.
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8
Q

What is the pathologic spectrum of adenocarcinoma?

A
  • Preinvasive AdenoCA
    • Atypical adenomatous hyperplasia (AAH) (preinvasive)
      • Preinvasive
      • GGN ≤ 0.5 cm
      • 10% grow, 1% develop into MIA or invasive adenocarcinoma
    • Adenocarcinoma in situ of lung (AIS) (≤3 cm) (malignant but preinvasive)
      • The most common subtype is non-mucinous and rarely mucinous or mixed subtypes
      • Histological pattern: no growth pattern other than lepidic and no feature of necrosis or invasion
    • Minimally invasive adenocarcinoma of the lung (MIA) ≤3 cm
      • Describes small solitary adenocarcinomas with either pure lepidic growth or predominant lepidic growth with ≤5 mm of stromal invasion

The two invasive adenocarcinomas previously termed non-mucinous and mucinous bronchoalveolar carcinoma have been renamed:

  • Invasive Adenocarcinoma
    • Lepidic-predominant adenocarcinoma describes invasive adenocarcinoma with a predominant lepidic pattern with >5 mm invasion; formerly known as non-mucinous bronchoalveolar carcinoma
      • Other types of invasive adenoCA = acinar, papillary, micropapillary, or solid predominant with mucin production.
    • Invasive mucinous adenocarcinoma is a variant of invasive adenocarcinoma; formerly known as mucinous bronchoalveolar carcinoma
      • Another variant of invasive adenoCA is colloid adenoCA.
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9
Q

Lepidic-predominant adenocarcinoma appearance?

Prognosis relative to invasive mucinous adenoCA?

A
  • Lepidic-predominant adenoCA (LPA) classically presents as a ground glass or solid nodule with air bronchograms and has a better prognosis compared to invasive mucinous adenoCA.
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10
Q

How does invasive mucinous adenocarcinoma present/appear?

Prognosis compared with LPA?

A
  • Invasive mucinous adenocarcinoma tends to present with chronic consolidation. It has a worse prognosis compared with non-mucinous BAC.
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11
Q

Pulmonary Squamous Cell CA

Prevalance relative to other lung cancers?

Where do these arise at? How may they present?

Common radiographic findings? What does SCC have a propensity to do?

A
  • Squamous cell carcinoma is slightly less common today than adenocarcinoma. Prior to filtered cigarettes, SCC was more common.
  • The majority of SCC arise centrally from main, lobar, or segmental bronchi, where the tumor tends to cause symptoms early due to bronchial obstruction. SCC may also present as a hilar mass.
  • Common radiographic findings are lobar atelectasis, mucoid impaction, consolidation, and bronchiectasis. SCC has a propensity to cavitate.
    • ​​MNEMONIC: “S’s” = Squamous, Smoker, Sentral, Syndrome (PTHtP)
      • s”Ca”umous
        • hypercalcemia
        • cavitates
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12
Q

Neuroendocrine Tumors

What are all of them? What cells do they arise from??

What are their characteristics?

  • Demographics
  • Pathology
  • Imaging Features
  • Clinical Features
A
  • Neuroendocrine tumors include high-grade tumors (small cell lung CA, large cell neuroendocrine CA), intermediate-grade = atypical carcinoid, low-grade = typical carcinoid, and preinvasive = diffuse idiopathic pulmonary neuroendocrine hyperplasia.
  • Neuroendocrine Kulchitsky cells!
  • note that LCNEC was formerly classified as a subtype of LCC.
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13
Q

Small Cell CA

Prevalence relative to other lung cancers?

Cell of origin?

Smoking association?

How do these typically present?

Treatment?

A
  • Small cell carcinoma is the third most common lung cancer cell type (after adenocarcinoma and squamous cell). Neoplastic cells are of neuroendocrine origin and are associated with various paraneoplastic syndromes.
  • Small cell carcinoma is strongly associated with smoking.
  • Small cell tends to occur in central bronchi with invasion through the bronchial wall, typically presenting as a large hilar or parahilar mass. Involvement of the SVC may cause SVC syndrome. Small cell rarely presents as a solitary pulmonary nodule.
  • Small cell is considered a disseminated disease and is generally not amenable to surgery.
    • MNEMONIC: “S’s” = Small cell, Smokers, Sentral, Syndromes (paraneoplastic like Eaton-Lambert, ADH, ACTH, and even paraneoplastic neurologic syndromes)
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14
Q

Carcinoid Tumor

Where do the neoplastic carcinoid cells originate from and where?

What is a common presentation of carcinoid tumor?

Types of carcinoid? Where do atypical carcinoids tend to arise and what is there prognosis?

What is diffuse idiopathic pulmonary neuroendocrine cell hyperplasia?

A
  • Neoplastic carcinoid cells originate from neuroendocrine cells in the bronchial walls.
  • A common presentation of carcinoid is an endobronchial mass distal to the carina, which may cause obstructive atelectasis. Up to 20% of cases present as a pulmonary nodule.
  • Carcinoid may be typical (low-grade) or the more aggressive atypical variant. Typical carcinoids without nodal or distant metastases have an excellent prognosis (92% 5-year survival). Atypical carcinoids tend to arise peripherally and have a worse prognosis.
  • Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) is an extremely uncommon precursor lesion to typical carcinoid tumor, characterized by multiple foci of neuroendocrine hyperplasia or tumorlets (carcinoid foci <5 mm in size) and bronchiolitis obliterans.
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15
Q

Large Cell CA

What are these?

Smoking association?

Prognosis?

Where do they occur in the lung?

How do they present?

A
  • Large cell carcinoma is a wastebasket pathologic diagnosis for tumors that are poorly differentiated squamous, adenocarcinoma, or neuroendocrine. Large cell carcinoma is strongly associated with smoking and has a poor prognosis.
  • Large cell carcinoma often occurs in the lung periphery, where it presents as a large mass.
    • Note that LCNEC is a new subtype under the neuroendocrine tumors and this is still a wastebasket of basically poorly differentiated versions of other things.
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16
Q

What are the radiologic presentations of lung cancer?

A
  • solitary pulmonary nodule or lung mass
  • segmental or lobar atelectasis
  • consolidation
  • hilar mass
  • superior sulcus tumor
  • lymphagitic carcinomatosis
  • pleural effusion
  • pneumothorax
17
Q

What is a noduled defined as? How about a mass?

Which lung cancer comprises about 50% of all cancers presenting as a solitary pulmonary lung nodule?

A
  • A nodule is defined as <3 cm and a mass is >3 cm.
  • Adenocarcinoma, including subtypes, comprises approximately 50% of cancers presenting as a solitary pulmonary nodule.
18
Q

Is it common to have atelectasis as a common presentation of lung cancer?

What is volume loss like in this scenario?

What is another presentation of lung cancer caused by bronchial obstruction?

What do you think is happening if two foci of atelectasis are present simultaneously that cannot be explained by a single endobronchial lesion?

A
  • Atelectasis due to bronchial obstruction is a common presentation of lung cancer.
  • Despite the presence of atelectasis, volume loss is variable, secondary to the volume displacing effects of desquamated cells, mucus, and fluid.
  • Obstructive pneumonia is a common presentation of lung cancer, caused by bronchial obstruction and parenchymal consolidation by inflammatory cells and lipid-laden macrophages.
  • If two foci of atelectasis are present simultaneously that cannot be explained by a single endobronchial lesion, a benign process is much more likely. However, CT and bronchoscopy are still needed for workup.
19
Q

Can cancer present as consolidation? What cancer can look just like a consolidation?

A
  • Consolidation that is indistinguishable from pneumonia can be seen with preinvasive adenoCA. Although AAH and pneumonia may appear similar, AAH is usually a non-resolving consolidation with (near) normal white blood cell count.
20
Q

Which cancers more commonly present as a hilar mass?

Hilar enlargement may be due to what two possibilities?

What can a tumor do to the bronchus? What is highly specific sign for cancer associated with the bronchus?

A
  • A hilar mass is a common presentation of squamous cell and small cell carcinoma.
  • Hilar enlargement may be due to a primary central tumor or nodal metastasis from a parenchymal neoplasm.
  • Tumor may compress and narrow the bronchus. A tapered bronchus is highly specific for lung cancer.
21
Q

What is a superior sulcus tumor?

What is a Pancoast tumor?

What tumor stage is a superior sulcus tumor?

A
  • A superior sulcus tumor is a lung cancer occurring in the lung apex.
  • A Pancoast tumor is a type of superior sulcus tumor with involvement of the sympathetic ganglia causing a Horner syndrome, with ipsilateral ptosis, miosis, and anhidrosis.
    • MNEMONIC: “Horny PAM - ptosis, anhydrosis, miosis, Pancoast”
  • A superior sulcus tumor is a stage T3 tumor.
22
Q

What is lymphangitic carcinomatosis?

Imaging appearance?

A
  • Lymphangitic carcinomatosis represents the diffuse spread of neoplasm through the pulmonary lymphatics, typically seen in late-stage disease.
  • On imaging, carcinomatosis manifests as nodular interlobular septal thickening, which is usually asymmetric.
23
Q

What is more common: cancer presenting as pleural effusion or pneumothorax?

How would a pleural effusion be caused by cancer?

What is a malignant effusion? What tumor stage are malignant effusions considered?

When could a cancer present as a pneumothorax?

A
  • Pleural effusions are relatively common in lung cancer and may be due to lymphatic obstruction or pleural metastases.
  • A malignant effusion is the presence of malignant cells within the effusion. A malignant effusion is an M1a lesion, which precludes curative resection. Not all effusions associated with lung cancer are malignant effusions, so cytologic evaluation is necessary.
  • Pneumothorax is not a common presentation of lung cancer but can be seen with peripheral tumors that cavitate or invade into the pleura.
24
Q

Staging of Lung Cancer

Treatment is based on what?

Primary tumor characteristics:

What is the T?

What is the N?

What is the M?

A
  • Treatment based on staging
    • For early stages up to IIB and sometimes IIIA, surgery is usually performed. Neoadjuvant or adjuvant chemotherapy and radiotherapy can be used.
    • Stage IIIB (N3 - contralateral or supraclavicular nodes; or T4/N2) is unresectable.
    • Stage IV disease is generally not treated surgically unless there is a solitary adrenal or brain metastasis.
  • T = Tumor size - look at the diagram for sizing.
  • N = Nodes - look at the first diagram for nodal staging of lung cancer.
  • M = Metastasis
    • Subsets of T, N, and M are grouped in certain stages because they share a similar prognosis - ie any mets is a stage IV.