Chapter 13: Lung tumors Flashcards Preview

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Flashcards in Chapter 13: Lung tumors Deck (58)
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1
Q

Carcinoma is a tumour that develops from *endothelial/epithelial* cells

A

Epithelial

2
Q

What types of tumors are most common in lung tumors?

A

95% are carcinomas (the remaining 5% span a miscellaneous group that includes carcinoids, mesenchymal malignancies, lymphomas and a few benign lesions)

3
Q

What is the most common benign lung tumour?

A

A spherical, small, discrete hematoma that often shows up as a so-called “coin lesion” on chest imaging (consisting of mature cartilage admixed with fat, fibrous tissue and blood vessels)

4
Q

Carcinoma of the lung is the *least/most* important cause of cancer-related deaths in industrialized countries

A

most

5
Q

In a ranking of incidence of cancers, at what place is lung cancer in males and females?

A

4th in place for both genders (colon (3rd), skin (2nd) and prostate/breast (1st) are above it)

6
Q

What is the 5-year survival rate

A

45%

7
Q

What are the four major histologic types of carcinomas of the lung?

A

Adenocarcinoma, squamous cell carcinoma, small cll carcinoma (a subtype of neuroendocrine carcinoma) and large cell carcinoma

8
Q

Which histologic cell types have the strongest association with smoking?

A

Squamous cell and small cell carcinomas, but there is also an association with adenocarcinoma (although it is more common in non-smokers)

9
Q

Fill in: Like other cancers, smoking-related carcinomas of the lung arise by a stepwise accumulation of driver … that result in transformation of benign progenitor cells in the lung into neoplastic cells possessing all of the hallmarks of cancer

A

mutations

10
Q

Before 2015 (when the WHO introduced a new classification), carcinomas were classified into: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). Why was that?

A

By the time SCLCs were diagnosed, virtually all have metastasized, thus chemotherapy is used. NSCLCs are more likely to be resectable and usually respons poorly to conventional chemotherapy

11
Q

Why was there a reorganization of the classification of lung tumors in 2015?

A

There are new therapies available that target specific onco-proteins that are found in subset of NSCLC (mainly adenocarcinomas). Thus, if adequate tissue is available, NSCLC is subjected to molecular analysis to determine if targeted therapy is warranted. In addition, new immunotherapy approaches are now approved for a subset and are being tested in SCLC

12
Q

The sequence of molecular changes is not random but tends to follow a sequence that parallels the histologic progression toward cancer. Explain these steps. (I don’t think you’re supposed to learn this (like 75% sure))

A

Inactivation of the putative tumor suppressor genes located on the short arm of chromosome 3 (3p) is a very common early event, whereas mutations in the TP53 tumor suppressor gene and the KRAS oncogene occur relatively late. Certain genetic changes, such as loss of chromosomal material on 3p, are found even in benign bronchial epithelium of smokers without lung cancer, suggesting that large areas of the respiratory mucosa are mutagenized by exposure to carcinogens (“field effect”). On this fertile soil, those cells that accumulate additional mutations ultimately develop into cancer.

13
Q

A subset of adenocarcinomas (about 10% in whites and 30% in Asians), particularly those arising in nonsmoking women, harbor mutations that activate the epidermal growth factor receptor (EGFR). What does this EGFR do?

A

It is a tyrosine kinase receptor that stimulates downstream pro-growth pathways involving RAS, PI3K and other signaling molecules

14
Q

With regard to carcinogenic influences, there is strong evidence that … and, to a much lesser extent, other environmental carcinogens are the main culprits responsible for the mutations that give rise to lung cancers

A

smoking (you should know this by now ;))

15
Q

Is there a linear correlation between the frequency of lung cancer and pack-years of cigarette smoking?

A

Yep (The increased risk is 60 times greater among habitual heavy smokers (two packs a day for 20 years) than among nonsmokers)

16
Q

True/false: Men are more susceptible to carcinogens in tobacco smoke than woman

A

False, woman are more susceptible than men (though for unclear reasons)

17
Q

Is is likely that the mutagenic effect of carcinogens is modified by hereditary (genetic) factors? Why?

A

Yes, very! Recall that many chemicals require metabolic activation via the P-450 monooxygenase enzyme system for conversion into ultimate carcinogens. Individuals with certain polymorphisms involving the P-450 genes have an increased capacity to activate procarcinogens found cigarette smoke, and are thus exposed to larger doses of carcinogens and incur a greater risk of developing lung cancer. Similarly, individuals whose peripheral blood lymphocytes undergo chromosomal breakages after exposure to tobacco-related carcinogens (mutagen sensitive genotype) have a greater than 10-fold increased risk for developing lung cancer over control subjects.

18
Q

The sequential changes leading development of squamous cell carcinomas are well documented; there is a linear correlation between the intensity of exposure to cigarette smoke and the appearance of ever more worrisome epithelial changes. What does this begin with and how does it progress?

A

It begins with rather innocuous basal cell hyperplasia and squamous metaplasia and progress to squamous dysplasia and carcinoma in situ, before culminating in invasive cancer

19
Q

Carcinomas of the lung begin as small lesions that are *firm/soft* and *grey-white/red-white*

A

firm and grey-white

20
Q

Where are adenocarcinomas usually located?

A

peripherically, but also may occur closer to the hilum

21
Q

Do carcinomas or adenocarcinomas grow slower?

A

Adenocarcinomas

22
Q

Which subtype is more likely to metastasize widely?

A

Adenocarcinomas (though they grow the slowest and form smaller masses)

23
Q

What variety of growth patterns can occur in adenocarcinomas?

A

Acinar (gland-forming), papillary, mucinous and solid types

24
Q

What is the putative precursor of adenocarcinoma?

A

Atypical adenomatous hyperplasia (AAH)

25
Q

Are squamous cell carcinomas more common in women or men?

A

men (and are closely related to smoking)

26
Q

What are large cell carcinomas?

A

Large cell carcinomas are undifferentiated malignant epi- thelial tumors that lack the cytologic features of neuroendocrine carcinoma and show no evidence of glandular or squamous dif- ferentiation. The cells typically have large nuclei, prominent nucle- oli, and moderate amounts of cytoplasm.

27
Q

Hoe doe small cell lung carcinomas (SCLCs) generally appear?

A

as pale gray, centrally located masses that extend into the lung parenchyma. These cancers are composed of relatively small tumor cells with a round to fusiform shape, scant cytoplasm, and finely granular chromatin with a salt and pepper appearance

28
Q

Precursor lesions of squamous cell carcinomas are shown in this figures. What are the subtypes displayed in the figures?

A
  • (A to C) Some of the earliest (and “mild”) changes in smoking-damaged respiratory epithelium include
    • goblet cell hyperplasia (A),
    • basal cell (or reserve cell) hyperplasia (B),
    • squamous metaplasia (C).
  • (D) More ominous changes include the appearance of squamous dysplasia, characterized by the presence of disordered squamous epithelium, with loss of nuclear polarity, nuclear hyperchromasia, pleomorphism, and mitotic figures.
  • (E and F) Squamous dysplasia may, in turn, progress through the stages of mild, moderate, and severe dysplasia. Carcinoma in situ (CIS) (E) is the stage that immediately precedes invasive squamous cell carcinoma (F). Apart from the lack of basement membrane disruption in CIS, the cytologic features of CIS are similar to those in frank carcinoma.
29
Q

True/false: carcinomas can already produce symptoms in the early stages

A

False, it is often only detected after symptoms because of metastasis occur (such as the brain, liver or bones)

30
Q

Overall, … (1) and … (2) carry a more favorable prognosis than … (3)

A

(1) squamous cell carcinoma, (2) adenocarcinoma and (3) SCLC

31
Q

When squamous cell carcinomas or adenocarcinomas are detected before metastasis or local spread, cure is possible by *chemotherapy/surgery*

A

Surgery (lobectomy or pneumonectomy)

32
Q

Unresectable adenocarcinomas associated with targetable mutations in tyrosine kinases such as EGFR may show remarkable responses to …

A

specific inhibitors (so no chemo/surgery!)

33
Q

Name some differences between small and non-small cell lung carcinoma

A

Don’t learn by heart, but you should be able to recognize this

34
Q

True/false: SCLCs have always already spread by the time they are detected

A

True (this is why surgery has no use)

35
Q

How is SCLC treated (chemo/surgery)

A

They respond well to chemo, but invariably recur (with treatment, only a year to live, 5% live for 10yrs)r

36
Q

Why are SCLCs likely to be immunogenic?

A

High mutation burden

37
Q

In addition to the direct effects of the tumor cells, it is estimated that 3% to 10% of patients with lung cancer develop paraneoplastic syndromes. What are some examples (I advise not to learn this)

A

(1) hypercalcemia caused by secretion of a parathyroid hormone–related peptide; (2) Cushing syndrome (from increased production of adrenocorticotropic hormone); (3) syndrome of inappropriate secretion of anti-diuretic hormone; (4) neuromuscular syndromes, including a myasthenic syndrome, peripheral neuropathy, and polymyositis; (5) clubbing of the fingers and hypertrophic pulmonary osteoarthropathy; and (6) coagulation abnormalities, including migratory thrombophlebitis, nonbacterial endocarditis, and disseminated intravascular coagulation

38
Q

What are carcinoid tumors?

A

Carcinoid tumors are malignant tumors composed of cells that contain dense-core neurosecretory granules in their cytoplasm and, rarely, may secrete hormonally active polypeptides. They are best thought of a low-grade neuroendocrine carcinomas and are subclassified as typical or atypical; both are often resectable and curable.

39
Q

Most carcinoids originate in main bronchi and grow in one of two patterns. Which two?

A

(1) an obstructing polypoid, spherical, intraluminal mass; or (2) a mucosal plaque penetrating the bronchial wall to fan out in the peribronchial tissue—the so-called collar-button lesion

40
Q

What are typical carcinoids composed of?

A

nests of uniform cells that have regular round nuclei with “salt-and-pepper” chromatin, absent or rare mitoses and little pleomorphism

41
Q

What are atypical carcinoids?

A

a higher mitotic rate and small foci of necrosis. These tumors have a higher incidence of lymph node and distant metastasis than typical carcinoids. Unlike typical carcinoids, the atypical tumors have TP53 mutations in 20% to 40% of cases

42
Q

Most carcinoid tumors manifest with signs and symptoms related to their intraluminal growth, such as?

A

cough, hemoptysis, and recurrent bronchial and pulmonary infections

43
Q

Disease of the pleura is usually *primary/secondary* (from this point onward was not discussed in the lecture, I tried to highlight the most important subjects in the book)

A

secondary, but important primary disorders are (1) primary intrapleural bacterial infections and (2) malignant mesothelioma, a primary neoplasm of the pleura.

44
Q

What is pleural effusion?

A

fluid in the pleural space

45
Q

What is transudates and exudates?

A

“Transudate” is fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system. “Exudate” is fluid buildup caused by tissue leakage due to inflammation or local cellular damage.

46
Q

Are pleural effusions transudate or exudate?

A

Can be either

47
Q

How is an effusion that is a transudate called?

A

hydrothorax

48
Q

What is the most common cause of bilateral hydrothorax?

A

Congestive heart failure

49
Q

What are the four principal causes of pleural exudate formation?

A

(1) microbial invasion through either direct extension of a pulmonary infection or blood-borne seeding (suppurative pleuritis or empyema); (2) cancer (lung carcinoma, metastatic neoplasms to the lung or pleural surface, mesothelioma); (3) pulmonary infarction; and (4) viral pleuritis

50
Q

True/false: Whatever the cause, transudates and serous exudates usually are resorbed without residual effects if the inciting cause is controlled or remits

A

True

51
Q

True/false: Fibrinous, hemorrhagic, and suppurative exudates may lead to fibrous organization, yielding adhesions or fibrous pleural thickenings that sometimes undergo calcification.

A

True

52
Q

What is pneumothorax?

A

Pneumothorax refers to presence of air or other gas in the pleural sac

53
Q

What is hemothorax?

A

Hemothorax, the collection of whole blood (in contrast with bloody effusion) in the pleural cavity, may be a complication of a ruptured intrathoracic aortic aneurysm, an event that is almost always fatal. With hemothorax, in contrast with bloody pleural effusions, the blood clots within the pleural cavity.

54
Q

What is chylothorax?

A

Chylothorax is a pleural collection of a milky lymphatic fluid containing microglobules of lipid. The total volume of fluid may not be large, but chylothorax is always significant because it implies obstruction of the major lymph ducts, usually by an intrathoracic cancer (e.g., a primary or secondary mediastinal neoplasm, such as a lymphoma).

55
Q

What is malignant mesothelioma related to?

A

Exposure to airborne asbestos

56
Q

How are ‘acute infections’ also called

A

‘common cold’

57
Q

What is nasopharyngeal carcinoma?

A

Nasopharyngeal carcinoma is a rare neoplasm that merits comment because of (1) the strong epidemiologic links to EBV and (2) the high frequency of this cancer among the Chinese, which raises the possibility of viral oncogenesis on a background of genetic susceptibility

58
Q

What types of laryngeal tumors can occur?

A

A variety of nonneoplastic, benign, and malignant neo- plasms of epithelial and mesenchymal origin may arise in the larynx, but only vocal cord nodules, papillomas, and squamous cell carcinomas are sufficiently common to merit comment

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