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The Respiratory System > The Pathology of Lung Cancer > Flashcards

The Pathology of Lung Cancer Flashcards

1
Q

What is the prognosis of lung cancer

A

Very poor - the prognosis for lung cancer is a lot poorer than for other common cancers.

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2
Q

When does lung cancer tend to present

A

Very late in the progression of the disease.

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3
Q

Which age group tends to present with lung cancer

A

The elderly - those in their 70s to 80s who have comorbidities although it is still common in younger people.

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4
Q

What is the main cause of lung cancer

A

Smoking - around 95% of lung cancer is attributable to smoking.

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5
Q

Other than smoking, what else can cause lung cancer

A
  • Occupational exposures including uranium mining and asbestos exposure
  • Environmental exposures including radon gas
  • Genetic conditions such as Li-Fraumeni Syndrome where there is a mutated p53 gene.
  • Possible viral infection
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6
Q

What kind of change does lung cancer bring about - obstructive or restrictive

A

Lung cancer causes an obstructive change.

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7
Q

What are the four types of lung cancer

A
  • Squamous carcinoma
  • Adenocarcinoma
  • Small cell carcinoma
  • Others - carcinoid tumours
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8
Q

Which type of lung cancer is most common

A

Adenocarcinoma. This is 40-50% and increasing.

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9
Q

What used to be the most common type of lung cancer

A

Squamous carcinoma. This is 30-40% and decreasing.

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10
Q

What is the origin of squamous carcinoma

A

Squamous carcinoma has an epithelial origin.

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11
Q

What kind of differentiation is shown in a squamous carcinoma

A

Although the origin of squamous carcinoma is epithelial, it shows squamous differentiation.

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12
Q

What is produced by squamous cell carcinomas

A

Keratin or “prickles”.

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13
Q

What growth pattern is shown by adenocarcinoma

A

A glandular growth pattern.

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14
Q

What is produced by adenocarcinomas

A

Mucus.

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15
Q

What kind of growth pattern is shown by a small cell carcinoma

A

Small cell carcinomas are very poorly differentiated carcinomas.

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16
Q

What kind of differentiation is there variable evidence of in small cell carcinoma

A

Neuroendocrine differentiation.

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17
Q

What is the issue with approaching treatment of small cell carcinomas compared to adenocarcinomas and small cell carcinomas

A

Surgery cannot be performed for small cell carcinomas.

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18
Q

In what age groups are carcinoid tumours of the lung seen

A

Most frequently in younger people.

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19
Q

What secondary condition often occurs as a result of carcinoid tumours

A

Pneumonia that does not improve with antibiotics.

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20
Q

What are the two types of carcinoid tumour

A

Typical and atypical carcinoid tumours.

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21
Q

What are the features of typical carcinoid tumours

A
  • There are less than 2 mitoses per 2mm squared
  • No necrosis
  • Very unlikely to return after surgery
  • There is less nodal involvement than atypical carcinoid tumours
  • Much better 5 and 10 year survival than atypical carcinoid tumours.
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22
Q

What are the features of atypical carcinoid tumours

A
  • More than 2 but less than 10 mitoses per 2mm squared.
  • More mitotic activity than typical carcinoid tumours.
  • Focal necrosis
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23
Q

When is a carcinoid tumour classified as a large cell neuroendocrine carcinoma (LCNEC)

A

When there are more than 10 mitoses per 2mm squared with usually extensive necrosis.

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24
Q

What is required for the development of a malignant tumour

A

This is a multi-step genetic process requiring the accumulation of many mutated genes.

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25
Q

What are oncogenes

A

Mutated genes encoding growth promoting proteins. These are overexpressed in neoplasia.

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26
Q

What are two examples of oncogenes

A

K-ras and cyclinD1.

27
Q

What are oncosuppressor genes

A

Mutated genes encoding growth-inhibitory proteins. Decreased expression can result in neoplasia.

28
Q

What is an example of an oncosuppressor gene

A

The retinoblastoma gene (Rb).

29
Q

What is the expression of oncosuppressor genes like in tumours

A

Oncosuppressor genes are inhibited in tumours.

30
Q

Other than oncogenes and oncosuppressor genes, what else can be mutated in tumour formation

A
  • Genes regulating apoptosis may be mutates, for example p53

- Genes regulating DNA repair may also be mutated.

31
Q

What do agents such as radiation and chemicals from cigarette smoke do when they come into contact with normal cells

A

If certain agents come into contact with normal cells this damages the DNA. DNA can be repaired unless there are inherited mutations in genes which affect DNA repair. This leads to mutations in the genome of somatic cells.

32
Q

What is the result of the accumulation of oncogenes, decreased apoptosis and mutated oncosuppressor genes

A

Clonal expansion, additional mutations, heterogeneity and finally malignant neoplasm.

33
Q

What is the process of parthenogenesis of squamous carcinoma

A

Squamous cells are not normally found in the lungs. There is squamous metaplasia in response to irritation from cigarette smoke. There is then squamous dysplasia leading to squamous carcinoma in situ and invasive squamous carcinoma.

34
Q

At what stage of squamous cell carcinoma is the pathogenesis reversible

A

Squamous metaplasia is reversible.

35
Q

What are the stages of pathogenesis of andenocarcinomas

A

1) Normal alveolar walls
2) Atypical adenomatous hyperplasia
3) Adenocarcinoma in-situ
4) Invasive adenocarcinoma

36
Q

What differences can be seen in the lungs in someone with adenocarcinoma

A

In adenocarcinoma the walls of the alveoli become thicker (hyperplasia) and columnar cells fill the air spaces of alveoli.

37
Q

What are some symptoms and sign of lung cancer

A
  • Cough
  • Dyspnoea
  • Haemoptysis
  • Weight loss
  • Chest/shoulder pain
  • Hoarseness
  • Fatigue
  • Slow to clear pneumonia
  • Finger clubbing
  • Liver, brain, bone metastases.
  • Pleural effusion
38
Q

What are the initial investigations that would be carried out for lung cancer

A
  • Radiology - X-ray and CT scan

- Blood tests - high calcium, abnormal liver function, low sodium,

39
Q

What two methods are used to try and deduce the type of lung cancer present

A
  • A tissue biopsy of the lung site and of any distant metastases
  • Cytology (looking at individual cells)
40
Q

How is cytology carried out

A
  • Bronchial brushings and washings
  • Sputum samples
  • Pleural fluid aspiration
  • Fine needle aspirates of metastases.
41
Q

Which type of cancer are we best at classifying from investigations

A

Small cell carcinoma - there is 90% accuracy.

42
Q

How do you differentiate between squamous cell carcinoma and adenocarcinoma

A

In squamous cell carcinoma there is production of keratin which makes it unique.

43
Q

What two types of lung cancer come under the classification “non small cell carcinoma” and why are they given this classification

A

Squamous cell carcinoma and adenocarcinoma because it is sometimes difficult to differentiate between these two types.

44
Q

What immunohistochemical markers are used for squamous cell carcinomas

A
  • CK5
  • CK14
  • p63
  • 34Be12
45
Q

Which immunohistochemical markers are used for adenocarcinomas

A
  • CK

- TTF1

46
Q

What are three behaviours of lung cancer

A
  • Intrapulmonary growth
  • Invasion of adjacent structures
  • Distant spread via the lymphatics and the blood.
47
Q

Which two complications can arise as a result of intrapulmonary growth of lung cancer

A
  • Obstructive pneumonia

- Lymphangitis carcinomatous

48
Q

Which adjacent structures may be invaded by lung cancer

A
  • The pleura
  • The chest wall
  • The mediastinum (containing the heart, the SVC, the IVC, the aorta, the phrenic nerve, the recurrent laryngeal nerve and the oesophagus)
  • the diaphragm
49
Q

Which distant sites may lung cancer spread to

A
  • Brain
  • Bone
  • Liver
  • Adrenals
50
Q

If there is adrenal metastasis what does this more than likely indicate

A

That the lung is the primary site of the cancer.

51
Q

What system is used for the staging of lung cancer

A

TNM staging

52
Q

What does TNM stand for

A

Tumour, node involvement, metastasis

53
Q

How does the TNM staging work

A 
T = a measure of the growth of the tumour (0,1,2,3)
N = indication of the extent of nodal involvement (0,1,2)
M = presence of absence of distant metastases (0,1)
54
Q

What are the four treatment modalities for lung cancer

A
  • Supportive/ palliative care
  • Chemotherapy
  • Radiotherpy
  • Surgery
55
Q

Why are only very few lung cancer patients offered the surgical treatment option

A

Because often lung cancer presents at a very late stage in the progression of the disease and also the patients often have comorbidities which would make the surgery less successful.

56
Q

What are the three oncogenic drivers in pulmonary adenocarcinoma

A

1) Unknown
2) Kras
3) Epidermal growth factor receptor (EGFR)

57
Q

What is the molecular pathology of the action of EGFR in the development of adenocarcinoma

A

Molecules such as epidermal growth factor, TGF-alpha etc. bind to EGFR.
There is phosphorylation of the intracellular domain of the receptor leading to a cascade of events inside the cell with several mediators. There is gene transcription and cell cycle progression resulting in cell proliferation, inhibition of apoptosis, angiogenesis and migration, adhesion and invasion.

58
Q

What is Crizotinib

A

This is a “designer drug” inhibiting tyrosine kinase. Crizotinib inhibits the enzyme anaplastic lymphoma kinase (ALK).

59
Q

Why is it important for crizotinib to inhibit the ALK enzyme

A

Because often in lung cancer patients there is a translocation between the EML4 gene and the ALK gene which results in constitutive kinase activity. contributing to carcinogenesis.

60
Q

What is the role of PDL1 in the pathogenesis of lung carcinomas

A

There is over expression of PDL1 in tumour cells. This activates the PD1 pathway by binding to the PD1 receptor. The PD1 pathway blocks the immune response by down-regulating T cells. There is therefore no T cell mediated rejection of the tumour.

61
Q

How is the activation of the PD1 pathway in tumour cells a target for therapy

A

It introduces the idea of creating anti-PD1 antibodies.

62
Q

What are 4 possible things which could be manipulated in the future to create personalised cancer therapy

A
  • Epidermal growth factor receptor mutations
  • ALK fusion
  • ROS1 translocation
  • PD1 expression
63
Q

What is meant by “personalised cancer therapy”

A

This targets characteristics of specific tumours in particular patients, not just the diagnosis of lung cancer.

64
Q

Since there is no cure for lung cancer, what is very important and needs to be emphasised

A

Prevention.

The Respiratory System (20 decks)

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