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Clinical Pathology in Action > L8 – Pulmonary–Lung Pathology > Flashcards

L8 – Pulmonary–Lung Pathology Flashcards

1
Q

What is the significance of lung cancer in terms of cancer mortality?

A

Lung cancer is one of the most common malignancies and accounts for one third of all cancer deaths in males.

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2
Q

What is the general 5-year survival rate for lung cancer in England?

A

The overall 5-year survival rate is around 16%, with significant differences between subtypes.

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3
Q

How does survival differ between NSCLC and small cell lung cancer?

A

NSCLC has a 5-year survival rate of approximately 26%, while small cell lung cancer is around 7%.

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4
Q

Which age group is most commonly affected by lung cancer?

A

Lung cancer most often occurs in individuals aged between 55 and 84 years, peaking between 65 and 74 years.

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5
Q

What are the main subtypes of non-small cell lung cancer (NSCLC)?

A

NSCLC includes squamous cell carcinoma, adenocarcinoma, large cell undifferentiated carcinoma, and adeno-squamous carcinoma.

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6
Q

How are lung carcinomas classified based on in situ versus invasive disease?

A

In situ lesions (e.g. adenocarcinoma in situ, squamous cell carcinoma in situ) are confined, while invasive carcinomas breach the basement membrane.

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7
Q

What are the recognised neuroendocrine tumours of the lung?

A

These include carcinoid tumours, atypical carcinoid, small cell carcinoma, and large cell neuroendocrine carcinoma.

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8
Q

How does tumour histology influence treatment decisions in lung cancer?

A

Histological subtype determines the choice of chemotherapy, targeted therapy, and eligibility for immunotherapy.

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9
Q

What is the role of cigarette smoking in lung cancer?

A

Smoking increases lung cancer risk dramatically, with heavy smokers facing a 20-fold increased risk.

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10
Q

How does asbestos exposure interact with smoking in lung cancer risk?

A

Asbestos exposure alone increases risk fivefold, but in combination with smoking, the risk can increase 50–90 times.

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11
Q

Which molecular genetic alterations are commonly found in adenocarcinomas?

A

Common alterations include mutations in EGFR, KRAS, ALK fusions, ROS1 rearrangements, and BRAF mutations.

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12
Q

Why are tumour suppressor gene mutations important in squamous cell carcinoma?

A

Mutations in TP53 and CDKN2A, along with amplification of FGFR1, are frequently observed and influence tumour behaviour.

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13
Q

What are common presenting symptoms of lung cancer?

A

Symptoms include cough, weight loss, haemoptysis, and sometimes paraneoplastic syndromes.

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14
Q

What local effects can lung tumours cause?

A

They may cause airway obstruction leading to pneumonia or lobar collapse, pleural effusions, and invasion of surrounding structures.

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15
Q

How do paraneoplastic syndromes manifest in lung cancer?

A

They can include ectopic hormone production (e.g. ACTH, ADH) leading to Cushing syndrome or hyponatraemia.

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16
Q

What is the clinical significance of lymph node metastasis in lung cancer?

A

Lymph node involvement is the strongest predictor of poor survival and guides the staging and treatment approach.

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17
Q

What is the role of tumour mutational burden (TMB) in lung cancer therapy?

A

A high TMB can predict better responses to immunotherapy by indicating a higher neoantigen load.

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18
Q

How do environmental exposures like radon contribute to lung cancer risk in non-smokers?

A

Radon gas induces DNA damage, thereby increasing lung cancer risk even in the absence of smoking.

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19
Q

What characteristic imaging features are associated with small cell lung carcinoma?

A

It often appears as a central mass with mediastinal involvement and may be accompanied by signs of paraneoplastic syndromes.

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20
Q

How is liquid biopsy transforming the management of lung cancer?

A

It offers a non-invasive method to detect circulating tumour DNA, monitor mutations, and assess treatment response.

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21
Q

What challenges exist in differentiating lung cancer subtypes histologically?

A

Overlapping morphological features and tumour heterogeneity can complicate the accurate classification of lung carcinomas.

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22
Q

How do targeted therapies revolutionise treatment for NSCLC?

A

Agents targeting specific mutations (e.g. EGFR, ALK) have significantly improved outcomes for patients with identifiable genetic alterations.

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23
Q

How does the expression of neuroendocrine markers help classify lung cancers?

A

They differentiate neuroendocrine tumours from other subtypes, aiding in precise diagnosis and appropriate therapy selection.

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24
Q

What is the significance of lung cancer in terms of cancer mortality?

A

Lung cancer is one of the most common malignancies and accounts for one third of all cancer deaths in males.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the general 5-year survival rate for lung cancer in England?
The overall 5-year survival rate is around 16%, with significant differences between subtypes.
26
How does survival differ between NSCLC and small cell lung cancer?
NSCLC has a 5-year survival rate of approximately 26%, while small cell lung cancer is around 7%.
27
Which age group is most commonly affected by lung cancer?
Lung cancer most often occurs in individuals aged between 55 and 84 years, peaking between 65 and 74 years.
28
What are the main subtypes of non-small cell lung cancer (NSCLC)?
NSCLC includes squamous cell carcinoma, adenocarcinoma, large cell undifferentiated carcinoma, and adeno-squamous carcinoma.
29
How are lung carcinomas classified based on in situ versus invasive disease?
In situ lesions (e.g. adenocarcinoma in situ, squamous cell carcinoma in situ) are confined, while invasive carcinomas breach the basement membrane.
30
What are the recognised neuroendocrine tumours of the lung?
These include carcinoid tumours, atypical carcinoid, small cell carcinoma, and large cell neuroendocrine carcinoma.
31
How does tumour histology influence treatment decisions in lung cancer?
Histological subtype determines the choice of chemotherapy, targeted therapy, and eligibility for immunotherapy.
32
What is the role of cigarette smoking in lung cancer?
Smoking increases lung cancer risk dramatically, with heavy smokers facing a 20-fold increased risk.
33
How does asbestos exposure interact with smoking in lung cancer risk?
Asbestos exposure alone increases risk fivefold, but in combination with smoking, the risk can increase 50–90 times.
34
Which molecular genetic alterations are commonly found in adenocarcinomas?
Common alterations include mutations in EGFR, KRAS, ALK fusions, ROS1 rearrangements, and BRAF mutations.
35
Why are tumour suppressor gene mutations important in squamous cell carcinoma?
Mutations in TP53 and CDKN2A, along with amplification of FGFR1, are frequently observed and influence tumour behaviour.
36
What are common presenting symptoms of lung cancer?
Symptoms include cough, weight loss, haemoptysis, and sometimes paraneoplastic syndromes.
37
What local effects can lung tumours cause?
They may cause airway obstruction leading to pneumonia or lobar collapse, pleural effusions, and invasion of surrounding structures.
38
How do paraneoplastic syndromes manifest in lung cancer?
They can include ectopic hormone production (e.g. ACTH, ADH) leading to Cushing syndrome or hyponatraemia.
39
What is the clinical significance of lymph node metastasis in lung cancer?
Lymph node involvement is the strongest predictor of poor survival and guides the staging and treatment approach.
40
What is the role of tumour mutational burden (TMB) in lung cancer therapy?
A high TMB can predict better responses to immunotherapy by indicating a higher neoantigen load.
41
How do environmental exposures like radon contribute to lung cancer risk in non-smokers?
Radon gas induces DNA damage, thereby increasing lung cancer risk even in the absence of smoking.
42
What characteristic imaging features are associated with small cell lung carcinoma?
It often appears as a central mass with mediastinal involvement and may be accompanied by signs of paraneoplastic syndromes.
43
How is liquid biopsy transforming the management of lung cancer?
It offers a non-invasive method to detect circulating tumour DNA, monitor mutations, and assess treatment response.
44
What challenges exist in differentiating lung cancer subtypes histologically?
Overlapping morphological features and tumour heterogeneity can complicate the accurate classification of lung carcinomas.
45
How do targeted therapies revolutionise treatment for NSCLC?
Agents targeting specific mutations (e.g. EGFR, ALK) have significantly improved outcomes for patients with identifiable genetic alterations.
46
How does the expression of neuroendocrine markers help classify lung cancers?
They differentiate neuroendocrine tumours from other subtypes, aiding in precise diagnosis and appropriate therapy selection.
47
Why do more people die from lung cancer compared to breast and prostate cancer despite lower incidence?
Because lung cancer often presents late and has poor response to current treatments.
48
What is the major prognostic difference between small cell and non-small cell lung cancers?
Small cell carcinoma has a much worse prognosis and faster progression.
49
Why is surgery rarely an option for small cell lung carcinoma?
Because small cell carcinoma is usually widely metastatic at diagnosis and very chemosensitive.
50
What classification change has occurred in lung cancer typing due to targeted therapies?
Lung cancers are now subtyped more specifically (e.g., squamous vs adenocarcinoma) to guide targeted therapy.
51
What type of lung tumour shows spindled or sarcomatoid features?
Sarcomatoid carcinoma.
52
What is the risk of lung cancer in heavy smokers compared to non-smokers?
Heavy smokers have a 24-fold increased risk compared to non-smokers.
53
What type of genetic polymorphism increases lung cancer risk from smoking?
Variants in cytochrome P450 enzymes that increase activation of procarcinogens.
54
How does a defect in DNA repair genes influence lung cancer risk in smokers?
Defects prevent effective repair of smoking-induced DNA damage, increasing cancer risk.
55
What is the typical latency period between asbestos exposure and lung cancer development?
Approximately 20 years.
56
What is the biological mechanism of radiation-induced carcinogenesis at low doses?
Low-dose radiation causes partial DNA damage, which can lead to oncogene activation instead of cell death.
57
Which genetic alterations are most commonly found in lung adenocarcinomas?
Mutations in EGFR, KRAS, ALK fusions, ROS1, and BRAF.
58
Which gene mutations are often found early in the development of squamous cell carcinoma of the lung?
TP53 mutations are common early events in squamous cell carcinoma.
59
What characterises the immunohistochemical profile of squamous cell carcinoma?
P63, CK5/6 positivity; strong cytokeratin expression.
60
What tumour suppressor genes are commonly inactivated in small cell carcinoma?
Inactivation of both TP53 and RB1 tumour suppressor genes.
61
How do patients with lung cancer sometimes present without respiratory symptoms?
By presenting first with lymph node metastasis or distant organ metastasis.
62
What clinical syndrome results from lung tumour invasion of the sympathetic chain?
Horner’s syndrome (ptosis, miosis, anhidrosis).
63
What paraneoplastic syndrome is associated with inappropriate ADH secretion?
Syndrome of inappropriate antidiuretic hormone secretion (SIADH).
64
What hormone is abnormally produced by some lung cancers, mimicking Cushing's syndrome?
ACTH production leading to paraneoplastic Cushing’s syndrome.
65
What radiological feature differentiates pneumonia from a lung mass on imaging?
Pneumonia consolidations usually resolve with antibiotics, while lung masses persist.
66
How can pleural fluid cytology help diagnose lung cancer?
Detection of malignant cells and immunoprofiling can suggest primary origin.
67
What feature differentiates adenocarcinoma in situ from minimally invasive adenocarcinoma?
In adenocarcinoma in situ, tumour cells are limited to alveolar surfaces without invasion; minimally invasive has ≤5 mm invasion.
68
Why can mucinous adenocarcinoma of the lung be confused with metastasis from other organs?
Mucinous adenocarcinomas resemble gastrointestinal tract tumours and share similar immunoprofiles.
69
Where in the lung are adenocarcinomas typically located?
Peripheral lung fields.
70
How does smoking prevalence influence the incidence of different lung cancer subtypes?
Lower smoking rates have shifted prevalence from squamous cell carcinoma to adenocarcinoma.
71
What is the primary histological feature seen in squamous cell carcinoma under the microscope?
Keratinisation and intracellular bridges.
72
How does PD-1 checkpoint inhibition therapy help treat lung cancers?
By reactivating T-cells to attack cancer cells blocked by tumour immune evasion.
73
What key feature helps distinguish small cell carcinoma from lymphocytes under microscopy?
Small cell carcinoma cells are about three times the size of a lymphocyte.
74
What is the typical survival time without treatment for small cell carcinoma?
6–17 weeks.
75
What is a typical site of metastasis for lung cancer besides the lungs themselves?
Brain, bone, and adrenal glands.
76
What neuroendocrine lung tumour has a good prognosis compared to others?
Typical carcinoid tumour.
77
What is the typical mitotic rate in typical carcinoid tumours?
Less than 2 mitoses per 2 mm² (less than 3 mitoses per 10 HPF).
78
What mutation often causes resistance to EGFR-targeted therapy in lung adenocarcinoma?
T790M mutation in EGFR.
79
Which lung cancer subtype shows scant cytoplasm and nuclear moulding?
Small cell carcinoma shows scant cytoplasm and nuclear moulding.
80
Why is it crucial to perform molecular profiling in non-small cell lung cancers today?
It identifies mutations like EGFR, ALK that guide use of targeted therapies.
81
What genetic mutation is associated with resistance to EGFR tyrosine kinase inhibitors?
T790M mutation.
82
What tumour marker is often positive in adenocarcinoma of the lung?
TTF-1 (thyroid transcription factor 1).
83
What is the importance of TTF-1 in diagnosing lung cancer subtypes?
TTF-1 positivity indicates pulmonary adenocarcinoma or small cell carcinoma origin.
84
How does pleural mesothelioma usually present radiologically?
Diffuse thickening of pleura encasing the lung.
85
What is the key risk factor for pleural mesothelioma?
Asbestos exposure.
86
Why is diagnosing mesothelioma particularly serious for prognosis?
Because median survival after diagnosis is only about 12 months.
87
What genetic marker loss can help distinguish malignant from benign mesothelial cells?
Loss of BAP1 or MTAP expression.
88
What immunohistochemical profile suggests mesothelioma over carcinoma?
Positive for CK5/6, calretinin, WT-1; negative for CEA, Ber-EP4.
89
How does biphasic mesothelioma differ from epithelioid or sarcomatoid types?
It contains both epithelial and spindle cell components.
90
Why is electron microscopy less used today in diagnosing mesothelioma?
Modern immunohistochemistry (IHC) markers provide faster, more accurate diagnosis.

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