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Respiratory > Pathology of Lung Cancer > Flashcards

Pathology of Lung Cancer Flashcards

1
Q

Describe the epidemiology of lung cancer

A

Current annual US death toll > 150,000 (more than breast, colon and prostate combined)
75.5 per 100,000 in Scotland
Two thirds of world smokers reside in China

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2
Q

Why are there less improvements in lung cancer mortality?

A
  • Late presentation with advanced disease
  • A disease of the elderly
  • Extensive co-morbidities especially cardiac and respiratory
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3
Q

What are the causes of lung cancer?

A
  • Smoking (>95%)= passive smoking effects difficult to quantify
  • Occupational exposures (uranium mining, asbestos exposure)
  • Environmental exposures= radon gas
  • Genetic= Li-Fraumeni Syndrome (mutated p53 gene)
  • Viral infection? = Retroviral infection in sheep leads to lung adenocarcinomas
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4
Q

What are the types of lung cancer?

A
  • Squamous Carcinoma (30-40% and decreasing)
  • Adenocarcinoma (40-50% and increasing)
  • Small cell carcinoma (20%)
  • Others (5%)= carcinoid tumours
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5
Q

What does a squamous carcinoma look like?

A
  • Tumour cells are showing squamous differentiation

- Keratin production or ‘prickles’

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6
Q

What does Adenocarcinoma look like?

A

Evidence of a glandular growth pattern or mucin production

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7
Q

What does a small cell (undifferentiated) carcinoma look like?

A

Very poorly differentiated carcinoma showing variable evidence of neuroendocrine differentiation

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8
Q

What are the classifications of Carcinoid/ Neuroendocrine Tumours in the Lung?

A
  • Typical (Classical) carcinoid

- Atypical carcinoid

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9
Q

What is Typical carcinoid?

A
  • <2 mitoses per 2mm^2

- No necrosis

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10
Q

What is Atypical carcinoid?

A
  • > 2 but <10 mitoses per 2mm^2
  • Focal necrosis (may be very focal commedo like)
  • > 10 mitoses per 2mm^2 with usually extensive necrosis then classified with LCNEC
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11
Q

What is the clinical significance of classical carcinoid?

A
  • 10-15% have hilar nodal involvement at diagnosis
  • 5-10% will eventually develop distant sites
  • 5 year survival 90-98%
  • 10 year survival 82-95%
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12
Q

What is the clinical significance of atypical carcinoid?

A
  • 40-50% have nodal metastases and 10% will have stage 4 disease at diagnosis
  • 5 year survival 61-73%
  • 10 year survival 35-59%
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13
Q

What are the mechanisms of Carcinogenesis?

A

Development of a malignant tumour is a multi-step genetic process requiring the accumulation of mutated genes
-adenoma carcinoma theory

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14
Q

What are oncogenes?

A

Mutated genes encoding growth-promoting proteins- these are overexpressed in neoplasia (k-Ras, cyclinD1)

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15
Q

What are oncosupressor genes?

A

Mutated genes encoding growth-inhibitory proteins= decreased expression can result in neoplasia (Rb)

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16
Q

Hoe is a malignant neoplasm formed?

A
  • Clonal expansion
  • Additional mutations
  • Heterogeneity
17
Q

Describe Pathogenesis of Squamous Carcinoma

A

Squamous metaplasia common in smokers, reversible

  • Metaplastic squamous epithelium
  • Squamous dysplasia
  • Squamous carcinoma in-situ
  • Invasive squamous carcinoma
18
Q

Describe Pathogenesis of Adenocarcinoma

A
  • Central tumours may arise in a similar manner to squamous carcinoma but pre-malignant states not really recognised
  • Peripheral tumours now believed to arise through a sequence of step-wise changes
  • Normal alveolar walls
  • Atypical adenomatous hyperplasia
  • Adenocarcinoma-in-situ
  • Invasive adenocarcinoma
19
Q

What are the symptoms and signs of lung cancer?

A
  • Cough
  • Dyspnoea
  • Haemoptysis
  • Weight loss
  • Chest/ shoulder pain
  • Hoarseness
  • Fatigue
  • Slow to clear pneumonia
  • Finger clubbing
  • Cervical lymphadenopathy
  • Liver, bone, brain metastases
  • Pleural effusion
20
Q

What are the initial investigations of lung cancer?

A
  • Radiology= chest x-ray, CT scan

- Bloods= High Ca, abnormal liver function tests, low serum Na

21
Q

How do we diagnose lung cancer?

A
  • Biopsies

- Cytology

22
Q

Describe biopsies

A
  • Bronchial biopsies
  • CT guided lung biopsies
  • Biopsies of distant metastases e.g. pleura, liver, lymph node
23
Q

Describe cytology

A
  • Bronchial brushings and washings
  • Sputum
  • Pleural fluid aspiration
  • Fine needle aspirates of metastases
24
Q

How good are we at classifying lung cancer on small biopsies and cytology samples?

A
  • Small cell carcinoma fairly robust >90% accuracy
  • Squamous carcinoma and adenocarcinoma generally poor 50-60% accuracy= often classified as ‘non-small cell’ carcinomas in diagnostic specimens recognising the poor predictive value of small biopsies/ cytology samples
25
Q

What can we do with the biopsies?

A

Immunohistochemistry

  • Squamous markers= CK5, CK14, p63, 34betaE12
  • Adenocarcinoma= CK7, TTF1 (c. 70-80% of primary lung tumours)
26
Q

Describe the behaviour of lung cancer

A
  • Intrapulmonary growth= Obstructive pneumonia, Lymphangitis carcinomatosis
  • Invasion of adjacent structures= pleura (with associated effusion), chest wall, mediastinum (SVC, phrenic nerve, recurrant laryngeal nerve, atrium, aorta, oesophagus), Diaphragm
27
Q

Where does the distant spread of lung cancer go via lymphatics and blood?

A
  • Hilar and mediastinal nodes
  • Liver
  • Bones
  • Adrenals
  • Brain
28
Q

Describe the process of Lung cancer staging

A
  • Staging is assessing the extent of tumour growth and spread
  • Allows patients to be grouped together for treatment schedules/ trials
  • Predictor of prognosis
  • TNM system
29
Q

What is the TNM system?

A
  • T= a measure of the growth of the primary tumour
  • N= indication of the extent of local nodal disease
  • M= presence or absence of distant metastases
30
Q

What are the treatment modalities?

A
  • Best supportive/ palliative care
  • Chemotherapy
  • Radiotherapy
  • Surgery (around 15%, advanced disease at presentation, co-morbidities emphysema, ischaemic heart disease)
31
Q

What drugs are being developed for lung cancer?

A
  • Tyrosine kinase inhibitors (check mutations by pcr from specimens)
  • Crizotinib (EML4-ALK Translocations)
32
Q

What is immunotherapy?

A

Immune check point regulation

  • Lung carcinomas may be associated with an inflammatory infiltrates
  • Suggested for decades that a lymphoid infiltrate within these tumours may be associated with a better outcome
33
Q

Hoe might personal medicine be used in lung cancer treatment?

A
  • EGFR mutation and ALK fusion testing is the first of a growing list of mutation/ genetic factors that are potential targets
  • Treatment not based on diagnosis but on specific characteristics any given tumour has in any given patient
34
Q

What do we do in routine practice for lung cancer?

A

-Epidermal growth factor receptor mutations
-ALK fusion
-ROS-1 translocation
-PDL-1 expression
Small number of cases suitable for specific targeted therapies

Respiratory (41 decks)

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