Lung Cancer (Respiratory Pathology 1) Flashcards

1
Q

RFx for lung cancer?

A
  • Smoking: amont, type, duration
  • Occupational hazards: asbestos, silica, radon, heavy metals etc.
  • Scarring: chronic scarring conditions of the lung
  • Molecular genetics: genetic predisposition
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2
Q

What are the clinical features of centrally located lung cancers?

A

Cough, dyspnoa, wheezing, haemoptysis.

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3
Q

What are the clinical features of peripherally located lung cancers?

A
  • Pleuritic chest pain

- Effusion

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4
Q

What are the 3 major secretions of tumours causing paraneoplastic syndrome?

A
  • ACTH
  • ADH
  • PTH
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5
Q

What are the biopsy methods of centrally located tumours?

A
  • Sputum
  • Bronchial washings/brushings
  • EBUS-TBNA (endobronchial ultrasound guided biopsy)
  • Bronchial biopsy
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6
Q

What are the biopsy methods of peripherally located tumours?

A
  • FNA (CT-guided, ENB)

- Pleural biopsy

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7
Q

What is the broad classification of lung cancer?

A

Most impt step: decide whether NSCC or SCC -> initial management v. different.

  1. Small cell lung carcinoma
  2. Non-small lung carcinoma
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8
Q

What are the types of non-small cell carcinoma?

A
  • Squamous cell carcinoma
  • Adenocarcinoma
  • Adenosquamous carcinoma
  • Large cell carcinoma
  • Sarcomatoid carcinoma
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9
Q

How should positive lung cancer biopsy be further investigated?

A
  • CT Chest - location, size, lymph nodes
  • CT Abdo - lung often spreads to adrenals
  • FBE: symptomatic investigation (e.g. haeoptysis)
  • UEC: baseline renal function
  • LFTs: liver mets, ALP evidence of bony mets
  • General surgical work up
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10
Q

What are the features of squamous cell carcinoma? (location, appearance, extent etc)

A
  • Generally central
  • Frequently involves large airways
  • Cavitation seen in 33% cases
  • Grey-white > yellow. Often with a dry, flaky appearance that reflects keratinisation.
  • Necrosis and haemorrhage common
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11
Q

What are the histological features of squamous cell tumours?

A

-Intercellular bridges
-Keratinisation
(poorly differentiated tumour may mean features are not obvious; need immunohistochemcial stains)

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12
Q

What are the characteristics of adenocarcinoma? (features, location, extent etc)

A
  • Most common non-small cell
  • Less correlation with smoking
  • Generally peripheral –> rapidly reach pleura causing effusions.
  • Grey-white with necrosis and haemorrhage
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13
Q

How can adenocarcinoma be differentiated as primary or metatastatic?

A
  • Immunohistochemistry -TTF1 (positive in lung alveolar stroma).
  • Diagnosis can be made on cytology but cancer line requires staining.
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14
Q

What is small cell carcinoma?

A
  • Tumour showing neuroendocrine differentiation.
  • Rapidly growing mass often with local obstruction, regional lymph node or distant metastases.
  • Associated with smoking
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15
Q

What are the histological features of small cell carcinoma?

A
  • Neuroendocrine type architecture: nests, trabeculae, ribbons.
  • Tumour cells have high N:C ration with enlarged ovoid nuclei, granular nuclear chromatin, inconspicuous nucleoli, nuclear holding and scanty cytoplasm.
  • Many mitoses seen + apoptotic bodies + necrosis.
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16
Q

What is large cell carcinoma?

A
  • Poorly differentiated - neither squamous nor adeno.
  • Undifferentiated non-small cell carcinoma that lacks cytological features of small cell, adeno or squamous carcinoma.
  • Only Dx when entire tumour examined by histology
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17
Q

What are the complications of lung cancer?

A
  • Lipoid pneumonia (due to distal obstructing tumour)
  • Atelectasis
  • bronchitis, bronchiectasis
  • cavitation and abscess formation
  • fistula formation
  • pleuritis/pleural effusion
  • vascular thrombosis
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18
Q

Why should small cell carcinomas be confirmed with immunohistochemistry?

A

Can mimic other types e.g. lymphoid, basal

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19
Q

How is lung cancer staged?

A

TNM

  • Tumour size
  • Number and location of LN mets
  • Metastases (distant)
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20
Q

Where does lung cancer metastasise?

A
  • adrenals - >50%
  • Liver - 30 - 50% cases
  • brain - 20% cases
  • bone - 20% cases
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21
Q

What are the two most important specific mutations in non-small cell adenocarcinomas?

A

EGFR and ALK
Treatment available to target specific mutations; treatment of using these inhibitors leads to superior response rate, prolong progression-free survival and improved QoL.

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22
Q

Who is most affected by EGFR mutations?

A

Young non- or light-smoking female Asians with low stage disease.
Incidence 30 -50% in this population; 10-20% in Western population.

23
Q

Epidemiology of lung cancer?

A
  • 18% cancer deaths (common)
  • 2.7M:1F
  • Age avg = 60
24
Q

Histology of adenocarcinoma?

A
  • Well to moderately differentitated tumour
  • Glandular and/or papillary structures
  • Produce mucin by showing cytoplasmic mutinous vacuoles or mucin extending into the stroma
25
Q

What is adenocarcinoma in situ?

A
Previously BAC (bronchiole-alveolar carcinoma in situ).
-adenocarcinoma showing growth of neoplastic cells along pre-existing alveolar structures (lepidic growth) w/o evidence of stromal, vascular or pleural invasion.
26
Q

How may adenocarcinoma in situ present?

A

-Well demarcated single
or
-multiple nodules
-pneumonic pattern (with involvement of entire lobe)

27
Q

What should be suspected if there is non-resolving consolidation / pneumonia?

A

Adenocarcinoma in situ

28
Q

What are the histological subtypes of adenocarcinoma in situ?

A
  • Non-mucinous (commonest)
  • Mucinous (~25%)
  • Mixed (very rare)
29
Q

Immunohistochemistry squamous cell carcinoma markers?

A
  • CK5/6

- p63

30
Q

Immunohistochemistry adenocarcinoma?

A
  • CK7

- TTF1

31
Q

Immunohistochemistry Small cell carcinoma?

A
  • synpatophysin
  • chromogranin
  • CD56
32
Q

Tumour morphology suggestive of EGFR mutation?

A

Well differentiated tumours with predominant lepidic growth; no necrosis.

33
Q

Are all EGFR mutations treatment sensitive?

A

No- different EGFR mutations occur. Some are resistant to treatment with inhibitors.

34
Q

Epidemiology ALK mutation?

A
  • Usually younger men; 40-60y.

- Light or non-smoking history.

35
Q

ALK tumour morphology?

A
  • Solid pattern
  • Signet ring cells
  • Prominent host inflammatory response
36
Q

What is ALK inhibitor therapy?

A

Crizotinib

37
Q

Epidemiology carcinoid tumours?

A
  • Mean age 55y

- Up to 50% incidental radiological finding

38
Q

Common symptoms carcinoid tumours?

A

Cough and haemoptysis. Relate to bronchial obstruction.

39
Q

Are carcinoid tumours benign?

A

No. All have metastatic potential and should not be considered benign.

40
Q

Macroscopic appearance carcinoid tumours?

A
  • Mostly ass/w large bronchus (peripheral lesions uncommonly seen)
  • Well demarcated
  • Soft tan colour
  • May have areas of congestion and haemorrhage
41
Q

Histology of carcinoid tumours?

A
  • Neuroendocrine architecture: nests, trabeculae, ribbons, rosettes.
  • Tumour cells: round to ovoid nuclei, granular chromatin, small nucleoli, moderate amts granular cytoplasm
42
Q

Histology of atypical carcinoid?

A

See more mitoses +/- necrosis

43
Q

How is carcinoid tumour diagnosis confirmed?

A

Diagnosis confirmed by immunostaining:

  • synaptophysin
  • chromogranin
  • CD56
44
Q

Prognosis carcinoid tumour?

A
  • Better cf small cell carcinoma

- up to 20% typical carcinoids have regional LN involvement; up to 70% in atypical carcinoids

45
Q

Prognosis large cell neuroendocrine carcinoma?

A

Poor. Similar to that of small cell carcinoma.

46
Q

Which sites commonly metastasise to lung?

A
  • Breast
  • Lower GIT
  • Melanoma
  • Renal cell carcinoma
47
Q

What are the patterns of lung mets?

A
  • Multiple nodules
  • Solitary met
  • Lymphangitis mets
  • Endobronchial mets
  • Pleural mets
  • Interstitial spread
48
Q

How is metastatic disease confirmed?

A
  • Clinical and radiological correlation
  • Histology with morphological assessment
  • Immunohistochemical staining
49
Q

What is superior vena cava syndrome?

A

Obstruction of SVC causing neck and facial swelling + dyspnoea + cough
(Other Sx: hoarseness, swollen tongue, epistaxis, haemoptysis)

50
Q

Signs of superior vena cava syndrome?

A
  • Dilated neck veins
  • Increased number of collateral veins covering anterior chest wall
  • Cyanosis
  • Oedema of face, arms, chest
  • Pemberton’s sign
51
Q

What is Pemberton’s sign?

A

Facial flushing, cyanosis and distension of neck veins on raising both arms above the head.

52
Q

Common sites of lung primary v met?

A
  • 2/3 primary in upper lung

- 2/3 of mets in lower lung

53
Q

CIx for surgical management lung Ca?

A
  • Spread to contralateral LN or distant sites
  • poor pulmonary status
  • SCLS (generally)