Bronchial Carcinoma Flashcards

1
Q

How common is it?

A
  • Accounts for ~1% of all cancers and 27% of cancer deaths. (40,000 cases/yr in UK).
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2
Q

Who does it affect?

A

Smokers, ex-smokers, people exposed to occupational carcinogens. Women who have never smoked at greater risk than men. Risk increases with age. Black men who have never smoked at greater risk.

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3
Q

What causes it?

A

Histology – Squamous (35%); adenocarcinoma (27%; small (oat) cell (20%); large cell (10%); alveolar cell carcinoma (rare, <1%). Clinically the most important division is between small cell (SCLC) and non-small cell (NSCLC).

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4
Q

What risk factors are there (and how can they be reduced)?

A

Cigarette smoking is major risk factor.

- Others = asbestos, chromium, arsenic, iron oxides and radiation (radon gas).

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5
Q

How does it present?

A

Symptoms
Cough (80%); haemoptysis (70%); dyspnoea (60%); chest pain (40%); recurrent or slowly resolving pneumonia; lethargy; anorexia; weight loss.

Signs
Cachexia; anaemia; clubbing; HPOA (hypertrophic pulmonary osteoarthropathy, causing wrist pain); supraclavicular or axillary nodes.

Chest signs
None, or: consolidation; collapse; pleural effusion.

Metastases
Bone tenderness; hepatomegaly; confusion; fits; focal CNS signs; cerebellar syndrome; proximal myopathy; peripheral neuropathy.

Complications
Local – recurrent laryngeal nerve palsy; phrenic nerve palsy; SVC obstruction; Horner’s syndrome (Pancoast’s tumour); rib erosion; pericarditis; AF.
Metastatic – brain; bone; liver; adrenals.
Endocrine – ectopic hormone secretion (eg SIADH and ACTH) by small cell tumours; PTH by squamous cell tumours.
Non-metastatic neurological – confusion; fits; cerebellar syndrome; proximal myopathy; neuropathy; polymyositis; Lambert-Eaton syndrome.
Other – clubbing, HPOa, dematomyoairia, acanthosis nigricans, thrombophlebitis migrans.

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6
Q

Which other conditions may present similarly?

A

Differential diagnoses of a nodule in lung on a CXR

  • Malignancy (1⁰ or 2⁰)
  • Abscesses
  • Granuloma
  • Carcinoid tumour
  • Pulmonary hamartoma
  • Aterio-venous malformation
  • Encysted effusion (fluid, blood, pus)
  • Cyst
  • Foreign body
  • Skin tumour
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7
Q

How would you investigate the patient?

A

Cytology – sputum and pleural fluid.
CXR – peripheral nodule, hilar enlargement, consolidation, lung collapse, pleural effusion, bony secondaries.
Peripheral lesions and superficial lymph nodes may be amenable to percutaneous fine needle aspiration or biopsy.
CT – to stage tumour and guide bronchoscopy.
Bronchoscopy – to give histology and assess operability ± endobronchial ultrasound for assessment and biopsy.
F-deoxyglucose PET or PET/CT scan – to help in staging.
Radionuclide bone scan – if suspected metastases.
Lung function tests – to assess suitability for lobectomy.

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8
Q

What treatment/s would you consider? What risks and benefits of treatment are there?

A

Non-small cell tumours

  • Excision is treatment of choice for peripheral tumours, with no metastatic spread: stage I/II.
  • Curative radiotherapy is an alternative if respiratory reserve is poor.
  • Chemotherapy ± radiotherapy for more advanced disease.

Small cell tumours =almost always disseminated at presentation. They may respond to chemotherapy but invariably relapse (cyclophosphamide + doxorubicin + vincristine + etoposide; or cisplatin ± radiotherapy if limited disease).

Pallitation

  • Radiotherapy – used for bronchial obstruction, SVC obstruction, haemoptysis, bone pain and cerebral metastases.
  • SVC stent + radiotherapy + dexamethasone for SVC obstruction.
  • Endobronchial therapy – tracheal stenting, cyrotherapy, laser, brachytherapy (radioactive source placed close to tumour).
  • Pleural draining/pleurodesis – for symptomatic pleural effusions.
  • Drugs – analgesia; steroids; antiemetics; cough linctus (codeine); bronchodilators; antidepressants.

Prognosis

  • Non-small cell: 50% 2 yr survival without spread; 10% with spread.
  • Small cell: median survival 3 months if untreated; 1-1½ yrs is treated.
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