lung cancer.txt

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lung cancer.txt
2010-05-12 18:28:16
lung malig

lung malig
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  1. what is a pulmonary hamartoma?
    • developmental disorder of CELL GROWTH.
    • excessive growth of cells and tissues normally present at that site
    • rare
  2. what is the most common fatal malignancy?
    bronchial carcinoma
  3. what are the risk factors for bronchial carcinoma?
    • tobacco smoking
    • industrial: uranium mining, asbestos, arsenic, nickel
    • radiation
    • air pollution: car exhausts, radon gas
  4. what is the stepwise pathogenesis of bronchial carcinoma?
    • normal epithelium
    • hyperplasia
    • squamous metaplasia
    • dysplasia
    • carcinoma in situ
    • invasive carcinoma
  5. what are the symptoms of bronchial carcinoma? and cause of them
    • cough - mucosal irritation
    • chest pain - invasion of chest wall
    • dyspnoea - atelectasis, obstruction
    • weight loss - cancer cachexia
    • present late so high mortality
  6. what are the clinical complications of bronchial carcinoma?
    • hoarseness of voice: left laryngeal nerve palsy
    • haemoptyis: vascular invasion
    • pneumonia, bronchiectasis, abscess: obstruction
    • dysphagia: oesophageal invasion
    • SVC syndrome: SVC obstruction
    • pleural effusion: pleural invasion
    • pericarditis: pericardial invasion
    • diaphragm paralysis: phrenic nerve invasion
    • horner's syndrome: sympathetic ganglia invasion
    • pancoast's humour: apical tumour causing hornets, shoulder, arm pain from brachial plexus involvement, hoarseness from laryngeal nerve palsy
  7. what causes the paraneoplastic syndromes of bronchial carcinoma?
    • often ectopic hormone production
    • NOT due to local or met spread
  8. name some endocrine paraneoplastic syndromes
    • hyperCa: PTH or PTHrP or PGE secertion esp scc
    • Cushing's syndrome: ACTH secreting tumour esp scc
    • SIADH: esp. in small cell carcinoma, get hyponatraemia leading to cerebral confusion and oedema
  9. what are the non-endocrine paraneoplastic syndromes?
    • Eaton-Lambert syndrome: autoAb against pre-synaptic VGCC on NMJ leading to muscle weakness
    • Hypertrophic pulmonary osteoarthropathy (HPOA): wrist and ankle pain due to periosteal new bone formation in small long bones also causing arthritis of adjacent joints; clubbing
    • Acanthosis nigricans: due to secretion of epidermal growth factor
    • Dermatomyositis: autoAb production
    • Trousseau's syndrome: migratory thrombophelbitis due to mucins that activate clotting
  10. what are the 3 types of non small cell lung cancer?
    • squamous cell carcinoma
    • adenocarcinoma
    • large cell carcinoma
  11. which type of bronchial carcinoma has the strongest association with smoking?
    • small cell carcinoma (99% are smokers)
    • squamous cell carcinoma (98% are smokers)
  12. what is the most common paraneoplastic syndrome in squamous cell carcinoma and where in the lung are they located?
    • hypercalcaemia
    • central location
  13. what are the histological signs of squamous cell carcinoma?
    • keratin production
    • intercellular bridges
  14. which bronchial carcinoma is least assoc. with smoking?
  15. what is the gender difference between squamous and adenocarcinoma of lung?
    • squamous cell: m>f
    • adenocarcinoma: f>m, but increase is in males
  16. what is the location of adenocarcinomas in lung? and which are associated with scarring?
    • peripheral as well as central
    • peripheral cancers associated with scarring
  17. what is the difference in pathogenesis of squamous cell and adenocarcinoma of lung?
    • squamous: metaplasia then dysplasia
    • adeno: dysplasia without metaplasia
  18. what is the histological feature of poorly differentiated adenocarcinoma of lung?
    • cells are vacuolated
    • cells produce lots of mucin WITHIN the individual cell, not as a gland
  19. what is bronchioalveolar carcinoma? where is it located? what does it arise from and where does it extend to?
    • rare subtype of adenocarcinoma
    • usually peripheral
    • arises from distal bronchi/bronchioles
    • extends to alveolar spaces
  20. what is the other name for large cell carcinoma? and why?
    • anaplastic carcinoma
    • lack of differentiation: no keratin/mucin/glands seen
    • when you cannot recognise if it is squamous or adeno
  21. what is the prognosis of large cell carcinoma compared to other NSCLC?
    • poorly differentiated so worse prognosis than squamous and adeno
    • paraneoplastic phenomena are rare
  22. where are large cell carcinomas located?
    centrally, with cavitation due to necrosis
  23. what do cells of large cell carcinoma look like?
    • large
    • nuclear pleomorphism
    • high mitotic activity
  24. which type of cells due squamous and adeno carcinoma arise from?
    stem cell population
  25. which type of cells do small cell carcinomas arise from?
    neuroendocrine cells
  26. which gender does small cell carcinoma affect more?
  27. what are the paraneoplastic syndromes of small cell carcinoma?
    • Cushing's: ectopic ACTH
    • SIADH: hyponatraemia
  28. where are small cell carcinomas located?
  29. what grade are small cell carcinomas? what is their stage at presentation?
    • high grade
    • already metastasised early even when the primary is small
  30. what are the cytological features of small cell carcinoma
    • small cells
    • little cytoplasm
    • speckled chromatin (salt and pepper)
  31. what is identifiable on electron microscopy and immunohistochemistry?
    • EM: neurosecretory granules
    • immunohistochemistry: secretory SUBSTANCES
    • confirm neuroendocrine tumour
  32. what are the 2 treatment options for small cell cancer?
    • chemotherapy: as already disseminated, cant resect
    • radiotherapy: is SVC obstruction
  33. what is the treatment of NSCLC?
    • 25% are resectable
    • if not: radiotherapy
    • if mets: chemotherapy, but poor response
  34. what is the difference between staging small cell and NSCLC?
    • NSCLC: TNM staging
    • small cell: not TNM as most already mets, so use limited v extensive
    • limited: disease confined to ipsilateral thorax, including supraclavicular fossa and pleural effusion. survival 1-2yrs
    • extensive: all other pts. survical 6-12months
  35. what age group do neuroendocrine tumours affect and are they more B or M?
    • young, under 40
    • 90% benign
    • no known relationship with smoking
  36. what is carcinoid syndrome due to?
    5HT production and enters SYSTEMIC circulation
  37. what are the symptoms of carcinoid syndrome?
    • skin: flushing
    • GI: abdo pain, N&V
    • lungs: bronchospasm: cough and wheeze
    • carcinoid heart disease: endocardial scarring affecting tricuspid and pulmonary valves - 5HT has damaging effects on right heart. rare on left as 5HT is broken down by MAO as it passes through the pulmonary system
  38. how are neuroendocrine tumours identified?
    immunohistochemistry: stains for 5HT
  39. where are the 3 most common lung mets originally from? and what histological type?
    • breast
    • GI
    • kidney
    • adenocarcinoma
  40. what are the 2 main ways of spread to lung and what do the mets look like?
    • haematogenous spread: discrete nodule
    • lymphatic spread: diffuse dissemination, aka lymphangitis carcinomatosa
  41. what is the differential for lymphangitis carcinomatosa on CXR?
    miliary TB
  42. what are the 2 main types of pleural tumours?
    • primary: malignant mesothelioma
    • secondary: i.e. metastatic (more common)
  43. what is a complication of pleural tumours?
    • pleural effusion
    • fibrous adhesions from pleural mets
  44. what are the most common primary sites of pleural mets? and what histological type?
    • lung
    • breast
    • GI
    • ovary
    • adenocarcinoma
  45. what is the way of spread to pleural mets?
  46. which cells does malignant mesothelioma arise from? and what do these look like in malignancy?
    • mesothelioma cells
    • atypical, multinucleate, pleomorphic
  47. what is the spread of mesothelioma like?
    • DIRECT invasion is aggressive: into lung and mediastinum
    • metastatic spread is less common
    • hilar nodes and liver are most common sites
  48. what is mesothelioma linked to?
    • asbestos exposure: mining, fabrication, insulation, electricians
    • latency period up to 40 years
  49. what is the presentation of mesothelioma?
    • cough
    • dyspnoea
    • pleural effusion
    • weight loss
    • chest pain
    • clubbing
    • fine end inspiratory crackles
  50. what is the main differential of mesothelioma? and why? how is it distinguished?
    • metastatic adenocarcinoma
    • as the histology is variable
    • can be spindle cell sarcoma like areas
    • or acinar adenocarcinoma like areas
    • distinguished: immunohistochemistry
  51. what is the macroscopic picture of mesotheioma?
    pleural thickening and extension into lung
  52. what is the treatment and prognosis of mesothelioma?
    • treatment: cant resect, chemo and radio give poor response
    • prognosis poor: 50% dead in a year
    • occupational exposure then unnatural cause of death so compensation
  53. at the death of a pt with mesothelioma, who must it be refered to?
    if diagnosis not confirmed in life then refer to Coroner at post portem. if diagnosed, it needs a Coroners inquest
  54. what different investigations are done in lung cancer diagnosis?
    • history: cough, haemoptysis, wt loss, cheeps pain, dyspnoea..paraneo
    • examination: consolidation (dull to percussion, reduced chest expansion), pleural effusion (stony dull, reduced air entry, reduced chest expansion), collapse (reduced expansion, dull percusion, reduced breath sounds)
    • CXR: but some not visible, need lateral view too. mimics consolidation
    • CT: high specificity
    • location: all central, adeno (inc bronchioalveolar) can be peripheral too
    • pathological diagnosis:
    • sputum cytology:gd if +ve as wont need invasive invest
    • pleural fluid
    • bronchoscopic specimens: bronchial washings, brushings, transbronchial FNA, (trans)bronchial biopsy. these are all best for central lesions
    • transthoracic FNA/biopsy (CT guided): best for peripheral lesions
  55. how are central lesions pathologically diagnosed?
    bronchoscopic sampling: washings, brushings, transbronch FNA or biopsy, bronch biopsy
  56. how are peripheral lesions pathologically diagnosed?
    CT guided transthoracic FNA or biopsy
  57. how are pleural lesions pathologically diagnosed?
    • pleural fluid cytology
    • CT guided transthoracic FNA or biopsy
  58. what is bronchoalveolar lavage used for?
    • samples the alveolar space
    • so good for pneumocystis (PCP), aspergillus, inflam lung disease
  59. What is the management of mesothelioma?
    • 1. breaking bad news, as poor prognosis
    • 2. radiotherapy to the drain site.. to prevent seeding to the skin
    • 3. refer to an oncologist to be put into a chemotherapy trial
    • 4. refer to palliative care for symptom control and for support for the patient and their family
    • 5. if asbestos exposure and mesothelioma – coroner’s inquest for compensation for the family
  60. Histology: for malignant mesothelioma, what 2 types of cells does it resemble?
    • 1. splindle cells – sarcoma
    • 2. acinar – adenocarcinoma
  61. if the atypical cells infiltrate the fat, what does this indicate?
    It is a MALIGNANT process, not just reactive mesothelial cells
  62. what are the different asbestos associated diseases?
    • 1.malignant mesothelioma
    • 2.asbestosis – interstitial fibrosis
    • 3.pleural plaques
    • 4.bronchial carcinoma
    • 5.extra pulmonary malignancy eg mesothelioma of peritoneal cavity or paratesticular
    • 6.Pleural effusion alone