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Systems: Resp. WK > 15. Pathology of Lung Cancer ( pulmonary neoplasia) > Flashcards

15. Pathology of Lung Cancer ( pulmonary neoplasia) Flashcards

1
Q

Does lung cancer kill more than breast and prostate cancers combined?

A

Yes; it’s the most common cause of cancer related deaths worldwide

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2
Q

What place is lung caner in terms of mortality?

A

1st for mortality accounting for 353,000 deaths (3rd for highest incidence of all cancer)

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3
Q

Name the 4 top cancers in Europe with highest incidences. (in 2012)

A
  1. female breast cancer
  2. colorectal cancer
  3. prostate cancer
  4. lung cancer
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4
Q

What percentage of deaths in Scotland does lung cancer approximate for?

A

6% of all deaths in Scotland (in males on the rise)

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5
Q

What are the 7 main aetiological factors (causes) for lung cancer from top cause to bottom?

A
  1. tobacco
  2. asbestos
  3. environmental radon (accumulation in granite-type rocks)
  4. other occupational exposure ( chromates, hydrocarbons, nickel)
  5. air pollution and urban environment
  6. other radiation
  7. pulmonary fibrosis
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6
Q

What is the current trend for males and females in terms of smoking?

A
  • for males smoking is decreasing

- for females smoking is increasing

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7
Q

What percentage of lung cancer patients are smokers?

A

> 85% (due to tobacco)

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8
Q

What percentage of smokers get lung cancer?

A

10% (but majority of other get other resp. failure disease and conditions)

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9
Q

By smoking, how much is the risk of getting cancer increased by for females and males?

A
  • For females, the risk is increased 22 times

- For males, the risk is increased 12 times

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10
Q

Are males or females more susceptible to tobacco smoke?

A

females

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11
Q

What is lung cancer risk directly related to?

A

Consumption; inhalation and pack years (packs per day per year)

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12
Q

What percentage of lung cancers are so-colled “non-smoking cancers”?

A

at least 25%

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13
Q

Through passive smoking, what is the increased percentage risk of getting cancer?

A

50-100%

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14
Q

Does risk of getting lung cancer reduces with smoking abstinence?

A

Yes but very slowly (over 50% lung cancers are ex-smokers)

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15
Q

What fraction of UK population smokes?

A

1/3 (worldwide 50% men and 12% women)

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16
Q

How many carcinogens are there roughly in a whiff of smoke?

A

~60 carcinogens

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17
Q

How many chemical compounds are found in a whiff of smoke?

A

over 4000

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18
Q

Which type of cancer are n-carcinogens more responsible for?

A

adenocarcinoma

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19
Q

Describe the multi-hit theory of carcinogenesis.

A
  • Approx. 3-12 key molecular changes in a specific sequence need to occur in a stem cell population to get clinical lung cancer (invasive phenotype). Depending on our genetics +detoxifying mechanisms, we deal with these differently.
  • host activation of pro-carcinogens are due to inherited polymorphisms which predispose.
  • metabolism for carcinogens and nicotine addiction influenced causing epithelial effects
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20
Q

What are 2 main pathways of carcinogenesis in the lung? (2 main areas where cancer development occurs)

A
  1. in lung periphery

2. in the central lung airways

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21
Q

What transformations occur in the lung periphery? What cancer do they lead to?

A
  • Bronchioalveolar epithelial stem cells transform

- adenocarcinoma

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22
Q

What transformations occur in the central lung airways? What cancer do they lead to?

A
  • bronchial epithelial stem cells transform

- more sensitive to polycyclic squamous cell carcinoma

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23
Q

What is squamous dysplasia forming carcinoma in-situ strongly associated with?

A

smoking

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24
Q

Does peripheral lung adenocarcinogenesis associated with smoking?

A

Less strongly, it also does occur in non- smokers (more than squamous dysplasia)

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25
Q

Describe the 3 stages of formation of an ademocarcinoma.

A
  1. atypical adenomatous hyperplasia (AAH)
  2. adenocarcinoma in situ
  3. invasive adenocarcinoma
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26
Q

What gene mutation is the most common in adenocarcinma patients and is therefore smoking induced?

A

KRAS mutation

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27
Q

Adenocarcinoma makes up what percentage of all lung cancers?

A

40%

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28
Q

Which 4 gene mutations are NOT related to tobacco carcinogenesis?

A
  1. EGFR
  2. BRAF
  3. HER2
  4. ALK rearrangements
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29
Q

What mechanism is the key driver for mutations?

A

oncogene addiction (by cells)

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30
Q

Is lung a common place for metastases?

A

Yes

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31
Q

What are the various types of “tumours” in the lung? (6)

A
  1. benign causes of mass lesion
  2. carcinoid tumour
  3. tumours of bronchial glands (V. RARE)
  4. Lymphoma
  5. Sarcoma
  6. Metastases to lungs from other body regions
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32
Q

What is a carcinoid tumour?

A
  • rare cancer of neuroendocrine system affecting hormone production
  • tends to grow very slowly
  • can affect; bowels, appendix, stomach, pancreas, kidneys, breast, ovaries, testes and lungs
  • low grade malignancy
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33
Q

Carcinoid tumours make up what percentage of lung neoplasms?

A

<5%

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34
Q

What are 3 types of tumour of bronchial glands?

A
  1. adenoic cystic carcinoma
  2. mucoepidermoid carcinoma
  3. benign adenomas
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35
Q

What are the 4 main types of carcinomas of the lung? (from most to least prevalent)

A
  1. squamous cell
  2. adenocarcinoma
  3. small cell carcinoma
  4. large cell carcinoma
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36
Q

What is the bronchioloalveolar cell carinoma (alveolar cell carcinoma) now walled?

A

adenocarcinoma in situ (subtype of adenocarcinoma)

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37
Q

Do small or non-small carcinomas make up 85% of all lung carcinomas?

A

Non-small cell carcinomas (NSCLC)

38
Q

What percentage of all lung cancers do small cell carcinomas (SCLC) make up?

A

~15%

39
Q

What are the main non-small cell carcinomas? (4)

A
  1. adenocarcinoma
  2. squamous cell carcinoma
  3. large cell carcinoma
  4. others
40
Q

Are non-small cell carcinomas a single type of lung carcinoma?

A
  • NO; NSCLC are not unified disease, it’s a GROUP of very biologically different and diverse diseases which have to be treated in different ways.
  • this term is used when non-small cell carcinomas cannot be distinguished on small biopsy samples
41
Q

How it can be identified if a person has a small or non-small cell carcinoma?

A

Using a microscope and looking at biopsy slides

42
Q

Does primary lung cancer present itself clinically early or late in its natural history?

A
  • grows clinically silent for many years in early stages
  • presents LATE
  • may have very little if any signs or symptoms until disease is advanced and progressed
43
Q

When is primary lung cancer often found in patients?

A

Sometimes incidentally during an investigation for something unrelated

44
Q

What does symptomatic lung cancer tell us about the disease?

A

most likely fatal and incurable

45
Q

When can surgeons resect the disease?

A

Only when it’s in early stages and no spread outside the thorax (no mets)

46
Q

What are 4 local effects of lung cancer?

A
  1. bronchial obstruction
  2. pleural
  3. direct invasion
  4. lymph node metastases
47
Q

What are 4 main effects of lung cancer specifically leading to bronchial obstruction?

A
  1. collapse
  2. endogenous lipoid pneumonia
  3. infection/ abscess
  4. bronchiectasis
    (mucous escalator in airways is blocked )
48
Q

What can yellow spots on a lung suggest?

A
  1. bronchial cartilages meaning lobe is collapsed (because of bronchiole obstruction)
  2. fat filled macrophages which accumulate in airways and obstruct
49
Q

What are the local effects of lung cancer on pleural regions? (2)

A
  1. inflammatory

2. malignant

50
Q

In local effects of lung cancer, where does the direct invasion occur?

A

invasion into the chest wall (it doesn’t necessarily rule out surgery)

51
Q

Lung cancer local effects can often lead to direct invasion into which nerves specifically? (4)

A
  1. phrenic nerves
  2. L recurrent laryngeal (branch of vagus nerve)
  3. brachial plexus
  4. cervical sympathetic
52
Q

What can local invasion into phrenic nerves lead to?

A

diaphragmatic paralysis

53
Q

What can local invasion into L recurrent laryngeal nerve lead to?

A

hoarse, bovine cough ( dry/ harsh cough)

54
Q

What can local invasion into brachial plexus lead to?

A

pancoast T1 damage

55
Q

What can local invasion into cervical sympathetic nerves lead to?

A

Horner’s syndrome

56
Q

Into which two regions in the mediastinum can direct invasion of lung cancer spread to?

A
  • superior vena cava (SVC)

- pericardium

57
Q

What symptom can invasion into superior vena cava cause?

A

excessive oedema and swelling (due to impaired circulation)

58
Q

What 2 local effects does direct invasion from lung cancer have on lymph node mets?

A
  1. mass effect

2. lymphangitis carcinomatose (inflammation of lymph vessels)

59
Q

Lymph nodes found where are most commonly involved in metastasis of lung cancer? (2)

A

Lymph nodes found in
1. head
2. neck
(spreads into hilum the mediastinal lymph nodes)

60
Q

Where do DISTANT metastases occur in lungs? (5)

A
  • liver
  • adrenals
  • bone
  • brain
  • skin
61
Q

What are distant effects of lung cancer which are secondary to local effects?

A
  1. neural

2. vascular

62
Q

What are 3 forms of distant effects of lung cancer in the body?

A
  1. distant metastases
  2. secondary to local effects
  3. non-metastatic effects (caused by hormonal changes in the body)
63
Q

Why do non-metastaitic effects of lung cancer cause so many changes in the body?

A

They are mediated by auto-imune system which tricks the tumour to damage its own cells

64
Q

What are the non-metastatic paraneoplastic effects of lung cancer on skeletal system? (2)

A
  1. clubbing

2. HPOA;hypertrophic osteoarthropathy (proliferation of skin and tissues, side effect of lung cancer)

65
Q

What are the non-metastatic paraneoplastic effects of lung cancer on endocrine system? (3)

A
  1. ACTH, ADH, PTH (adenocorticotrophic hormone, antidiruetic hormone, parathyroid hormone)
  2. carcinoid syndrome (mets in liver usually release seratonin causing a collection of symptoms)
  3. gynecomastia
66
Q

What are the non-metastatic paraneoplastic effects of lung cancer on neurological system? (4)

A
  1. polyneuropathy
  2. encephalopathy (general term for disease affecting structure and function of brain)
  3. cerebellar degeneration
  4. myasthenia (Eaton-Lambert; muscle weakness)
67
Q

What are the non-metastatic paraneoplastic effects of lung cancer on cutaneous system? (2)

A
  1. acanthosis nigricans (hyperpigmentation of skin)

2. dermatomyositis (inflammation, causes rash)

68
Q

What are the non-metastatic paraneoplastic effects of lung cancer on haematologic system? (3)

A
  1. granulocytosis (increase in granulocutes whihc are neutrophils)
  2. eosinophilia
  3. DIC; disseminated intravascular coagulation (overreactive coagulation)
69
Q

What are the non-metastatic paraneoplastic effects of lung cancer on renal system? (1)

A
  1. nephrotic syndrome (proteins are leaked into urine from kidneys)
70
Q

Small cell carcinomas are what type what types of tumours?

A

neuroendocrine tumours (they secrete hormones; ADH and ACTH etc and other molecules)

71
Q

A person with abnormal ADH levels due to a neuroendocrine tumour can appear to have what condition? (common clinical misdiagnosis)

A

diabetes

72
Q

Squamous carcinomas lead to abnormal levels of which hormone?

A

PTH; parathyroid hormone

73
Q

What are 7 main investigation done for lung cancers?

A
  1. chest x ray
  2. sputum cytology (rarely used)
  3. bronchoscopy
  4. trans-thoracic fine needle aspiration
  5. trans-thoracic core biopsy
  6. pleural effusion
  7. advanced techniques (CT, MRI, PET, other imaging)
74
Q

What are 3 forms of bronchoscopy?

A
  1. bronchial biopsy
  2. bronchial brushings and washings
  3. endobronchial ultrasound guided aspiration (EBUS)
75
Q

What is the main disadvantage of less invasive procedures used for investigation of lung cancer?

A

Smaller samples are sent to labs for diagnosis; this means it’s harder to fully diagnose and establish cancer type and staging

76
Q

What are 2 main prognostic factors which need to be identified in lung cancer?

A
  1. STAGE of disease

2. CLASSIFICATION (type of disease)

77
Q

What is adjuvant therapy?

A
  • “additional therapy”
  • chemotherapy, hormone therapy or radiotherapy follows surgery to improve the patient’s prognosis/ outcome
  • decreases the risk of cancer recurring following surgery
    (neoadjuvant is the therapy step BEFORE the main treatment e.g. surgery)
78
Q

What is used to select patients for adjuvant therapy or any forms of treatment?

A

Prognostic predictive biomarkers

79
Q

What is the usual prognosis for lung cancer?

A
  • Generally dreadful; <7%
  • survive 5 year survival rate
  • overall correlation with stage
80
Q

What is prognosis in % for Stage 1 lung cancer (operable)?

A

> 60% 5YS (5 year survival)

81
Q

What is prognosis in % for Stage 2 lung cancer (operable)?

A

35% 5YS (5 year survival)

82
Q

In Scotland, what percentage of patients with lung cancer receive surgical treatment?

A

around 10%

83
Q

What stages are “operable” lung cancers?

A

stages 1 and 2

84
Q

What is the survival rate range for non-small cell carcinomas?

A

from 10-25%

85
Q

What is the survival rate range for small cell carcinomas?

A
  • 4% (median survival is 9 months)

- very little can be done

86
Q

What main mutations occur in adenocarciomas? (non-small) (5)

A
  1. EGFR
  2. KRAS
  3. HER2
  4. BRAF
  5. ALK translocations etc
87
Q

What main mutations occur in squamous cell carcinomas? (non small) (3)

A
  1. FGFR1 gene copy number
  2. DDR2
  3. FGFR2 mutations etc
88
Q

What 2 mutations only have drugs to treat them?

A
  1. EGFR

2. ALK translocations

89
Q

What are immune checkpoints?

A
  • control immune reactions

- adopted by tumours to avoid immune destruction

90
Q

What 3 mutations are involved in immune checkpoints in tumours and have drugs developed against them (immune checkpoint inhibitors) which are becoming more popular in lung cancer therapy?

A
  1. PD1
  2. PD-L1
  3. CTLA4
    (they switch our immune system off and make tumour evade it)
91
Q

What is immunotherapy trying to achieve?

A
  • Aims to have our immune system attack cancer as a foreign invader
  • It aims to suppress PD1, PD-L1 and CTLA4 mutations which give tumours the property of escaping the immune system

Systems: Resp. WK (40 decks)

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