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1Principles of Biomedicine - MD1 > 94 - Neoplasia 3 > Flashcards

94 - Neoplasia 3 Flashcards

1
Q

*Four appearances of intraepithelial neoplasia

A
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2
Q

Process that precedes many carcinomas

A

Intraepithelial neoplasia

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3
Q

Most-common cancers

A

Carcinomas/epithelial cancers

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4
Q

Stages of intraepithelial neoplasia 1 2 3 4

A

1) Normal 2) Dysplasia (EG: simple columnar cell takes on several mutations) 3) In situ neoplasm 4) Invasive neoplasm

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5
Q

Stages of intraepithelial neoplasia 1 2 3 4

A

1) Normal 2) Dysplasia (EG: simple columnar cell takes on several mutations, increased mitotic activity, pleiomorphic nuclei. Changes are restricted to epithelial cells) 3) In situ neoplasm 4) Invasive neoplasm

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6
Q

Stages of intraepithelial neoplasia 1 2 3 4

A

1) Normal 2) Dysplasia (EG: simple columnar cell takes on several mutations, increased mitotic activity, pleiomorphic nuclei. Changes are restricted to epithelial cells) 3) In situ carcinoma (architecture is no longer organised) 4) Invasive neoplasm

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7
Q

Appearance of dysplasic cells

A

Increased mitotic activity. Pleiomorphic nuclei Large nucleoli Premalignant.

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8
Q

What is in situ carcinoma?

A

When dysplasic cells become malignant.

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9
Q

Dysplasia

A

Abnormality of development; alteration in size, shape and organisation ofcells

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10
Q

Meaning of grades of dysplasia

A

Higher the grade -> more likely to progress to malignancy (grades 1, 2 and 3)

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11
Q

Grade 3 dysplasia

A

In situ carcinoma. Non-invasive.

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12
Q

Differences between normal stratified squamous epithelium and squamous dysplasia

A

Dysplasic: Enlarged nuclei, pleomorphic nuclei, disorganised cells, increased proliferation, incomplete cellular maturation (should only have mitosis in basal layer)

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13
Q

Differences between normal stratified squamous epithelium and squamous dysplasia

A

Dysplasic: Enlarged nuclei, pleomorphic nuclei, disorganised cells, increased proliferation, incomplete cellular maturation (should only have mitosis in basal layer)

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14
Q

What do glandular dysplastic lesions arising from lining epithelium often form?

A

Polyps (protuberances of tissue into the lumen)

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15
Q

Difference between hyperplasia and neoplasia

A

Hyperplasia is controlled.

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16
Q

When can hyperplasia predispose to cancer?

A

Hyperplasia in certain situations can confer increased risk of malignancy (risk of mutations developing). NOT premalignant.

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17
Q

When can metaplasia predispose to neoplasia?

A

Influences that lead to pathologic metaplasia can also predispose to malignant transformation of metaplastic epithelium

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18
Q

Risk of intraepithelial neoplasias to become malignant

A

Reasonable risk (therefore considered premalignant). Greater risk than most other benign lesions

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19
Q

Risk of intraepithelial neoplasias to become malignant

A

Reasonable risk (therefore considered premalignant). Greater risk than most other benign lesions

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20
Q

Lymphadenopathy

A

Enlarged lymph nodes

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21
Q

Examples of effects of metastases 1 2 3 4

A

– Local lymphadenopathy (draining to local lymph node) – Bone pain or features related to hypercalcaemia – Jaundice (to liver) – Seizures (if in brain)

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22
Q

Examples of effects of metastases 1 2 3 4

A

– Local lymphadenopathy (draining to local lymph node) – Bone pain or features related to hypercalcaemia – Jaundice (to liver) – Seizures (if in brain)

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23
Q

Malignancies often associated with weight loss, fever

A

Late-stage

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24
Q

Where do TNFa and IL-1 come from in some cancers?

A

Produced by either tumour cells or cells in the tumour microenvironment (EG: macrophages)

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25
Q

Paraneoplastic effects

A

Effects of malignancy, not caused directly by tumour mass

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26
Q

Examples of paraneoplastic endocrine effects 1 2 3 4 5

A

1) Cushing’s syndrome 2) Inappropriate ADH syndrome 3) Hypercalcaemia 4) Hypoglycaemia 5) Polycythaemia

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27
Q

Cushing’s syndrome

A

ACTH (adrenocorticotropic hormone) release.

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28
Q

Hypercalcaemia in cancer

A

Squamous cell carcinoma releases parathyroid hormone-like substance.

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29
Q

Hypercalcaemia in cancer

A

Squamous cell carcinoma releases parathyroid hormone-like substance. Can lead to excessive breakdown of bone (increase osteoclast activity)

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30
Q

Immunological paraneoplastic effects 1 2 3 4

A

1) Dermatologic (rashes, lesions) 2) Neuropathy (injuries to nerves) 3) Inflammation of muscle (weakness) 4) Nephrotic syndrome

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31
Q

Paraneoplastic effects of lung cancer 1 2 3 4

A

Clubbing Hypertrophic osteoarthropathy Venous thrombosis Non-bacterial thrombotic endocarditis

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32
Q

Paraneoplastic effects 1 2 3 4

A

1) Clubbing 2) Hypertrophic osteoarthropathy 3) Venous thrombosis 4) Non-bacterial thrombotic endocarditis

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33
Q

Local effects of primary lung cancer 1 2 3 4 5 6

A

1) Cough 2) Haemoptysis 3) Wheeze 4) Dyspnoea 5) Pneumonia 6) Pancoast’s syndrome

34
Q

Cancer that can lead to anaemia

A

Colon cancer (lose blood into colon)

35
Q

Tests that can be useful in diagnosing cancers

A

1) Haemoglobin level 2) Liver function tests 3) Radiology (CXR, CT scan) 4) Endoscopy

36
Q

Prostate specific antigen

A

Can be elevated in prostate, pancreatic cancer. Can also be elevated in non-malignant tumours, non-cancer conditions. Used in diagnosis, but is hard to use because of some non-specificity.

37
Q

What can CXR be used for? 1 2 3

A

1) Investigation of primary cancer 2) Staging of cancer (progression) 3) Follow up (to see if there is remission, relapse, etc)

38
Q

Tests that can be useful in diagnosing cancers 1 2 3 4

A

1) Haemoglobin level 2) Liver function tests 3) Radiology (CXR, CT scan) 4) Endoscopy

39
Q

What can CXR be used for? 1 2 3

A

1) Investigation of primary cancer 2) Staging of cancer (progression) 3) Follow up (to see if there is remission, relapse, etc)

40
Q

Uses of endoscopy

A

Visualisation and biopsy of suspicious-looking lesions

41
Q

Anatomical pathologist

A

Specialises in looking at biopsy results under a microscope, diagnosing cancers.

42
Q

Samples essential for diagnosis of cancer

A

Histopathological specimens

43
Q

Two principle ways to biopsy a tumour

A

1) Histopathology 2) Cytology

44
Q

Histopathology

A

Take a piece of tissue, stain it (HE, immunohistochemistry). Can see tissue architecture.

45
Q

Cytology

A

Take fine needle aspiration, exfoliative cytology (scrape cells from a surface). Place cells onto a slide. Can’t see stroma, tissue architecture.

46
Q

Examples of molecular, cytogenic techniques for diagnosing cancers 1 2 3 4

A

1) In situ hybridisation 2) PCR 3) Chromosomal rearrangements 4) Flow cytometry

47
Q

Cytologic tissue sampling in lung tumours 1) 2) 3) 4)

A

• Sputum • Bronchial brush and wash at bronchoscopy • Endobronchial ultrasound transbronchial aspiration (EBUS-TBNA) • FNA under radiological guidance for more peripheral lesions

48
Q

Tissue/histopathology specimens for diagnosing lung tumours 1) 2) 3) 4)

A

• Tissue core biopsy for peripheral lesions • Surgical resection specimen (if performed) • H&E • Immunohistochemistry: may help distinguish primary from metastatic lesions

49
Q

Things we need to know once diagnosis of malignancy is made 1 2 3 4

A

• Specific tumour type and subtype (cell lineage) • Grade • Stage • Presence of lymphovascular invasion

50
Q

Two broad groups of lung cancers

A

Non-small cell Neuroendocrine

51
Q

Neuroendocrine carcinomas

A

Show features of neuroendocrine cells.

52
Q

Small cell carcinoma

A

Very aggressive neuroendocrine cardcinoma

53
Q

Main types of non-small cell carcinomas

A

Squamous cell carcinoma, adenocarcinoma, large-cell (undifferentiated) carcinoma

54
Q

Most-common cancer in smokers and non smokers

A

Adenocarcinomas

55
Q

Pre-neoplastic changes in squamous cell carcinoma (lung) 1 2 3 4

A

Stratified squamous cell epithelium present (in smokers) Large, pleomorphic nuclei. Necrosis Invasive

56
Q

Pre-neoplastic changes in squamous cell carcinoma (lung) 1 2 3 4

A

Stratified squamous cell epithelium present (in smokers) Large, pleomorphic nuclei. Necrosis Invasive

57
Q

Name for pre-malignancy of squamous cell carcinoma

A

Dysplasia-carcinoma sequence

58
Q

Gross appearance of squamous cell carcinoma

A

Pale mass. Arise in main bronchi. Can form cavities.

59
Q

Location of adenocarcinomas

A

In bronchiolar epithelial cells. More peripheral. Not in main airways.

60
Q

Desmoplasia

A

When a lot of the tumour isn’t actually neoplastic cells, but stroma.

61
Q

What determines how hard a tumour is?

A

Degree of desmoplasia (amount of stroma)

62
Q

Classic histological feature of adenocarcinoma

A

Form ducts

63
Q

Classic histological feature squamous cell carcinoma

A

Keratinisation

64
Q

Degrees of cancer differentiation

A

Well-differentiated (resemble mature cells) Moderately-differentiated Poorly-differentiated (only poorly resemble mature cells, more aggressive)

65
Q

Stage of cancer

A

Refers to progression of malignancy (in terms of local spread, metastasis)

66
Q

What is used to determine stage of cancer?

A

Radiological and pathological assessment

67
Q

TNM

A

T: Extent of primary tumour (1 - 4) N: Regional lymph node metastases (0 - 3) M: Presence or absence of metastases (0 or 1) These are combined to give a score out of four.

68
Q

Histological suggestion of metastasis

A

Lympho-vascular invasion (even if can’t see metastases radiologically). Gives a poorer prognosis

69
Q

Examples of predictive factors in breast cancers

A

HER2 amplification in breast cancer Oestrogen and progesterone receptors Predictive factors can suggest potential therapies

70
Q

Examples of predictive factors in breast cancers

A

HER2 amplification in breast cancer Oestrogen and progesterone receptors Predictive factors can suggest potential therapies

71
Q

Management of a tumour 1 2 3 4 5

A

1) Surgery 2) Radiotherapy 3) Chemotherapy 4) Targeted therapy 5) Immunotherapy, bone marrow transplant (these are less-widely applicable)

72
Q

Things on a path report for a cancer 1 2 3 4 5 6

A

• Confirmation/further information on type and subtype of malignancy • Grade • Size of tumour/depth of invasion • Presence/absence of microscopic vascular invasion • Completeness of excision • Presence and number of lymph node metastases (which may only be microscopic so histologic examination is necessary)

73
Q

Targeted therapy

A

Targeted therapies block the growth of cancer cells by interfering with the function of specific molecules (e.g. oncoproteins) resulting from genetic alterations that drive carcinogenesis and tumour growth

74
Q

Advantages of targeted therapies

A

Less damaging to normal cells, target neoplastic cells

75
Q

Two broad types of targeted therapies

A

Monoclonal antibodies Small molecules

76
Q

Most important mutations in non-small cell carcinomas

A

EGFR ALK

77
Q

EGFR

A

Transmembrane tyrosine kinase receptors Growth factor receptor. When stimulated, causes cell to divide.

78
Q

Examples of anti-EGFR therapies

A

Gefitinib Erlotinib Both inhibit EGFR tyrosine kinase.

79
Q

Examples of anti-EGFR therapies 1 2

A

Gefitinib Erlotinib Both inhibit EGFR tyrosine kinase.

80
Q

Causes of death in cancer 1 2 3

A

1) Cachexia 2) Secondary infection from poor nutrition, effects of treatment (pneumonia is common) 3) Damage to vital organ or system by either primary or secondary tumour

1Principles of Biomedicine - MD1 (157 decks)

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