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Phase 2a Medicine > Cancer > Flashcards

Cancer Flashcards

1
Q

What is important about basal cell carcinoma?

A

Never spreads to other parts of the body

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2
Q

What happens if you carry out a complete local excision of a basal cell carcinoma?

A

The patient is completely cured.

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3
Q

Leukaemia definition

A

Malignant cancer of both bone marrow and other blood-forming organs. Usually involves WBC.

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4
Q

Why can’t you treat leukaemia with surgery?

A

Because it’s in your blood- all over your body.

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5
Q

What often happens to lymph nodes during breast cancer?

A

Lymph nodes drain the site of the carcinoma, and become cancerous themselves.

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6
Q

Can carcinomas spread to bone?

A

Yes. Carcinomas can spread through the blood to bone.

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7
Q

What are the cancers that commonly spread to bone?

A

Breast, prostate, lung, thyroid and kidney.

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8
Q

How do you confirm that someone has breast cancer?

A

A core needle biopsy.

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9
Q

After you confirm someone has breast cancer, where do you check next?

A

The axilla. If it has spread, node clearance is needed.

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10
Q

What are micro metastases?

A

Metastases that may still be present even if a tumour is completely excised.

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11
Q

How do you remove micro metastases?

A

Adjuvant radiotherapy.

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12
Q

What are recovered breast cancer patients often prescribed?

A

Anti-oestrogens.

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13
Q

What is the name of neoplasms starting in epithelial tissue or the skin?

A

Carcinomas.

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14
Q

What is the name of neoplasms starting in bones or soft tissues?

A

Sarcomas.

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15
Q

What is the most common type of cancer?

A

Carcinomas.

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16
Q

What is the name of neoplasms starting in plasma cells?

A

Myeloma.

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17
Q

What is the name of neoplasms most linked to WBCs?

A

Leukaemia.

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18
Q

What is the name of neoplasms starting in the lymphatic system?

A

Lymphoma.

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19
Q

What are the 3 classes of neoplasms based on their behaviour?

A

Benign, borderline and malignant.

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20
Q

What is a tumour?

A

Any mass or lump of tissue that may resemble swelling. A tumour may be: a neoplasm, an inflammation, hypertrophy or a hyperplasia.

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21
Q

Neoplasm definition

A

An abnormal mass of tissue that forms when cells grow and divide more than they should or do not die when they should.

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22
Q

What are 4 characteristics of neoplasia?

A

AN autonomous, abnormal, persistent new growth.

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23
Q

What is the suffix of all neoplasms?

A

‘-oma’

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24
Q

What are the 2 main types of benign epithelial neoplasms?

A

Papillomas and adenomas.

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25
Q

What is a papilloma?

A

Benign tumour of non-glandular, non-secretory epithelium.

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26
Q

What is an adenoma?

A

Benign tumour of glandular or secretory epithelium.

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27
Q

What is a malignant epithelial neoplasm known as?

A

Carcinoma

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28
Q

How do you name benign connective tissue neoplasms?

A

According to the cell of origin, suffixed by ‘-oma’. E.g. lipoma: adipocytes.

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29
Q

What is the prefix referring to adipocytes?

A

‘Lip-‘

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30
Q

What is the prefix referring to cartilage?

A

‘Chondr-‘

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31
Q

What is the prefix referring to bone?

A

‘Oste-‘

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32
Q

What is the prefix referring to vascular?

A

‘Angi-‘

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33
Q

What is the prefix referring to striated muscle?

A

‘Rhabdomy-‘

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34
Q

What is the prefix referring to smooth muscle?

A

‘Leiomy-‘

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35
Q

What is the prefix referring to nerves?

A

‘Neur-‘

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36
Q

What is a malignant connective tissue neoplasm?

A

Sarcoma

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37
Q

How are sarcomas named?

A

‘-sarcoma’ prefixed with by cell type of origin.

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38
Q

What is the definition of anaplastic?

A

Cancer cells that divide rapidly and have little or no resemblance to normal cells.

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39
Q

Where do neoplastic cells derive from?

A

Nucleated cells.

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40
Q

What is the definition of monoclonal?

A

Forming a clone which is derived asexually from a single individual or cell. Neoplasms are usually monoclonal.

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41
Q

How does the parent cell affect the growth pattern of the neoplasm?

A

Synthetic activity is related to the the parent cell.

42
Q

How does the stroma support the development of the neoplasm.

A

Connective tissue framework. Mechanical support and nutrition.

43
Q

What is tumour angiogenesis?

A

The growth of new blood vessels that tumours need to grow.

44
Q

What is the name of striated muscle cancer?

A

Rhabdomyosarcoma

45
Q

What is a cancer in situ?

A

Cancer that has not broken through the basement membrane.

46
Q

What cancer does Hep C cause?

A

Hepatocellular carcinoma

47
Q

What is the name of a benign tumour of fat cells?

A

Lipoma

48
Q

What is the name of malignant tumour of glandular epithelium?

A

Adenocarcinoma

49
Q

Does ovarian cancer commonly spread to the peritoneum?

A

Yes

50
Q

Definition of carcinogenesis

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations.

51
Q

Does carcinogenesis apply to benign neoplasms, malignant neoplasms or both?

A

Malignant neoplasms

52
Q

Does oncogenesis apply to benign neoplasms, malignant neoplasms or both?

A

Both benign and malignant neoplasms.

53
Q

Is carcinogenesis a single or multistep process?

A

A multistep process.

54
Q

What is a carcinogen?

A

Agents known or suspected to cause tumours.

55
Q

What is the difference between carcinogenic and oncogenic?

A

Carcinogenic is cancer causing. Oncogenic is tumour causing?

56
Q

Definition of mutagenic

A

Inducing or capable of inducing genetic mutation.

57
Q

What percentage of cancer risks are environmental?

A

85%

58
Q

What are the problems with identifying carcinogens?

A

Latent interval may be decades. Complexity of environment. Ethical constraints (can’t just give people cancer)

59
Q

What is hepatocellular carcinoma?

A

Most common type of primary liver cancer. Uncommon in UK/USA. Common in areas with high hep B/C and mycotoxins.

60
Q

How does thorotrast provide direct evidence of carcinogenesis?

A

Colloidal suspension of thorium.
Radiographic contrast medium 1930-1950.
Irreversibly ingested by phagocytes.

61
Q

Evidence linked to thyroid irradiation?

A

Chernobyl nuclear reactor explodes.
Release of radioactive iodine isotopes.
Increased incidence of thyroid cancer in Ukrainian children.

62
Q

How do you ethically collect evidence for carcinogens?

A

Incidence of tumours in laboratory animals.
Cell/tissue cultures.
Mutagenicity testing in bacterial cultures.

63
Q

What are the problems with cancer research on animals and cultures.

A

Animals / cultures may metabolise agents differently to humans. Bacterial mutation may not mean carcinogenicity.

64
Q

What are the classes of carcinogens?

A

Chemical, viral, ionising and non-ionising radiation, hormones parasites and mycotoxins and miscellaneous.

65
Q

Are there common features of chemical carcinogens?

A

There are no common structural features.

66
Q

How many of the chemical carcinogens act directly?

A

Some act directly, but most require metabolic conversion from pro-carcinogens to ultimate carcinogens.

67
Q

Where does alcohol cause cancer?

A

Oropharynx, larynx, oesophagus, liver, breast, colorectal

68
Q

How does cancer assist other cancer development?

A

Makes it easier for cells in oropharynx to absorb other carcinogens. Also increases oestrogen levels.

69
Q

What cancers does UV light (UVA and UVB) increase the risk of?

A

BCC, melanoma and SCC. The risk is increased in xeroderma pigmentosum.

70
Q

What is radiant energy and what time frame does the effect have?

A

Ionising radiation. Long term effect.

71
Q

What cancers is increased oestrogen associated with?

A

Increase in mammary/endometrial cancer.

72
Q

What cancer is anabolic steroids associated with?

A

Increased risk of hepatocellular carcinoma.

73
Q

What are 2 examples of miscellaneous carcinogens?

A

Asbestos and metals.

74
Q

What host factors affect the risk of cancer?

A

Race, diet, premalignant lesions, transplacental exposure and constitutional factors (age, gender etc.)

75
Q

What are identifiable local abnormalities associated with an increased risk of malignancy at the site?

A

Colonic polyps, cervical dysplasia (CIN), ulcerative colitis, undescended testis.

76
Q

Why can’t carcinoma in situ spread anywhere?

A

The cancer is enclosed by the basement membrane.

77
Q

What is an invasive carcinoma?

A

When the cancer leaves the basement membrane and escapes somewhere with blood and lymph vessels.

78
Q

What is a micro-invasive carcinoma?

A

Carcinomas that have not invaded very far.

79
Q

How does the tumour break through the basement membrane?

A

Proteases - matrix metalloproteinases, collagenase, cathepsin D, urokinase-type, plasminogen activator, cell motility.

80
Q

What are the first 4 steps of metastasis?

A

Cross the basement membrane. Get through the connective tissue. Enter a small vessel (blood or lymph). Avoid WBC’s.

81
Q

What are the last 4 steps of metastasis?

A

Lodge somewhere in the vessel. Cross the basement membrane again. Lodge itself in the connective tissue (metastatic site). Develop its own blood supply.

82
Q

What is tumour cell motility?

A

Tumour derived motility factors, often derived by the tumour cells often breakdown the products of extracellular matrices.

83
Q

How do spreading cancers evade host immune defence?

A

Aggregation with platelets. Shedding of surface antigens. Adhesion to other tumour cells.

84
Q

What is needed for growth of the metastatic site?

A

Growth factors. The cancers often produce their own.

85
Q

What is angiogenesis?

A

The formation of new blood vessels.

86
Q

What growth factors promote angiogenesis?

A

Vascular endothelial growth factor.

87
Q

What inhibits angiogenesis?

A

Angiostatin, endostatin and vasculostatin.

88
Q

Where do cancers first formed in the heart commonly metastasise?

A

In the lungs.

89
Q

Where do cancers first formed in the colon often metastasise?

A

In the liver via the portal vein. Other cancers that commonly metastasis in the liver are Colon, stomach, pancreas, carcinoid tumours of intestine.

90
Q

Which tumours commonly metastasise to bone?

A

Prostate, breast, thyroid lung and kidney.

91
Q

Definition of chemotherapy

A

The treatment of disease by the use of chemical substances, especially the treatment of cancer by cytotoxic and other drugs

92
Q

What type of cells does conventional chemotherapy act on?

A

Dividing cells

93
Q

How does conventional chemotherapy work?

A

It prevents microtubules pulling DNA apart to stop cell division. Cross links DNA to prevent replication

94
Q

Why does chemotherapy cause side effects?

A

It doesn’t just target cancer cells; targets all cells that are dividing

95
Q

What are side effects of conventional chemotherapy?

A

Fatigue, hair loss, myelosuppression (anaemia), nausea and vomiting and changes to bowel movements

96
Q

What 2 factors result in the increase in tumour size?

A

Cell division. Lack of cell death (apoptosis)

97
Q

What sort of tumour is conventional chemotherapy good for?

A

Fast dividing tumour e.g. germ cell tumours of testis, acute leukaemia, lymphomas, embryonal paediatric tumours, choriocarcinoma

98
Q

How does targeted chemotherapy work?

A

Exploits some difference between cancer cells and normal cells to target drugs to the cancer cells

99
Q

How can differences between cancer cells and normal cells be found?

A

Gene arrays, proteomics and tissue microarrays

100
Q

How are the differences between cancer cells and normal cells be exploited?

A

Make a monoclonal antibody against growth factor A receptor. Binds to the outside of the growth factor. No activation because the receptor is blocked by the antibody.

101
Q

What is cetuximab?

A

Monoclonal antibody against epidermal growth factor receptor (EGFR).

Phase 2a Medicine (6 decks)

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