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ΩΩ 2a Bateman - Introductory Clinical Sciences > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What is a cancer called contained within a basement membrane?

A

Carcinoma in situ

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2
Q

What is a cancer called when a cancer breaks through the basement membrane?

A

Invasive cancer.

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3
Q

What are the different classifications of invasive cancer?

A

Micro-invasive cancer. (Small amount of cancer cells released)

Invasive cancer. (Large amount of cancer cells released)

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4
Q

How does the cancer get out of the basement membrane?

A

Uses proteases.

Needs cell motility.

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5
Q

What proteases does a cancer use to get out of the basement membrane?

A

Collagenase

Cathepsin D

Urokinase-type plasminogen activator

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6
Q

What do cancers have to do to metastasise?

A

Grow.

Invade basement membrane.

Move.

Lymphatic vessels or blood vessel.

Travel without getting eaten.

Find another site to live.

Invade.

Growth.

Blood supply.

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7
Q

How could you treat some cancers?

A

Inhibit some enzymes a tumour needs to eat threw the basement membrane.

Stop them travelling around.

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8
Q

How can cancers evade the lymphocytes in the blood?

A

Aggregation with platelets.

Shredding of surface antigens.

Adhesion of other tumour cells.

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9
Q

What do cancers need for tumour cell motiltiy?

A

Tumour cell derived motility factors

Breakdown products of extracellular matrix

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10
Q

What do cancers need to enter the blood?

A

Collagenases

Cell motility

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11
Q

What do cancers need to exit the blood?

A

Adhesion receptors.

Collagenases.

Cell motility.

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12
Q

What do cancers need after they exit the blood?

A

growth factors.

Angiogenesis.

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13
Q

What are some angiogenesis promoters?

A

Vascular endothelial growth factor.

Basic fibroblast growth factor.

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14
Q

What are some angiogenesis inhibitors?

A

Vasculostatin.

Endostatin.

Angiostatin.

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15
Q

Give an example of an inhibitor of angiogenesis?

A

Avastin.

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16
Q

Where is an easy place for a tumour to get stuck in the body?

A

The lung capillaries.

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17
Q

Is a vein or artery easy for a tumour to metastasise to?

A

Vein.

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18
Q

Which tumours commonly metastasises to the lung?

A

Sarcomas or any common cancers.

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19
Q

Where is the first place a cancer cell will spread to in colon cancer?

A

Liver.

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20
Q

What are common cancers which metastasise to the liver?

A

Colon, stomach, pancreas, carcinoid tumours of intestine.

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21
Q

What are the tumours which commonly metastasise to bone?

A

Prostate, breast, thyroid, lung and kidney.

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22
Q

What happens when a tumour invades bone?

A

Either eat the bone or lay new bone down.

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23
Q

What is chewing up bone called in cancer?

A

Osteolytic metastasise.

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24
Q

What is laying new bone down called in cancer?

A

Osteosclerotic metastasise.

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25
Q

What does Vinblastine do?

A

Binds to mitotic spindels and stops them contracting.

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26
Q

What drug inhibits topoisomerase 2?

A

Etoposide.

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27
Q

What does ifasemide and cisplatin do?

A

Cross links DNA so can’t divide.

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28
Q

What are the side effects of conventional chemotherapy?

A

Not selective for tumour cells.

-Except that they might be dividing faster.

Usually hits normal cells which are dividing

  • Myelosuppresion.
  • Hair loss.
  • Diarrhoea.
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29
Q

What is Myelosuppresion?

A

A condition in which bone marrow activity is decreased, resulting in fewer red blood cells, white blood cells, and platelets.

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30
Q

What do cancer cells need to do to increase in size?

A

Cell division.

Lack of cell death (apoptosis).

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31
Q

What are the pros and cons of conventional chemotherapy? Give some examples of types of cancers?

A

-Good for fast dividing tumours

germ cell tumours of testis

acute leukaemias

lymphomas

embryonal paediatric tumours

choriocarcinoma

-Not so good for slower dividing tumours

most other tumours.

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32
Q

What are the benefits of targeted chemotherapy?

A

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

  • more effective
  • less side effects.
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33
Q

What can you do to work out if different diseases are present?

A

Gene arrays.

Proteomics.

Tissue Microarrays.

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34
Q

What is an example of a cancer cell proliferation?

A

over expression of a receptor or the receptor is always on despite no growth factor being bound to it.

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35
Q

How can you block a receptor which is being overexpressed?

A

Produce monoclonal antibodies against the receptor to block anything binding.

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36
Q

How can you block a receptor which is constantly on?

A

A small molecular inhibitor of the receptor. CAN also block over expression.

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37
Q

What is an example of a monoclonal antibody which blocks a receptor?

A

Cetuximab - blocks epidermal growth factor receptor.

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38
Q

What is an example of a drug which combats breast cancer?

A

Herceptin.

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39
Q

What does Herceptin bind to?

A

Her-2.

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40
Q

How does Herceptin work?

A

Binds to Her-2 receptors on the cell surface and make them become endocytosed, therefore there is less Her-2 on the surface to bump into each other and produce a reaction. Also cause lymphocytes to come along and destroy the cell.

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41
Q

What is Her-2 associated with?

A

large size

high grade

aneuploidy

negative oestrogen receptor status

independent adverse prognostic factor.

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42
Q

What can Her-2 not do?

A

Cross the blood brain barrier.

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43
Q

What is Gleevac?

A

inhibitor of c-kit tyrosine kinase originally developed as inhibitor of BCR-ABL protein to treat CML also found to inhibit c-kit protein.

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44
Q

What is a tumour?

A

Any abnormal swelling.

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45
Q

What is a neoplasm?

A

A lesion resulting from the AUTONOMOUS or relatively autonomous ABNORMAL growth of cells which persists after the initiating stimulus has been removed.

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46
Q

Which is worse malignant or benign?

A

Malignant.

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47
Q

What is the structure of a neoplasm?

A

Neoplastic cells and Stroma.

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48
Q

What are neoplastic cells of a neoplasm?

A

Derive from nucleated cells.

Usually monoclonal.

Growth pattern related to parent cell.

Synthetic activity related to parent cell:

Collagen, mucin, keratin, hormones.

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49
Q

What is the stroma of a neoplasm?

A

Mattress.

Connective tissue framework.

Mechanical support.

Nutrition. Stroma grows by growth factors from neoplastic cells.

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50
Q

What cell and tissue types would you therefore expect to find within a neoplasm’s stroma?

A

Fibrous connective tissue.

Unorganised.

Blood vessels.

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51
Q

What is essential to tumour growth?

A

Angiogenesis. 2mm small takes oxygen by diffusion.

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52
Q

How do you classify a neoplasm?

A

Behavioural: benign/malignant

Histogenetic: cell of origin.

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53
Q

Why do we classify a neoplasm?

A

To determine appropriate treatment

To provide prognostic information.

54
Q

How may a neoplasm be classified?

A

benign

borderline

malignant.

55
Q

What do borderline tumours do?

A

defy precise classification.

56
Q

What are the features of benign neoplasms at low magnification?

A

Localised, non-invasive

Slow growth rate

Low mitotic activity

Close resemblance to normal tissue

Circumscribed or encapsulated.

57
Q

What are the features of benign neoplasms at high magnification?

A

Nuclear morphometry often normal

Necrosis rare

Ulceration rare

Growth on mucosal surfaces

often exophytic

58
Q

Why should we worry about benign neoplasm?

A

Pressure on adjacent structures

Obstruct flow

Production of hormones

Transformation to malignant neoplasm

Anxiety.

59
Q

What are the features of malignant neoplasms at low magnification?

A

Invasive

Metastases (Not always)

Rapid growth rate

Variable resemblance to normal tissue

Poorly defined or irregular border

60
Q

What are the features of malignant neoplasms at high magnification?

A

Hyperchromatic nuclei (lots)

Pleomorphic nuclei (Different shaped)

Increased mitotic activity

Necrosis common

Ulceration common

Growth on mucosal surfaces and skin often endophytic

61
Q

What are the key features of a malignant neoplasm?

A

Encroach upon and destroy surrounding tissue

Are poorly circumscribed

Have a ‘crab-like’ cut surface (Latin: cancer)

Metastasise

62
Q

Why do we need to worry about malignant neoplasms?

A

Destruction of adjacent tissue

Metastases

Blood loss from ulcers

Obstruction of flow

Hormone production

Paraneoplastic effects

Anxiety and pain.

63
Q

What is histogenesis?

A

The specific cell of origin of a tumour.

64
Q

Where can neoplasms arise from?

A

Epithelial cells

Connective tissues

Lymphoid/haemopoietic organs.

65
Q

What do neoplasms end in?

A

OMA.

66
Q

What is a papilloma?

A

Benign tumour of non-glandular, non-secretory epithelium

Prefix with cell type of origin

e.g. squamous cell papilloma.

67
Q

What is an adenoma?

A

Benign tumour of glandular or secretory epithelium

Prefix with cell type of origin

e.g. colonic adenoma, thyroid adenoma.

68
Q

What is a Carcinoma?

A

Malignant epithelial neoplasm.

Malignant tumour of epithelial cells

Prefixed by name of epithelial cell type

e.g. transitional cell Ca.

69
Q

What is a adenocarcinoma?

A

Malignant tumour of epithelial cells,

Carcinomas of glandular epithelium.

70
Q

What is a: Lipoma Chondroma Osteoma Angioma?

A

adipocytes cartilage bone vascular

71
Q

What is a rhabdomyoma?

A

Benign neoplasm of striated muscle.

72
Q

What is a leiomyoma?

A

Benign neoplasm of smooth muscle.

73
Q

What is a neoplasm of nerves called?

A

Neuroma.

74
Q

What do you call connective tissue malignant neoplasms?

A

Sarcoma.

75
Q

How can you further classify carcinomas and sarcomas?

A

Degree of differentiation.

76
Q

What is it called when the cell-type is unknown?

A

Anaplastic.

77
Q

What words have Oma but are not neoplasms?

A

Granuloma, mycetoma and tuberculoma.

78
Q

What are some exceptions to malignant tumours being carcinomas or sarcomas?

A

melanoma: malignant neoplasm of melanocytes

Mesothelioma: malignant tumour of mesothelial cells

lymphoma: malignant neoplasm of lymphoid cells

79
Q

What is carcinogenesis?

A

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

80
Q

What does carcinogenesis apply to?

A

Malignant neoplasms.

81
Q

What is oncogenesis?

A

Benign and malignant tumours.

82
Q

What are carcinogens?

A

Agents known or suspected to cause tumours.

83
Q

What is carcinogenic?

A

Cancer causing.

84
Q

What is oncogenic?

A

Tumour causing.

85
Q

How much of cancer risk is environmental?

A

85%.

86
Q

What are the problems with identification of carcinogens?

A

Latent interval may be decades.

Complexity of environment.

Ethical constraints.

87
Q

What are the different classes of carcinogens?

A

Chemical.

Viral.

Ionising and non-ionising radiation.

Hormones, parasites and mycotoxins.

Miscellaneous.

88
Q

What are chemical carcinogens features?

A

No common structural features

Some act directly

Most require metabolic conversion from pro-carcinogens to ultimate carcinogens

Enzyme required may be ubiquitous or confined to certain organs.

89
Q

What are polycyclic aromatic hydrocarbons tumours and how do people obtain them?

A

Lung cancer and skin cancer. Smoking and mineral oils.

90
Q

What are aromatic amines tumours and how do people obtain them?

A

Bladder cancer. Rubber/dye works.

91
Q

What are Nitrosamines tumours and how do people obtain them?

A

Gut cancer. Proven in animals.

92
Q

What are alkylating agent tumours and how do people obtain them?

A

Leukaemia. Small risk in humans.

93
Q

What is xeroderma pigmentosum?

A

Repair DNA mechanism is defective

94
Q

What does radiation energy cause?

A

UV light Increase Exposure to UVA or UVB causes Increase BCC, melanoma, SCC

95
Q

What are some biological agents for causing cancer?

A

Hormones. Mycotoxins. Parasites.

96
Q

How hormones cause cancer.

A

Increase Oestrogen leads to an increase mammary/endometrial cancer Anabolic steroids leads to hepatocellular carcinoma

97
Q

How can mycotoxins cause cancer?

A

Alfatoxin B1 leads to hepatocellular carcinoma

98
Q

How can parasites cause cancer?

A

Chlonorchis sinensis leads to cholangiocarcinoma

Shistosoma leads to bladder cancer

99
Q

What are the host factors for cancer?

A

Race

Diet

Constitutional factors - age, gender etc

Premalignant lesions

Transplacental exposure.

100
Q

What race factors are there in cancer.

A

Increase Oral cancer in India, SE Asia (reverse smoking, betal chewing) Decrease Skin cancer in blacks (melanin)

101
Q

What are some premalignant conditions?

A

Colonic polyps

Cervical dysplasia (CIN)

Ulcerative colitis

Undescended testis

102
Q

Where does a basal cell carcinoma spread?

A

Basal cell carcinoma of the skin only invades locally - it never spreads to other parts of the body.

103
Q

How can you treat a basal cell carcinoma?

A

Cut it out

104
Q

Why can’t you just cut out leukaemia?

A

White blood cells circulate round the body and so will any tumour of white blood cells

105
Q

Where are cancer cells most likely to spread to first?

A

Lymph nodes.

106
Q

Where does the cancer spread to in breast cancer?

A

Axillary lymph nodes.

107
Q

Where can carcinomas spread?

A

To bone from the blood.

108
Q

What are the common cancers that spread to bone?

A

breast, prostate, lung, thyroid and kidney.

109
Q

What do you need to do if a cancer has spread to the axilla?

A

Axilla clearance is needed.

110
Q

What do you need to do if a cancer has spread to the rest of the body?

A

Chemo therapy is needed.

111
Q

What do you need to do if a cancer has not spread to the rest of the body?

A

surgery with or without lymph node clearance.

112
Q

Once a tumour has been excised will the tumour be gone?

A

Even if a tumour is completely excised micro metastases could be present.

113
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision.

114
Q

What is an example of adjuvant therapy?

A

Radiotherapy after breast excision.

115
Q

What is hypertrophy?

A

increase in size of a tissue caused by an increase in size of the constituent cells.

116
Q

What can divide in skeletal muscle?

A

Myofibrils.

117
Q

What is hyperplasia?

A

Increase in size of a tissue caused by an increase in number of the constituent cells.

118
Q

What is an example of hyperplasia?

A

Prostate in older age.

119
Q

What is an example of hypertrophy and hyperplasia?

A

Smooth muscle in pregnancy.

120
Q

What is atrophy?

A

decrease in size of a tissue caused by a decrease in number of the constituent cells or a decrease in their size.

121
Q

What is metaplasia?

A

change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type.

122
Q

What is an example of metaplasia?

A

metaplasia in bronchi of a smoker. Ciliated columnar epithelium to squamous epithelium.

123
Q

What is dysplasia?

A

imprecise term for the morphological changes seen in cells in the progression to becoming cancer.

124
Q

What limits the number of divisions in a cell?

A

Telomeres.

125
Q

What can telemeres be used to predict?

A

Lifespan.

126
Q

What damage can happen at DNA replication?

A

Telomere shortening.

Free radical generation.

Cross-linking or mutations of DNA.

Loss of calcium influx controls.

Damage to mitochondrial DNA.

Loss of DNA repair mechanisms.

127
Q

How does UV-B light affect the skin?

A

Cross links proteins and cause wrinkling.

128
Q

What is osteoporosis?

A

Loss of bone matrix.

129
Q

What causes osteoporosis?

A

increased bone resorption - lack of oestrogen.

decreased bone formation - lack of oestrogen.

130
Q

What happens later in life to hormones?

A

decreased growth hormone.

decreased testosterone.

increased catabolic cytokines.

131
Q

What can a cancer cell do?

A

Either undergo apoptosis and go away. Grow and multiply.

ΩΩ 2a Bateman - Introductory Clinical Sciences (4 decks)

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