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Pathology > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Define neoplasm

A

Abnormal growth of tissue, which is partly or completely autonomous of normal growth controls

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2
Q

How are tumours graded

A

According to the degree of histological resemblance to the cell of origin

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3
Q

What are tumours labelled if they defy histogenetic classification

A

Anaplastic

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4
Q

What is a carcinoma

A

Malignant epithelial neoplasm

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5
Q

What is a sarcoma

A

Malignant connective tissue neoplasm

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6
Q

Define carcinoma in situ

A

A lesion with all the cytological features of cancer but no evidence of invasion through the epithelial basement membrane

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7
Q

Define teratoma

A

Germ cell neoplasm representing all three germ layers i.e. ectoderm, mesoderm, endoderm

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8
Q

Define blastoma.

A

Tumours bearing histological resemblance to the embryonic form of the organ which they arise

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9
Q

Define hamartoma

A

Tumour-like lesion which lacks autonomy but in which the elements are fully differentiated and are normally found in the tissue of origin

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10
Q

What is a labile cell

A

Cell that is constantly renewed

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11
Q

What is a stable cell

A

Usually quiescent but can be stimulated to divide (e.g. hepatocyte)

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12
Q

What is a permanent cell

A

Do not undergo mitoses in postnatal life

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13
Q

List the 4 DNA amino acids

A
  • Adenine
  • Thymine
  • Cytosine
  • Guanine
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14
Q

In what form is DNA stored in the cell nucleus

A

Chromatin - which are wrapped around histones to form nucleosome complexes

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15
Q

Describe G1 phase of the cell cycle

A

Pre-synthetic phase - cellular contents, excluding chromosomes, are duplicated

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16
Q

Describe the S phase of the cel cycle

A

DNA synthesis - each of the 46 chromosomes is duplicated

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17
Q

Describe G2 phase of the cell cyclce

A

Premitotic - the cell double checks the duplicated chromosomes for errors and makes repairs

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18
Q

What is G0 phase of the cell cycle

A

Quiescent (resting) phase

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19
Q

List the phases of mitosis (7)

A
  1. Interphase
  2. Prophase
  3. Prometaphase
  4. Metaphase
  5. Anaphase
  6. Telophase
  7. Cytokinesis
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20
Q

Describe Interphase

A

Comprises G1, S, and G2 phases of the cell cycle when the cell is in preparation for division

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21
Q

Describe Prophase

A
  • Chromatin begins to condense and is seen as chromosomes

- Centrioles move to the opposing end of the cell and the mitotic spindle is formed

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22
Q

Describe Prometaphase

A
  • Nuclear membrane dissolves

- Chromosomes start to move to the centre of the cell under the control of microtubules

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23
Q

Describe Metaphase

A

Spindle fibres align with the chromosomes along the metaphase plate

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24
Q

Describe Anaphase

A

The paired chromosomes separate and are dragged to the poles of the cell

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25
Q

Describe Telophase

A

Chromatids arrive at the opposite ends of the cell and disperse after new nuclear membranes are formed

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26
Q

Describe Cytokinesis

A

Actin fibre forms around the centre of the cell and contracts to pinch off two daughter cells

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27
Q

When are the two crucial regulatory points of the cell cycle

A
  1. Entry of G0 cells into G1

2. G1 to S phase

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28
Q

What causes the cell to move from G1 to S phase and also G2 to M phase

A

Cyclin-dependent Kinases (CDKs)

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29
Q

What blocks the cells in G1 if DNA is damaged

A

Protein p53

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30
Q

What occupation is associated with scrotal cancer and why

A

Chimney Sweeps - polycyclic aromatic hydrocarbon exposure

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31
Q

What cancer is associated with Beta-naphthylamine

A

Bladder TCC

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32
Q

What cancers are associated with EBV

A
  • Burkitt’s lymphoma
  • Nasopharyngeal carcinoma
  • Beta-cell lymphoma in the immunocompromised
33
Q

What virus is strongly associated with cervical cancer

A

HPV 16 and 18

34
Q

What cancer is associated with wood dust

A

Paranasal sinus cancer

35
Q

What gene is affected in Li-Fraumeni syndrome

A

p53

36
Q

What neoplasms result from Li-Fraumeni syndrome

A
  • Breast
  • Ovarian
  • Astrocytoma
  • Sarcoma
37
Q

What gene is affected in retinoblastoma

A

Rb1

38
Q

What other neoplasms are associated with retinoblastoma

A

Osteosarcoma

39
Q

What gene is affected in Familial polyposis coli

A

APC

40
Q

What cancers are associated with Von-Hippel-Lindau syndrome

A
  • Renal
  • Phaeochromocytoma
  • Haemangioblastoma
41
Q

What gene is affected in MEN syndromes

A

RET

42
Q

What gene is affected in Von-Hippel-Lindau syndrome

A

VHL

43
Q

What causes the conversion of hyperproliferative colonic epithelium to adenoma

A
  • APC inactivation

- K-ras mutation

44
Q

What causes the conversion of colonic adenoma to carcinoma

A
  • DCC deletion

- p53 deletion

45
Q

What cancer may develop from Paget’s disease of the bone

A

Osteogenic sarcoma

46
Q

What haematological malignancy is associated with Down’s Syndrome

A

Acute Leukaemia

47
Q

How do oncogenes contribute to cancer development

A

Instruct cells to make proteins that stimulate excessive growth and cell division

48
Q

What is a proto-oncogene

A

Family of normal genes that code for proteins involved in the normal growth-control pathway of cels

49
Q

How do oncogenes arise

A

From mutation of proto-oncogenes

50
Q

What are the 2 classes of tumour suppressor genes

A
  1. Caretaker genes

2. Gatekeeper genes

51
Q

What is the role of caretaker genes

A

Maintain integrity of the genome by repairing DNA damage

52
Q

What is the role of gatekeeper genes

A

Inhibit proliferation, or promote the death of cells with damaged DNA

53
Q

How many tumour suppressor genes must be affected to cause cancer

A

Both of the gene PAIR

54
Q

Where is the p53 gene situated

A

Short-arm of chromosome 17

55
Q

What type of tumour suppressor genes are BRCA 1 and 2

A

Caretaker

56
Q

What does the rate of cell proliferation within a population of cells depend on

A
  1. Rate of tumour cell division
  2. Fraction of cells within the population undergoing division
  3. Rate of cell loss from the replicating pool due to regulated apoptosis
57
Q

Define ‘Growth Fraction’

A

The fraction of cells within a population undergoing cell division - typically 20% of rapidly growing tumours

58
Q

What is Gompertzian growth

A

The way neoplasms initially grow exponentially and then slow as they increase in size

59
Q

Why does Gompertzian growth occur

A
  • Decrease in growth fraction
  • Increase in cell loss e.g. necrosis
  • Nutritional depletion of tumour cells as they outgrow blood supply
60
Q

Why does ‘debulking’ or radiation improve the effectiveness of chemotherapy

A

Pushes more cells into the cell cycle and therefore increases the number of cells susceptible to chemotherapy

61
Q

What are the 4 routes of metastases

A
  1. Lymphatic
  2. Haematogenous
  3. Transcoelomic
  4. Seeding
62
Q

Which cancers favour haematogenous spread to the bone

A
  1. Breast
  2. Prostate
  3. Lung
  4. Kidney
  5. Thyroid (follicular)
63
Q

How do sarcomas metastasise

A

Haematogenous

64
Q

Tumour marker for B-cell lymphoma

A

CD20

65
Q

Investigation for suspected lymphoma

A

Excision biopsy

66
Q

Tumour marker for choriocarcinoma

A

beta-HCG

67
Q

Tumour markers for testicular cancer

A
  • Beta-HCG
  • AFP
  • Placental alkaline phosphatase
68
Q

What has been the outcome of the UK breast screening programme

A

35% reduction in mortality from breast cancer among screened women for 50-69

69
Q

What is the structure of the UK breast screening programme

A

Women aged 50 (47) -70 are invited for screening every 3 years

70
Q

What is the structure of the UK cervical screening programme

A

All women aged 25-64:

  • 25-49 screened 3-yearly
  • 50-64 screened 5-yearly
71
Q

What is the structure of the UK colorectal cancer screening programme

A

2-yearly FIT test for men and women aged 60 (56) - 74

72
Q

Define Resection en bloc

A

Surgical removal of the entirety of the tumour without disrupting its capsule

73
Q

What type of radiotherapy is used to treat cutaneous and subcutaneous lesions

A

Particulate radiotherapy

74
Q

Which phase of the cell cycle are cells most sensitive to radiotherapy

A

S phase

75
Q

Describe stereotactic radiotherapy

A

Radiotherapy that is given from many different angles around the body e.g. used in brain tumours

76
Q

What is the mechanism of action of classic alkylating agents e.g. cyclophosphamide

A

Act by forming covalent bonds with nucleic acids, proteins, nucleotides, and amino acids, and so inactivate the enzymes involved in DNA production

77
Q

What is the mechanism of action of non-classic alkylating agents e.g. Cisplatin

A

Act by causing cross-linking of DNA strands

78
Q

What is the mechanism of action of antimetabolites e.g. Methotrexate

A

Act by interfering with purine or pyrimidine synthesis and hence interfere with DNA synthesis

79
Q

What is the mechanism of action of Vinca Alkaloids e.g. Vincristine

A

Act by inhibiting mitosis, by preventing spindle formation (they are M-phase specific)

Pathology (7 decks)

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