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Principles of Disease HQ > Tumour Pathology > Flashcards

Tumour Pathology Flashcards

1
Q

What is a tumour?

A

Abnormal growing mass of tissue
Uncoordinated with surrounding normal tissue
Growth continues after stimulus removal, meaning it is an irreversible change

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2
Q

What are benign tumours of the glandular epithelium/squamous epithelium called?

A

Adenoma/Squamous papilloma

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3
Q

Malignant of glandular epithelium/squamous epithelium?

A

Adeno-carcinoma/Squamous carcinoma

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4
Q

Benign of bone/fat/fibrous tissue?

A

Osteoma/Lipoma/Fibroma

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5
Q

Malignant of bone/fat/fibrous tissue?

A

Osteo-sarcoma/Lipo-sarcoma/Fibro-sarcoma

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6
Q

What are tumours of the white blood cells/lymphoid tissue called?

A

Leukaemia/Lymphoma

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7
Q

Tumours of the CNS/PNS?

A

Astrocytoma/Schwannoma

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8
Q

Tumours of the germ cells?

A 
Ovarian teratoma (usually benign)
Testicular treatoma (usually malignant)
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9
Q

Give features of benign tumours

A 
Non-invasive growth
Well differentiated
Encapsulated
No metastases
Rarely cause death
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10
Q

Give features of malignant tumours

A 
Invasive growth
Poorly differentiated
Not encapsulated
Metastases present
Frequently cause death
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11
Q

Give feature of cancer cells

A
  • altered genetics (tumour suppressor genes and oncogenes)
  • altered cellular function (caused by tumour-related proteins)
  • abnormal morphology
  • loss of cell/cell and cell/matrix adhesion (for movement)
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12
Q

What are tumour related proteins?

A

Biomarkers whose presence predict the type of cancer present/prognosis/appropriate therapy

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13
Q

How is the presence of tumour biomarkers detected?

A

A specific cancer drug will only work when the biomarker is active in the body

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14
Q

Give some examples of tumour biomarkers and the cancers they can be used to predict

A 
Kras - colorectal
EGFR - lung
Her2 - breast/gastric
Braf - melanoma
Alpha-fetoprotein - testicular/liver
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15
Q

What is angiogenesis?

A

Formation of new blood vessels to supple the tumour

Provides a mechanism for metastasis

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16
Q

What is metastasis?

A

Spreading of cancer cells following capsule degradation and transport in the blood/lymph

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17
Q

What is the term given to the special spread of cancer across a body cavity?

A

Trans-coelomic spread

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18
Q

What are common sites of metastasis?

A

Places of high blood flow;

Liver/lungs/brain/axial skeleton

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19
Q

What are uncommon sites of metastasis?

A

Spleen/heart/kidney

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20
Q

Where do the following tumours specifically metastasise to?

Breast
Colorectal
Prostate

A

Bone
Bone
Liver

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21
Q

What are the local effects of benign tumours?

A

Pressure and obstruction

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22
Q

What are the local effects of malignant tumours?

A

Pressure
Obstruction
Tissue destruction (ulceration and infection)
Bleeding (anaemia and haemorrhage)
Pain (pressure on nerves/pathological bone fractures)

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23
Q

What are the systemic effects of malignant tumours?

A

Normal and abnormal hormone secretion

24
Q

What is ‘normal’ hormone secretion in relation to the systemic effects of malignant tumours?

A

Secretion by cancer cells where it is normally expected in physiology, but at an abnormal level

25
Q

What is ‘abnormal’ hormone secretion in relation to the systemic effects of malignant tumours?

A

Secretions of unexpected origin; e.g. ADH/ACTH

26
Q

What is dysplasia?

A

a pre-malignant change (organ/tissue enlargement), the earliest change in the malignancy process that can be detected

  • in epithelium
  • no invasion
  • can progress to cancer
27
Q

Give some features of dysplasia?

A

Increased nuclear size
Increased mitotic activity
Abnormal mitoses

28
Q

How is the cell cycle externally controlled?

A

by:

  • hormones
  • growth factors
  • cytokines
  • stroma
29
Q

How is the cell cycle intrinsically controlled?

A

by restriction points (R)

30
Q

When does external control of the cell cycle occur?

A

before the restriction point

31
Q

How is the cell cycle controlled after the restriction point?

A

autonomous control

32
Q

What happens during the G0 stage of the cell cycle?

A

resting phase, no division occurring

33
Q

G1 stage?

A
  • cells increase in size

- G1 checkpoint control occurs

34
Q

S stage?

A

DNA replication occurs

35
Q

G2 stage?

A
  • cells continue to increase in size

- G2 checkpoint control occurs

36
Q

M stage?

A
  • no more cell growth
  • mitosis occurs
  • metaphase checkpoint control occurs (to ensure cell is ready to complete division
37
Q

What causes G1 to stop?

A
  • inadequate cell size
  • inadequate nutrient supply
  • no external stimuli present
  • DNA damage isn’t detected
38
Q

What causes G2 to stop?

A
  • inadequate cell size

- DNA damage isn’t detected

39
Q

What causes S to stop?

A
  • DNA isn’t replicated
40
Q

What causes M to stop?

A
  • chromosomes mis-align
41
Q

What are checkpoints?

A
  • cyclically active/inactive enzymes (CDK/cyclin complex)

- catalytic sub-units activated by regulatory sub-units

42
Q

What are the catalytic sub-units called?

A

Cyclin-dependent kinases (CDKs)

43
Q

What are the regulatory sub-units called?

A

Cyclins

44
Q

What is the function of the CDK/cyclin complex?

A
  • phosphorylates target proteins
  • causes activation/inactivation of substrates
  • regulates the next phase in the cell cycle
45
Q

How are CDKs expressed?

A

constitutively in inactive form

46
Q

What happens to cyclins in the cell cycle?

A

accumulate and are destroyed as the cycle progresses

47
Q

What is the function of the retinoblastoma gene?

A
  • encodes pRb (phosphoprotein) in almost every cell
  • pRb is hypophosphorylated by CDK/cyclin complexes
  • E2F transcription is inactivated by Rb
48
Q

What is the function of active E2F?

A
  • activates viral target genes

- stimulates cell cycle entry (potent; leads to cancer)

49
Q

What causes carcinogenesis?

A
  • mutation of genetic material that unbalances proliferation and apoptosis
  • in genes that regulate division/apoptosis/DNA repair
  • uncontrolled proliferation leads to cancer
50
Q

How can this genetic damage occur?

A
  • environmental

- inherited

51
Q

How does environmental genetic damage occur?

A
  • chemicals
  • radiation
  • oncogenes
52
Q

How can chemicals give rise to carcinogenesis?

A
  • DNA bases damaged by oxidising and alkylating agents
  • chemical carcinogens/active metabolites react with DNA to form DNA adduct (covalent bonds)
  • adducts at certain chromosomes can lead to cancer
53
Q

How can radiation give rise to carcinogenesis?

A
  • damages DNA bases

- when received in high doses e.g. UV rays/X-rays/Gamma radiation

54
Q

What two pathways can carcinogenesis disrupt?

A
  • cyclin D-pRb-E2F pathway (retinoblastoma)

- p53 pathway

55
Q

What is the physiological function of p53?

A
  • usually present in higher levels in damaged cells
  • stops cell cycle at G1
  • facilitates DNA repair/induces apoptosis

Principles of Disease HQ (26 decks)

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