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EMS MOD > behaviour of tumours > Flashcards

behaviour of tumours Flashcards

1
Q

what is neoplasia?

A

an autonomous proliferation of cells with the loss of normal growth control

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2
Q

what is a tumour?

A

it is any swelling that can be benign or malignant

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3
Q

what is benign?

A

when there is no local invasion and no metastasis

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4
Q

what is malignant?

A

when there is local invasion and metastasis

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5
Q

what is hypertrophy and hyperplasia?

A

hypertrophy is an increase in individual cell size and hyperplasia is an increase in the number of cells

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6
Q

what is metaplasia?

A

it is the replacement of mature tissue types

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7
Q

what is dysplasia?

A

commonly it is an abnormality that indicative of the precursor change of malignancy

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8
Q

what is anaplasia?

A

failure to differentiate in malignancy

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9
Q

what is the AAA, BCSP, BSP and the CSP programmes?

A

the abdominal aortic aneurysm, bowel cancer, breast screening and cervical screening programme

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10
Q

what are the DES, FASP, IDPS, and NIPE programmes?

A

the diabetic eye, fetal abnormality, infectious diseases in pregnancy and newborn and infant physical examination programmes

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11
Q

what are the NBS, NHSP, SCT?

A

the newborn blood spot, newborn hearing screening and the sickle cell and thalassaemia programmes

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12
Q

what is the name for all programmes and how are they assessed?

A

the screening and quality assurance programmes

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13
Q

what are three characteristics imperative in tumour behaviour?

A

invasion, metastasis and angiogenesis

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14
Q

what is the difference between invasion and metastasis?

A

invasion is invading the adjacent normal tissue and destroying normal tissue whereas metastasis is when it spreads from the site of origin to distant sites and forms secondary tumours here

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15
Q

what is the result of metastasis and invasion?

A

can result in local disease forming a systemic disease

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16
Q

how do clinicians characterise the tumours?

A

using staging and grading

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17
Q

which cancer is unlikely to metastasise?

A

basal cell carcinoma

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18
Q

which cancer is very likely to metastasise?

A

lung cancer and 1/3 of breast

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19
Q

how do paediatric patients present?

A

majority will already have metastasised

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20
Q

what happens with metastasis in adults?

A

around half of all adult patients will metastasise

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21
Q

how does invasion occur?

A

there is increased motility, decreased adhesion, production of proteolytic enzymes and mechanical pressure

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22
Q

how to cells adhere to one another?

A

cell to cell adhesion molecules called cadherins

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23
Q

what happens if there is a mutation in E-cadherin?

A

there is the loss of cell to cell adhesion and contact inhibition

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24
Q

where else can cells adhere to?

A

the matrix through cell-matrix adhesion molecules

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25
Q

what are cell-matrix adhesion molecules and how can changes in these lead to motility changes?

A

integrins

changes in integrin expression can result in the decreased cell-matrix adhesion

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26
Q

what changes happen in epithelial cells in cancer?

A

epithelial cells are usually tightly connected, polarised and tethered
mesenchymal cells are loosely connected and able to migrate
in cancer epithelial cells with gain mesenchymal cell properties making them able to migrate and invade

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27
Q

what changes occur in ECM during caner?

A

in the ECM there are matrix metalloproteinases and in normal tissue regulation there is a balance between the matrix and the metalloproteins, with tissue inhibitors of metalloproteins. In cancer the balance tips as the inhibitors become more dense and therefore favours ECM breakdown meaning that there is local invasion

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28
Q

what role does mechanical pressure play in tumour formation?

A

the uncontrolled proliferation forms a mass, this puts pressure on vessels and results in occlusion and pressure atrophy. The tumour will spread along the lines of least resistance

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29
Q

what are examples of proteolytic enzymes in the ECM?

A

interstitial collagenases, gelatinases and stomolysins

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30
Q

what do stomolysins break down?

A

collagen type IV and proteoglycans

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31
Q

what do gelatinases break down?

A

collagen IV and gelatin

32
Q

what do interstitial collagenases break down?

A

collagen types I, II and III

33
Q

what is the issue with metastasis?

A

there is an unknown primary site and this metastasis is often the presenting tumour. The secondary tumour burden is often greater than that of the first

34
Q

why does metastasis make it difficult to grade?

A

they occur at different stages of the natural history in different tumours - may occur early, or be a late relapse commonly

35
Q

what are the main routes of metastasis?

A

canalicular
haematogenous
lymphatic
transcoelomic

36
Q

what is meant by canalicular?

A

some tumours especially carcinomas will metastasise along anatomical canalicular spaces such as the urinary tract or the bile duct, the airways or the subarachnoid space

37
Q

what is meant by lymphatic?

A

it spreads through local or distant lymph nodes

38
Q

what cancers often spread haematogenously?

A

liver, brain, lung and bone

39
Q

what is transcoelomic?

A

it is when there is metastasis across the peritoneal, pleural or pericardial cavities or the CSF

40
Q

what is another way of tumour metastasis?

A

implantation - spillage of tumour during biopsy or surgery

41
Q

how do carcinomas and sarcomas initially spread?

A

carcinoma through lymphatic and sarcoma through the blood

42
Q

which cancers often result in bone metastasis?

A

breast, prostate (sclerotic), lung (lytic), kidney and thyroid

43
Q

what cancer spreads through the transcoelomic route?

A

ovarian

44
Q

where does lung cancer often spread to?

A

the adrenal and the brain

45
Q

what is the mechanical hypothesis?

A

that metastasis is dictated by anatomy - liver metastasising to the GIT

46
Q

what is the seed and soil hypothesis?

A

the spread can go anywhere but can only grow if the conditions are right - tissue environment is important as it influences the organ selectivity for metastases

47
Q

what is the issue with metastatic cells?

A

they can remain dormant for years

48
Q

what are the stages of metastasis?

A

detachment, invasion, adherence loss and extravasation, intravasation,, survival against the host defences, growth and angiogenesis

49
Q

what is angiogenesis?

A

new vessel formation that is derived from existing vessels

50
Q

which cells are we unsure about the role of but know that they are involved?

A

the bone marrow derived endothelial stem cells

51
Q

what is the function of angiogenesis?

A

it has a role in healing and development and is essential if a metastases are to grow larger than 1-2cm

52
Q

what are the inhibitors of angiogenesis?

A

thrombospondin, endostatin, canstatin, and ECM proteins

53
Q

what promotes angiogenesis?

A

inflammatory cells producing TGFbeta, stromal cells producing PDGF and tumour cells producing promoters such as VEGF

54
Q

what is staging and graded needed for?

A

research for comparison of therapies, prognosis - survival time and QoL, treatment

55
Q

what is the stage?

A

how far along the tumour is = how advanced it is, i.e has it metastasised and to what extent

56
Q

what is the grade?

A

how quickly to tumour is progressing and how aggressive it is - how differentiated is it and how different to the cells of origin is it

57
Q

what do stage and grade allow us to determine?

A

if the cancer is the primary site or if it is a secondary tumour resulting from metastasis

58
Q

how are tumours graded?

A

G1-4 which is near normal to undifferentiated

59
Q

how is staging determined?

A

pre-invasive, early tumour, locally advanced, metastases - I-IV
TMN system

60
Q

what is the TMN system?

A

it is tumour, metastasis and nodes - each can be clinical, radiological or pathological

61
Q

what is T?

A

it is the size and or the extent of the tumour

62
Q

what is M?

A

it is the presence and extent of distant metastases

63
Q

what is N?

A

it is the presence and number of lymph node metastases

64
Q

in breast cancer screening what does Ti-T4 mean?

A 
Ti - in situ stage
T1 - less than 2cm
T2 - 2-5cm
T3 >5cm 
T4 - involving the chest wall or skin
65
Q

in breast cancer screening what is the N section?

A

N0 - no nodes
N1 - ipsilateral nodes
N2 - more than ipsilateral nodes

66
Q

in breast cancer screening what is the M part?

A

M0 - no distant metastases

M1 - distant metastases

67
Q

all parts of the TMN system are combined to make an overall stage. Describe the stages? List the treatments.

A

stage 0 - Tis - surgery only
stage 1 - T1, N0, M0 - RT, surgery
stage 2 - T1-2, N1 OR T3 - RT and surgery
stage 3 - T(any), N2 or T4 - chemo and surgery
stage 4 - T(any), N(any), M1 - chemo

68
Q

where is there correlation is staging?

A

between staging and outcome

69
Q

what system is used to stage CRC?

A

Duke’s ABCD

70
Q

what is A and the survival rate for Duke’s?

A

invades into, but not through the bowel wall - >90% survival chance for 5 years

71
Q

what is B and the survival rate for Duke’s?

A

B - invades through the bowel wall but with no lymph node involvement - 70% 5 year

72
Q

what is C and the survival rate for Duke’s?

A

local lymph nodes are involved - 30% 5 year survival

73
Q

what is D and the survival rate for Duke’s?

A

distant metastases - 5-10% 5 year survival

74
Q

what is the differentiation level?

A

it is the grade - how much the tumour resembles it’s original form

75
Q

who performs grading?

A

histopathologists and therefore it is subjective

76
Q

what else is involved in grading?

A

nuclear pleomorphism and size, mitotic activity and necrosis

EMS MOD (28 decks)

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