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EMS - MoD > 18. Characteristic of tumours > Flashcards

18. Characteristic of tumours Flashcards

1
Q

Different malignancies show varied growth rates. What are slow-growing tumours associated with?

A

Long survival

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2
Q

Different malignancies show varied growth rates. What are rapidly-growing tumours associated with?

A

Lethal within a short time

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3
Q

What is the definition of ‘differentiation’ in terms of tumours?

A

The extent that neoplastic cells resemble the corresponding normal parenchymal cells, morphologically and functionally

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4
Q

What are the characteristics of benign tumours in terms of differentiation?

A
  • usually well-differentiated

- mitoses are rare

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5
Q

What are the characteristics of malignant neoplasms in terms of differentiation?

A
  • wide range of parenchymal differentiation

- most exhibit morphologic alterations showing malignant nature

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6
Q

Do benign and malignant tumours look different histologically?

A

Well-differentiated malignant tumours and benign tumours can look very similar

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7
Q

What is anaplasia?

A

Poorly-differentiated cells

A condition whereby cells lose the morphological characteristics of mature cells

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8
Q

How are neoplasms comprised of poorly-differentiated cells described?

A

Anaplastic

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9
Q

What condition is a “telltale sign of malignancy”

A

Anaplasia

Neoplasms comprised of poorly-differentiated cells

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10
Q

What are some possible morphological changes in cells?

A
  • pleomorphism
  • abnormal nuclear morphology
  • mitoses
  • loss of polarity
  • other changes
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11
Q

What is pleomorphism?

A

Describes variability in the size, shape and staining of cells and/or their nuclei. It is a feature characteristic of malignant neoplasms, and dysplasia

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12
Q

Give some examples of the huge differences shown in pleomorphism

A
  • small cells with little differentiation
  • large cells with one massive nucleus
  • large cells with multinucleation
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13
Q

Cells can have abnormal nuclear morphology. Give some examples of this

A
  • nuclei appear too large for the cell
  • variability in nuclear shape
  • chromatin distribution
  • hyperchromatism
  • abnormally large nucleoli
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14
Q

In abnormal nuclear morphology, nuclei may appear too large for the cell that they are in. What is normal?

A

Normal nuclear to cytoplasmic ratio = 1:4 or 1:6

When abnormal, it can reach 1:!

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15
Q

In abnormal nuclear morphology, there can be variability in nuclear shape. Give examples

A
  • irregular

- making pictures (raisins, faces etc)

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16
Q

In abnormal nuclear morphology, there can be abnormal chromatin distribution. Give examples

A
  • coarsely clumped

- along cell membrane

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17
Q

In abnormal nuclear morphology, there can be hyperchromatism. What does this look like?

A

Dark colour

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18
Q

What are mitoses an indication of and what are they seen in?

A

An indication of proliferation

Therefore seen in normal tissues with a rapid turnover and in hyperplasias

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19
Q

In malignancy, atypical bizzare mitotic figures are seen. Give examples

A
  • tripolar division
  • quadripolar division
  • multiple spindles
    etc
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20
Q

What occurs in loss of polarity in cells?

A
  • orientation of cells disturbed

- disorganised growth

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21
Q

In summary, what are the main characteristics of well differentiated tissues?

A
  • closely resembles normal tissue or origin
  • little or no evidence of anaplasia
  • benign and occasional malignant
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22
Q

In summary, what are the main characteristics of poorly differentiated tissues?

A
  • little resemblance to tissue of origin

- highly anaplastic appearance

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23
Q

In summary, what are the main characteristics of undifferentiated/anaplastic tissues?

A
  • cannot be identified by morphology alone

- need molecular techniques

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24
Q

What is ‘grade’ in terms of tumour classification?

A
  • closely related to differentiation/clinical behaviour

well differentiated = low grade/grade 1

moderately differentiate = intermediate/grade 2

poorly differentiated = high grade/grade 3

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25
Q

What is ‘stage’ in terms of classification of tumours?

A

A measure of prognostication/therapeutic decisions

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26
Q

Better differentiation = ?

A

Better retention of normal function

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27
Q

How can benign and well-differentiated carcinomas of the endocrine glands be detected?

A

They frequently secrete hormones characteristic of origin

Increased levels in the blood can be used to detect and to follow up tumours

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28
Q

How can changes in function of tumours give clinical clues?

A
  • some tumours express foetal proteins not seen in adults

- some express proteins only normally found in other adult cells

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29
Q

Change in function of tumours can lead to paraneoplastic syndromes. For example, in bronchogenic carcinomas, what is released which leads to secondary effects on the body?

A
  • corticotropin
  • parathyroid-like hormone
  • insulin
  • glucagon
  • others
30
Q

What are the general differences between cancer and benign tumours in terms of local invasion?

A

Cancer =

  • infiltration
  • invasion
  • destruction

Benign =

  • cohesive expansile masses
  • localised to site of origin
  • no capacity to infiltrate, invade or metastasise
31
Q

Can benign tumours invade other areas of the body?

A

No, they are localised to their site of origin and cannot infiltrate, invade or metastasise

32
Q

What is encapsulation? (in terms of benign tumours)

A

The tumour grows in a contained area usually surrounded by a fibrous connective tissue capsule

33
Q

In encapsulation of benign tumours, ECM is deposited by stromal cells. How is this activated?

A

Activated by hypoxia from the pressure of the tumour

34
Q

In benign tumours, what are the characteristics of the tissue plane?

A

Easy to identify because they are

  • discrete, moveable
  • easily palpable
  • easily excised
35
Q

The fibrous capsule around benign tumours consists of extracellular matrix (ECM). What is ECM deposited by?

A

Stromal cells

This process is activated by hypoxia from pressure of the tumour

36
Q

Whereas you get encapsulation of benign tumours, what can sometimes occur in malignant tumours?

A

Pseudoencapsulation

Happens in the more slow-growing tumours

37
Q

What is pseudoencapsulation?

A

Happens in slow-growing malignant tumours

Looks like encapsulation but microscopically there are actually rows of cells penetrating the margin

38
Q

Do malignant tumours respect anatomical boundaries?

A

No

Penetration of organ surfaces and skin

39
Q

Is surgical resection easy in malignant tumours?

A

No

Requires resection of adjacent macroscopically normal tissue (margin)

40
Q

What is metastasis?

A

Spread of a tumour to sites physically discontinuous with the primary tumour

41
Q

What does pathognomic mean?

A

Characteristic of a particular disease

42
Q

What is metastasis pathognomic of?

A

Malignancy

If a tumour metastasises, it is NOT benign

43
Q

What proportion of cancers metastasise?

A

30% of non-skin malignancies have metastasised at diagnosis

44
Q

Metastasis is generally correlated which what features? (but with lots of exceptions)

A
  • lack of differentiation
  • local invasion
  • rapid growth
  • large size
45
Q

What are the possible pathways for metastasis?

A
  • direct seeding
  • lymphatic spread
  • haematogenous spread
46
Q

What is direct seeding? (a pathway for metastasis)

A

The neoplasm penetrates a natural open field without physical barriers

Can remain confined to surface of peritoneal structures without penetrating eg. pseudomyxoma peritonea

47
Q

In direct seeding, a neoplasm penetrates a natural open field without physical barriers. Give some examples of these

A
  • peritoneal cavity
  • pleural cavity
  • pericardial space
  • subarachnoid space
  • joint spaces
48
Q

What is the most common pathway for metastasis?

A

Lymphatic spread

49
Q

Describe lymphatic spread

A
  • tumours do not contain lymphatic channels
  • lymphatic vessels at the tumour margins
  • pattern of lymph node involvement follows the routes of lymphatic drainage
50
Q

What is the pattern of lymphatic spread in breast cancers?

A
  • most commonly presents in upper outer quadrant
  • disseminate first to axillary nodes
  • then infraclavicular and supraclavicular nodes become involved
51
Q

What determines future course of disease and what therapy is most suitable for a patient with breast cancer?

A

Determination of axillary node status

52
Q

What are sentinel nodes?

A

The first node in a regional lymphatic basin that receives lymph flow from the primary tumour

(the first few lymph nodes into which a tumour drains)

53
Q

How are sentinel nodes identified?

A

Injection of radiolabelled tracers/coloured dyes

54
Q

Despite being a passage of spread for tumours, how can regional nodes be beneficial?

A

Effective barriers to further tumour dissemination

Cells arrest within node and then can be destroyed by a tumour-specific immune response

55
Q

Does every enlarged node next to a tumour have cancer in it?

A

No!

Drainage of tumour cell debris and tumour antigens induces a reactive change in nodes

56
Q

What is haematogenous spread seen in?

A

Typical of sarcomas

But also seen in carcinomas!

57
Q

Describe haematogenous spread

A

Bloodborne cells follow the venous flow drainage site of the neoplasm

Often come to rest in the first encountered capillary bed

58
Q

In haematogneous spread, the cells often come to rest in the first encountered capillary bed, what is most frequently involved?

A

Liver (portal)

Lungs (caval)

59
Q

In haemotogenous spread, why are veins involved?

A

They are more easily penetrated because they have thinner walls

60
Q

What is the stroma?

A

Connective tissue framework that neoplastic cells are embedded in

61
Q

What does the stroma provide?

A
  • mechanical support
  • intercellular signalling
  • nutrition
62
Q

What is a desmoplastic reaction?

A

Fibrous stroma formation due to induction of connective tissue fibroblast proliferation by growth factors from the tumour cells

63
Q

What does the stroma contain? (in a desmoplastic reaction)

A
  • cancer-associated fibroblasts
  • myofibroblasts (see puckering of skin)
  • blood vessels (blood to tumour)
  • lymphatics
64
Q

What are the clinical complications of tumours dependent on?

A
  • location
  • cell of origin
  • behaviour
65
Q

In what general classifications can effects of tumours be?

A
  • local
  • metabolic
  • due to metastases
66
Q

What are some LOCAL complications of tumours?

A
  • compression

- destruction

67
Q

Compression is a local complication of tumours. Describe this

A

Displacement of adjacent tissue

  • benign eg. pituitary adenomas obliterate adjacent functioning pituitary tissue leading to hypopituitarism
68
Q

Destruction is a local complication of tumours. Describe this

A

Invasion

Rapidly fatal is vital structures are invaded e.g. artery

Mucosal surfaces - ulceration eg. GI - anaemia

69
Q

Describe tumour type-specific METABOLIC complications of tumours?

A
  • well differentiated endocrine tumours can retain functional properties
  • autonomous
  • number of cells exceeds normal organ
  • eg. thyrotoxicosis in thyroid adenoma
  • if inappropriate (paraneoplastic) eg. ACTH/ADH in small cells lung cancer
70
Q

Give some non-specific METABOLIC complications of tumours

A
  • cachexia
  • warburg effect
  • neuropathies
  • myopathies
  • venous thrombosis
71
Q

What is cachexia?

A

Profound weight-loss despite apparently adequate nutrition

Tumour-derived humoral effects that interfere with protein metabolism

72
Q

What is the Warburg effect?

A

Produces energy by high rate of glycolysis with fermentation of lactic acid

Used in imagine - PET scanning (FDG uptake)

Observation seen in most cancer cells

EMS - MoD (17 decks)

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