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Sophie - Principles of Pathology - Year 2 > 43.1 Pathology of Neoplasia > Flashcards

43.1 Pathology of Neoplasia Flashcards

1
Q

Describe the characteristics of benign tumours.

A
  • Loss of growth control
  • Limited to the site of origin, often encapsulated
  • Clinical signs related to the occupying space or due to production of hormones/active molecules
  • Often cured by surgery
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2
Q

Describe the characteristics of malignant tumours.

A

*Invasion
*Metastasis
*Progression
*Aberrant differentiation
*Pleomorphism and anaplasia
*Distinct from benign tumours

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3
Q

What is the difference in level of differentiation between benign and malignant tumours?

A
  • Benign: well-differentiated, closely resemble normal structure and function (just high numbers of cells)
  • Malignant: wide range of differentiation with significant alterations - such as different cell and nucleus sizes, hyperchromatic nuclei, loss of polarity
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4
Q

What are the examples of benign tumours that you need to know?

A
  • Papilloma (warts) -> Epithelial tumour
  • Gliomata -> Glial cell tumour (CNS)
  • Adenoma (e.g. colonic polyps) -> Glandular tumour
  • Leiomyoma (e.g. uterine fibroids) -> Smooth muscle tumour
  • Lipoma -> Fat cell tumour
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5
Q

What are the examples of malignant tumours that you need to know?

A
  • Squamous cell carcinoma -> Skin tumour
  • Adenocarcinoma -> Glandular tumour
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6
Q

What are the potential damaging effects of benign tumours?

A
  • Bleeding
  • Pressure
  • Endocrine toxicity (if glandular tissue affected)
  • Possible progression to malignancy
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7
Q

How can glioma be harmful?

A
  • Cause intracranial hypertension and headaches
  • Impact local structures e.g. compress optic nerve –> visual disturbances
  • Affect connectivity –> seizures
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8
Q

What % of deaths from cancer are caused by benign primary tumours?

A

10%

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9
Q

What is a benign tumour?

A

A local growth of cells that does not invade nearby tissues

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10
Q

What is a glioma?

A

A tumour of the glial cells in the CNS (astrocytes, oligodendrocytes, ependymal cells)

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11
Q

What is a leiomyoma? Give a specific example

A

A smooth muscle tumour

Uterine leiomyoma –> uterine fibroids

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12
Q

What is a papilloma?

A

A tumour of the skin usually derived from the keratinocytes in the stratum basale
= Wart

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13
Q

What is an adenoma? Give two specific examples

A

Arenal adenoma (Cushing’s disease)
Colonic polyps

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14
Q

What is lipoma?

A

Tumour of fat cells

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15
Q

Why do benign tumours not invade local tissues?

A

They are confined within a rim of compressed fibrous tissue (capsule)

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16
Q

They are confined within a rim of compressed fibrous tissue (capsule)

A

Grow into blood vessels –> rupture them

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17
Q

How does a malignant tumour cause local infection?

A

Local modulation of immune system, loss of protective structures such as barriers
Makes nearby structures more susceptible to infection

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18
Q

How does a tumour cause intussusception?

A

Tumour obstructs lumen, weight causes abnormal folding
Tumour serves as the leading edge of the fold

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19
Q

How does cancer cause anaemia?

A

Involves inflammation that reduces RBC production

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20
Q

What are examples of local effects of malignant tumours?

A

Direct:
- Pressure on other structures
- Occupation of space (e.g. intra-thoracic or intra-cranial)
- Obstruction of vessels/ducts

Indirect:
- Intussusception of gut
- Haemorrhage
- Infection

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21
Q

What is intussusception of the gut?

A

When part of the gut slides into another - like a crumpling sock

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22
Q

What are examples of systemic effects of malignant tumours?

A
  • Cachexia (weight-loss, nausea, anorexia, lethargy)
  • Hormonal effects
  • Marrow destruction (leukaemias) leading to neutropenia –> infection, Bleeding (thrombocytopenia), or anaemia.
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23
Q

What are the hormonal effects that can be caused by malignant tumours?

A

Over-secretion, ectopic secretion (e.g. ACTH release from tumours in lungs), or destruction of endocrine tissue.

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24
Q

What is pleomorphism?

A
  • The variability in the size, shape and staining of cells and/or their nuclei.
  • Several key determinants of cell and nuclear size, like ploidy and the regulation of cellular metabolism, are commonly disrupted in tumours.
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25
Q

What is anaplasia?

A
  • A condition of cells with poor cellular differentiation, losing the morphological characteristics of mature cells and their orientation with respect to each other and to endothelial cells.
  • This is a feature of malignant tumours.
  • In other words, the cells become less differentiated in tumours.
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26
Q

What is invasion of tumours? Do all tumours do it?

[IMPORTANT]

A
  • The direct extension and penetration by cancer cells into neighbouring tissues.
  • It is a characteristic of malignant tumours.
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27
Q

What is meant by infiltration and permeation in cancers?

A
  • Infiltration -> Spread beyond the layer of tissue in which it developed and is growing into surrounding, healthy tissues.
  • Permeation -> Spread of cancer cells in continuous columns within the lymph vessels.
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28
Q

What is the benign to malignant transformation?

A

Benign → malignant transformation: Malignant acquire invasive, aggressive phenotype.
*Accumulation of more mutations (from genome instability/ loss of checkpoint reg etc)
*Benign → confined to origin site
*Malignant → rapid growth/ invasion/ destruction of surroundings.
- May metastasise + form 2o tumours.

29
Q

How may an organ/tissue be made favourable for metastatic extravasation?

A
  • Exosome delivery –> regulatory molecules that send many signals to recipient cells at once
  • Growth factor release
  • Cytokine release –> inflammation, immunosuppression

Overall: angiogenesis, vascular permeability, reprogrammed energy metabolism, modulated immunity, induced EMT

30
Q

What are adenocarcinomas? Give examples

A

Tumours of specialised cells of epithelia that secrete substances into ducts or cavities

Examples:
lung, colon, breast, pancreas, stomach, ovary, prostate

31
Q

What are squamous cell carcinomas? Give examples

A

Tumours of epithelial sheets that protect a cavity or channel and the underlying cell populations

Examples:
skin (keratinocytes), nasal, lung, oesophagus, cervix

32
Q

What are micrometastases?

A

Small metastatic deposits that stay dormant for months/years

33
Q

What are the four key features of malignant tumours that benign tumours do not have?

A
  • Dedifferentiation (anaplasia)
  • High rate of growth
  • Local invasion
  • Metastasis
34
Q

What are the most common sites of secondary tumours?

A
  • Lungs
  • Liver
  • Lymph nodes
  • Bones
  • Brain
  • Skin
35
Q

What are the three routes of metastasis?

A
  • Grow directly into surrounding tissue (infiltration)
  • Travel through bloodstream to distant locations
  • Travel through lymph system to nearby or distant lymph nodes
36
Q

What are the two events after local invasion?

A

Intravasation (entry into circulation)
Extravasation (leaving circulation)

37
Q

Explain the seed and soil hypothesis of metastasis. What are its shortcomings?

A

(Paget, 1889):

  • The theory that metastatic tumor cells will metastasise to a site where the local microenvironment is favorable, similar to how a seed grow only if it lands on fertile soil.
  • This has been shown to be largely true and we now know that endosomes released by tumour cells can influence which sites in the body become favourable for metastasis development (see flashcards).
  • However, the theory does not account for why the contralateral organ is rarely a site of metastasis (e.g. one lung to the other), since it would be
38
Q

Summarise the main theories about what determines the location of metastatic tumour formation.

A
  • Seed and soil hypothesis -> The theory that metastatic tumor cells will metastasise to a site where the local microenvironment is favourable. How favourable a site is is largely determined by exosome release (from tumour cells), which bind to a specific tissue based on their integrins and create a pre-metastatic niche there.
  • Mechanical mechanisms hypothesis -> The theory that patterns of blood flow determine the site of tumour formation.

Neither of these can fully explain trends for all metastatic tumours seen clinically, so it is likely that both contribute somewhat.

39
Q

What is the half-life of a circulating tumour?

A

1-2.4 hours

40
Q

What is the key event to allow local invasion?

A

*Remodelling of b.membrane enables invasion
- Due to protease secretion (e.g. MMP) + changes in cell-cell/ matrix adhesion molecules.
*EMT = key phenotype switch allowing cancer cells to detach from 10 tumour + intravasate into lumen of blood/ lymphatic vessel.

41
Q

What is thrombocytopenia?

A

Low platelet count

42
Q

Which processes permit tumour extravasation?

A
  • Adhesion molecules
  • Local thrombin proteolysis which retracts the endothelial membrane - allows tumour cells through
  • Local proliferation and secretion of proteases - can lead to eventual membrane rupture
43
Q

Why are certain sites more common for secondary tumour growth?

A

More easily reachable from the primary tumour

44
Q

Why are micro-metastases not destroyed by antimitotic chemo- or radiotherapy?

A

They are negative for markers of replication

45
Q

Why do most metastatic tumours die before extravasation?

A
  • High shear forces in circulation
  • Loss of cell-cell contact; less signalling etc
46
Q

Why is spread via lymphatics more likely than via blood vessels?

A

Less shear force

47
Q

Is metastasis always the same?

A

It is common and serious, but variable

48
Q

How can immunodeficiency give an increased risk of digestive tract tumours?

A
  • More likely to get chronic infections of H. pylori - which is potentially carcinogenic
  • H. pylori induces upregulation of oncogenes and silencing of tumour suppressor genes
  • Also generates inflammatory response - that releases ROS that induce DNA breaks
  • Increased levels of nitrate –> promotes progression to intestinal metaplasia/dysplasia
49
Q

How can immunodeficiency give an increased risk of lymphomas?

A
  • More likely to get infections that increase risk of developing lymphoma - e.g. HIV, which invades lymphocytes and may cause DNA changes
    –> increases risk of Burkitt lymphoma, Hodgkin lymphoma, and more
  • More likely to get infections that make immune system overactive and make too many lymphocytes
50
Q

How can immunodeficiency give an increased risk of virus-associated tumours?

A

More likely to get infected by potentially carcinogenic viruses

51
Q

How do lymphomas cause immunodeficiency/suppression?

A
  • Lymphocytes are growing rapidly and lose normal function
  • Take up space in bone marrow so there are less other types of immune cells too
  • Lymphoma cells use excessive energy –> affects general immune system’s ability to work well
52
Q

What % of global cancer burden is attributable to viral infection?

A

15%

53
Q

What are examples of virus-associated tumours?

A
  • Cervical carcinoma (HPV)
  • Kaposi’s sarcoma (HHV-8)
  • Hepatocellular carcinoma (HBV)
54
Q

Which three types of tumours are at a higher risk of developing when a person has immunodeficiency or immunosuppression?

A
  • Lymphomas
  • Digestive tract tumours
  • Virus-associated tumours
55
Q

Which type of carcinomas is there an immunisation program in the UK for?

A

Papilloma-associated carcinomas…

Cervical carcinoma
Ano-genitcal carcinomas
Head and neck squamous cell carcinoma

56
Q

Generally, what is the ending for the names of mesenchymal malignant tumours?

A

-sarcoma

57
Q

Generally, what is the ending for the names of parenchymal malignant tumours?

A

-carcinoma

58
Q

Generally, what is the ending for the names of parenchymal or mesenchymal benign tumours?

A

-oma

59
Q

Give examples of mesenchymal benign tumours

A

Fibroma, lipoma, chondroma, osteoma

60
Q

Give examples of mesenchymal malignant tumours

A

Fibrosarcoma, liposarcoma, chondrosarcoma, osteosarcoma

61
Q

Mesenchymal refers to…

A

Connective tissue

62
Q

Parenchymal refers to…

A

epithelium

63
Q

What is the term for a benign glandular epithelial tumour?

A

Adenoma

64
Q

What is the term for a benign surface epithelial tumour?

A

Papiloma

65
Q

What is the term for a malignant glandular epithelial tumour?

A

Adenocarcinoma

66
Q

What is the term for a malignant surface epithelial tumour?

A

Carcinoma

67
Q

What is the term for benign OR malignant bone marrow tumours?

A

Leukaemia

68
Q

What is the term for benign OR malignant lymphoid tumours?

A

Lymphoma

Sophie - Principles of Pathology - Year 2 (43 decks)

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