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Mechanisms of Disease > Session 9 - Neoplasm 2 > Flashcards

Session 9 - Neoplasm 2 Flashcards

1
Q

What 3 steps are necessary for a tumour to metastasise?

A

1) Growth and invasion at the primary site
2) Enter a transport system and lodge at a secondary site
3) Grow at the secondary site to form a new tumour

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2
Q

What is colonisation?

A

-The growth of a new tumour into a clinical entity at a distal site to become a metastasis (otherwise micrometastasis)

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3
Q

Why is colonisation a difficult process?

A
  • The malignant cells often get sheared and destroyed in BVs

- Tiny clusers of cells which do get lodged die or fail to grow into clinically detectable tumours

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4
Q

Malignant cells must evade…

A

…destruction by the immune system during metastasising

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5
Q

What three important alterations are required for invasion of carcinomas?

A

1) Altered adhesion
2) Stromal proteolysis
3) Motility

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6
Q

What are the most lethal features of a malignant neoplasm?

A

-Invasion and metastasis

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7
Q

What is epithelial to mesenchymal transition?

A

-The alterations in adhesion, stromal proteolysis and motility create a carcinoma cell phenotype that appears more like a mesenchymal cell

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8
Q

What are micrometastises?

A

-Surviving microscopic deposits which fail to grow

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9
Q

What are the most common entry routes of malignant cells into the bloodstream?

A

-Capillaries and veins as they have very thin walls

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10
Q

How is adhesion between malignant cells altered?

A

-Initial reduction in E-cadherin expression -> re-expression upon entering blood stream to make cells viable for travel-> down regulation at distal site

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11
Q

How do renal cell carcinomas pass into the right heart?

A

-Invades the renal vein, forma a plug which grows along the inferior vena cava into the right heart

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12
Q

How is adhesion altered between malignant cells and stromal proteins?

A

-Changes in integrin expression

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13
Q

How is proteolysis altered for invasion?

A

-Altered expression of protesases, specifically matric metalloproteases which degrade the basement membrane and stroma

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14
Q

Why do metastases often become necrotic in the centre?

A

-The rate of growth is rapid and a blood supply cannot be generated quick enough to supply the centre so it become necrotic

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15
Q

Why do metastases increase tumour burden?

A
  • There are more malignant cells in the body

- Metastases can produces metastases

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16
Q

What is the primary site of metastases in organs drained by the portal system?

A

-Liver

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17
Q

Brochial carcinomas often metastasise in the…

A

…adrenal glands

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18
Q

What are kruckenberg tumours?

A

-Bilateral metatastic tumours of the ovaries

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19
Q

What is meant by the seed and the soil?

A
  • The seed is the malignant cells which develop into a tumour/metastasis
  • The soil is the secondary organ which favours the growth of particular seeds
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20
Q

What is the most common way of spread of carcinomas?

A

-Lymphatics to draining lymph nodes and then to blood-borne distal sites

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21
Q

What is a cancer niche?

A

-Forms when malignant cells take advantage of surrounding non-neoplastic cells for their growth factors and proteases

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22
Q

How is mobility altered for invasion in carcinoma cells?

A
  • Changes in the actin cytoskeleton

- Glycoproteins interact with integrins to cause stromal re-arrangement

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23
Q

Is penetration of the lymphatics a destructive process?

A

-No, malignant cells penetrate without destroying the epithelium

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24
Q

What happens once carcinomas are in the lymphatics?

A

-They travel to the next lymph node where they settle and grow

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25
Q

What are the three modes of transport of malignant cells to distal sites?

A
  • Bloodstream
  • Lymphatics
  • Fluid in body cavities
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26
Q

What is transcoelemic spread?

A

-Tumours invade body cavity eg peritoneum, pleura, and spreads to other sites within that space

27
Q

Why do lymph nodes downstream from a tumour become swollen?

A
  • Due to antigens and irritating material that leaches out of the tumour, especially if it is necrotic, ulcerated or infarcted
  • Draining lymph nodes can then undergo hyperplasia (not due to metastases)
28
Q

When does the peritoneum become seeded?

A

-Complication of malignancies in abdominal organs

29
Q

Why does ascites develop with peritoneal seeding?

A
  • Hundreds of metastatic nodules can develop

- Leakage of fluid from peritoneal membrane

30
Q

What is the greatest barrier to successful formation of metastasis?

A

-Colonisation

31
Q

What is tumour dormancy?

A

-When an apparently disease-free person harbours many micrometastases which causes a malignant neoplasm relapse years later as they have started to grow

32
Q

What determines the secondary site of neoplasms?

A
  • Regional drainage of blood, lymph or coelomic fluid

- Seed and the soil phenomenon

33
Q

What is the most common secondary site for lymphatic drainage?

A

-Draining lymph nodes

34
Q

What is the common secondary site for transcoelomic spread?

A

-Other areas in coelomic space or adjacent organs

35
Q

What is the most common way sarcomas spread?

A

-Via blood stream

36
Q

What are common sites of blood-borne metastases?

A

-Ling, bone, liver and brain

37
Q

What is meant by osteolytic?

A

-Dissolution of bone

38
Q

What is meant by osteosclerotic?

A

-Increase in bone density

39
Q

What tumours commonly spread to bone?

A

-Breast, bronchus, kidney, thyroid and prostate

40
Q

What correlates with the presence of metastases?

A

-The size of the primary tumour

41
Q

Name a malignant tumour which almost never metastasises?

A

-Basal cell carcinoma

42
Q

Is a small cell bronchial carcinoma aggressive?

A

-Yes it metastasises very early on in its course

43
Q

What is cancer staging based on?

A

-The aggression and metastases of a tumour ie tumour burden

44
Q

What are the two classification of effects which neoplasms can have?

A
  • Direct local effects

- Indirect systemic effects

45
Q

What are direct local effects of a neoplasm?

A
  • Those effects which are due to the physical presence of the primary and/or secondary neoplasm
    1) Direct invasion and destruction of normal tissue
    2) Ulceration of the surface leading to bleeding
    3) Compression of adjacent structures
    4) Blocking of tubes or orifices
46
Q

What are indirect systemic effects?

A
  • Those effects caused by tumour burden, secreted hormones or miscellaneous effects
  • Cachexia, malaise, immunosuppression, thrombosis
47
Q

What are paraneoplastic syndromes?

A

-Symptom complexex that accompany tumours and concern distant targets whether the mechanisms be hormonal, immunologic or unknown

48
Q

Provide an example of direct invasion of a tumour which destroys local tissue

A

-Osteosarcoma and the osteolytic lesions in young people

49
Q

What can be the result of ulceration and bleeding of malignancies in the bowel?

A

-Perforation leading to peritonitis

50
Q

What is cachexia?

A

-Reduced appetite and weghtloss due to fat and muscle wastage as body in catabolic state

51
Q

Why can thromobosis occur due to malignant neoplasms?

A
  • Irregular tubes
  • Irregular constituents
  • Irregular flow
52
Q

Why do benign tumours of endocrine glands typically produce hormones?

A

-They are well differentiated

53
Q

Provide an example of a benign endocrine tumour secreting a hormone

A

-Thyroid adenoma producing thyroxine

54
Q

What hormone does bronchial small cell carcinoma often produce? What is the result of this?

A
  • ACTH -> cushings

- ADH -> hyponatramia-> confusion, convulsion and coma

55
Q

What hormones does bronchial squamous cell carcinoma produce? What is the result of this?

A

-PTH-like hormone -> hypercalcaemia-> constipation, polyuria, polydipsia, vomiting, phsycosis and coma

56
Q

Name some miscellaneous effects of malignant neoplasms

A
  • Neuropathies of brain and peripheral nerves
  • Puritis (increased skin itching) and abnormal pigmentation
  • Fever
  • Finger clubbing
  • Myositis
57
Q

Briefly, what is the mechanism of invasion and metasasis?

A
  • Alter adhesion and separate from tumour mass
  • Digest intercellular martrix and basement membrane to enter lumen of vessel
  • Evade the immune system during transport
  • Embolise a small vessel and survive the impact and mechanical squeeze
  • Penetrate the endothelium and basement mambrane -> further evasion of immune system
  • Multiply, induce angiogenesis and establish as a tumour
58
Q

Is the metastatic process an efficient one?

A

-No, only 0.1-0.01% of cells succeed

59
Q

In which organ are direct local effects most critical?

A

-Brain -> SOL no room for compensation

60
Q

What is different between benign tumour secreting hormones and malignant tumour secreting hormones?

A
  • Malignant tumour often secrete hormones unrelated to the tissue of origin (ectopic hormone secretion)
  • Benign tumours secrete origin-related hormones
61
Q

Why do malignant tumours often cause a hypercoagulable state?

A
  • Platelets can be activated by tumour products eg ADP

- Tumours can secrete procoagulants eg tissue factor

62
Q

What is tumour lysis syndrome?

A

-Extensive necrosis of a tumour by chemotherapy releases toxic amounts of K or uric acid

63
Q

What is the most common ways cancer kills?

A
  • Infection
  • Haemorrhage and thromboembolic phenomena
  • Cachexia
  • Respiratory failue
  • Renal failure

Mechanisms of Disease (11 decks)

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