Neoplasia Flashcards

1
Q

What is oncology?

A

Branch of medicine which studies malignant tumours and treatment

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2
Q

What is a neoplasm?

A
  • new growth (tumour)
  • genetic disorder of cell growth triggered by acquired or less commonly inherited mutations (single cell)
  • abnormal mass of tissue
  • uncoordinated growth which exceeds that of normal tissues
  • growth persist after stimuli is removed
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3
Q

What are the two categories within the classification of tumours?

A
  • clinical behaviour
  • histogenesis (tissue of origin)
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4
Q

What are classifications of tumours within clinical behaviour?

A
  • benign
  • malignant
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5
Q

What are classifications of tumours within histogenesis?

A
  • epithelial
  • connective tissue
  • other tissue
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6
Q

Growth pattern benign vs malignant?

A
  • benign grow by method of localised expansion due to them being encapsulated (easier to remove)
  • malignant grow by metastasis (they can travel to other organs/sites in the body to form a new tumour) invasion/infiltration as they have no surrounding capsule
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7
Q

Growth rate benign vs malignant?

A
  • benign tumour growth tends to be slow
  • malignant tumour can grow rapidly, but this is variable
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8
Q

Histology benign vs malignant?

A
  • benign tumour cells resemble the tissue of origin (differentiation), they are the same size and shape and there may be a few mitotic cells (within normal limit)
  • malignant cells have variable resemblance to their tissue of origin, cellular and nuclear pleomorphism (different size/shapes), many mitotic cells (abnormal amount)
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9
Q

Clinical effects benign vs malignant?

A
  • a benign tumour can cause a lump or pressure or obstruction in the area depending on the site and size, if the arise from endocrine gland there can be an increase/decrease in hormone production, treated by local excision (surgery)
  • a malignant tumour can cause pressure or infiltration or destruction to the area, if endocrine can also affect hormone secretion, treated by local excision and chemotherapy or radiation (if metastases present)
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10
Q

What are the effects of benign tumours?

A
  • varies depending on size, site and tumour
  • palpable lump
  • pressure
  • obstruction
  • function eg hormone secretion
  • the effect may not always be benign
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11
Q

What is an examples of a benign tumour in the head and neck?

A
  • benign tumour affecting salivary gland - pleomorphic adenoma (potential to cause pressure on facial nerve)
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12
Q

What is an example of a malignant tumour in the head and neck?

A
  • squamous cell carcinoma of tongue and larynx
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13
Q

What are the two components which compose all tumours?

A
  • neoplastic cells
  • reactive stroma
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14
Q

What do neoplastic cells constitute?

A

The tumour parenchyma

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15
Q

What is the reactive stoma made up of?

A

Connective tissue, blood vessels and cells of adaptive/innate immune cells

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16
Q

What is a malignant epithelium called?

A

Carcinoma

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17
Q

What is a benign squamous epithelium?

A

Papilloma

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18
Q

What shows a malignant connective tissue?

A

Sarcoma

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19
Q

What is a benign glandular epithelium?

A

Adenoma

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20
Q

What is a malignant squamous epithelium?

A

Squamous cell carcinoma

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21
Q

What is a malignant glandular epithelium?

A

Adenocarcinoma

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22
Q

what do potentially malignant disorders of the oral cavity indicate?

A

Risk of likely future malignancies occurring in the oral mucosa

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23
Q

What is a leukoplakia?

A

Which patch that cannot be rubbed off or attributed to any other cause

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24
Q

How is the potential of a malignancy assessed?

A

By taking a biopsy and assessing for dysplasia

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25
Q

What does a tissue which shows dysplasia indicate?

A

Potential to become malignant

26
Q

What is dysplasia?

A

Abnormality (changes in shape/size) confined to epithelium

27
Q

What are potential aetiology for oral cancer?

A
  • tobacco
  • betel quid
  • alcohol
  • diet/nutrition
  • oral hygiene
  • viruses eg HPV
  • immunodeficiency
  • socioeconomic factors (deprived area)
  • GORD
28
Q

What are the two groups of factors within carcinogenesis?

A

Environmental (carcinogens)
And
Genetic

29
Q

What are carcinogens for benign tumours?

A
  • inherited
  • viruses
30
Q

What are carcinogens for malignant tumours?

A
  • chemical agents
  • physical agents
  • viruses
  • may affect tissue directly or indirectly
31
Q

What is the multi-step theory of carcinogenesis?

A
  • initiation
  • promotion
  • progression
  • latency period
32
Q

Describe the initiation step of carcinogenesis

A

Carcinogen induces a genetic change resulting in a neoplastic potential

33
Q

Describe the promotion stage of carcinogenesis

A

Another factor stimulates the initiated cell for division (clinal proliferation)

34
Q

Describe the progression step in carcinogenesis

A

Additional mutations resulting in malignancy

35
Q

What are examples of chemical carcinogens?

A
  • smoking polycyclic hydrocarbons (includes tars)
  • diet
  • drugs
  • alcohol
  • asbestos
36
Q

What are examples of physical carcinogenesis?

A
  • ionising radiation (damages DNA causing mutations)
  • radioactive metals and gases (radium bone and bone marrow tumours)
  • UV light damages skin leading to skin cancer (sun beds)
37
Q

Which type of tissues are most sensitive to radiation?

A

Embryonic tissues

38
Q

What are examples of viral carcinogenesis?

A
  • DNA viruses
  • RNA viruses
39
Q

What are the genes which accelerate cancer?

A

Oncogenes

40
Q

What are the genes which prevent cancer?

A

Tumour suppressor genes

41
Q

What are protooncogenes?

A

Normal genes which regulate cell division

42
Q

What do oncogenes produce?

A

Oncoproteins

43
Q

How do genes become deregulated?

A

Tight regulation is lost
- mutation (increased activity of product)
- excess normal product (duplication of gene/viral product)
- enhanced transcription (translocation/chromosome rearrangement)

44
Q

How do tumour suppressor genes act?

A
  • act to inhibit cell division and suppress growth
  • act as anti oncogenes
  • require loss of both alleles
  • retinoblastoma gene
45
Q

TP53

A
  • acts just before the restriction point in the cell cycle
  • stops the cell cycle to allow for DNA repair
  • initiates apoptosis if repair isn’t possible
  • often inactivated in cancer (common in HPV)
46
Q

What are examples of genetic susceptibility to cancer?

A
  • inherited cancer syndromes (single mutant genes, eg retinoblastoma)
  • familial cancer (family clusters, genes and inheritance patterns unclear, eg breast cancer)
  • defective DNA repair (increased sensitivity to carcinogens and general increased cancer risk eg xeroderma pigmetosum)
47
Q

How may a cancer cell differ

A
48
Q

What are modes of spread of malignant tumours?

A
  • local spread
  • lymphatic spread
  • blood spread (haematogenous)
  • transcoelomic spread
  • intraepithelial spread
49
Q

What is metastasis?

A

Spread of the malignant cells to distant organs forming secondary tumours

50
Q

What is the pattern of spread of carcinomas?

A
  • lymphatics first
  • then blood later
51
Q

What is the pattern of spread of sarcomas?

A

Blood spread (rarely lymphatic

52
Q

What is used for tumour grading?

A

Microscope

53
Q

What is used for tumour staging?

A

Clinical tests

54
Q

Describe grading of tumours

A

Histological assessment of:
- invasion into underlying tissue
- cellular atypia
- many methods eg numerical grades/low-high/degree of differentiation

55
Q

What does cancer staging describe?

A

The extent or severity of a persons cancer
- helps treatment planning
- helps estimate the persons prognosis
Methods include:
- physical exams
- imaging procedures
- lab tests
Etc.

56
Q

What clinical staging system is used for oral cancer?

A

TNM (tumour size, lymph node involvement, presence of metastases)

57
Q

How does the immune system recognise tumour cells?

A
  • tumour associate dantigens TAAs
  • neoantigens
  • products of mutated genes
  • overexpressed proteins
  • viral proteins eg HPV
58
Q

What is the tumour response to tumour antigens?

A

A cell mediated immune response
- CD8+
- NKC
- macrophages

59
Q

How do tumour cells escape immune response?

A
  • alter tumour antigen expression
  • activation of immunoregulatory pathways leading to T cell unresponsiveness and apoptosis
  • immunosuppressive factors eg cytokines which inhibit T cell response
60
Q

What is immunotherapy?

A

Uses the patients own immune response to control and destroy malignant cells
- active immunisation
- reversal of immunosuppression
- adopted cell transfer
- strengthening natural immune responses