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BDS1 BAMS: Pathology > Neoplasia 1 + 2 > Flashcards

Neoplasia 1 + 2 Flashcards

1
Q

Define ‘neoplasia’

A

An abnormal mass of tissue
Growth is uncoordinated and exceeds that of normal tissues
Persists after removal of stimuli that initiated the change

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2
Q

Describe the growth pattern of benign tumours

A

Expansion
May be encapsulated
Localised
Slow growth rate

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3
Q

Describe the growth pattern of malignant tumours

A

Invasion/infiltration
No capsule
Metastasis
Rapid growth rate

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4
Q

Describe the histological appearance of a benign tumour

A

Resembles tissue of origin
Uniform cell/nuclear shape and size
Few mitoses

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5
Q

Describe the histological appearance of a malignant tumour

A

Variable resemblance to tissue of origin
Cellular and nuclear pleomorphism
Many mitoses, abnormal

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6
Q

How do you treat a benign growth?

A

Local excision

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7
Q

How do you treat a malignant growth?

A

Local excision and and chemotherapy or radiation if metastases present

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8
Q

What are the effects of a benign tumour?

A

Palpable lump, pressure, obstruction, function (especially hormone secretion)
The effects are not always benign

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9
Q

What is a squamous cell carcinoma?

A

A malignant tumour of the squamous epithelium

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10
Q

What is a papilloma?

A

A benign tumour of the squamous epithelium

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11
Q

What is an adenoma?

A

A benign tumour of the glandular epithelium

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12
Q

What is an adenocarcinoma?

A

A malignant tumour of the glandular epithelium

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13
Q

What does the suffix -sarcoma usually mean?

A

Malignant tumour

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14
Q

What is a lymphoma?

A

A malignant tumour of lymphoid tissue

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15
Q

What is leukaemia?

A

A malignant tumour of haematopoietic tissue

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16
Q

What is a melanoma?

A

A malignant tumour that develops from melanocytes

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17
Q

What causes benign tumours?

A

Little is known - may be inherited factors or viruses

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18
Q

What causes malignant tumours?

A

Chemical agents, physical agents, viruses

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19
Q

What are some examples of chemical carcinogens?

A

Tobacco, drugs, alcohol, asbestos

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20
Q

What are the two stages of chemical carcinogenesis?

A
  1. Initiation - permanent DNA damage (mutations)
  2. Promotion - agent promotes proliferation
    Most chemicals are pro-carcinogen and require metabolic activation
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21
Q

Describe ‘initiation’ in chemical carcinogenesis

A

When a carcinogen induces a chemical change resulting in a neoplastic potential

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22
Q

Describe ‘promotion’ in chemical carcinogenesis

A

Another factor stimulates the imitated cell for division. Does not act on non-initiated cells.

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23
Q

Describe ‘progression’ in chemical carcinogenesis

A

Additional mutations occur resulting in malignancy

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24
Q

What are some examples of physical carcinogens?

A 
Ionising radiation (e.g. UV light) - damages DNA causing mutations
Radioactive metals and gases (e.g. radium)
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25
Q

Which are the most sensitive tissues to radiation?

A

Those in which cells are most rapidly renewed (embryonic tissues are the most sensitive)

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26
Q

Give some examples of viral carcinogenesis

A
  1. Epstein-Barr virus: Burkitt’s lymphoma, nasopharyngeal carcinoma
  2. Hepatitis B/C: Hepatocellular carcinoma
  3. Human papillomavirus (HPV): cervical and oropharyngeal carcinoma
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27
Q

What is the 2nd most frequent cause of death worldwide?

A

Cancer

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28
Q

What is the most common form of cancer?

A

Carcinoma - develops from epithelium

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29
Q

Name the risk factors for developing oral cancer.

A

Multifactorial: tobacco, alcohol, viruses (HPV), alcohol, diet and nutrition, socioeconomic factors, GERD, betal quid, immunodeficiency, oral hygiene

30
Q

What is leukoplakia?

A

Leukoplakia is a white patch that cannot be rubbed off or attributed to any other cause. Potentially a malignant lesion.

31
Q

What is dysplasia?

A

The presence of cells of an abnormal type within a tissue, which may signify a stage preceding the development of cancer

32
Q

Which histopathological feature is currently the ‘gold standard’ for assessing whether a tissue has the potential to become malignant?

A

Dysplasia - the presence of cells of an abnormal type within a tissue

33
Q

How is dysplasia identified?

A

Histological examination

Looking for cellular atypia i.e. changes in cells’ appearance and arrangement

34
Q

What is cellular atypia?

A

Changes in cells’ appearance and arrangement

35
Q

What are the 2 main (broad) factors that lead to carcinogenesis?

A

Genetic factors

Environmental factors

36
Q

What are oncogenes?

A

A gene which under certain circumstances can transform a cell into a tumour cell - “accelerators”

37
Q

What are tumour suppressor genes?

A

Anti-oncogenes - they act as “brakes” on cell division. They also repair DNA and send cells into apoptosis.

38
Q

What are proto-oncogenes?

A

Normal genes which regulate cell division

39
Q

What are abnormal variants of proto-oncogenes?

A

Oncogenes

40
Q

What do oncogenes produce?

A

Oncoproteins

41
Q

What can oncogenes cause?

A

Mutations: increased activity of product
Excess of normal product: duplication of the gene
Enhanced transcription: translocation, chromosomes rearrangement

42
Q

What is the Knudson’s “two hit” hypothesis?

A

Most loss of function mutations in tumour suppressor genes are recessive and so both need to be mutated for the cell to become cancerous. This occurs in the RB gene in retinoblastoma.

43
Q

Give examples of inherited cancer syndromes.

A

Retinoblastoma, some colon cancers

44
Q

Give examples of familial cancers.

A

Breast cancer, ovarian cancer, colon cancer

45
Q

What is p53?

A

“the guardian of the genome”

Acts just before the restriction point in the cell cycle to check for DNA damage

46
Q

What are the functions of p53 in response to DNA damage?

A
  1. Stops the cell cycle to allow DNA repair

2. Apoptosis (if repair not possible)

47
Q

Which gene is often inactivated in cancer?

A

p53

48
Q

What are some hallmarks of cancer?

A

Increased growth rate, growth potential - may be immortal, differentiation, invasion/destruction, ability to avoid apoptosis, angiogenesis, evasion of host defences, cell surface changes

49
Q

What are the 3 steps of carcinogenesis?

A
  1. Initiation
  2. Promotion
  3. Progression
50
Q

What is metastasis?

A

The spread of malignant cells to distant organs forming secondary tumours

51
Q

How do carcinomas (epithelial tissues) commonly metastasise?

A

Lymphatics, blood

52
Q

How do sarcomas (connective tissues, non-epithelial tissues) commonly metastasise?

A

Blood (lymphatic spread is rare)

53
Q

What are the 4 stages of metastasis?

A
  1. Direct spread and invasiveness
  2. Angiogenesis
  3. Vascular invasion and spread
  4. Establishment of a new colony
54
Q

What does tumour grading refer to?

A

Grade - the biological nature of the tumour

histopathology

55
Q

What does tumour staging refer to?

A

Stage - the extent of the spread (clinical)

56
Q

Which 2 processes are essential in predicting tumour behaviour and in treatment planning?

A

Grading and staging

57
Q

Which features are pathologists looking for during tumour grading?

A

Histological assessment of:

  • invasion into underlying tissue
  • cellular atypia (mitotic activity, nuclear pleomorphism, differentiation, necrosis.
58
Q

Name some methods of grading.

A
  1. Numerical grades (1,2,3)
  2. Low, intermediate, high
  3. Degree of differentiation
59
Q

What is pleomorphism?

A

Variation in cell/nuclear shape and size

60
Q

How is staging determined?

A 
Physical exams
Imaging procedures
Laboratory tests
Pathology
Surgical reports
61
Q

Which clinical staging system is used for oral cancer?

A

TNM
T = tumour size
N = lymph node involvement
M = metastases

62
Q

Why might patients with cancer experience systemic effects?

A

Often caused by cytokines or hormones released by tumour cells or dysfunction of the organ.

63
Q

How can malignant tumours be treated?

A

Depends on type, grade and stage

  • Surgery
  • Radiotherapy
  • Chemotherapy
64
Q

How does the immune system recognise tumour cells?

A

Tumour associated antigens (TAAs)

65
Q

Give some examples of tumour associated antigens.

A

Products of mutated genes
Overexpressed proteins
Viral proteins

66
Q

What is ‘Elimination-Equilibrium-Escape?”

A

Immunoediting

Immune system components try to protect the host against primary tumour development

67
Q

What happens in the Elimination phase of Elimination-Equilibrium-Escape?

A

Cell mediated immune response
Cytotoxic T cells (CD8+)
NK cells
Macrophages

68
Q

Which immune cells are the primary defence against tumour cells?

A

NK cells

69
Q

What happens in the Escape phase of Elimination-Equilibrium-Escape?

A

Tumours evade the immune response.
Alter tumour antigen expression
Activate immunoregulatory pathways that lead to T-cell unresponsiveness and apoptosis
Release immunosuppressive factors to inhibit T-cell responses

70
Q

What does immunotherapy refer to?

A

Using the patient’s own immune response control and destroy malignant cells

71
Q

What happens during the Equilibrium phase of Elimination-Equilibrium-Escape?

A

The immune system can still control the tumours but no longer eradicate them

72
Q

Define “immunoediting”

A

The relationship between the immune system and the tumour cells
Consists of immunosurveillance and tumour progression

BDS1 BAMS: Pathology (11 decks)

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