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aPATH P COPY (SC) > Neoplasia 1 > Flashcards

Neoplasia 1 Flashcards

1
Q

a tumour

A

a swelling (any clinical detectable lump or swelling)

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2
Q

neoplasm

A

‘ a neoplasm is an abnormal growth of cells that persists after the initial stimulus is removed’ - new growth - just one type of tumour

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3
Q

oncology

A

study of tumours and neoplasm

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4
Q

hyperplasia

A

increase in cell number

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5
Q

hypertrophy

A

increase in cell size

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6
Q

regeneration

A

return to normal mechanisms e.g. the liver

  • stimulated by GF
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7
Q

benign neoplasia

A

gross and microscopic appearances are considered to be innocent, implying that it will remain localised and not spread to other sites

  • less well differentiated
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8
Q

cancer

A

a malignant neoplasm

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9
Q

neoplasm

A

an abnormal growth of cells that persists after the initial stimulus and invades surrounding tissues with the potential to spread to distant sites

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10
Q

metastasis

A

where a malignant neoplasm has spread from its original site to a new non-contiguous site

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11
Q

dysplasia

A

A pre-neoplastic alteration in which the cells how disordered tissue organisation.

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12
Q

characteristics of dysplasia

A

Reversible

Can exhibit considerable pleomorphism, with large hyperchromatic nuclei and high nuclear to cytoplasmic ratio

If detected early it can be prevented from progressing to cancer

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13
Q

summary of how a tumour can be defined

A
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14
Q

primary site

A

original location of malignant neoplasm

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15
Q

secondary site

A

place to which it has spread

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16
Q

how do we tell the difference between benign and malignant tumours

A
  1. Behaviour of the tumour
    • E.g. if its metastases = probably malignant
  2. Appears different to the naked eye
  3. Differentiation
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17
Q

behaviour of benign neoplasms

A
  • remain confined to their site of origin and do not produce metastases
  • Grow in a confined area- capsule
  • Pushing outer margin
  • Rarely dangerous (depends on location)
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18
Q

where could a benign tumour be dangerous

A

in the brain- confined space

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19
Q

behaviour of malignant neoplasms

A
  • invade and have the potential to metastasise
  • Irregular outer margin and shape
  • May have ulcerations and necrosis
  • Infiltrative
  • Grow very rapidly
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20
Q
A
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21
Q

definititon of differentitation

A

process of becoming different by growth or differentiation

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22
Q

differentitation and benign tumours

A

closely resemble the parent tissue- well differentiated

23
Q

differentiation and malignant neoplasms

A

range from well to poorly differentiated dependent on how closely they resemble the cell origin

24
Q

cells with no resemblance to any tissue are called

A

anaplastic

25
Q

characteristics of poorly differentiated cells (6)

A
  1. Increased nuclear size
  2. Increases nuclear to cytoplasmic size
  3. Increased nuclear staining (hyperchromasia)
  4. Increased mitotic figures
  5. Abnormal mitotic figures
  6. Variation in size and shape of cells and nuclei (pleomorphism)
26
Q

what term do clinicians use to indicate differentition

A

grade

  • a high grade tumour is usually poorly differentiated
27
Q

melanoma

A
  • poorly differneited
  • pigment= melanin
28
Q

summary of behaviour of benign tumour

A
  • grows locally
  • retained functions of their cells of origin
29
Q

histology of benign tumour

A
  • resembles cells/tissue of origin
  • few mitoses
  • normal or mild increase in nuclear to cytoplasmic ration
  • cells are unifrom throughout the tumour
30
Q

summary of behaviour of malignant tumour

A
  • expansive and invasive
  • potential to metastasise
  • less likely to retain functions of cells of origin and may soemtimes acquired unexpected functions
31
Q

histology of malignant tumour

A
  • failure ot fully differentiate
  • many mitoses
  • high nuclear to cytoplasmic ration
  • cells/ nuceli vary in size and shape (pleomorphism)
32
Q

pleomorphism

A

cells/ nuceli vary in size and shape

33
Q

example of grade

A

grade 1- well differentiated

grade 3- poorly differnetiated

34
Q

gradding pattern for the breast

A

Gleasons pattern

35
Q

the higher the grade

A

the less liekly to survive

36
Q

dysplasia and differentiation

A

Altered differentiation

Not yet invasive

Mild, moderate and severe- worsening differentiation

37
Q

Dysplasia in the cervice

A

CIN1- mild dysplasia

Malignant changes just affecting lower third of epithelium

CIN2- moderate dysplasia

Lower 2/3rd

CIN3- severe dysplasia

Full thickness of the epithelium

38
Q

why do we get neoplasia (2)

A
  1. Cacrinogenesis
  2. Non-lethal genetic damage (can be genetic, can be spontaneous, can be environmental)
39
Q

mutations and neoplasia

A
  • Accumulated mutations in somatic cells
  • Mutations are caused by initiators- mutagenic agents
  • Promoters then cause cell proliferation
  • A tumour is formed by the clonal expansion of a single precursor cell that has incurred genetic damage
40
Q

give 4 intiators

A
  • Chemicals
    • smoking
    • alcohol
    • diet and obesity
  • Infectious agents
    • HOV
  • Radiation
  • Inherited mutation
41
Q

progression of a normal cell to neoplastic cells due to mutation

A

1) normal cell population
2) Intiator causes mutation in one cell
3) Mitosis of cell and vertical transmsision of mutation
4) most cells start to have mutation

42
Q

germline mutations

A

e.g. BRCA1 skips out this progressing stage*

43
Q

a selection of cell is monoclonal if

A

they all originated from a single founding cell

44
Q

neoplasms emerges from

A

this group of cells by a process called progression

  • characterised by an accumulation of more mutations
  • mutations may give the cell advanatges such as faster growth
45
Q

4 classes of normal regulatory genes

A
  • Growth promoting proto-oncogenes
  • Growth inhibiting tumour suppressor genes
  • Genes that regulated programmed cell death – apoptosis
  • Genes involved in DNA repair
46
Q

proto-oncogenes

A
  • participate in signalling pathwyas which drive proliferation
  • ‘increase in function’ mutation
  • when mutated become Oncogenes
47
Q

oncoge

A
48
Q

oncogenes

A
  • are created by mutations in proto-oncogenes and encode proteins called oncoproteins that have the ability to promote cell growth in the absence of normal growth promoting signals
  • They can transform cells despite a normal copy of the same gene
  • Oncogenes are dominant over their normal counterparts (allele)
49
Q

oncogene mutations can be targeted by

A

inhibitors eg.g. BRAF inhibitor

  • therefoe eimportnant to identify oncogene causing cancer
50
Q

tumour suppressor genes

A
  • Normal function is to stop cell proliferation
  • Generally cause a loss of function
  • In most instances both alleles must be damaged for transformation to occur
  • Abnormalities in these genes leads to failure of growth inhibition (e.g. TP53)
51
Q

apoptosis regulating genes

A
  • May acquire abnormalities that result in less cell death and enhanced survival of mutated cells
  • E.g. follicular B cell lymphoma
52
Q

DNA repair genes

A
  • Loss of function mutations
  • Contribute indirectly to carcinogenesis
  • Impair the ability of cell to recognise and repair non-lethal genetic damage in other genes
  • As a result affected cells acquire mutations at an accelerated rate, a state referred to as a mutator phenotype and is marked by genomic instability
53
Q
A

aPATH P COPY (SC) (19 decks)

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