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MBBS IASM > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What is the definition of neoplasia

A

An abnormal mass of tissue, the growth of which exceeds and is UNCOORDINATED

with that of normal tissues

and persists in the same excessive manner after cessation of the stimuli which evoke the change

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2
Q

How can u identify Neoplasia

A

-Loss of response to normal growth control mechanisms
- Continued proliferation even without a recognizable stimulus
- Loss of differentiation (especially for malignant neoplasm)
- Aberrant differentiation function (especially for malignant neoplasm)
- Expression of ‘embryonal’ characteristics (especially for malignant neoplasm)

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3
Q

Embryonic development is somehow similar to neoplasia in some way

How are they similar

How are they different

A

Both have rapid growth and are mitotic figures

Embryonic development is coordinated

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4
Q

What is hypertrophy

What is Hyperplasia

How are they different from neoplasia

A

Hypertrophy= Increase in size of cell (Muscle in response to exercise)

Hyperplasia= Increase in number of cell (uterine muscle in respoonse to pregnancy

They are cordianted and Reversible hence different from neoplasia

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5
Q

What are the difference between a benign and a maligant neoplasia in terms of their ability to invade

A

Benign is expansive yet limited by Basement membrane

malignant is infiltrative and expansive, and they can invade BEYOND Basement membrane

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6
Q

What are the difference in gross appearance between a benign and a malignant neoplasia

A

Benign is circumscribed and encapsulated

Malignant has a poorly defined margin

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7
Q

What are differences between benign and malignant neoplasia in terms of their rate of growth

A

Benign is slow and may cease

Malignant is fast, and it is common for it to outgrow it’s blood vessel supply to cause irregular necrosis

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8
Q

If a tumour has crab-foot like extensions, do u think it is benign or malignant

A

Malignant

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9
Q

How can benign and malignant neoplasia be classified according to microscopic appearance (6 difference)

A

Benign has

–> Normochromatic nuclei
–> Low Nucleus-to-cytoplasm ratio
-> well-differentiated and it closely resembles tissue of origin
–> It has regular cell shape
–> Mitosis is absent or scanty
–> It has mild architectural disturbance and with maintained polarity (ie they grow toward the same side)

Malignant is
–> Hyperchromatic nuclei
–> High nuclei-to-cytoplasm ratio
(The cytoplasm is small as it contains protien for function)
(The nuclei is enlarged due to replication, expression and division)
–> It has vary degree of differentiation (well/poor)
–> It shows cellular pleomorphism (Variation in size and shape of nucleus and overall cell)
–> It is active mitosis and there are abnormal mitosis (Indicated by tripolar or multipolar spindles)
–> it has lost the polarity and with marked architectural disturbance

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10
Q

Why the malignant neoplasia exhibits genetic instability

A

The nuclear sizes are irregular,

and the abnormal alignment of chromatin leads to unequal division of genetic materials in mitosis

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11
Q

For benign neoplasia,
What is meant by the term Polarity

What are the 2 situations called when benign tumour grows to increase the surface area

A

Polarity means they grow towards the same side

Grow outward to form papillary lesion: Papilloma

Invaginated: Adenoma

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12
Q

If a malignant cancer occurs at the epithelium, what will it usually do

A

Grows into the connective tissue and invade through the basement membrane

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13
Q

What is meant by the term differentiation

In embryonic development

And in neoplasia

A

It means the cell becomes specific cell types that performs specific functions

It means the cell resembles the tissue it originates both morphologically and functionally

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14
Q

What is the difference between the carcinoma and sarcoma in terms of the tissue they invade and the way they spread

A

Carcinoma: Epithelial . Spread by lymphatics

Sarcoma: Connective Tissue: Spread by blood

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15
Q

What is the term for

Benign

Malignant

At epithelium

A

Papilloma

Adenoma

Carcinoma

Adenocarcinoma

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16
Q

What is the term for

Benign

Malignant

At Fibrous tissue

A

Fibroma

Fibrosarcoma

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17
Q

What is the term for

Benign

Malignant

At Bone

A

Osteoma

Osteosarcoma (aka osteogenic sarcoma)

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18
Q

What is the term for

Benign

Malignant

At Fat

A

Lipoma

Liposarcoma

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19
Q

What is the term for

Benign

Malignant

At Cartilage

A

Chondroma

Chondrosarcoma

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20
Q

What is the term for

Benign

Malignant

At Smooth muscle

A

leiomyoma

leiomyosarcoma

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21
Q

What is the term for

Benign

Malignant

At Striated muscle

A

Rhabdomyoma

Rhabdomyosarcoma

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22
Q

What is the term for

Benign

Malignant

At blood vessel

A

Haemangloma

Angiosarcoma

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23
Q

What is the term for

Benign

Malignant

At Nervous tissue

A

Benign: Nil

Astrocytoma

Oligodendroglioma

Ependymoma

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24
Q

What is the term for

Benign

Malignant

At trophoblast

A

Hydatidiform mole

Chorion carcinoma

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25
Q

What is the term for

Benign

Malignant

At Totipotent cell of Embryonic tissue

A

Benign Teratoma

Malignant Teratoma

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26
Q

What is the term for

Benign

Malignant

At Pluripotent cell

A

Benign: Nil

Malignant:
Nephroblastoma

Hepatoblastoma

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27
Q

What is the term for

Benign

Malignant

At Unipotent cell

A

Benign: Ganglioneuroma

Malignant
Medulloblastoma
Retinoblastoma
Neuroblastoma (Sympathetic nerve)

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28
Q

What is dysplasia

A

It has cellular change similar to malignant neoplasia but there is no evidence of invasion and actual tumour formation

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29
Q

Does dysplasia Has maintained it’s polarity and architecture

A

It has maintained the polarity

And preserved Architecture

30
Q

How can we define the seriousness of dysplasia

A

Graded as mild/ moderate/ severe:

  • Mild/ moderate: some reluctance to differentiate, but will differentiate when forced without increase in size or any mass effect

Moderate dysplasia is still considered
- Severe: nuclear pleomorphism, hyperchromatism up to surface, mitosis in upper layers and also refuse to differentiate (but no loss of polarity yet, architecture preserved)

31
Q

What is the situation when dysplasia involves the whole thickness of surface epithelium

A

Carcinom-in-situ

32
Q

What is the problem of dysplasia

A

It increase chance for invasive carcinoma

It maybe reversible

33
Q

For colorectal cancer, is the molecular change stepwise．What genes are affected

Name a crucial mutation on chromosome

A

APC gene: A Tumour suppressor gene

Ras gene: A oncogene, activated to benign adenoma with dysplasia

Chromosome 18q is needed

p53 is inactivated (Tumour suppressor)

34
Q

What is the Concept of clonality and heterogeneity in malignant neoplasm

A

There are random mutations in our DNA everyday
- Competition in cells of our body:
nutrients, space, etc.
→ selection pressure
→ mutated cells may outcompete and become the dominant clone/ progeny
→ accumulation of mutations leads to formation of malignant cell (clonal expansion)

  • By the time a malignant tumour is formed, the malignant cells are usually clonal in origin but have developed heterogeneity with varying ability to invade and metastasize
  • Clonality in some situation helps us to distinguish a neoplastic from a hyperplastic situation clinically
  • E.g. lymphoid hyperplasia in reaction to
    antigen are polyclonal, whereas
    lymphoid neoplasm are monoclonal →
    distinguished by a clonality marker
35
Q

How is the idea of clonal and heterogenity affect the treatment for cancer

A

Treatment induces new selection pressure
- Since there is variation within the tumour cell population, some cells will
survive the selection pressure and undergo clonal expansion again →
recurrence

36
Q

How can the carcinoma or adenocarcinoma invade through the Connective tissue

A

it cleaves the basement membrane with enzymes like Type IV Collagenase

It also pause the anoikis (a strong program which signals the epthelial cell to die if not attached basement membrane/ neighbouring cell

Hence it can survive after detached from the Basement membrane and in the connective tissue

37
Q

How is the metestatis done. What are the body defences kicknig in

A

The tumour can find a vessel and invade it to enter the blood

Platelet will clot it while the host immune cells will attack it but it is uneffective

it then adhere to the basement membrane of the blood vessel and do extravasation.

It then induce the formation of new blood vessel via angiogenesis to establish colony

38
Q

Name 3 media for tumour to do metastatis ead and what is the speed

A

Via lymph: Slow

Via blood: Quick

via transcoelomic spread (pleural cavity or peritoneal cavity)

39
Q

Other than metastatis, name 2 ways for it to spread

A

Local invasion

Nerve invasion

40
Q

What is the movement of tumour when it spread along lymph

A

Primary organ –> regional lymph node -> More central lymph node

41
Q

What is the movement of tumour in haematogenous route

A

Veins to heart to organs

42
Q

What is the route of peritoneal metastatis

A

Invasde through muscle wall then disseminate in the peritoneal cavity

43
Q

What is the route of pagetoid spread

A

Crawling along the epithelium as each individual gland cell can invade a single layer or stratified squamous epithelium

44
Q

What is the route of Perineural spread

A

Less resistant in nerves, easier to travel along them

45
Q

What are the T N M stages of cancer

A

T: Local extension
N: Extent of lymph node metastatis
M: Extent of distant metastatis

46
Q

What are the instrinsic factor for tumour growth

A

Cell proliferation rate, Cell death, cell maturation and stop dividing

47
Q

What contributes to the net growth rate of a neoplasia

A

Balance between the proliferation and differentation

Tumour enhances Proloferation and avoids differentiation and cell death

48
Q

What are the hall marks of the neoplasia

A
  • Deregulate the cellular energy requirement
  • Resist cell death
  • Activate invasion and metastasis mechanisms
  • Promote inflammation
  • Enable them to replicate limitlessly (telomeres)
  • Sustain proliferation signal
  • Evade growth suppressive signal
  • Avoid immune destruction
  • To induce angiogenesis
  • Show genomic instability and increased mutation rate to facilitate the development of
    heterogeneity to overcome environmental constraints
  • [DRAPE SEATS or GRAPE CGI II]
49
Q

What are the term of Normal gene for proliferation and differentiation

Cancer-causing gene

Gene that prevent development of tumour

A

Proto-oncogene

Oncogene

Tumour Suppressor gene/ antioncogene

50
Q

How can

Viral infection

Chromosomal arrangement

Mutation

Gene amplification

Turns an protooncogene into Oncogene

A

a virus may insert own promoter above 5’-end of protooncogene
→ activity of proto-oncogene become controlled by the viral
promoter leading to aberrant activation

Chromosomal arrangement/ gene fusion – chromosomes break and
another fragment of the chromosome is connected to the 5’-end of the gene,
so the hybrid gene activity is controlled by an active cellular gene that is
normally active in certain cell types → uncontrolled activity

aberrant activation of proto-oncogenes

copies of proto-oncogene is duplicated (up to 30-40 copies of the same gene in the genome) and contributes to the net overactivity

51
Q

how to inactivate the tumour suppressor gene

A
  • Deletion (whole or part of the gene)
  • Truncating mutation (frameshift, nonsense or splice site mutation) [shortening]
  • Point mutation
  • Promoter methylation
52
Q

How does accumulation of multiple events cause the development of tumour

A
  • Cells have altered, overactive oncogenes and loss of regulator tumour suppressor genes
  • If there is growth advantage, there will be clonal expansion of the cells that have accumulated these changes
  • Lead to a population of cells that divide faster and lead to additional genomic instability
    (acquire additional genetic alterations more rapidly)
  • Development of heterogeneity
53
Q

What is the major type of cancer in Child

A

46% leukaemia/lymphoma (hematopoietic or lymphoid
cells), 28% CNS tumours

54
Q

What is the most 5 prevalent type of cancer in Male

A

Colorectal, lung, prostate, liver, stomach

55
Q

What is the most 5 prevalent type of cancer in Female

A

Breast, colorectal, lung, corpus uteri, thyroid

56
Q

What can chemical agents do to cause cancer

Under what circumstances will clonal expansion occur

A

Electrophilic, mutagenic, cause rapid irreversible DNA alteration in isolated cells
- Only when they are pushed to divide can they form clonal expansion/ pass mutation to the progeny

57
Q

What does Pott suggest

A

Soot can enhance the risk of Scrotal cancer

58
Q

Name 4 characteristics of chemical carcinogens

A

Long latent period
- Great individual variation in susceptibility
- Many are indirect carcinogens requiring metabolic activation but can also be destroyed by
detoxification pathway
- Hereditary factors may contribute to mild difference in activity of these pathways

59
Q

How can Radiation cause Cancer

A
  • DNA damage, if unrepaired, can cause cancer
  • Depend of linear energy transfer (e.g. UV, gamma irradiation)
  • UV is much weaker, so required very long exposure to cause mutations in DNA that can
    develop into cancer
  • Related cancer types: e.g. Leukaemia, osteogenic sarcoma
60
Q

Name 4 virus-linked cancer

A

Human papilloma virus (HPV) and cervical cancer

Epstein-barr virus and nasopharyngeal carcinoma

Hepatitis B virus and hepatocellular carcinoma

Epstein-barr virus and Burkitt lymphoma

61
Q

What is the characteristic of Viral DNA when it is corporated into the host genome to cause cancer

A

incorporated and remains in cells as
they develop into cancer (viral DNA integration into the host genome)

Site of viral DNA integration into host genome not constant but clonal
- Every progeny cells have the virus in the same integration site
- Process is very critical in the early events of the cancer development

62
Q

How does HBV cause hepatocellular carcinoma

A

The HBV induces chronic injury to the liver, which enhances cellular proliferation

The viral DNA integrated to the host DNA in clonal form, and activate proto-oncogenes and PKC

63
Q

How can hormones induce Neoplasia

Name an example

A

Hormones are involved in stimulating the proliferation of the target
organs → increased risk of mutations or genetic aberrations →
increased incidence of specific cancer types

  • E.g. Endometrial carcinoma and high oestrogen level
64
Q

Name 2 other factors causing cancer

A

-Chronic irritation and trauma
- Immunological

65
Q

How can one inherit Neoplasia

A

They receive defective tumour suppressor gene

66
Q

What is the Knudson’s Hypothesis

A

2 Hit inactivation of antioncogene can allow unrestricted cell proliferation

67
Q

Does oncogene need 1 or more copies to activate neoplasia

A

1 is alrd enough

68
Q

For Lynch Syndrome

What is the gene mutated

What is the cancer caused

Why the offspring of Lynch syndrome is more prone to the cancer

A

MLH1 (a DNA repair mismatch gene)

Colorectal cancer

They have inherited a defective copy of MLH 1

69
Q

For Familial Adenomatous polyposis (FAP)

is that autosomal dominant or recessive

What is the gene affected

What is the Cancer associated

A

Dominant

APC gene

adenocarcinoma (at colon epithelial cell)

70
Q

What is microsatellite

How can we detect microsatellite

A

a tract of repetitive DNA

Measure length of satellite – in normal situations, the length of cancer and normal bands should be the same

  • If there are multiple loci showing the phenomenon (displacement/ unequal length) then there is
    microsatellite instability
71
Q

Is Inherited Neoplasia Dominant or recessive

A

mostly dominant

MBBS IASM (24 decks)

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