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Pathology > Disorders of Growth & Neoplasia 4/5 > Flashcards

Disorders of Growth & Neoplasia 4/5 Flashcards

1
Q

how do the cells in a tumour appear

A

monoclonal
from one parent cell which has undergone genetic change
PROGENY

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2
Q

how does the clone expand in a tumour

A

uncontrolled proliferation as lack normal control mechanism

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3
Q

tumours become —-

A

heterogenous
mix genetic profiles
diff properties and mutations

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4
Q

what is the tumour progression

A

normal cell

transformed cell - mutation

clonal expansion

tumour progression

further tumour progression

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5
Q

what is metastatic property

A

can go spread elsewhere

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6
Q

what are some examples of changes in a transformed cell

A

altered nuclear/cyto ratio

altered DNA content

altered surface change

growth at very low cell densities in vitro

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7
Q

what si the aetiology of cancer

A 
not single disease
diff forms
other factors involved 
-geographic
- age
- gender
-geentic
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8
Q

what are some environmental factors assc with carcinogenesis

A

chemicals
radiation
viruses
unknown

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9
Q

what is chemical carcinogenesis

A

chems implications to cause cancer
animal studies
epidemiology

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10
Q

what are some cancers linked to smoking

A

lung
laryngeal
oral
bladder

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11
Q

is smoke a bur chemical

A

no

  • polyacrylic hydrocarbons
  • Ni + Cd
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12
Q

wha does asbestos and nitrosamines cause

A

asbestos - insulation - mesothelioma

nitrosamines - diet - gastric carcinoma

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13
Q

what re the nurses of action of chems

A

direct action
metab conv to active form
weak/strong carcinogens
synergistic effects

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14
Q

what is a simplified theory of carcinogens

A

initiation - DNA damage and mutation

promotion - clonal expansion of abnormal cells leading to cancer

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15
Q

what can radiotherapy do

A

lead to later development of second cancer

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16
Q

what is radiation evidence linked to cancer

A

ionising radiation can induce cancers

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17
Q

what does ionising radiation do to dn

A

damages dna

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18
Q

how does ionising radiation damage dan

A

break single strand - repaired… inaccurate

break double strand - chromo break… chromo rearrange

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19
Q

what is UV radiation strongly implicated with

A

development of skin cancers

  • basal cell carcinoma
  • squamous cell carcinoma
  • malignant melanoma
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20
Q

how does UV light effect the body

A

does not penetrate deeply therefore damage limited to skin

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21
Q

what does UV light induce formation of

A

pyramidine dimers =base pair sub during rep

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22
Q

can viruses cause cancer

A

yes

and contribute to development in diff ways

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23
Q

what is a retrovirus

A

RNA tumour virus

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24
Q

what are the genes retrovirus contains

A

viral oncogenes

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25
Q

what are viral oncogenes responsible for

A

malignant transformation in cells

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26
Q

how does the Viral RNA genome have an effect

A

copied into DNA by revise transcriptase and inserted into host genome — can influence adjacent genes

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27
Q

how do viruses act indirectly

A

cause tissue damage, lead to inc ell prolif and increased risk of mutations - HEP C

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28
Q

give some viruses examples

A

HPV
EBV
Hep C & B

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29
Q

what can HPV give rise to

A

cervical/anal/penile/oropharyngeal carcinoma

30
Q

what can EBV give rise to

A

epstein-barr virus

nasopharyngeal carcinoma, burkitts/hogkins lymphoma

31
Q

what does Hep B & C give rise to

A

hepatocellular carcinoma

32
Q

give an example of a non malignant disease caused by virus

A

EBV
- infectious mononucleosis
oral hairy leukoplakia

33
Q

what are some hosts defences

A

immune cells target tumour cells - destruct
lymphoid infiltrate
regression some cancers
immunodef states assc increase risk

34
Q

is neoplasia genetic

A

yes genetic disease

35
Q

what happens in consideration of neoplasia

A

tumour cells breed
all carcinogens mutagens
tumour cells - nuc abnormalities
altered DNA content

36
Q

what are oncogenes

A

normal genes switched on when cell is needed and promote cell div when expressed are “porto-oncogenes”

37
Q

what happens if oncogenes are inappropriately switch don

A

cell div at wrong time

oncogene –> oncoprotein

38
Q

how do oncogenes act in manner

A

dominant

39
Q

what are the categories of photo- oncogenes

A

genes prod GF/ GF receps

gene overexressed or muataed = diff recep

gene encode signal transducers

gene activate other genes to promote growth transcription factors

40
Q

how are oncogenes activated

A

point mutations

gene amplification translocation between chromos

41
Q

wha are tumour suppressor genes

A

genes that normally stop a cell grow, promote diff of cell to terminal state OR trigger checkP’s = cell arrest if dna damage occurs

42
Q

how can normal tumour suppressor function be lost

A

inactivating mutations
deletions
viral protein = complexes
loss both copies f tumour suppressor gene

43
Q

what re some examples of tumour suppressor genes

A

APC
TP53
Rb

44
Q

what does activation of p53 do

A

regulation of transcription of down streak target genes

cell cycle arrest
cell death - apoptosis

45
Q

how is tumour suppressor genes known

A

inherited cancers

46
Q

what are 3 broad groups of familial cancer syndromes

A

familial cancer syndromes
familial cancers
autosomal recessive disorders (DNA repair defects)

47
Q

what are familial cancer syndromes

A

increased risk of cancer due to transmission of single gene

Rb

48
Q

who is retinoblastoma inherited

A

abnormal allele is inherited and has an effect after a sporadic occurrence previous

49
Q

what ar familial cancers

A

in some fams is marked increase in incidence of common cancers

  • breast
  • ovary
50
Q

what are some responsible genes in familial cancers

A

BRCA -1/2 in breast cancer

51
Q

what are autosomal recessive disorders ) due to DNA repair defects)

A

eg lynch syndrome
due to impaired na repair
fail to mismatch

52
Q

what can be done for relatives of affected ppl

A

screening, counselling and early treatment

53
Q

what are telomeres

A

repeating DNA sequences found at end of chromosome

54
Q

what are tele mores imp for

A

regulating the number of cells divisions a cell is capable of

55
Q

what happens to the telemere after each division

A

shortens until cannot replicate anymore

56
Q

what is telomerase

A

enzyme that lengthens teleomres in stem cells

- tumours have more of this

57
Q

what are epigenetic effects

A

reversible, heritable altered gene expression without mutation

58
Q

give some examples of epigenetic events

A

histone mod
dna mthylation
silenced tumour suppressors by hypermethylation

59
Q

what is molecular carcinogenesis

A

multiple genetic abnormalities

60
Q

what does molecular carcinogenesis involve

A

oncogenes and tumour suppressors

61
Q

what si the presentation of cancer like

A

very vary
incidental screening
effect of primary OR metatstic lesion
dept on site

62
Q

what can tumours present as consequence of

A

local disease
distant spread
non metatstic manifestation of malignancy
incidental findings

63
Q

what are the symptoms of cancer

A

asymptomatic

vague
- tired, weight loss, fever, anorexia

sp symptoms
- primary/secondayr lesions
- skin/rash
paraneoplastic syndomres

64
Q

what are paraneoplastic syndromes

A

symptoms that cannot be explained by effects of local or distant tumours

65
Q

why is it imp ro recog paraneoplastic syndormes

A

may be first sign of underlying cancer
significant clinical effect itself
mimic metasstaci disease

66
Q

give some examples of paraneoplastic syndromes

A

endocrinopathy
- hypercalcaemia

neuromuscular
- myasthenia

vascular
- nonbac thrombotic endocraditis

67
Q

what si the presentation of oral cancer

A 
vary 
white patch
red speck patch
lump
ulcer
not pain 
no sympt
68
Q

what is commonly cancer screened

A

breast
ceervix
colorectal

69
Q

what is the diagnosis

A 
clinical signs 
cytology
histopathology
immunohistochem
biomarkers
imaging
70
Q

what are courses of treatment

A 
intent - curative/palliative 
surgery
radiotherapy
chemotherapy
novel molecularly targeted therapies
none

Pathology (13 decks)

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