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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
what are viral oncogenes responsible for
malignant transformation in cells
26
how does the Viral RNA genome have an effect
copied into DNA by revise transcriptase and inserted into host genome --- can influence adjacent genes
27
how do viruses act indirectly
cause tissue damage, lead to inc ell prolif and increased risk of mutations - HEP C
28
give some viruses examples
HPV EBV Hep C & B
29
what can HPV give rise to
cervical/anal/penile/oropharyngeal carcinoma
30
what can EBV give rise to
epstein-barr virus nasopharyngeal carcinoma, burkitts/hogkins lymphoma
31
what does Hep B & C give rise to
hepatocellular carcinoma
32
give an example of a non malignant disease caused by virus
EBV - infectious mononucleosis oral hairy leukoplakia
33
what are some hosts defences
immune cells target tumour cells - destruct lymphoid infiltrate regression some cancers immunodef states assc increase risk
34
is neoplasia genetic
yes genetic disease
35
what happens in consideration of neoplasia
tumour cells breed all carcinogens mutagens tumour cells - nuc abnormalities altered DNA content
36
what are oncogenes
normal genes switched on when cell is needed and promote cell div when expressed are "porto-oncogenes"
37
what happens if oncogenes are inappropriately switch don
cell div at wrong time | oncogene --> oncoprotein
38
how do oncogenes act in manner
dominant
39
what are the categories of photo- oncogenes
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
how are oncogenes activated
point mutations | gene amplification translocation between chromos
41
wha are tumour suppressor genes
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
how can normal tumour suppressor function be lost
inactivating mutations deletions viral protein = complexes loss both copies f tumour suppressor gene
43
what re some examples of tumour suppressor genes
APC TP53 Rb
44
what does activation of p53 do
regulation of transcription of down streak target genes cell cycle arrest cell death - apoptosis
45
how is tumour suppressor genes known
inherited cancers
46
what are 3 broad groups of familial cancer syndromes
familial cancer syndromes familial cancers autosomal recessive disorders (DNA repair defects)
47
what are familial cancer syndromes
increased risk of cancer due to transmission of single gene | Rb
48
who is retinoblastoma inherited
abnormal allele is inherited and has an effect after a sporadic occurrence previous
49
what ar familial cancers
in some fams is marked increase in incidence of common cancers - breast - ovary
50
what are some responsible genes in familial cancers
BRCA -1/2 in breast cancer
51
what are autosomal recessive disorders ) due to DNA repair defects)
eg lynch syndrome due to impaired na repair fail to mismatch
52
what can be done for relatives of affected ppl
screening, counselling and early treatment
53
what are telomeres
repeating DNA sequences found at end of chromosome
54
what are tele mores imp for
regulating the number of cells divisions a cell is capable of
55
what happens to the telemere after each division
shortens until cannot replicate anymore
56
what is telomerase
enzyme that lengthens teleomres in stem cells | - tumours have more of this
57
what are epigenetic effects
reversible, heritable altered gene expression without mutation
58
give some examples of epigenetic events
histone mod dna mthylation silenced tumour suppressors by hypermethylation
59
what is molecular carcinogenesis
multiple genetic abnormalities
60
what does molecular carcinogenesis involve
oncogenes and tumour suppressors
61
what si the presentation of cancer like
very vary incidental screening effect of primary OR metatstic lesion dept on site
62
what can tumours present as consequence of
local disease distant spread non metatstic manifestation of malignancy incidental findings
63
what are the symptoms of cancer
asymptomatic vague - tired, weight loss, fever, anorexia sp symptoms - primary/secondayr lesions - skin/rash paraneoplastic syndomres
64
what are paraneoplastic syndromes
symptoms that cannot be explained by effects of local or distant tumours
65
why is it imp ro recog paraneoplastic syndormes
may be first sign of underlying cancer significant clinical effect itself mimic metasstaci disease
66
give some examples of paraneoplastic syndromes
endocrinopathy - hypercalcaemia neuromuscular - myasthenia vascular - nonbac thrombotic endocraditis
67
what si the presentation of oral cancer
``` vary white patch red speck patch lump ulcer not pain no sympt ```
68
what is commonly cancer screened
breast ceervix colorectal
69
what is the diagnosis
``` clinical signs cytology histopathology immunohistochem biomarkers imaging ```
70
what are courses of treatment
``` intent - curative/palliative surgery radiotherapy chemotherapy novel molecularly targeted therapies none ```

Pathology (13 decks)

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