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BDS4 BAMS Oral Disease, Medicine, Virology > potentially malignant lesions > Flashcards

potentially malignant lesions Flashcards

1
Q

potentially malignant lesion

WHO defintion

A

altered tissue in which cancer is more likely to form

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2
Q

potentially malignant condition

WHO definition

A

generalised state with increased cancer risk (systemic)

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3
Q

potentially malignant disorder

A

umbrella term which covers both potentially malignant lesions and conditions

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4
Q

what terms are no longer used and why

A

premalignant, precancerous, preneoplastic

pre gives defintiive indication
* not every single one will be so potentially is better

use potentially malignant

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5
Q

4 potentially malignant disorders

A

lichen planus

oral submucous fibrosis

iron deficiency

tertiary syphillis

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6
Q

is lichen planus a potentially malignant disorder

A

sometimes

can affect skin and mucous membranes - esp if oral cavity

not all types are at risk of developing malignancy
* eroisve and ulcerative on tongue and gingiva are high risk

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7
Q

what is oral submucous fibrosis

A

Betal nut chewing can lead to dev
Abnormal collagen deposited in epithelium
* Makes tissues of oral cavity hard to expand or move
* Muscles undergo liquidation
* Pt have limited mouth opening

Higher risk of oral cancer

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8
Q

is iron deficiency a potentially malignant disorder

A

Oral epithelium thinner than normal – issue as important barrier against pathogens and carcinogens

More at risk of infection and carcinogens as result

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9
Q

is tertiary syphillis a potentially malignant disorder

A

rare now

massive granulation tissue on the tongue, predispose to develop oral cancer
can get white leukoplakia like lesion on tongue as well

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10
Q

lesions that are potentially malignant

4

A

leukoplakia
erythroplakia
erytholeukoplakia
chronic hyperplastic candidosis

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11
Q

leuko and erythoplakia are

A

clinical dx
can’t determine underlying cause

form a list of diff dx
* try scraping off
* candida albicans? –> acute pseudomembranous candidiasis (thrush)

if investigations still unclear –> leukoplakia

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12
Q

most carcinomas in the UK arise from

A

clinically normal mucosa

other areas have a higher incidence from potentially malignant lesions (e.g. India)

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13
Q

leukoplakia is X more likely to progress to cancer than clinically normal mucosa

A

50-100 times

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14
Q

will all leukoplakias develop into cancer?

A

no

unable to predict which ones will

pt factors have a role - habits, where they are from etc

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15
Q

clinical factors that play a role on chance of cancer development from leukoplakia

5

A
  • age
  • gender
  • idiopathic
  • site
  • clinical appearance
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16
Q

age impact on cancer progression

A

older the pt more likely

inc incidence with age

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17
Q

gender impact on leukoplakia progression to cancer

A

more likely in females

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18
Q

idiopathic leukoplakia progression into cancer

A

more likely if pt has no other risk factors
e.g. no smoking, no tobacco use, no/limited alcohol, good diet but have an unexplained white patch on tongue

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19
Q

sites that have inc progression to cancer from leukoplakia

A

floor of mouth
tongue
gingiva

sublingual keratosis - extreme high risk

buccal mucosa - low risk

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20
Q

clincial appearance that has inc progression to oral cancer from leukoplakia

A

non-homogenous
* verrucous, ulcerated leuko-erythroplakia
* warty, knobbly, ulcerated, mix red and white - higher risk
* Biopsy and manage quickly - Some parts may already be malignant

homogenous appearance less - all same colour, consistency

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21
Q

gold standard for assessing malignant potential

A

histopathology

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22
Q

histopathology preditors of malignant change

4

A

dysplasia

atrophy - thinner, esp in erythro lesions

candida infection - chronic hyperplastic candiasis or candida leukoplakia
* get mixed colour lesion or pure white
* associated with smoking
* has potential to become malignant

biological markers: DNA content in leukoplakia
* inc DNA due to inc in chromosomes or amplification of genes
* Signs the cells is acquiring characteristics or hallmarks

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23
Q

molecular markers in oral epithelium dysplasia

A

wide variety
* Signalling pathways - EGFR
* Cell cycle - Ki67; p53; pRB
* Immortalization -Telomerase
* Apoptosis - p53, p21
* Angiogenesis - VEGF
* COX-1&2 enzymes
* Proliferation and differentiation markers
* Viruses: HPV +, HPV-
* Loss of heterozygosity (LOH) 3p, 9p,13q ( retinoblastoma),17p

no markers (single/combination) ID to help determine progression

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24
Q

p53

A

tumour suppression gene
* makes protein that helps cell division when irreparable genetic damage

Cancer has it deleted, inactivated or mutation - 80% Head and neck cancer
**Strong indicator lesion is on its way to malignancy **

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25
HPV
inc incidence of oropharyngeal cancer * Different from oral cancer Tumours positive for HPV have better prognosis than negative HPV tumours
26
first thing to look for histopathologicaly
epithelial dysplasia
27
dysplasia definition
disordered maturation (growth) in a **tissue** types: fibrous, osseous, renal, *epithelial (oral)*
28
atypia definition
changes in **cells** | dysplaisa - tissue
29
describe this
Cellular atypia Cells normal, well stratified in top 2/3 White spaces between them, not so well arranged, separated from each other, irregular shape - cells showing signs of atypia – bottom 1/3
30
potentially malignant lesions - criteria for diagnosis | 2 groups
**assess arichitectural changes then cytology** boundaries between categories not well defined How much involved in changes * layers – stratified (arranged in normal manner) or not * individual cell changes
31
architectural changes
abnormal maturation and stratification
32
cytological abnormalities
cellular atypia
33
grading of epithelial dysplasia by
microscope (NOT clinical)
34
WHO grading of epithelial dysplasia 2005 | 6
* dysplasia * hyperplasia * mild * moderate * severe * carcinoma-in-situ
35
basal hyperplasia
inc basal cell numbers architecture * regular statification * basal compartment is larger no cellular atypia
36
basal hyperplasia
inc basal cell numbers architecture * regular statification * basal compartment is larger no cellular atypia
37
basal cells
divide at membrane then progress through layers of epithelium
38
describe this
basal cell hyperplasia increased basal cell numbers no cellular atypia architecture * regular stratification * basal compartment is larger
39
mild epithelial dysplasia
architecture changes in lower third cytology mild atypia - generally only show a few signs of cellular atypia (not all the signs) * pleomorphism * hyperchromatism * basal cell hyperplasia
40
possible cause of mild epithelial dysplasia
can be reactive - smoker, infection, inflammation, trauma remove cause and likely regress
41
pleomorphism
variety in shape and size of nuclei/cell or both
42
hyperchromatism
darker stained nuclei due to inc DNA content
43
describe this
mild epithelial dysplasia architecture: changes in lower third cytology: mild atypia * generally only show a few signs of cellular atypia (not all the signs) here - pleomorphism, hyperchromatism, basal cell hyperplasia
44
moderate dysplasia
architecture * change extends to middle third (2/3 changed) cytology * rete pegs rounder and more bulbous * separation and increased cell motility
45
describe this
moderate dysplasia architecture: change extends into middle third (2/3 changed) cytology: moderate atypia * Rete pegs rounder and more bulbous * Separation and increased cell motility
46
describe this
moderate dysplasia architecture: change extends into middle third (2/3 changed) cytology: moderate atypia * Rete pegs rounder and more bulbous * Separation and increased cell motility
47
severe dysplasia
architecture * changes extend to upper third (most layers affected) cytology * severe atypia and numerous mitoses, abnormally high mitotic figures not at basal cell layer (white circles - 5 here) * location and number abnormal - stong malignant indicator
48
describe this
severe dysplasia architecture * changes extend to upper third (most layers affected) cytology * severe atypia and numerous mitoses, abnormally high mitotic figures not at basal cell layer (white circles - 5 here) * location and number abnormal - stong malignant indicator see loss of polarity, hyperchromatism, pleomorphism
49
describe this
carcinoma in situ theoretic concept malignant but not invasive abnormal architecture * full thickness (or almost full) of viable cell layers * confined to basal epithelium, no invasion to underlying connective tissue pronounced cytological atypia * mitotic abnormalities frequent * hyperchromatism – dark spots * pleomorphism – wide and look like pushing down
50
carcinoma-in-situ
theoretic concept malignant but not invasive abnormal architecture * full thickness (or almost full) of viable cell layers * confined to basal epithelium, no invasion to underlying connective tissue pronounced cytological atypia * mitotic abnormalities frequent * hyperchromatism – dark spots * pleomorphism – wide and look like pushing down
51
management of carcinoma-in-situ
lesion needs immediate removal
52
malignancy always has X associated with in
inflammation Indication of good immune response - lacking indicates the immunocompromised More severe dysplasia - more inflammation in underlying CT
53
at present detection of potentially malignant lesion by confirmation by
detection by oral visual examination confirmation by histopathology
54
cons of histopathology | 3
* invasive - biopsy * cannot monitor tissue response to tx effectively (invasive, load on NHS) * not suitable for mass screening
55
possible future options for detection of potentially malignant lesions | 3
Salivary biomarkers * easy, cheap, can be used to monitor and can help indicate recurrence of tumour before clinical detection possible Next generation sequencing * Detect disease in people or people at risk of disease Artificial intelligence AI * Esp for mass screening in rural areas
56
2 main factors for carcinogenesis
genetic environmental (carcinogens)
57
molecular basis of cancer | 3 stages
**damage** * inactivated, useless or over/under express **alterd gene expression** * Gene responsible for protein which has a function **altered cell function** * if gene expression is changed and target for protein (function) is changed causes alteration in cell function
58
molecular basis of cancer | 3 stages
**damage** * inactivated, useless or over/under express **alterd gene expression** * Gene responsible for protein which has a function **altered cell function** * if gene expression is changed and target for protein (function) is changed causes alteration in cell function
59
carcinogenesis
Multi step Initiation * Mutation to gene * Cell continues to divide with genetic mutation that wasn’t repaired * Not enough to form malignant cell Promotion * Another mutation in genes that are responsible for repairing DNA * Cell harbours more genetic mutation due to def DNA repair system * Whole genome unstable * Cell becomes malignant Can be years between initiation and malignant presentation | REVISE BDS1
60
possible changes to chromosomes | 3
aneuploidy translocations amplifications
61
aneuploidy to chromosomes
increase/decrease in number of chromosomes
62
translocations to chromosomes
break off and add to another part, *can cause certain leukaemias*
63
amplifications to chromosomes
extra copy of genes so make extra factors can cause malignancy* (esp if growth factors)*
64
3 possible changes to genes | which can cause malignancy
mutations deletions amplifications
65
epigenetic changes | which can cause maliganancy
chemical changes in DNA, such as * methylation - methyl silence genes, stop from functions * modification of the histones that package DNA - small molecules attach to histones, also regulate gene expression
66
classes of changes to DNA that can occur in initiaion/promotion during carcinogenesis
changes to chromosomes * aneuploidy * translocations * amplifications changes to genes * mutations * deletions * amplifications epigenetic changes * chemical changes to DNA e.g. methlyation, modificaiton to histones
67
growth in the body is an equilibrium between
oncogenes and tumoursupressor genes
68
oncogenes
have normal roles within the cells (produce normal growth factors), differeing oncogenes can be activated
69
tumour suppressor genes
supres the growth of cells most imp is Tp53
70
Knudson's "two-hit" hypothesis of carconogenesis
Have a pair of tumour suppressor genes – one on each chromosome * So lose 1 have the other to still function * But lose both -> two hit hypotheses, cell becomes malignant Oncogenes (that produce growth factors), * One becomes mutated - enough for cell to require malignant characterises - not 2 hit *Onco - 1 word 1 knocked needs to work Tumour suppressor - 2 words need both knocked out*
71
oral cancer genetics possible pathways | 5
equilibrium between oncogenes and tumour suppressor genes genes that regulate apoptosis * if stopped continue to divide forever, no natural programmed cell death genes involved in DNA repoar miRNA - strands of RNA that can play a part in neoplastic transformation * don't code to produce protein, regulate things * target of many drugs viral component - HPV
72
HPV and cancer
HPV 16 and 18 are carcinogenic have E6 protein which degrades p53 - so nothing to stop them passing on this inactivation of tumour suppressor genes
73
6 hallmarks of cancer
evading apoptosis self-sufficient in growth signals insensitivity to anti-growth signals sustained angiogenesis limitless replication potential tissue invasion and metastasis
74
update to hallmarks of cancer that is key for oral cancer | 2011
polymorphic microbiomes * bacteria have protective function against oral cancer Connective tissue has effect on cells capacity and needs for malignant growth drugs developed to target 6 hallmarks (outer circle)
75
variation in process of carcinogenesis
* “multistep” - initiation, promotion, progression * sum of genetic changes, not order, important * how many changes needed? Differs between malignancy
76
field change theory
**all the area may be susceptible to developing oral cancer * Not just the potentially malignant lesion ** genetic instability increasing the possibility of developing cancer * clinically may appear normal * difficult to estimate extent of field * includes pharynx, larynx and respiratory tract. multiple primaries - 15 to 20% Can develop a whole new tumour (not a recurrence) * synchronous – 6 months to 1 year after primary tumour * metachronous - several years after primary tumour
77
synchronous tumour
new malignancy 6 months to 1 year after primary tumour | field of change theory
78
metachronous tumour
new malignancy several years after primary tumour | field of change theory
79
oral cancer pathology report points | biosy report 4 points
Dx differentiation and grading pattern of invasive front local extension of disease
80
Dx of oral cancer from pathology report
most are squamous cell carcinomas
81
squamous cell carcinomas gradings/differentiations | done by micrscope 4
* well * moderate (most are) * poly * anaplastic
82
anaplastic SCC
so de differentiated, impossible to know where it came from
83
pattern of invasive front is
related to nodal spread help predict if lymph nodes involved
84
cohesive front
wave like
85
non cohesive front
advancing in strands, possible correlation with lymph node involvement despite no clinical changes detected
86
spread of oral cancer | biopsy report
Local extension of disease varies according to site * mucosal extension * muscle (tongue etc) * bone * nerve * salivary gland Lymphatic spread Haematogenous spread
87
signs malignancy spread to bone
Can cause destruction In pt with good standard OH but have unexplained mobility - needs further investigation, malignancy underlying in bone
88
perineural spread of malignancy | how management
Along myelin sheath of nerves * possible correlation with lymph nodes spread * Difficult to manage * Recurrence high *Perineural spread involving small nerves at advancing edge predicts nodal spread Extensive spread related to inferior alveolar nerve, may give recurrence*
89
3 modes of lymphatic spread of malignancy
Permeation – grow inside lymph nodes Break of emboli - circulate and attach and grow to lymph nodes Extracapsular spread – grow outside the lymph node, can spread easily
90
sentinel node biopsy
Principle draining lymph node of area of malignancy is taken out and examined to ID any small malignant lesions (micrometasis), that wouldn’t cause lymph node enlargement but are malignant
91
lymph permeation of malignancy
grow inside lymph node
92
maligannt emboli spread to lymph
circulate and attach and grow to lymph nodes
93
extracapsular spread of malignancy to lymph node
grow outside the lymph node, can spread easily
94
staging of oral cancer
clincal procedure by examination TNM
95
TNM staging
Tumour - width, Node - lymph node involvement, number and symmetry Metastases - distal spread
96
haematogenous spread of malignancy
late feature enter veins in neck * Emboli or grow in neck Metastasis to lungs, and spine * ? other sites
97
OSCC subtypes | 3
rare types Verrucous - better prognosis, warty, knobble, slow invasion, rare metastases Basaloid - assoc with HPV Spindle cell - aggressive, cells like fibroblasts, hard to ID, poor prognosis

BDS4 BAMS Oral Disease, Medicine, Virology (23 decks)

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