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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
Q

HPV

A

inc incidence of oropharyngeal cancer
* Different from oral cancer

Tumours positive for HPV have better prognosis than negative HPV tumours

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26
Q

first thing to look for histopathologicaly

A

epithelial dysplasia

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27
Q

dysplasia definition

A

disordered maturation (growth) in a tissue

types: fibrous, osseous, renal, epithelial (oral)

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28
Q

atypia definition

A

changes in cells

dysplaisa - tissue

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29
Q

describe this

A

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

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30
Q

potentially malignant lesions - criteria for diagnosis

2 groups

A

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

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31
Q

architectural changes

A

abnormal maturation and stratification

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32
Q

cytological abnormalities

A

cellular atypia

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33
Q

grading of epithelial dysplasia by

A

microscope (NOT clinical)

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34
Q

WHO grading of epithelial dysplasia 2005

6

A
  • dysplasia
  • hyperplasia
  • mild
  • moderate
  • severe
  • carcinoma-in-situ
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35
Q

basal hyperplasia

A

inc basal cell numbers

architecture
* regular statification
* basal compartment is larger

no cellular atypia

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36
Q

basal hyperplasia

A

inc basal cell numbers

architecture
* regular statification
* basal compartment is larger

no cellular atypia

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37
Q

basal cells

A

divide at membrane then progress through layers of epithelium

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38
Q

describe this

A

basal cell hyperplasia

increased basal cell numbers
no cellular atypia
architecture
* regular stratification
* basal compartment is larger

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39
Q

mild epithelial dysplasia

A

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
Q

possible cause of mild epithelial dysplasia

A

can be reactive - smoker, infection, inflammation, trauma
remove cause and likely regress

41
Q

pleomorphism

A

variety in shape and size of nuclei/cell or both

42
Q

hyperchromatism

A

darker stained nuclei due to inc DNA content

43
Q

describe this

A

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
Q

moderate dysplasia

A

architecture
* change extends to middle third (2/3 changed)

cytology
* rete pegs rounder and more bulbous
* separation and increased cell motility

45
Q

describe this

A

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
Q

describe this

A

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
Q

severe dysplasia

A

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
Q

describe this

A

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
Q

describe this

A

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
Q

carcinoma-in-situ

A

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
Q

management of carcinoma-in-situ

A

lesion needs immediate removal

52
Q

malignancy always has X associated with in

A

inflammation

Indication of good immune response - lacking indicates the immunocompromised

More severe dysplasia - more inflammation in underlying CT

53
Q

at present detection of potentially malignant lesion by

confirmation by

A

detection by oral visual examination

confirmation by histopathology

54
Q

cons of histopathology

3

A
  • invasive - biopsy
  • cannot monitor tissue response to tx effectively (invasive, load on NHS)
  • not suitable for mass screening
55
Q

possible future options for detection of potentially malignant lesions

3

A

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
Q

2 main factors for carcinogenesis

A

genetic

environmental (carcinogens)

57
Q

molecular basis of cancer

3 stages

A

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
Q

molecular basis of cancer

3 stages

A

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
Q

carcinogenesis

A

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
Q

possible changes to chromosomes

3

A

aneuploidy

translocations

amplifications

61
Q

aneuploidy to chromosomes

A

increase/decrease in number of chromosomes

62
Q

translocations to chromosomes

A

break off and add to another part,

can cause certain leukaemias

63
Q

amplifications to chromosomes

A

extra copy of genes

so make extra factors

can cause malignancy* (esp if growth factors)*

64
Q

3 possible changes to genes

which can cause malignancy

A

mutations

deletions

amplifications

65
Q

epigenetic changes

which can cause maliganancy

A

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
Q

classes of changes to DNA that can occur in initiaion/promotion during carcinogenesis

A

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
Q

growth in the body is an equilibrium between

A

oncogenes and tumoursupressor genes

68
Q

oncogenes

A

have normal roles within the cells (produce normal growth factors), differeing oncogenes can be activated

69
Q

tumour suppressor genes

A

supres the growth of cells

most imp is Tp53

70
Q

Knudson’s “two-hit” hypothesis of carconogenesis

A

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
Q

oral cancer genetics possible pathways

5

A

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
Q

HPV and cancer

A

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
Q

6 hallmarks of cancer

A

evading apoptosis

self-sufficient in growth signals

insensitivity to anti-growth signals

sustained angiogenesis

limitless replication potential

tissue invasion and metastasis

74
Q

update to hallmarks of cancer that is key for oral cancer

2011

A

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
Q

variation in process of carcinogenesis

A
  • “multistep” - initiation, promotion, progression
  • sum of genetic changes, not order, important
  • how many changes needed?
    Differs between malignancy
76
Q

field change theory

A

**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
Q

synchronous tumour

A

new malignancy 6 months to 1 year after primary tumour

field of change theory

78
Q

metachronous tumour

A

new malignancy several years after primary tumour

field of change theory

79
Q

oral cancer pathology report points

biosy report
4 points

A

Dx

differentiation and grading

pattern of invasive front

local extension of disease

80
Q

Dx of oral cancer from pathology report

A

most are squamous cell carcinomas

81
Q

squamous cell carcinomas
gradings/differentiations

done by micrscope
4

A
  • well
  • moderate (most are)
  • poly
  • anaplastic
82
Q

anaplastic SCC

A

so de differentiated, impossible to know where it came from

83
Q

pattern of invasive front is

A

related to nodal spread

help predict if lymph nodes involved

84
Q

cohesive front

A

wave like

85
Q

non cohesive front

A

advancing in strands, possible correlation with lymph node involvement despite no clinical changes detected

86
Q

spread of oral cancer

biopsy report

A

Local extension of disease
varies according to site
* mucosal extension
* muscle (tongue etc)
* bone
* nerve
* salivary gland

Lymphatic spread

Haematogenous spread

87
Q

signs malignancy spread to bone

A

Can cause destruction

In pt with good standard OH but have unexplained mobility - needs further investigation, malignancy underlying in bone

88
Q

perineural spread of malignancy

how
management

A

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
Q

3 modes of lymphatic spread of malignancy

A

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
Q

sentinel node biopsy

A

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
Q

lymph permeation of malignancy

A

grow inside lymph node

92
Q

maligannt emboli spread to lymph

A

circulate and attach and grow to lymph nodes

93
Q

extracapsular spread of malignancy to lymph node

A

grow outside the lymph node, can spread easily

94
Q

staging of oral cancer

A

clincal procedure by examination

TNM

95
Q

TNM staging

A

Tumour - width,

Node - lymph node involvement, number and symmetry

Metastases - distal spread

96
Q

haematogenous spread of malignancy

A

late feature

enter veins in neck
* Emboli or grow in neck

Metastasis to lungs, and spine
* ? other sites

97
Q

OSCC subtypes

3

A

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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