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Oral Med > Oral Cancer > Flashcards

Oral Cancer Flashcards

1
Q

What are the risk factors for oral cancer?

A

tobacco?betel
alcohol
premalignant lesions
emerging rrisk factors

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2
Q

What is the effect of tobacco and alcohol?

A

Synergistic effect

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3
Q

How does alcohol cause oral cancer?

A

alters permeability of oral mucosa therfor carcinogens can more easily enter the blood
causes liver damage so body is less able to get rid of toxins
causes immune supression
alcohol induces senescence in the underlying stroma

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4
Q

What factors of alcohol are important?

A

quality

quantity

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5
Q

What are the emerging risk factors?

A 
chronic infection/OH
HPV
HIV
Immunosupression
DIet and Nutrition
UV light
Hereditary
Socioeconomic 
Marajuiana
Nicotine replacement
Alcohol in mouth rinses
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6
Q

Which chronic infections are associated with an increased risk of OC?

A

Chronic hyperplastic candida
Syphylis
Viruses (HPV, HIV)
Oral microbes break down thanol to acetalydehyde in chronic alchoholcs
chronic irration which is thought to be a co factor only

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7
Q

What is the effect of HPV on OC?

A

6 and 16 associated with oral cancer and pharyngeal through oro-genital contact

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8
Q

What factors increase risk of developing HPV related OC?

A

more than 6 sexual partners
more than 4 oral sex partners
for males who had an early age of first intercourse

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9
Q

What is the prognosis of HPV related OC?

A

better prognosis

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10
Q

what is the relationship between HIV and oral cancer?

A

More likely to be kaposis and lymphoma not SCC

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11
Q

What is the effect of immunosupresssion and OC?

A

Kidney transplants associated with lip and tongue cancer

drugs involved are azothirpine and ciclsoporin

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12
Q

What is the effect of diet and nutrition on OC?

A

Plummer vinson syndrome and not enough veg increases chances of OC

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13
Q

What is the effect of UV light and OC?

A

UV light increases chances of Lip SCC

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14
Q

Which premalignant lesions may preceded Lip cancer?

A

actinic keratosis

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15
Q

What is the view on hereditary links between OC?

A

likely that OC linked in family due to shared risk factors
BUT inherited problems in gatekeeper (Tumour suppressor genes) no increased risk of cancer
BUT inherited problems in caretakeer genes (DNA repair) 100,000 times more likely to develop OC

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16
Q

What is the relationship between SES and OC?

A

not a great link

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17
Q

What is the effect of marijuana on OC?

A

unsure

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18
Q

What is the effect on nictoine replacement on OC?

A

no association

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19
Q

What is the efect of alcohol in mouth rinses on OC?

A

unsure

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20
Q

What are the features of OC?

A 
Consider RF
Erythroplasia
lymph node palpable
ulcer with a granular floor and exophytic margins
indurated and fixated
non healing ulcer
red or white lesion
swelling
unexplained pain
unexplained mobile teeth
dysphagia
referred pain
high risk sites
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21
Q

What three ways can oral cancer spread?

A

local
lymphatic
distant

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22
Q

What are sites for local tumour invasion?

A 
soft tissues
Fixation
bone
vessels
perineural
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23
Q

What are the sites for distant metastases?

A

bone
lung
liver

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24
Q

What are the prognostic indicators for oral cancer?

A 
STNMP staging
S=Site
T=tumour size
N=Nodal status
M=metaastes
P=Pathology
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25
Q

What sites are high risk for SCC?

A

Lip and cheek
Anterior tongue, FOM, retromolar region
Posterior third of tongue
Soft palate and antrum

prognosis decreases towards back of the mouth

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26
Q

T/F faster growing tumours have a better prognosis?

A

F

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27
Q

By what percentage does positive lymph nodes decrease liklihood of survival?

A

50%

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28
Q

What is the five year survival rate for OC?

A

stage 1: 51%
stage 2: 40%
stage 3: 21%
stage 4: 8%

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29
Q

How can you treat OC?

A 
Palliative
Radiotherapy
chemotherapy
immunotherapy
photodynamic therapy
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30
Q

what are the surgical compications of treating OC?

A

infection, pain, swelling, resection, psychological

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31
Q

What are the complications of radiotherapy?

A

mucositis, ulceration, dermatitis
drymouth, fibrosis and trismus
osteoradionecrosis

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32
Q

What are the side effects of chemotherapy?

A

mucosisits, ulceration
Bone marrow priblems
pain

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33
Q

how does radiation cause ORN?

A

radiation causes endoarterirtis obliterans which is occlusion of rthe lumen of an artery

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34
Q

When are people at greatest risk of ORN?

A

3-12 months post radiation

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35
Q

What are the three main skin cancers of Head and NEck?

A

Malignant melanoma
BCC
SCC

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36
Q

What are the riskk factors for malignant melanoma?

A 
UV light (even short bursts)
Immunocompiormised
family history
freckling 
light eyes and hait colour
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37
Q

What are the 8 subtypes of malignant melanoma?

A 
Superfifcal
nodular
lentigo
amelonotic
acroa
mucosal
occular
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38
Q

Which are major signs when suspicous of malignant melanoma?

A

change in size, shape and colour

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39
Q

What are the minor signs when suspicious of skin cancer malignancy?

A

inflammation
cursting
sensory change
diameter of more than 7mm

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40
Q

How can we stage malignant melanoma?

A

Stage 1: local tumour
stage 2: local lymoph nodes
stage 3: disseminated disease

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41
Q

How can we assesss the extent of tumour growth?

A

clarkes level

breslow thickness

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42
Q

WHat are the clarkes levels?

A 
5 layers to the skin 
1:pre invasive
2: thinly invasive
3 and 4: mod inasive
5: extensive

qualtitiave assesment

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43
Q

What are the breslows thickness?

A

<4mm thick: mod risk

more than or equal to 4mm thick: higher risk

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44
Q

Where do malignant melanomas usually metastisise to?

A

eye
brain
liver
lung

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45
Q

What is BCC? and which syndrome is it associated with?

A

Gorlin Goltz

slowly invading malignancy of akin

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46
Q

WHat is the pattern of invasion of a BCC?

A

3D pattern

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47
Q

T/F. Metastese are rare in BCC?

A

T

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48
Q

What are the types of BCC?

A 
nodular
superfical
ulcerating
morphoeic
keratotic
pigmented
cystic
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49
Q

What are thr RF for BCC?

A

Gorlin Goltz
Chronic UV exposure
males who freckle
increased age

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50
Q

What are the factors influencing prognosis of BCC?

A

tumour size, site, type
growth pattern
recurrent tumout
Immunocom

51
Q

What are the 2 treatment surgical options for skin cancer?

A

destroy

excise

52
Q

What are the destructive methods for BCC?

A

cryosuurgery
CO2 laser
currettage

53
Q

What non surgical options are there for sBCC?

A 
radiotherapy
chemotherapy
intralesion interferon
retinoids
palliative
54
Q

which pre malignant skin lesions are there?

A

actinic keratosis

actinic chelitis

55
Q

What is the clinical appearance of actinc keratosis?

A

rough scaly light brown patch up WHat ito 2cm in diamter

can be brown or red

56
Q

WHat is actinic chelitis?

A

type of actinic keratosis which occurs on the lips
causes the lips to becomes dry and scaly
mainly occurs on lower lip

57
Q

WHat percentage of people with actinic keratosis will become malignant?

A

10%

more likely in those that are older

58
Q

what is a pre-malignant lesions?

A

a morphologically altered tissue which cancer is more likely to arise in than its normal counterpart

59
Q

What is a pre malignant condition?

A

a generalised state associated with an increased risk of cancer

60
Q

What is the differential diagnosis of a normal white patch?

A

Fordyce spots caused by ectopic sebaceous glands

61
Q

What is the differential diagnosis of transient white patches?

A

thrush

chemical burn

62
Q

WHat is the differential diagnosis for persistant white plaques?

A

congenital: dyskeratosis congitia, white sponge naeuve, leukoedema
keratosis: smokers, frictional, idiopathic, sublingual
Lichen planus
SCC
syphilitic leukplkia
Hairy leukoploka
chronic hyper plastic candida

63
Q

What is leukoplakia?

A

idiopathic keratosis

A white patch which cannot be removed by scraping and cannot be attributed to any disease

64
Q

what is the maligant potential leukoplakia?

A

10 years 2%

20 years 4%

65
Q

How can leukoplakia be classified?

A

Homogenous or speckled

66
Q

What are the high risk sites for leukoplakia?

A

FOM

ventral tonguE

67
Q

wHAT PERCENTAGE OF LEUKOPLAKIA ARE ASSOCIATE WITH scc?

A

15-30%

68
Q

What 4 features raise your index of suscpsion for malignant features?

A

SIte: FOM/Tongue
Lack of aetoloogical factors
Clinical features
Path: degree of dysplasia

69
Q

What are the features of subligual keratosis?

A

Ventral of tongue
Bilateral and symmetrtical
ebbing tide and sharply demarcate

70
Q

subligual keratosis is more common in M or F?

A

F

71
Q

What percentage of sub lingual keratosis become malignant?

A

25%

72
Q

What is erthroplasia?

A

A rare red velvety lesion which is more commonly seen in elderly patetins

73
Q

Where is eryhttoplasia more commonly seen?

A

FOM and Palate

74
Q

What percentage of erythroplasia show dysplasia?

A

75%

75
Q

What is submucous fibrosis?

A

this is when the palate and buccal mucasa appear white

caused by developement of firbous tissue in mucosa

76
Q

What is theough to cause sub mucous fibrosis?

A

Chewing betal quid

Fe or B vitamin defiecneiy

77
Q

What is the pathology behind Sub mucous fibrosis?

A

too much collagen being laid down
insuffiecient collagen destruction
firbroelastic change in the coreum

78
Q

How do you diagnosise submucosa fibrosis and what must you warn the pateint of?

A

biopsy, but this often makes the lesion worse since more scar tissue is formed

79
Q

How do you manage submucosa fibrosis?

A

Inject steroids into lesion
hyluronidases into lesion
excise the bands

80
Q

What percentage of people with submucous fibrosis will develop cancer?

A

8%

81
Q

What is the potetnial malignancy change for chronic hyperplastic candida?

A

30%

9-40%

82
Q

Which sites are most commonly affected by chronic hyperplastic candida?

A

buccal mucosa, lips, tongue and palate

83
Q

What are the types of chronic hyperplasitc candida?

A

soliitary
mucocutanoues
candida endocrine syndromes

84
Q

What is the pathology behind chronic hyperplastic candida?

A

unsure if candida has invaded the tissue or whether the altered tissue has been secondarily invaded by candida

85
Q

where is a high risk site for chronic hyper plastic candida?

A

buccal mucosa

86
Q

what is the liklihood for malignant transformation of lichen planus?

A

2% for erosive lichen planus

87
Q

What is the potential for syphylitic leukoplakia to become malignant?

A

10-30%

88
Q

which site is most commonly affected by syphilitic leukoplkia?

A

dorsum of the otngue

89
Q

what is sideropanic dysphagia associated with?

A

glossitis, dysphagia, anaemia

90
Q

which type of cancer are people with sideropaenic dysphagia associated with?

A

oral and pharyngeal cancer

91
Q

What is white sponge naevus?

A

benign condition inherited in AD fashion

caused by mutation in keratin protein

92
Q

what is the clinical presentation of white sponge naevus?

A

deeply folded white lesions

may also be associated with anus and vagina lesions

93
Q

When would you consider active eradication of a pre malignant lesion?

A 
speckled
FOM
Tongue
Patient fit
accessible
no obvious aetiology
dysplsia
94
Q

What are the three histological features of pre malignancy?

A

CEF
Cytological features
Epithelial architecture
Functional asepcts

95
Q

What are the cytological features of pre malignancy?

A 
pleiromorphic cells
increase cell size
loss of polarity
loss of cellular adhesions
nuclear pleiomorphisms and hyperchromatism
high nucleus to cytoplasm ratio
prominent nucleoli
96
Q

What re the epithelial architectural changes?

A

disruption of the layers

basal cell hyperplasia (replaces prickel cell layer)

97
Q

What happens to the rete ridges in pre malignancy?

A

THEY BECOME DROP SHAPED

98
Q

What happens to the basement membrane in premaliganancy?

A

it remains intact

99
Q

What are the functional aspects of premalig?

A

Mitotic figures increase and are located in the suprabasal epithlium with abnormal forms

dyskeratosis

100
Q

how can dysplasia be classified?

A

mild moderate or severe

101
Q

What happens in SCC?

A

basement membrane becomes invaded

102
Q

How can you remove pre malignant lesions?

A

cryosurgery
scalpel
electro surgery/laser

103
Q

What imaging modalities are available for head and neck cancers?

A 
plain film
US
CT
MRI
PET
104
Q

how dpes US work?

A

provides a topographical map of the tissue interface

105
Q

What are the disadvantage of US?

A

Low resolution
limited penetration
poor for bone or air filled structures

106
Q

What are the advantages of US?

A

flexible and quick
no ionising radiation
best initial assessment for neck masses

107
Q

What type of radiation is CT?

A

ionising

108
Q

What are the disadvantage of CT?

A

need IV contrast media which is iodine bases (allergy)

Not great for soft tissue

109
Q

what are the advantages of CT?

A

excellent resolution especially for cortical bone and air filled structures
guided intervention for deep structures

110
Q

What type of radiation does MRI use?

A

radiofrequency uses a magnetic filed

111
Q

What are the disadvantages to MRI?

A

foreign body hazard
enclosed
slow image production and prone to artefact

112
Q

What are the advantages of MRI?

A

no ionising radaition

excellens tsoft tissues analysis

113
Q

what is PET-CT scanning?

A

combine CT with PET

114
Q

What is used in PET scan?

A

biologically labelled agent with a positron emitter

injected into pateint

115
Q

How does the agent used in PET work?

A

it distributes itself around the body depending upon the metabolic activity of that tissue

116
Q

Which agent is used in PET?

A

FDG, glucose with a single oxygen atom replaced with F18

117
Q

When would you use imaging for cancer?

A

When there is suspected cancer, to aid diagnosis. To assist with staging for a probable cancerous lesion
To follow uo

118
Q

when would you use US?

A

obviously benign lesion

119
Q

When would you do an US guided biopsy?

A

more significant lesions:
Salivary gland tumour
thyroid nodule
lymph node

120
Q

What else could you do if you were worries about malignancy of salivary gland?

A

MRI if complex

CT chest

121
Q

What else could you do for a thyroid nodule if you were concerned other than US?

A

MRI if invasive

122
Q

If there was a pathological lymph node and unsure where the primary malignancy is what investigation could you do?

A

MRI oral cavity
CT chest
PETCT

123
Q

Which vitamin deficiencies are most closely implicated in oral cancer?

A

Vit c and a def

124
Q

What are the three types of chemotherapy available for oral cancer?

A

Neoadjuvant: chemo prior
Concurrent: chemo during radio
Adjuvant: chemo after

Oral Med (31 decks)

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