Oral Cancer Flashcards
1
Q
What are the risk factors for oral cancer?
A
tobacco?betel
alcohol
premalignant lesions
emerging rrisk factors
2
Q
What is the effect of tobacco and alcohol?
A
Synergistic effect
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
4
Q
What factors of alcohol are important?
A
quality
quantity
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
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
7
Q
What is the effect of HPV on OC?
A
6 and 16 associated with oral cancer and pharyngeal through oro-genital contact
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
9
Q
What is the prognosis of HPV related OC?
A
better prognosis
10
Q
what is the relationship between HIV and oral cancer?
A
More likely to be kaposis and lymphoma not SCC
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
12
Q
What is the effect of diet and nutrition on OC?
A
Plummer vinson syndrome and not enough veg increases chances of OC
13
Q
What is the effect of UV light and OC?
A
UV light increases chances of Lip SCC
14
Q
Which premalignant lesions may preceded Lip cancer?
A
actinic keratosis
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
16
Q
What is the relationship between SES and OC?
A
not a great link
17
Q
What is the effect of marijuana on OC?
A
unsure
18
Q
What is the effect on nictoine replacement on OC?
A
no association
19
Q
What is the efect of alcohol in mouth rinses on OC?
A
unsure
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
21
Q
What three ways can oral cancer spread?
A
local
lymphatic
distant
22
Q
What are sites for local tumour invasion?
A
soft tissues Fixation bone vessels perineural
23
Q
What are the sites for distant metastases?
A
bone
lung
liver
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
25
What sites are high risk for SCC?
Lip and cheek
Anterior tongue, FOM, retromolar region
Posterior third of tongue
Soft palate and antrum
prognosis decreases towards back of the mouth
26
T/F faster growing tumours have a better prognosis?
F
27
By what percentage does positive lymph nodes decrease liklihood of survival?
50%
28
What is the five year survival rate for OC?
stage 1: 51%
stage 2: 40%
stage 3: 21%
stage 4: 8%
29
How can you treat OC?
```
Palliative
Radiotherapy
chemotherapy
immunotherapy
photodynamic therapy
```
30
what are the surgical compications of treating OC?
infection, pain, swelling, resection, psychological
31
What are the complications of radiotherapy?
mucositis, ulceration, dermatitis
drymouth, fibrosis and trismus
osteoradionecrosis
32
What are the side effects of chemotherapy?
mucosisits, ulceration
Bone marrow priblems
pain
33
how does radiation cause ORN?
radiation causes endoarterirtis obliterans which is occlusion of rthe lumen of an artery
34
When are people at greatest risk of ORN?
3-12 months post radiation
35
What are the three main skin cancers of Head and NEck?
Malignant melanoma
BCC
SCC
36
What are the riskk factors for malignant melanoma?
```
UV light (even short bursts)
Immunocompiormised
family history
freckling
light eyes and hait colour
```
37
What are the 8 subtypes of malignant melanoma?
```
Superfifcal
nodular
lentigo
amelonotic
acroa
mucosal
occular
```
38
Which are major signs when suspicous of malignant melanoma?
change in size, shape and colour
39
What are the minor signs when suspicious of skin cancer malignancy?
inflammation
cursting
sensory change
diameter of more than 7mm
40
How can we stage malignant melanoma?
Stage 1: local tumour
stage 2: local lymoph nodes
stage 3: disseminated disease
41
How can we assesss the extent of tumour growth?
clarkes level
| breslow thickness
42
WHat are the clarkes levels?
```
5 layers to the skin
1:pre invasive
2: thinly invasive
3 and 4: mod inasive
5: extensive
```
qualtitiave assesment
43
What are the breslows thickness?
<4mm thick: mod risk
| more than or equal to 4mm thick: higher risk
44
Where do malignant melanomas usually metastisise to?
eye
brain
liver
lung
45
What is BCC? and which syndrome is it associated with?
Gorlin Goltz
slowly invading malignancy of akin
46
WHat is the pattern of invasion of a BCC?
3D pattern
47
T/F. Metastese are rare in BCC?
T
48
What are the types of BCC?
```
nodular
superfical
ulcerating
morphoeic
keratotic
pigmented
cystic
```
49
What are thr RF for BCC?
Gorlin Goltz
Chronic UV exposure
males who freckle
increased age
50
What are the factors influencing prognosis of BCC?
tumour size, site, type
growth pattern
recurrent tumout
Immunocom
51
What are the 2 treatment surgical options for skin cancer?
destroy
| excise
52
What are the destructive methods for BCC?
cryosuurgery
CO2 laser
currettage
53
What non surgical options are there for sBCC?
```
radiotherapy
chemotherapy
intralesion interferon
retinoids
palliative
```
54
which pre malignant skin lesions are there?
actinic keratosis
| actinic chelitis
55
What is the clinical appearance of actinc keratosis?
rough scaly light brown patch up WHat ito 2cm in diamter
| can be brown or red
56
WHat is actinic chelitis?
type of actinic keratosis which occurs on the lips
causes the lips to becomes dry and scaly
mainly occurs on lower lip
57
WHat percentage of people with actinic keratosis will become malignant?
10%
| more likely in those that are older
58
what is a pre-malignant lesions?
a morphologically altered tissue which cancer is more likely to arise in than its normal counterpart
59
What is a pre malignant condition?
a generalised state associated with an increased risk of cancer
60
What is the differential diagnosis of a normal white patch?
Fordyce spots caused by ectopic sebaceous glands
61
What is the differential diagnosis of transient white patches?
thrush
| chemical burn
62
WHat is the differential diagnosis for persistant white plaques?
congenital: dyskeratosis congitia, white sponge naeuve, leukoedema
keratosis: smokers, frictional, idiopathic, sublingual
Lichen planus
SCC
syphilitic leukplkia
Hairy leukoploka
chronic hyper plastic candida
63
What is leukoplakia?
idiopathic keratosis
| A white patch which cannot be removed by scraping and cannot be attributed to any disease
64
what is the maligant potential leukoplakia?
10 years 2%
| 20 years 4%
65
How can leukoplakia be classified?
Homogenous or speckled
66
What are the high risk sites for leukoplakia?
FOM
| ventral tonguE
67
wHAT PERCENTAGE OF LEUKOPLAKIA ARE ASSOCIATE WITH scc?
15-30%
68
What 4 features raise your index of suscpsion for malignant features?
SIte: FOM/Tongue
Lack of aetoloogical factors
Clinical features
Path: degree of dysplasia
69
What are the features of subligual keratosis?
Ventral of tongue
Bilateral and symmetrtical
ebbing tide and sharply demarcate
70
subligual keratosis is more common in M or F?
F
71
What percentage of sub lingual keratosis become malignant?
25%
72
What is erthroplasia?
A rare red velvety lesion which is more commonly seen in elderly patetins
73
Where is eryhttoplasia more commonly seen?
FOM and Palate
74
What percentage of erythroplasia show dysplasia?
75%
75
What is submucous fibrosis?
this is when the palate and buccal mucasa appear white
| caused by developement of firbous tissue in mucosa
76
What is theough to cause sub mucous fibrosis?
Chewing betal quid
| Fe or B vitamin defiecneiy
77
What is the pathology behind Sub mucous fibrosis?
too much collagen being laid down
insuffiecient collagen destruction
firbroelastic change in the coreum
78
How do you diagnosise submucosa fibrosis and what must you warn the pateint of?
biopsy, but this often makes the lesion worse since more scar tissue is formed
79
How do you manage submucosa fibrosis?
Inject steroids into lesion
hyluronidases into lesion
excise the bands
80
What percentage of people with submucous fibrosis will develop cancer?
8%
81
What is the potetnial malignancy change for chronic hyperplastic candida?
30%
| 9-40%
82
Which sites are most commonly affected by chronic hyperplastic candida?
buccal mucosa, lips, tongue and palate
83
What are the types of chronic hyperplasitc candida?
soliitary
mucocutanoues
candida endocrine syndromes
84
What is the pathology behind chronic hyperplastic candida?
unsure if candida has invaded the tissue or whether the altered tissue has been secondarily invaded by candida
85
where is a high risk site for chronic hyper plastic candida?
buccal mucosa
86
what is the liklihood for malignant transformation of lichen planus?
2% for erosive lichen planus
87
What is the potential for syphylitic leukoplakia to become malignant?
10-30%
88
which site is most commonly affected by syphilitic leukoplkia?
dorsum of the otngue
89
what is sideropanic dysphagia associated with?
glossitis, dysphagia, anaemia
90
which type of cancer are people with sideropaenic dysphagia associated with?
oral and pharyngeal cancer
91
What is white sponge naevus?
benign condition inherited in AD fashion
| caused by mutation in keratin protein
92
what is the clinical presentation of white sponge naevus?
deeply folded white lesions
| may also be associated with anus and vagina lesions
93
When would you consider active eradication of a pre malignant lesion?
```
speckled
FOM
Tongue
Patient fit
accessible
no obvious aetiology
dysplsia
```
94
What are the three histological features of pre malignancy?
CEF
Cytological features
Epithelial architecture
Functional asepcts
95
What are the cytological features of pre malignancy?
```
pleiromorphic cells
increase cell size
loss of polarity
loss of cellular adhesions
nuclear pleiomorphisms and hyperchromatism
high nucleus to cytoplasm ratio
prominent nucleoli
```
96
What re the epithelial architectural changes?
disruption of the layers
| basal cell hyperplasia (replaces prickel cell layer)
97
What happens to the rete ridges in pre malignancy?
THEY BECOME DROP SHAPED
98
What happens to the basement membrane in premaliganancy?
it remains intact
99
What are the functional aspects of premalig?
Mitotic figures increase and are located in the suprabasal epithlium with abnormal forms
dyskeratosis
100
how can dysplasia be classified?
mild moderate or severe
101
What happens in SCC?
basement membrane becomes invaded
102
How can you remove pre malignant lesions?
cryosurgery
scalpel
electro surgery/laser
103
What imaging modalities are available for head and neck cancers?
```
plain film
US
CT
MRI
PET
```
104
how dpes US work?
provides a topographical map of the tissue interface
105
What are the disadvantage of US?
Low resolution
limited penetration
poor for bone or air filled structures
106
What are the advantages of US?
flexible and quick
no ionising radiation
best initial assessment for neck masses
107
What type of radiation is CT?
ionising
108
What are the disadvantage of CT?
need IV contrast media which is iodine bases (allergy)
| Not great for soft tissue
109
what are the advantages of CT?
excellent resolution especially for cortical bone and air filled structures
guided intervention for deep structures
110
What type of radiation does MRI use?
radiofrequency uses a magnetic filed
111
What are the disadvantages to MRI?
foreign body hazard
enclosed
slow image production and prone to artefact
112
What are the advantages of MRI?
no ionising radaition
| excellens tsoft tissues analysis
113
what is PET-CT scanning?
combine CT with PET
114
What is used in PET scan?
biologically labelled agent with a positron emitter
| injected into pateint
115
How does the agent used in PET work?
it distributes itself around the body depending upon the metabolic activity of that tissue
116
Which agent is used in PET?
FDG, glucose with a single oxygen atom replaced with F18
117
When would you use imaging for cancer?
When there is suspected cancer, to aid diagnosis. To assist with staging for a probable cancerous lesion
To follow uo
118
when would you use US?
obviously benign lesion
119
When would you do an US guided biopsy?
more significant lesions:
Salivary gland tumour
thyroid nodule
lymph node
120
What else could you do if you were worries about malignancy of salivary gland?
MRI if complex
| CT chest
121
What else could you do for a thyroid nodule if you were concerned other than US?
MRI if invasive
122
If there was a pathological lymph node and unsure where the primary malignancy is what investigation could you do?
MRI oral cavity
CT chest
PETCT
123
Which vitamin deficiencies are most closely implicated in oral cancer?
Vit c and a def
124
What are the three types of chemotherapy available for oral cancer?
Neoadjuvant: chemo prior
Concurrent: chemo during radio
Adjuvant: chemo after
