cancer Flashcards
1
Q
list some signs/symptoms of oral cancer (up to 11)
A
- visible oral lesions = red/white/speckled, ulcerated, indurated or indistinct borders, mass/lump
- neck mass (>50%)
- sore throat, dysphagia, sensation of lump in throat
- difficulty opening jaw
- jaw swelling, change in denture fit
- dysaesthesia, paraesthesia, loss of sensory/motor function
- tongue stiffness, “hot potato dysarthria”
- otalgia
- non-specific pain, bleeding
- rapidly loose teeth
- non-healing extraction socket
2
Q
what visual features of a lesion may raise suspicions of oral cancer?
A
- white, red or speckled
- ulcerated
- indistinct or indurated borders
3
Q
what characteristics of a lesion may raise suspicions of oral cancer? (6)
A
- sudden onset
- fast-growing
- non-responsive to non-opioid analgesics, RCT and antibiotics
- resorption of structures
- no identifiable cause
- lasting longer than 2 weeks
4
Q
high risk sites for oral cancer (3)
A
tongue
FOM
retromolar pad
5
Q
common sites for HPV positive oral
cancer (2)
A
tonsil
base of tongue
6
Q
common sites for HPV negative oral
cancer (3)
A
FOM
lateral tongue
retromolar
7
Q
major risk factors for oral cancer (4)
A
- smoking or smokeless tobacco
- betel quid, betel/areca nut chewing
- alcohol intake >14u/wk
- UV radiation
8
Q
how much does smoking increase the risk of oral cancer?
A
10x
9
Q
how much does alcohol increase the risk of oral cancer?
A
4x
10
Q
how much does smoking and alcohol increase the risk of oral cancer?
A
40x
11
Q
what is the biggest lip cancer risk factor?
A
UV radiation
12
Q
where is betel quid chewing common?
A
SE Asia, Indian subcontinent
13
Q
low risk factors for oral cancer (4)
A
- diet, antioxidants (lack of)
- chronic candidiasis
- HPV 16 or 18
- lichen planus
14
Q
in what type of patients will you be more suspicious for oral cancer? (6)
A
- > 45yo
- male
- previous malignancy
- potentially malignant lesions
- long-term immunosuppression
- socially deprived
15
Q
list some potentially malignant oral lesions (up to 13)
A
- oral submucous fibrosis
- lichen planus/oral lichenoid lesions
- dyskeratosis congenita
- Fanconi’s anaemia
- tertiary syphilis
- discoid lupus erythematosus
- proliferative verrucous leukoplakia
- pipe smoker’s keratosis
- palatal keratosis
- snuff dipper’s keratosis
- xeroderma pigmentosum
- Patterson-Kelly syndrome/sideropenic dysphagia
- erythroplakia
16
Q
describe oral submucous fibrosis (what, cause, s/s)
A
- potentially malignant oral lesion
- caused by betel quid or areca/betel nut chewing
- thick fibrous bands in BM (collagen I) = marbled texture of mucosa,
progressive trismus - ulceration, burning, pain
- depapillation of tongue
- loss of pigmentation
17
Q
cause of oral submucous fibrosis
A
betel quid or areca/betel nut chewing (paan)
18
Q
oral submucous fibrosis s/s
A
- thick fibrous bands in BM (collagen I) = marbled texture of mucosa,
progressive trismus - ulceration, burning, pain
- depapillation of tongue
- loss of pigmentation
19
Q
describe dyskeratosis congenita (what, s/s)
A
- X-linked AD/AR condition which increases the risk of cancer when young
- oral leukoplakia (30% malignant by 30yo)
- rapid periodontal disease
- abnormal skin hyperpigmentation, reticulated
- nail dystrophy
- premature aging
- progressive marrow failure (thrombocytopaenia, aplastic anaemia)
20
Q
s/s of dyskeratosis congenita (7)
A
- cancer when young
- oral leukoplakia (30% malignant by 30yo)
- rapid periodontal disease
- abnormal skin hyperpigmentation, reticulated
- nail dystrophy
- premature aging
- progressive marrow failure (thrombocytopaenia, aplastic anaemia)
21
Q
describe Fanconi’s anaemia (what, s/s)
A
- AR mutation = defective DNA repair gene
- marrow failure, acute leukaemia when young
- mucosal malignancies
22
Q
what is the triad of Patterson-Kelly syndrome/sideropenic dysphagia?
A
iron deficiency anaemia
oesophageal web
dysphagia
23
Q
describe proliferative verrucous leukoplakia (what, demographic, lesion)
A
- uncommon potentially malignant oral lesion
- older females, tobacco users
- corrugated widespread keratoses
- shows relentless growth and high likelihood of progressing to SCC
- unusual areas = gingiva, alveolar ridge
24
Q
proliferative verrucous leukoplakia demographic (2)
A
older females
tobacco users
25
proliferative verrucous leukoplakia common sites (2)
gingiva
alveolar ridge
26
WHO definition of erythroplakia
"fiery red patch that cannot be characterised clinically or pathologically as any other definable disease"
27
erythroplakia malignant transformation rate
5-10%
28
erythroplakia differential diagnosis (many)
- benign migratory glossitis
- non-homogenous leukoplakia
Inflammatory/immune:
- desquamative gingivitis (MMP, LP)
- erythematous or atrophic LP
- DLE
- hypersensitivity reaction
- Reiter’s disease (reactive arthritis)
Infection – histoplasmosis, erythematous candidiasis
Hamartomas/neoplasm – haemangioma, Kaposi’s sarcoma
29
describe erythroplakia (definition, lesion, demographic)
"fiery red patch that cannot be characterised clinically or pathologically as any other definable disease"
- smooth, velvety, red
- tobacco and alcohol users
- FOM most often
- often dysplasias or carcinomas in situ
30
how are erythroplakias managed? (2)
depending on dysplasia degree - excised if >moderate dysplasia
risk factors eliminated
31
differences between HPV+ and HPV- cancers (5)
- sites = tonsil/base of tongue (HPV+), FOM/lateral tongue/retromolar (HPV-)
- HPV+ incidence increasing
- RFs = sexual behaviour (HPV+) vs smoking/alcohol
- HPV+ usually non-keratinising
- HPV+ has better survival
32
describe the TNM staging system briefly
- determines spread of a cancer
T = tumour size (1-4 and is)
N = node involvement (0-3)
M0/1 = metastases
- as it increases, chance of survival decreases
- 1-4A/B/C
33
describe the T part of staging cancers
T = tumour size
- T1 = ≤2cm (≤5mm depth of invasion)
- T2 = 2-4cm (5-10mm depth)
- T3 = >4cm (>10mm depth)
- T4 = into adjacent tissues/bone
- T4a = through cortical bone of mandible/sinus or skin of face
- T4b = invades masticator space, pterygoid plates, skull base, encases internal carotid artery
- Tis = carcinoma in situ, not invasive, dysplasia only
34
describe the N part of staging cancers
N = nodal involvement
- N0 = no metastases
- N1 = ≥1 node involved (ipsilateral, all <3cm)
- N2 = contralateral/bilateral involvement (all <6cm):
-- N2a = extranodal extension or 3-6cm diameter with no extranodal extension
-- N2b = metastasis in multiple ipsilateral LNs, without extranodal extension
-- N2c = metastasis in bilateral or contralateral LNs, without extranodal extension
- N3 = at least 1 node >6cm
-- N3a = without extranodal extension
-- N3b = >3cm with extranodal extension or multiple with extranodal extension
35
describe the M part of staging cancers
M = metastasis
- M0 = no distant metastases
- M1 = metastases present
36
what does stage 1 cancer include?
T1 with no N/M (≤2cm)
37
what does stage 2 cancer include?
T2 with no N/M (2-4cm)
38
what does stage 3 cancer include?
T3 only (>4cm)
T1-3 with N1
39
what does stage 4 cancer include?
4A = T4a, N0/1 OR T1-4a, N2
4B = N3 OR T4b with any N
4C = M1 (metastases)
40
what tumour size often indicates elective neck dissection?
T2 - 2-4cm (5-10mm depth)
(and above)
41
describe the classification of dysplasia and features that would indicate SCC
mainly classified by features present, severity of these features and how widespread (histology)
1 Mild dysplasia – abnormal cells, hyperchromatic, more nuclei, pleomorphic, increased number; lower third of epithelium
2 Moderate dysplasia – >1/3 thickness of epithelium but not into the lamina propria
3 Severe dysplasia
4 SCC – no basal cell layer, INVASION
- para/orthokeratosis, dyskeratosis
- hyperplasia/atrophy
- disordered architecture – bulbous/drop-shaped rete processes, verrucous surface profile
- decreased intercellular cohesion
- irregular stratification
- pleomorphism, anisonucleosis, nuclear hyperchromatism, increased nuclear/cytoplasmic ratio
- abnormal mitoses (morphological and location)
42
what histological features may be present in dysplasia? (up to 9)
- abnormal cells - hyperchromatic, pleomorphic
- anisonucleosis or more nuclei
- increased nuclear/cytoplasmic ratio
- hyperplasia/atrophy
- para/orthokeratosis, dyskeratosis
- disordered architecture – bulbous/drop-shaped rete processes, verrucous surface profile
- decreased intercellular cohesion
- irregular stratification
- abnormal mitoses (morphological and location)
43
what is the TNM staging for? (2)
- establish extent of the tumour spread
- to guide treatment and determine prognosis
44
what is the difference between cancer staging and grading?
staging = assessing spread of tumour to guide treatment and determine prognosis
grading = histological, assessing cell differentiation and hence how the cancer may behave
45
describe how cancers are graded
- based on degree of cell differentiation, histological
- well-differentiated (only nuclear differences)
- moderately-differentiated (can recognise tissue of origin)
- poorly-differentiated
- undifferentiated – pleomorphic, spindle cells; likely to spread and progress faster, more dangerous
46
why are cancers graded?
determine how aggressively the cancer is likely to behave (spread, progress)
47
what grade of cancer is most likely to progress/spread?
undifferentiated
48
describe multistep carcinogenesis
describes the transformation of a normal cell into a cancer from a series of events/mutations
1 initiation (by carcinogens, radiation, viruses) = event that induces the genetic alteration that gives neoplastic potential, potentially reversible
2 promotion = event that stimulates clonal proliferation of the initiated cell (usually into a benign tumour)
3 progression = process culminating in malignant behaviour
49
what is the most common type of cancer in the oral cavity
squamous cell carcinoma
50
why do we histological analyse excised precancerous oral lesions? (4)
- check if there is already a carcinoma within the clinically visible lesion
- grade any dysplasia
- ploidy analysis
- assess excision of dysplasia (complete or incomplete)
51
what is the current best predictor of malignant change in a potentially malignant oral lesion?
degree of dysplasia
52
what may contraindicate taking a biopsy? (6)
- MH
- specialist to see the undisturbed lesion
- need for complex or specialist treatment
- anxiety
- diagnostic difficulty
- cost, time and resources
53
what/when should you NOT biopsy in general practice? (7)
- likely malignant lesions
- haemangiomas, vascular lesions (excessive bleeding)
- extensive cystic lesion in bone (infection risk to pt)
- salivary lumps other than probable mucoceles
- soft palate lesion where tearing of tissue and retching makes it difficult
- lack of experience (non-ideal specimen)
- needs hospital care/tx once diagnosis is made
54
most common primary sites for jaw metastases (6)
- breast
- bronchus
- prostate (radiopaque)
- thyroid
- kidney
- colon, rectum
