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BDS5 oral disease > cancer > Flashcards

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
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2
Q

what visual features of a lesion may raise suspicions of oral cancer?

A
  • white, red or speckled
  • ulcerated
  • indistinct or indurated borders
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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
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4
Q

high risk sites for oral cancer (3)

A

tongue
FOM
retromolar pad

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5
Q

common sites for HPV positive oral
cancer (2)

A

tonsil
base of tongue

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6
Q

common sites for HPV negative oral
cancer (3)

A

FOM
lateral tongue
retromolar

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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
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8
Q

how much does smoking increase the risk of oral cancer?

A

10x

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9
Q

how much does alcohol increase the risk of oral cancer?

A

4x

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10
Q

how much does smoking and alcohol increase the risk of oral cancer?

A

40x

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11
Q

what is the biggest lip cancer risk factor?

A

UV radiation

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12
Q

where is betel quid chewing common?

A

SE Asia, Indian subcontinent

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13
Q

low risk factors for oral cancer (4)

A
  • diet, antioxidants (lack of)
  • chronic candidiasis
  • HPV 16 or 18
  • lichen planus
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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
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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
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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
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17
Q

cause of oral submucous fibrosis

A

betel quid or areca/betel nut chewing (paan)

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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
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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)
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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)
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21
Q

describe Fanconi’s anaemia (what, s/s)

A
  • AR mutation = defective DNA repair gene
  • marrow failure, acute leukaemia when young
  • mucosal malignancies
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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
Q

proliferative verrucous leukoplakia common sites (2)

A

gingiva
alveolar ridge

26
Q

WHO definition of erythroplakia

A

“fiery red patch that cannot be characterised clinically or pathologically as any other definable disease”

27
Q

erythroplakia malignant transformation rate

A

5-10%

28
Q

erythroplakia differential diagnosis (many)

A
  • 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
Q

describe erythroplakia (definition, lesion, demographic)

A

“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
Q

how are erythroplakias managed? (2)

A

depending on dysplasia degree - excised if >moderate dysplasia
risk factors eliminated

31
Q

differences between HPV+ and HPV- cancers (5)

A
  • 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
Q

describe the TNM staging system briefly

A
  • 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
Q

describe the T part of staging cancers

A

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
Q

describe the N part of staging cancers

A

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
Q

describe the M part of staging cancers

A

M = metastasis
- M0 = no distant metastases
- M1 = metastases present

36
Q

what does stage 1 cancer include?

A

T1 with no N/M (≤2cm)

37
Q

what does stage 2 cancer include?

A

T2 with no N/M (2-4cm)

38
Q

what does stage 3 cancer include?

A

T3 only (>4cm)
T1-3 with N1

39
Q

what does stage 4 cancer include?

A

4A = T4a, N0/1 OR T1-4a, N2
4B = N3 OR T4b with any N
4C = M1 (metastases)

40
Q

what tumour size often indicates elective neck dissection?

A

T2 - 2-4cm (5-10mm depth)
(and above)

41
Q

describe the classification of dysplasia and features that would indicate SCC

A

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
Q

what histological features may be present in dysplasia? (up to 9)

A
  • 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
Q

what is the TNM staging for? (2)

A
  • establish extent of the tumour spread
  • to guide treatment and determine prognosis
44
Q

what is the difference between cancer staging and grading?

A

staging = assessing spread of tumour to guide treatment and determine prognosis
grading = histological, assessing cell differentiation and hence how the cancer may behave

45
Q

describe how cancers are graded

A
  • 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
Q

why are cancers graded?

A

determine how aggressively the cancer is likely to behave (spread, progress)

47
Q

what grade of cancer is most likely to progress/spread?

A

undifferentiated

48
Q

describe multistep carcinogenesis

A

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
Q

what is the most common type of cancer in the oral cavity

A

squamous cell carcinoma

50
Q

why do we histological analyse excised precancerous oral lesions? (4)

A
  • 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
Q

what is the current best predictor of malignant change in a potentially malignant oral lesion?

A

degree of dysplasia

52
Q

what may contraindicate taking a biopsy? (6)

A
  • MH
  • specialist to see the undisturbed lesion
  • need for complex or specialist treatment
  • anxiety
  • diagnostic difficulty
  • cost, time and resources
53
Q

what/when should you NOT biopsy in general practice? (7)

A
  • 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
Q

most common primary sites for jaw metastases (6)

A
  • breast
  • bronchus
  • prostate (radiopaque)
  • thyroid
  • kidney
  • colon, rectum

BDS5 oral disease (26 decks)

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