Benedict oral cancer and OPMD Flashcards

(28 cards)

1
Q

What is a neoplasm

A
  • Abnormal and excessive new growth of cells
  • Arises spontaneously
  • Proceeds irrespective or potential stimuli
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2
Q

Describe benign neoplasms

A
  • slower growth
  • cells similar to normal
  • mat be encapsulated
  • compresses normal tissues
  • remains localised
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3
Q

Describe malignant neoplasms

A
  • more rapid growth
  • cells not similar to normal
  • often non-encapsulated
  • invades normal tissues
  • spreads throughout the body (metastasis
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4
Q

Describe benign oral epithelial neoplasms

A

epithelial
- papilloma: surface epithelium
- Adenoma: glandular
connective tissue
- fibroma: fibrous connective tissue
- lipoma: fat
- osteoma: bone

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5
Q

What are some papillomas

A
  • squamous papilloma
  • verruca vulgaris
    cauliflower like, finger projection
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6
Q

What suffix usually indicates a benign tumor?

A

-oma

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7
Q

Describe epithelial malignant oral neoplasms

A

Carcinoma
- squamous cell carcinoma (surface epithelium)
- adenocarcinoma (glandular)

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8
Q

Describe connective tissue malignant oral neoplasms

A

Sarcoma
- fibrosarcoma: fibrous connective tissue
- liposarcoma: fat
- osteosarcoma: bone

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9
Q

Describe oral squamous cell carcinoma

A

An invasive epithelial neoplasm with varying degrees of squamous differentiation and a propensity to early and extensive lymph node metastases

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10
Q

When and in who is oral squamous cell carcinoma most likely to appear

A
  • 40+
  • whites>maori
  • M>F???
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11
Q

Where does OSCC occur

A
  • Lateral tongue then FoM
  • In whites, lower lip then tongue then FoM
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12
Q

What is the aetiology of OSCC

A
  • radiation
  • tobacco use
  • betel nut
  • alcohol
  • nutritional deficiencies
  • viruses (HPV)
  • candidosis
  • immunosupression
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13
Q

Describe carcinogenesis

A
  • abberation of normal regulatory genes
  • multistep process
  • initiation, promotion, progression
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14
Q

Describe how carcinogens work

A

carcinogens are metabolised and either excreted, or they damage DNA. This DNA is either repaired, or if not it can cause mutation, deletion, or amplification.

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15
Q

What about a lesion may indicate SSC?

A

irregular border

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16
Q

Describe OSSC staging

A
  • TNM system
  • tumor: primary tumor size
  • nodes: cervical metastasis
  • metastasis: distant metastasis
    Staged 1-4
    5yr survival
    1-85%
    2-65%
    3-40%
    4-10%
17
Q

Describe development of SSC

A
  • usually evolves from benign oral neoplasms
  • most of these go through a potentially malignant or precancerous phase before they invade and become malignant
18
Q

list 8 oral potentially malignant disorders

A
  • Leukoplakia
  • erythroplakia
  • palatal lesions in reverse smokers
  • oral submucous fibrosis
  • actinic keratosis
  • lichen planus
  • discoid lupus erythmatosus
  • hereditary disorders w/ increased risk
19
Q

describe diagnosis of leukoplakia

A

elimination- only when all other known disorders or diseases with no increased risk of cancer have been ruled out

20
Q

Describe the two types of leukoplakia

A

Homogenous (90%)
- flat, corrugates, wrinkled, pumice-like
- low risk of transformation (5%)

Non-homogenous (10%)
- verrucous, nodular, ulcerated, erythroplakia
- higher risk of transformation (30%)

21
Q

Describe erythroplakia

A
  • red, cannot be characterised clinically or pathologically as any other definable lesion
  • high risk of malignant transformation (30%)
22
Q

What is a reverse smoker and what does this cause

A

people who smoke with the lit end in their mouth-causes palatal lesions

23
Q

How to predict behaviour of a lesion

A

-clinical exam
- biopsy to assess presence or absence of dysplasia

24
Q

Describe assessment of lesion colour

A
  • risk of transformation increases with redness
  • association with candidal infection?? has many appearances-take a swab
25
Describe assessment of lesion texture
- homogenous? low risk of transformation - non homogenous? increased risk
26
Describe assessment of lesion site
FOM- increased risk of transformation
27
Describe assessment of dysplasia
- gold standard is still biopsy - increased dysplasia shows increased risk of transformation - good indicator of behaviour of high grade lesions but poor for lesions with minimal or no dysplasia
28
to conclude what are some clinical considerations with OPMD
- examine pt thoroughly - carefully review MH - note any abnormalities - 2-3 week rule: if lesion persists despite removal of/lack of causative factors, refer to oral surg.