premalignant oral lesions Flashcards

(37 cards)

1
Q

What is a premalignant lesion?

A

A morphologically altered oral lesion with higher risk of transforming into oral cancer.

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2
Q

What are the three possible cellular reactions to a carcinogen?

A

Hyperplasia, Atrophy, Irreversible cell damage.

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3
Q

What genetic changes lead to neoplastic transformation?

A

Oncogene activation, mutations/deletions in suppressor genes and DNA repair genes.

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4
Q

How are premalignant lesions identified?

A

Through clinical, morphological, and molecular means.

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5
Q

What is leukoplakia?

A

A white patch on oral mucosa that cannot be diagnosed as another disease; a diagnosis of exclusion.

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6
Q

Is leukoplakia a histopathologic diagnosis?

A

No, it’s a clinical term.

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7
Q

What percent of oral carcinoma arises near leukoplakia?

A

More than one-third.

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8
Q

How much more likely are leukoplakia patients to develop oral cancer?

A

Fivefold higher risk.

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9
Q

What is the malignant transformation rate of speckled leukoplakia?

A

0.47

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10
Q

Name three local etiological factors of leukoplakia.

A

Tobacco, alcohol, chronic irritation.

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11
Q

Name two systemic etiological factors of leukoplakia.

A

Endocrine dysfunction, infections like HSV and HPV.

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12
Q

List three clinical types of leukoplakia.

A

Homogeneous, Speckled (erythroleukoplakia), Verrucous.

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13
Q

Which leukoplakia type has the highest malignant potential?

A

Speckled leukoplakia.

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14
Q

What is the significance of a biopsy in leukoplakia?

A

It confirms the presence of dysplasia, carcinoma in situ, or carcinoma.

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15
Q

Define epithelial dysplasia.

A

Disordered growth of epithelium with cytological and architectural atypia.

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16
Q

Is dysplasia reversible?

A

Yes, if the causative stimulus is removed.

17
Q

What are the three grades of dysplasia?

A

Mild, Moderate, Severe.

18
Q

How deep does mild dysplasia extend?

A

Lower third of the epithelium.

19
Q

How deep does severe dysplasia extend?

A

More than two-thirds of the epithelium.

20
Q

What is carcinoma in situ?

A

Full-thickness dysplasia without invasion past basement membrane.

21
Q

What organism is associated with candidal leukoplakia?

A

Candida albicans.

22
Q

What is another name for candidal leukoplakia?

A

Chronic hyperplastic candidiasis.

23
Q

What are common sites for candidal leukoplakia?

A

Dorsum of the tongue and commissural buccal mucosa.

24
Q

What is seen histologically in candidal leukoplakia?

A

Hyperparakeratosis, candida hyphae, chronic inflammation, dysplasia.

25
What is erythroplakia?
A red velvety lesion that cannot be classified as any other disease.
26
How likely is erythroplakia to show dysplasia or carcinoma?
0.9
27
What causes the red appearance of erythroplakia?
Increased subepithelial vessels, epithelial thinning, lack of keratin.
28
What are the three types of erythroplakia?
Homogeneous, erythroleukoplakia, speckled.
29
What is the diagnostic approach to persistent red oral lesions?
Biopsy after 2 weeks if not resolved.
30
What syndromes cause oral epithelial atrophy?
Plummer-Vinson syndrome and submucous fibrosis.
31
What are oral signs of Plummer-Vinson syndrome?
Burning tongue, angular cheilitis, atrophy of lingual papillae.
32
What substance in betel nut causes submucous fibrosis?
Alkaloids that stimulate fibroblast proliferation.
33
What is a hallmark clinical sign of submucous fibrosis?
Trismus and whitish-yellow mucosa.
34
What causes actinic cheilitis?
Chronic exposure to UV light.
35
Which lip is more commonly affected by actinic cheilitis?
Lower lip.
36
What is seen histologically in actinic cheilitis?
Atrophic epithelium, epithelial dysplasia, collagen degeneration.
37
Who is most at risk for actinic cheilitis?
Fair-skinned males with high sun exposure (e.g., farmers, sailors).