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AU'18 Oral Path II > Premalignant Epithelial Lesions > Flashcards

Premalignant Epithelial Lesions Flashcards

1
Q

premalignant epithelial lesions

A
  1. leukoplakia
  2. proliferative verrucous leukoplakia (PVL)
  3. erythroplakia
  4. oral submucous fibrosis
  5. actinic keratosis
  6. actinic cheilitis
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2
Q

what is the most common oral precancer?

A

leukoplakia

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3
Q

is a biopsy mandatory for leukoplakia?

A

yes

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4
Q

what causes the white color in leukoplakia?

A

white color due to thickened keratin

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5
Q

can leukoplakia white patches be wiped off?

A

NO

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6
Q

T/F: leukoplakia can be diagnosed clinically or microscopically as any other condition

A

false

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7
Q

how is leukoplakia diagnosed?

A

by exclusion

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8
Q

T/F: ill-fitting dentures, poor oral hygiene and broken teeth do NOT increase oral cancer risk

A

true

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9
Q

what causes tobacco pouch keratosis?

A

use of smokeless tobacco

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10
Q

3 main types of smokeless tobacco in US

A
  1. chewing tobacco
  2. dry snuff
  3. moist snuff
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11
Q

dry snuff is primarily used by who?

A

women in southern US

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12
Q

T/F: moist snuff is often supplied in prepackaged pouches called snus

A

true

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13
Q

clinical features of tobacco pouch keratosis

A

white or gray often corrugated, can appear thin and translucent or thick and white

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14
Q

does tobacco pouch keratosis disappear when the mucosa is stretched?

A

no

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15
Q

what can tobacco pouch keratosis cause?

A
  1. gingival recession
  2. facial or buccal alveolar bone loss at site of use
  3. tooth staining and halitosis often noted
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16
Q

what causes the gray, translucent appearance in tobacco pouch keratosis?

A

contact irritation

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17
Q

treatment of tobacco pouch keratosis?

A

cessation of habit and lesion resolves within 5-6 weeks

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18
Q

what will happen if there is any remaining leukoplakia after cessation of smokeless tobacco habit?

A

biopsy

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19
Q

T/F: prognosis of tobacco pouch keratosis is not completely without risk but is significantly MORE than cigarettes

A

false, it’s less

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20
Q

what can affect the risk of developing tobacco pouch keratosis?

A

frequency, dose, length of time and type of tobacco especially with concurrent cigarette use

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21
Q

what is the risk of malignant transformation of tobacco pouch keratosis?

A

low

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22
Q

T/F: dry snuff has a higher associated risk for transformation than moist or wet

A

true

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23
Q

epithelial dysplasia

A

disturbances of proliferation and maturation as seen microscopically

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24
Q

grades of epithelial dysplasia

A
  1. normal
  2. mild
  3. moderate
  4. severe
  5. carcinoma in-situ
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25
Q

mild grade epithelial dysplasia

A

~ lower ⅓ of epithelium

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26
Q

moderate grade epithelial dysplasia

A

~ lower ½ of epithelium

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27
Q

severe grade epithelial dysplasia

A

involves upper ⅓ of epithelium

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28
Q

carcinoma in-situ epithelial dysplasia

A

involves full thickness of

epithelium

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29
Q

severity of dysplasia increases as what?

A

as the changes approach the surface

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30
Q

phases of leukoplakia/erythroleukoplakia

A
  1. normal mucosa
  2. think, smooth leukoplakia
  3. thick, fissured leukoplakia
  4. granular, verruciform leukoplakia
  5. erythroleukoplakia (speckled leukoplakia)
  6. erythroplakia
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31
Q

dysplastic epithelial cells of thick, fissured leukoplakia

A

mild/moderate dysplasia

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32
Q

dysplastic epithelial cells of granular, verruciform leukoplakia

A

moderate/severe dysplasia

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33
Q

dysplastic epithelial cells of erythroleukoplakia

A

carcinoma in-situ

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34
Q

histopathologic features of leukoplakia

A
  1. some degree of keratosis
  2. often sharply demarcated from normal epithelium
  3. can show mild, moderate, severe epithelial dysplasia or carcinoma-in-situ
  4. some have shown squamous cell carcinoma
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35
Q

what percent of leukoplakias show hyperkeratosis without epithelial dysplasia?

A

80%

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36
Q

at what phase does irregular hyperkeratosis occur?

A

granular, verruciform leukoplakia

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37
Q

at what phase does bulbous rete pegs occur?

A

granular, verruciform leukoplakia

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38
Q

at what phase can candida hyphae occur?

A

granular, verruciform leukoplakia

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39
Q

at what phase does congested vessels occur?

A

granular, verruciform leukoplakia

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40
Q

at what phase does epithelial atrophy occur?

A

erythroleukoplakia (speckled leukoplakia)

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41
Q

histo of carcinoma in-situ

A
  1. abnormal maturational pattern
  2. variation in nuclear size and shape
  3. mitosis
  4. hyperchromatic nuclei
42
Q

risk factors for premalignant epithelial lesions

A
  1. male >50 y.o.
  2. tobacco use, esp cigs (products of combustion)
  3. sanguinaria (bloodroot)
  4. UV radiation
  5. use of betel quid, paan, masala, gutkha, mawa
  6. biopsy-proven oral epithelial dysplasia or squamous cell carcinoma
  7. immunocompromised state
43
Q

what percentage of patients with leukoplakia are smokers?

A

80%

44
Q

T/F: tobacco use with alcohol simultaneously with have a synergistic effect?

A

true

45
Q

reverse-smoker’s palate clinical feature

A

diffuse keratosis of palate

46
Q

what is the risk of reverse smoking?

A

significant risk of epithelial dysplasia/carcinoma

47
Q

pack/year

A

number of packs of cigarettes per day x number of years smoked

48
Q

pk/yr TOB is an estimate of what?

A

lifetime tobacco exposure

49
Q

T/F: pk/yr TOB is a risk factor

A

true

50
Q

sanguinaria (bloodroot)

A
  • effective against plaque and gingivitis

- was in old formulation of Viadent

51
Q

UV radiation

A

leukoplakia lower lip vermilion zone

52
Q

leukoplakia clinical features

A
  1. older adult males (>50 y.o.)
  2. white plaque with SHARPLY DEMARCATED, crisp borders
  3. smooth, verrucous or micronodular surface
  4. flat to slightly elevated
  5. thin or thick
53
Q

overall most common site for leukoplakia

A

buccal mucosa

54
Q

erythroleukoplakia (speckled leukoplakia) clinical features

A

red and white components

55
Q

treatment for leukoplakia

A

biopsy mandatory to guide treatment

56
Q

treatment for no or mild dysplasia

A

discontinue carcinogenic habits

57
Q

treatment for moderate and severe dysplasia

A

discontinue carcinogenic habits, remove by most convenient means available

58
Q

treatment after initial treatment of leukoplakia

A
  1. close clinical follow-up
  2. re-biopsy any suspicious area
  3. laser ablation
59
Q

T/F: laser ablation of leukoplakia negates ability for microscopic exam

A

true

60
Q

prognosis of leukoplakia

A

guarded

61
Q

what percent of non-dysplastic lesions will transform to squamous cell carcinoma if not treated?

A

15%

62
Q

what percent of dysplastic lesions will transform?

A

33%

63
Q

what percent of leukoplakias will recur, even after complete clinical excision

A

30%

64
Q

proliferative verrucous leukoplakia (PVL) clinical features

A
  1. grows laterally
  2. slow, persistent spreading
  3. involves multiple sites
  4. keratotic plaques, “warty” rough surface projections
65
Q

T/F: PVL has a 4:1 female predilection but only 1/3rd have traditional risk factors (minimal association with tobacco use)

A

true

66
Q

mean age female for PVL

A

65 y.o.

67
Q

mean age male for PVL

A

49 y.o.

68
Q

treatment for PVL

A
  1. close clinical follow-up
  2. biopsy any suspicious area
  3. laser ablation
69
Q

T/F: it is uncommon for patients who have PVL to have multiple biopsies/surgeries

A

false; it is common

70
Q

persistent growth of PVL usually develops what?

A

epithelial dysplasia

71
Q

how many years does it take for PVL to transform into SCC?

A

within 8 years

72
Q

erythroplakia

A

red patch that cannot be wipped off AND cannot be diagnosed clinically or microscopically as any other condition

73
Q

risk factors of erythroplakia

A

same as leukoplakia but NO GENDER PREDILECTION

74
Q

T/F: erythroplakia is less serious/severe than leukoplakia

A

false, more serious/severe

75
Q

erythroplakia clinical features

A
  1. velvety red
  2. well-demarcated
  3. usually asymptomatic
76
Q

what causes erythroplakia to be velvety red?

A
  1. due to the lack of keratin production on the surface of the lesion
  2. mucosa is atrophic; underlying vasculature shows through
77
Q

what are the most common sites for erythroplakia?

A

lateral tongue, floor of mouth (FoM) or soft palate

78
Q

what percent of erythroplakia show severe epithelial dysplasia or worse at the time of biopsy?

A

90%

79
Q

treatment for erythroplakia

A
  • same as leukoplakia with a similar degree of epithelial dysplasia
  • if biopsy shows cancer, protocol for cancer treatment
80
Q

high-risk sites for leukoplakia

A
  1. ventral tongue
  2. floor of mouth
  3. soft palate/tonsillar pillars
81
Q

what does a high-risk site mean?

A

lesions in these sites are more likely to be dysplastic or worse as compared to similar lesions in sites that are not considered high-risk

82
Q

risk factor for oral submucous fibrosis

A

betel quid, paan, masala, gutkha, mawa

83
Q

oral submucous fibrosis clinical features

A
  1. pallor and fibrosis of soft palate
  2. uvula retains normal color
  3. stomatopyrosis (burning) and intolerance to spicy foods
  4. vesicles, petechiae, melanosis, dry mouth
  5. progressive scarring “piano wires”
  6. limited incisal opening
  7. saliva becomes red and stains teeth
84
Q

where does oral submucous fibrosis affect?

A
  1. tongue
  2. buccal mucosa
  3. retromolar area
85
Q

treatment of oral submucous fibrosis

A
  1. intralesional steroid injection mild lesions
  2. surgical splitting of fibrous bands
  3. physical therapy lifelong
  4. close clinical follow-up
86
Q

what causes actinic keratosis

A

sun-induced by UV rays

87
Q

where does actinic keratosis affect?

A

skin - any sun-exposed area

88
Q

most common head and neck sites for actinic keratosis

A
  1. face
  2. scalp
  3. ears
89
Q

actinic keratosis clinical features

A
  1. fair or light-skinned people
  2. over 40 y.o.
  3. scaly plaque with sandpaper texture
  4. may have erythematous base
90
Q

actinic keratosis histopathologic features

A
  1. hyperkeratosis (usually parakeratin)
  2. solar elastosis (degeneration of CT)
  3. some degree of epithelial dysplasia or superficially invasive SCC
91
Q

treatment for actinic keratosis

A
  1. skin lesions treated with topical liquid nitrogen, 5-fluoro-uracil, imiquimod, surgical excision, laser ablation
  2. Mohs micrographic surgery
  3. reduce sun exposure; hats, sunscreen
92
Q

prognosis for actinic keratosis

A

fair to good

  • patient must be monitored for development of new lesions
  • biopsy/re-biopsy any suspicious areas
93
Q

what causes actinic cheilitis (actinic cheilosis)?

A

chronic UV exposure

94
Q

actinic cheilitis

A

term for actinic keratosis involving vermilion zone of lips (especially lower lip)

95
Q

actinic cheilitis clinical features

A
  1. male predilection
  2. fair skinned
  3. over 45 y.o.
  4. develops slowly
  5. atrophy
  6. dryness
  7. fissures
  8. blended or blurred vermilion border
  9. rough, scaly areas on dry portions may thicken and become leukoplakias
  10. may develop chronic ulceration
96
Q

epithelium of actinic cheilitis histopathologically may exhibit what?

A
  1. hyperkeratosis
  2. acanthosis (thickening)
  3. atrophy (thinning) and/or ulceration
  4. dysplasia
97
Q

CT of actinic cheilitis histopathologically may show what?

A

solar elastosis

98
Q

treatment for actinic cheilitis

A
  1. laser ablation of vermilion zone
  2. electrodessication, 5-FU, cryotherapy
  3. vermilionectomy (lip shave)
  4. reduce sun exposure; hats, sunscreen
  5. biopsy/re-biopsy any suspicious areas
99
Q

how long does it take for actinic cheilitis to transform into SCC?

A

may take many years

100
Q

the risk for transformation of actinic cheilitis to SCC is how much greater than for actinic keratosis?

A

2.5x greater

101
Q

T/F: actinic cheilitis has a worse off prognosis than intraoral SCC

A

false, better prognosis than intraoral SCC

AU'18 Oral Path II (31 decks)

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