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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
mild grade epithelial dysplasia
~ lower ⅓ of epithelium
26
moderate grade epithelial dysplasia
~ lower ½ of epithelium
27
severe grade epithelial dysplasia
involves upper ⅓ of epithelium
28
carcinoma in-situ epithelial dysplasia
involves full thickness of | epithelium
29
severity of dysplasia increases as what?
as the changes approach the surface
30
phases of leukoplakia/erythroleukoplakia
1. normal mucosa 2. think, smooth leukoplakia 3. thick, fissured leukoplakia 4. granular, verruciform leukoplakia 5. erythroleukoplakia (speckled leukoplakia) 6. erythroplakia
31
dysplastic epithelial cells of thick, fissured leukoplakia
mild/moderate dysplasia
32
dysplastic epithelial cells of granular, verruciform leukoplakia
moderate/severe dysplasia
33
dysplastic epithelial cells of erythroleukoplakia
carcinoma in-situ
34
histopathologic features of leukoplakia
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
35
what percent of leukoplakias show hyperkeratosis without epithelial dysplasia?
80%
36
at what phase does irregular hyperkeratosis occur?
granular, verruciform leukoplakia
37
at what phase does bulbous rete pegs occur?
granular, verruciform leukoplakia
38
at what phase can candida hyphae occur?
granular, verruciform leukoplakia
39
at what phase does congested vessels occur?
granular, verruciform leukoplakia
40
at what phase does epithelial atrophy occur?
erythroleukoplakia (speckled leukoplakia)
41
histo of carcinoma in-situ
1. abnormal maturational pattern 2. variation in nuclear size and shape 3. mitosis 4. hyperchromatic nuclei
42
risk factors for premalignant epithelial lesions
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
what percentage of patients with leukoplakia are smokers?
80%
44
T/F: tobacco use with alcohol simultaneously with have a synergistic effect?
true
45
reverse-smoker's palate clinical feature
diffuse keratosis of palate
46
what is the risk of reverse smoking?
significant risk of epithelial dysplasia/carcinoma
47
pack/year
number of packs of cigarettes per day x number of years smoked
48
pk/yr TOB is an estimate of what?
lifetime tobacco exposure
49
T/F: pk/yr TOB is a risk factor
true
50
sanguinaria (bloodroot)
- effective against plaque and gingivitis | - was in old formulation of Viadent
51
UV radiation
leukoplakia lower lip vermilion zone
52
leukoplakia clinical features
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
overall most common site for leukoplakia
buccal mucosa
54
erythroleukoplakia (speckled leukoplakia) clinical features
red and white components
55
treatment for leukoplakia
biopsy mandatory to guide treatment
56
treatment for no or mild dysplasia
discontinue carcinogenic habits
57
treatment for moderate and severe dysplasia
discontinue carcinogenic habits, remove by most convenient means available
58
treatment after initial treatment of leukoplakia
1. close clinical follow-up 2. re-biopsy any suspicious area 3. laser ablation
59
T/F: laser ablation of leukoplakia negates ability for microscopic exam
true
60
prognosis of leukoplakia
guarded
61
what percent of non-dysplastic lesions will transform to squamous cell carcinoma if not treated?
15%
62
what percent of dysplastic lesions will transform?
33%
63
what percent of leukoplakias will recur, even after complete clinical excision
30%
64
proliferative verrucous leukoplakia (PVL) clinical features
1. grows laterally 2. slow, persistent spreading 3. involves multiple sites 4. keratotic plaques, "warty" rough surface projections
65
T/F: PVL has a 4:1 female predilection but only 1/3rd have traditional risk factors (minimal association with tobacco use)
true
66
mean age female for PVL
65 y.o.
67
mean age male for PVL
49 y.o.
68
treatment for PVL
1. close clinical follow-up 2. biopsy any suspicious area 3. laser ablation
69
T/F: it is uncommon for patients who have PVL to have multiple biopsies/surgeries
false; it is common
70
persistent growth of PVL usually develops what?
epithelial dysplasia
71
how many years does it take for PVL to transform into SCC?
within 8 years
72
erythroplakia
red patch that cannot be wipped off AND cannot be diagnosed clinically or microscopically as any other condition
73
risk factors of erythroplakia
same as leukoplakia but NO GENDER PREDILECTION
74
T/F: erythroplakia is less serious/severe than leukoplakia
false, more serious/severe
75
erythroplakia clinical features
1. velvety red 2. well-demarcated 3. usually asymptomatic
76
what causes erythroplakia to be velvety red?
1. due to the lack of keratin production on the surface of the lesion 2. mucosa is atrophic; underlying vasculature shows through
77
what are the most common sites for erythroplakia?
lateral tongue, floor of mouth (FoM) or soft palate
78
what percent of erythroplakia show severe epithelial dysplasia or worse at the time of biopsy?
90%
79
treatment for erythroplakia
- same as leukoplakia with a similar degree of epithelial dysplasia - if biopsy shows cancer, protocol for cancer treatment
80
high-risk sites for leukoplakia
1. ventral tongue 2. floor of mouth 3. soft palate/tonsillar pillars
81
what does a high-risk site mean?
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
risk factor for oral submucous fibrosis
betel quid, paan, masala, gutkha, mawa
83
oral submucous fibrosis clinical features
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
where does oral submucous fibrosis affect?
1. tongue 2. buccal mucosa 3. retromolar area
85
treatment of oral submucous fibrosis
1. intralesional steroid injection mild lesions 2. surgical splitting of fibrous bands 3. physical therapy lifelong 4. close clinical follow-up
86
what causes actinic keratosis
sun-induced by UV rays
87
where does actinic keratosis affect?
skin - any sun-exposed area
88
most common head and neck sites for actinic keratosis
1. face 2. scalp 3. ears
89
actinic keratosis clinical features
1. fair or light-skinned people 2. over 40 y.o. 3. scaly plaque with sandpaper texture 3. may have erythematous base
90
actinic keratosis histopathologic features
1. hyperkeratosis (usually parakeratin) 2. solar elastosis (degeneration of CT) 3. some degree of epithelial dysplasia or superficially invasive SCC
91
treatment for actinic keratosis
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
prognosis for actinic keratosis
fair to good - patient must be monitored for development of new lesions - biopsy/re-biopsy any suspicious areas
93
what causes actinic cheilitis (actinic cheilosis)?
chronic UV exposure
94
actinic cheilitis
term for actinic keratosis involving vermilion zone of lips (especially lower lip)
95
actinic cheilitis clinical features
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
epithelium of actinic cheilitis histopathologically may exhibit what?
1. hyperkeratosis 2. acanthosis (thickening) 3. atrophy (thinning) and/or ulceration 4. dysplasia
97
CT of actinic cheilitis histopathologically may show what?
solar elastosis
98
treatment for actinic cheilitis
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
how long does it take for actinic cheilitis to transform into SCC?
may take many years
100
the risk for transformation of actinic cheilitis to SCC is how much greater than for actinic keratosis?
2.5x greater
101
T/F: actinic cheilitis has a worse off prognosis than intraoral SCC
false, better prognosis than intraoral SCC

AU'18 Oral Path II (31 decks)

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