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Opath > Block 4 > Flashcards

Block 4 Flashcards

1
Q

squamous papilloma = bpsse

what does this result in?

A

benign proliferation stratisfied squamous epitelium

papillary or verruciform mass

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2
Q

what induces squamous papilloma? How do you id it?

A
  1. Human Papilloma Virus 6 and 11
  2. ways:
    1. PCR
    2. immunohistochemistry analysis
    3. in situ hybridization
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3
Q

Sq pap is identified _____ in oral papilloma and _____ in normal mucosal cells

A
  • 50 % oral papilloma
  • 5% in normal mucosal cells
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4
Q

Clincal features of sq papilloma:

sppec

A
  1. s = soft
  2. p = painless
  3. p= pedunculated
  4. e = exophytic nodule with finger-like surface projections
  5. c = look cauliflower or wartlike
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5
Q

what is the most common SOFT TISSUE MASS arising from the SOFT PALATE?

A

squamous papilloma

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6
Q

sq pap occurs ____ in men and women and at any age but specifically at ages _____?

A
  • equally among men and women
  • 30 - 50 yo
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7
Q

Finger-like projections can be _____ or ____ and _____, _____, _____ in color depending on the amt of surface keratinization

A
  1. blunted or pointed
  2. white, slightly red, normal in color
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8
Q

what are the histo features of sq papilloma? 3 things

A
  1. psep = pedunculated surface epithelial proliferation
  2. fct = fibrovascular connective tissue core
  3. koilocytes
    1. virus altered epithelial clear cells
    2. with dark nuclei [pyknotic]
    3. seen high in prickle cell layer
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9
Q

true or false:

If left untreated, they rarely transform into malignancy, continuous enlargement, or dissemination to other parts of the oral cavity

A

true

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10
Q

true or false

  1. Conservative surgical excision [w/ base of the lesion] is adequate;
  2. recurrence is likely.
A
  1. true
  2. false, unlikely for recurrence
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11
Q

What are the 3 Oral warts?

A

1) Verruca Vulgaris
2) Condyloma Acuminatum
3) Focal Epithelial Hyperplasia

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12
Q

Verruca Vulgaris is Benign, virus-induced, ________plasia of stratified squamous epithelium.

A

focal hyperplasia

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13
Q

true or false

HPV types 2, 4, 6, and 40 are found in virtually all examples of verruca vulgaris

and what are found for HPV 6 and 11?

A
  1. true
  2. squamous papilloma
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14
Q

Verruca vulgaris is Contagious, can spread to other parts of a person’s _______ or ______ by way of autoinoculation.

A
  1. skin
  2. mucous membranes
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15
Q

true or false

  1. Verruca vulgaris frequently develops on oral mucosa,
  2. extremely common on the skin
A
  1. false, infrequently develops on oral mucosa
  2. true
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16
Q

define Cutaneous horn/keratin horn which is a clinical feature of verruca vulgaris

A
  1. extreme accumulation of compact keratin
  2. results in hard projection several millimeters in height
  3. = keratin horn aka cutaneous horn
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17
Q

what are 3 other cutaneous lesions that creates cutaneous horns?

A

SAS

1) seborrheic keratosis,
2) actinic keratosis,
3) squamous cell carcinoma.

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18
Q

what are the 3 histofeatures of the verruca vulgaris ?

A

1) hyperkeratotic stratisfied squamous epithelium
2) elongated rete pegs at the EDGES of the lesion that converge at the CENTER
3) koilocytes in the upper epithelial layer

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19
Q

Skin verrucae – topical _____ acid, topical ______ acid, or liquid ________.

A

salicylic acid

lactic acid

nitrogen cyrotherapy

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20
Q

true of false verruca vulgaris

Surgical excision is always indicated for cases with an__________ in which the dx is uncertain.

A

false, ONLY FOR atypical clinical presentation for dx uncertain

typical cases use:

salicylic acid, lactic acid, or lq nitrogen cyrotherapy

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21
Q

Verruca vulgaris, Oral lesions – uses what 4 treatments?

A

surgical excision,

laser,

cryotherapy,

electrosurgery

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22
Q

verruca vulgaris, Recurrence – seen in a _____ portion of treated cases

A

small

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23
Q

w/out treatment, verrucae ____ transform into malignancy, and ____ will disappear spontaneously w/in 2 years

A

do NOT

2/3s disappear spontaneously in 2 years

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24
Q

what is the most common skin wart?

A

verruca vulgaris

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25
Q

waht is another name for condyloma acuminatum?

A

veneral wart

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26
Q

condyloma acuminatum, Virus-induced proliferation of stratified squamous epithelium of the 4______?

A

genitalia

perianal region

mouth

larynx

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27
Q

waht 2 types of HPV are often found in veneral wart? and waht it similar to?

A

6 and 11 just like squamous papilloma

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28
Q

condyloma acuminatum, Represents ___ of all STDs diagnosed in STD clinics and may be an indicator of sexual abuse when diagnosed in ____

A

20%

young children = may be an indicator of sexual abuse

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29
Q

true of false can veneral wart

be passed from mother to child in utero.

A

true

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30
Q

condyloma acuminatum can occur in:

mouth

larynx

genitalial

perianal region,

but specifically for the papillary lesions in the mouth, which 3 areas?

A

lingual frenum

labial mucosa

soft palate

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31
Q

4 veneral wart clinical features?

A

1) Sessile,
2) pink,
3) well-demarcated,
4) nontender exophytic mass w/ short, blunted surface projections.

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32
Q

Histo features of condyloma acuminatum, _______stratified squamous epithelium forming a ______ projection

Koilocytes in the ______ [arrows]

A

acanthotic stratisfied squamous epi

blunted projections

koilocytes in the spinous layer

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33
Q

what are the 2 treatments for ORAL condyloma acuminatum?

A

conservative surgical excision

laser ablation

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34
Q

what are the cons of laser ablation?

what treatment is this used for?

A
  1. causes aerosolized microdroplets

–> to airborne spread of HPV

  1. ORAL condyloma acuminatum
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35
Q

veneral wart, treatment of Anogenital, non-oral lesions = Nonsurgical, patient-applied topical agents 2___?

A

imiquimod

podophyllotoxin

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36
Q

true or false

Condyloma infected w/ ____ or ____ are associated w/ an increased risk of malignant transformation to squamous cell carcinoma

A

HPV-16 or HPV-18

true

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37
Q

true of false

veneral wart, Should be removed b/c it is contagious and can spread to other oral surfaces and to other persons through direct (sexual) contact

what else is also contagious?

A

true

verruca vulgaris

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38
Q

what is typically low risk lesions of HPV 6 and 11 and are dome shaped?

A

condyloma acuminatum

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39
Q

“accumulation of little hills”

A

veneral wart

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40
Q

waht is another name for multifocal epithelial hyperplasia?

A

Heck’s disease

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41
Q

multi focal epi hyperplasia, Virus-induced, localized proliferation of oral squamous epithelium is induced by?

A

HPV 13 and 32

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42
Q

multifocal epi hyperplasia

May be related to eithery _______ or _____ transmitted by _________ .

Association w/ ________.

A

genetic suscpetibility

HPV transmitted by

family members

HLA-DR4 allele

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43
Q

what are the risk factors of multifocal epi hyperplasia?

A

lower socioeconomc status

crowded living conditions

poor oral hygiene

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44
Q

multifocal epithelial hyperplasia

Lesions arise more often in people with ____.

A

aids

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45
Q

multifocal epi hyperplasia

Usually _______ condition, but can affect young and middle-aged adults

Slight ______ predilection, or no significant gender bias

A

childhood

female

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46
Q

Common sites of multifocal epi hyperplasia?

Rarely seen?

A

common:

labial, buccal, lingual mucosa

gingival, palatal, and tonsillar regions

rarely:

conjunctiva region

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47
Q

what are the histo features of multifocal epi hyperplasia?

A
  1. acanthotic epithelium with broad and elongated rete pegs
  2. mitosoid cells containing altered nuclei in otherwise mature and well-differentiated stratisfied squamous epithelium
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48
Q

true or false of mutlifocal epi hyperplasia

Spontaneous regression of these lesions has been reported after months or years and is inferred from the rarity of the disease in adults.

A

true

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49
Q

4 backgound information of molluscum contagiosum

A
  1. epithelial hyperplasia
  2. molluscum contagiousum virus [DNA pox virus]
  3. sexual and non sexual transmission
  4. lesions have predilection for warm skin and recent injury
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50
Q

what are the non sexual ways for transmission of molluscum contagiosum

A

bathing

swimming

wresting

sharing clothing

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51
Q

who does molluscum contigosum affect?

A

immunocompromised

HIV [5 - 18%}

atopic dermatitis pt

Darier’s Disease

children and young adults

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52
Q

molluscum contagiosum is like verruca vulgaris in two ways

what are the two ways

A
  1. like verruca vulgaris and condyloma acuminatum - multiple papules [non solitary]
  2. like verruca vulgaris **commonly **affects SKIN - skin of head, neck eyelids, trunk and genitial
  3. oral involement is - buccal mucosa, lips, gingiva or palate
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53
Q

like multifocal epi hyperplasia, molluscum contagiousum is similar for the treatment

A

no TX

spontaneous regression in 6 - 9 MONTHS

tx can be given to decrease risk of transmission or provide symptomatic relief

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54
Q

Leukoplakia is what?

A
  1. white plaque or patch that cant be rubbed off
  2. CAN NOT be clinically or pathologically identified as another disaese
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55
Q

leukoplakia is waht type of term?

A

clinical term, NOT a specific tissue alteration

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56
Q

waht are the clinical COLORS of leukoplakia?

A
  1. thickened keratin surface epi [white when wet]
  2. thickened spinous layer [masks vascularity of underlying CT]
57
Q

4 causes of leukoplakia

A
  1. tobacco [highly correlated]
  2. UV radiation [caustive factor for leukoplakia on the vermillion border of the lower lip]
  3. micro-o = HPV 16 and 18
  4. sanguinaria [maxillary vestibule and alveolar max mucosa]
58
Q

what is the most common INDICATOR of evolving or actual malignancy

A

leukoplakia

59
Q

most common ORAL precancer or premalignant lesion

A

leukoplakia

60
Q

who does leukoplakia affect

+40

5

70%

A

> +40 yo

prevalence increases with age

found to occur 5 years earlier than SCC

70% vermillion border, buccal mucosa, and gingiva

61
Q

give me the order of change in leukoplakia from plaque to projections

A

early grary plaque

mild/thin leukoplakia

homogenous/ thick leukoplkia [leathery]

granular / nodule leukoplakia

verrucous / verruciform leukoplakia [projections]

62
Q

what is PVL and what are the info

A

Proliferative VERRUCOUS leukoplakia

  1. high risk, slowly spread
  2. development of multiple keratotic plaque with rough surface projections
  3. GINGIVA FREQ involved
  4. STRONG FEMALE predilection
  5. looks like verrucous carcinoma, but this will have dysplastic changes and in 8 year will turn to SCC
  6. simple flat hyperkeratosis -> persistent growth -> exophytic and verruca in nature
63
Q

development of multiple keratotic plaque with rough surface projections, is what?

A

proliferative verrucous leukoplakia

64
Q

speckled leukoplakia aka waht and give the descriptio

A

erythroleukoplakia

  1. intermixed red and white lesion
  2. lesions ahve scattered red patches
  3. epi cells are immature or atrophic cant make keratin
  4. reveals advaced dysplakia on biopsy
65
Q

waht is reveals advaced dysplakia on biopsy

A

speckled leukoplakia

66
Q

Hyperkeratosis

A

thickened surface keratin epithelium with or WITHOUT acanthosis = thickened spinous layer

67
Q

Leukoplakia four description

A
  1. hyperkeratosis
  2. chronic inflammatory cells in the subadjacent CT
  3. underlying epi can be thinning or atrophic even with hyperkatosis
  4. keratin layer can be parakeratin [nuclei but no granular cell layer] or orthokeratin [granular cell layer but no nuclei]
68
Q

Alterations of dysplactic epithelial cells

A
  1. large nuclei and cells
  2. large and prominent nucleolus
  3. incraesed nucleus to cytoplasm ratio
  4. hyperchromatic [dark stain nuceli
  5. pleomorhphic [abnormal cells and nuceli]
  6. dyskeratosis = premature keratinization
  7. abnrmal mitotic activity [tripolar]
  8. increased mitotic activity
  9. bulbous and tear shaped RETE RIDGES
  10. loss of polarity [lack proliferation maturation towards surface
  11. keratain and epithelial pearls
69
Q

spectrum of epithelial dysplasia

A

mild = basal or parabasal layer

moderate = basal -> mid spinous layer

severe = basal -> mid epithelial layer

carcinoma in situ = entire thickness of epi

ductal dysplasia = down the duct of minor salivary glands

70
Q

waht is the FIRST STEP of tx for leukoplakia

A

biopsy

71
Q

___ % of oral leukoplakia turns in to SCC

A

4%

72
Q

what factors INCREASE the risk of cancer in leukoplakic lesions

A
  1. non smoker
  2. female
  3. persistence over many years
  4. on the ORAL FLOOR OR VENTRAL TONGUE
73
Q

what are the risk factors for INCREASED MALIGNANT TRANSFORMATION for leukoplaskic lesions

A
  1. loss of heterogenicity
  2. microsatellite instability
  3. incrase telomerase activity
  4. change in expression of biomarkers
74
Q

true or false

change in expression of biomarkers = increase malig trans

  1. on the oral floor or ventral tongue = incrase malig trans
A
  1. true
  2. false, increase risk of cancer in leukoplastic lesions
75
Q

what 2 things can eliminate or reduce leukoplakia

A
  1. iso tre ti noin
  2. betacarotene
76
Q

what other diseases have white plaques

A
  1. leukoedema
  2. leukoplakia
  3. frictional keratosis
  4. tobacco pouch keratosis
  5. white sponge nevus
  6. nicotinic stomatitis
  7. lichen planus
  8. mor sica tio
77
Q

waht is erythroplakia

A

red patch that CAN NOT be clinically or pathologically identifed as another diease

78
Q

____ is LESS common than leukoplakia but has a ___ potential to be SEVERELY DYSPLATIC CHANGES at the time of biopsy or invasive malignancy later in time

A

erythroplakia is less common than leukoplakia

greater potential for severely dysplastic

79
Q

waht is asymptomatic and associated with erythroleukoplakia

A

erythroplakia

80
Q

clincal features of erythroplakia

A
  1. altered mucosa and well demarcated
  2. erythematous MACULE or PLAQUE
  3. with soft velvety texture
  • assymptomatic
  • associated with erythroleukoplakia
  • biopsy REQUIRED to distinguish bt psoriasis and candidiasis
81
Q

true or false

biopsy is required for erythroplakia to distinguish bt psoriasis and candidiasis

A

true

82
Q

what are the histofeatures of erythroplakia

A

90% erythroplakic lesions represent S C Sscc

  • severly epithelial dysplasia
  • carcinoma in situ
  • superficially invasive squamous cell carcinoma
    2. epi of erythroplakia lacks keratin production, thin, and shows underlying vasculature = red
    3. underlying CT has chronic inflammatory cells
83
Q

treatments of erythroplakia

A
  1. biopsy
  2. if moderat dsyplasia or worst need to:
    - completely destroy
    - remove

by means of leukoplakia methods

  1. reoccurence = common

mom = multifocal oral mucosal involvement = common

84
Q

true of false

long term follow up is necessary for erythroplakia because of reoccurence is common

A

true

85
Q

Nicotine stomatitis is a general- ized white palatal alteration that seems to be a hyper- keratotic response to the _______ by tobacco smoking (usually a pipe), rather than a _______ .

A

HEAT from the tobacco smoke

NOT response to the carcinogens within the smoke

86
Q

true or false nicotine stomatitis malignant transformation is low

A

true

87
Q

true or falase

  1. Erythroplakia also may occur in conjunction with leukoplakia
  2. has been found concur- rently with a large proportion of early invasive oral carcinomas.
A

true

true

88
Q

waht are the 3 most common types of smokeless tobacco

A

chewing tobacco

snuff:
- dry snuff
- moist snuff

89
Q

waht is the most popular type of snuff

A

moist

90
Q

true or false

  1. chronic users of smokless tobacco are carcinogenic
  2. its more carcinogenic than cigs
A
  1. true
  2. false LESS CARCINOGNEIC than cigs
91
Q

resorption of smokless tobacco of nicotine and other molecues through _____

A

resorption through oral mucosa

92
Q

local oral alterations in chronic users of smokless tobacco

A
  1. most common = gingival recession
  2. halitosis [bad breath]
  3. destruction of facial surface of alveolar bone
  4. DENTAL CARIES
  5. localized or generalized wear on occlusal and incisal surfaces
  6. smokeless tobacco keratosis [white plaque where you put the tobacco
  7. mucosal is fissured and rippled
  8. soft velvety texture to mucosa
  9. lesions thickens appear leathery
93
Q

are induration, pain, and ulceration assocaited with smokless tobacco

A

no

94
Q

the epithelium of smokless tobacco appears?

A
  1. hyperkeratosis
  2. acanthosis
  3. chevron formation
95
Q

waht is chevron formation and where do you see this

A
  1. pointed projections ABOVE or WITHIN superficial epithelial layers
  2. seen with smokelss tobacco
96
Q

true or false

smokeless tobacco,

  1. epithelial dsyplasia is uncommon
  2. significant dysplasia and SCC can be present
A

true

true

97
Q

in smokeless tobacco when is biopsy ONLY need?

A
  1. severe lesions
  2. if lesion remains after 6 WEEKS without tobacco contact
98
Q

waht is the treamtnet for smokeless tobacco

A

NO TX

unless, dsyplasia or malignant

99
Q

waht are the pros and cons of alterating smokeless tobacco use

A

pro = reduce smokeless tobacco keratosis [white plaque lesions]

con = 2 sites instead of 1

100
Q

waht is the most common malignancy with smokeless tobacco

A

SCC

101
Q

smokless tobacco, habit cessation leads to normal mucosa appearance in ___ %

A

98%

102
Q

what condition involves chronic progressive scarring

A

oral submucous fibrosis

103
Q

oral submucous fibrosis involves

____ risk,

pre cancerous condition

oral mucosa

A

high risk

104
Q

oral submucous fibrosis

chronic placement of betel quid in the mouth, prevalence in these people:

A

indians

SEA

southern China

taiwan

105
Q

4 Conditions characterized by oral submucous fibrosis

A
  1. mucosal rigidity
  2. fibro-elastic hyperplasia with
  3. changes to:
    - superficial CT
    • submucosal changes from areca nut: [cytokines, growthfactors, and copper]
    • epithelial changes and CARCINOGENSIS from tobacco contact
106
Q

The underlying pathogenetic mechanism for oral submucous fibrosis is hypothesized to involve the role of the areca nut in disrupting the _____.

A

homeostatic equilib- rium between

synthesis and degradation of the

extra- cellular matrix

107
Q

waht is the main chief complaint for oral submucous fibrosis

A

trismus and associated with mucosal pain

an 20 cm interincisal distance = severe

108
Q

which sex is more suceptible to oral submucosal fibrosis

A

females

109
Q

clinical features of oral submucous fibrosis

A
  1. first found in young adults chewing betel quid
  2. females > males
  3. chief complaint trismus and some mucosal pain [20 mm interincisal distance or less = severe]
  4. signs and symptoms: X Men S VP
  • X = xerostomia

M = melanosis

S = stomatopyrosis [generalized oral burning sensation]

V = vesicles

P = petechiae

110
Q

waht are the most common areas affected by oral submucous fibrosis

A
  1. buccal mucosa

retromolar area

soft palate

111
Q

3 Histo features of oral submucous fibrosis

A
  1. submucosal deposition

DENSE and HYPOvascular

collagenous CT

with chronic inflammatory cells

  1. hyperkeratosis, basilar hyperplasia, fibrosis of LAMINA PROPRIA
  2. ragged keratinaceous surface

covered by

encrusted betel quid ingredients

112
Q

Unlike ____, oral submucous fibrosis does NOT regress with habit cessation.

A

tobacco pouch keratosis,

113
Q
  1. Frequent evaluation for development of oral SCC

is essential because a ______ YEAR malignant transformation 2. At a rate of ___ % has been determined for betel quid users in India.

A

17 years

8%

114
Q

people with oral submucous fibrosis are ___ x more likely to develop oral cancer than people without

A

19 times

115
Q

true or false

nicotinic stomatitis is a generalized MUCOSAL alteration to the hard palate

A

true

116
Q

true or false

Once a common mucosal change of the hard palate, nicotine stomatitis has become less common as cigar and pipe smoking have lost popularity.

A

true

117
Q

white keratotic change

with tobacco smoking

A

nicotinic stomatitis

118
Q

nicotinic stomatitis, does have a premalignant nature

A

false DOES NOT have premalignant in nature

119
Q

true or false

nicotinic stomatitis, reverse smokers palate has potential to develop to dysplasia or carcinoma

A

true, reverse smokers plalate can turn to dysplasia or carcinoma

120
Q

waht are the 3 clinical features of nicotinic stomatitis

A
  1. WE GIS of hard palate
    - white kertotic changes
    - extensive leathery
    - generalized mucosal alteration
    - inflamed salivary duct openings which represent
    - sprinkled red papules
  2. ducts have white keratotic rings surrounding them
  3. gingival mucosal also keratotic
121
Q

what are the 2 histofeatures of nicotinic stomatitis

A
  1. hyperkeratosis and acanthosis

PALATAL epithelium

  1. squamous METAplasia of

minor salivary gland ducts

122
Q

true or false

  1. nicotinic stomatitis is completely reversible
  2. also, non precancerous lesion and not malignant, so thus doesnt need treatment
A

true

true

123
Q

nicotinic stomatitis

any white lesion of the PALATAL MUCOSA persisting 1 month after cessation is considered a true _____ and should be ____ for tx.

A

leukoplakia and should be biopsied for treatment

124
Q

actinic keratosis is a ____ ___ lesion and is ______ in nature

A

cutaneous premalignant lesion

and

precancerous is nature

125
Q

waht is actinic keratosis caused by?

A

CUMULATIVE UV radiation

sun exposed skin

esp fair skinned people

126
Q

actinic keratosis

lesions develop on the skin of more than ___% ___ adults with SIGNIFICANT LIFETIME SUN EXPOSURE

A

50% ALL white adults

with

significant lifetime sun exposure

127
Q

clinical features of actinic keratosis

A
  1. seldom occurs in people YOUNGER than 40 yo
  2. common sites:
    - face and neck
    - scalp of balding men

dorsum of hands

forearm

  1. **irregular scaly plaques **

VARY IN COLOR

can be superimposed on erythematous background

  1. keratotic scales can PEEL OFF
  2. palpation reveals rough, sandpaper feel
  3. minimal elevation, but may produce cutaneous horn
128
Q

waht are the 4 histofeatures of actinic keratosis

A
  1. hyperPARAkeratosis and acanthosis
  2. excessive amount of parakertain on the surface epithelium
  3. tear drop rete ridges
  4. hyperchromatic and pleomorphic epidermal cells
129
Q

what are 4 ways to destroy actinic keratosis

A
  1. lq nitrogen cyrotherapy
  2. electrodessication
  3. surgical excision
  4. CURETTAGE
130
Q

true or false actinic keratosis

  1. reoccurance is likely
  2. additonal lesions freq arise in adj sun damaged skin
A

false, recurrence is RARE

true add lesions can arise in adj sun damaged skin

131
Q

just like erythroplakia, actinic keratosis has long term follow up?

A

true

132
Q

what is actinic cheilosis

A
  1. premalignant lesion of

lower lip vermillion border

  1. caused by: excessive UV radiation from sun
  2. mostly confined to fair skin people and people that sunburn easily
  3. outdoor jobs: sailer’s lip and farmer’s lip
133
Q

actinic cheilosis, lesions develop rapidly

true or false

A

false, lesions develop SLOWLy that pts are NOT aware of changes

134
Q

what are the clinical changes of actinic cheilosis

A
  1. EARLIEST CHANGE:
    - **atrophy **lower lip vermillion border
    - smooth surface
    - blotchy pale areas
  2. **blurring **of margin bt vermillion zone and cutaneous portion of lip
  3. rough scaly areas develop

lesion progress

thicken and appear like LEUKOPLAKIC LESION

135
Q

waht are the 4 histofeatures of actinic kertaosis

A
  1. atrophic SSE w/

marked keratin production

  1. hyperkeratosis and epithelial atrophy
  2. mild chronic INFLAMMATORY INFILTRATE present

subadjacent dysplastic epithelium

  1. underlying CT shows:

solar [actinic]

elastosis

136
Q

waht is elastosis and which diseaease do you see it in the underlying CT histofeatures

A
  1. elastosis = UV light induceed alteration of COLLAGEN and ELASTIC FIBERS
  2. actinic cheilosis
137
Q

true or false actinic cheilosis

  1. many changes are irreversible
  2. to prevent further damage use lip balm with sunscreen
A

true IRREVERSIBLE for ACTINIC CHEILOSIS

true

138
Q

actinic cheilosis

any areas with 4_____ should be biopsy

A
  1. induration
  2. ulceration
  3. thickening
  4. leukoplakia

SHOULD BIOPSY

139
Q
A

Opath (6 decks)

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