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Dr. Murrahs class > Chapter 10: Epithelial Pathology PART 2 > Flashcards

Chapter 10: Epithelial Pathology PART 2 Flashcards

1
Q

___ is an oral counterpart to ephelis

A

oral melanotic macule

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2
Q

___ is a brown asymptomatic macule produced by a focal increase in melanin deposition

A

oral melanotic macule

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3
Q

are oral melanotic macules dependent on sun exposure?

A

no

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4
Q

what is the most common site of oral melanotic macules?

A

vermillion zone of the lower lip (labial melanotic macule)

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5
Q

___% of oral melanotic macules are solitary

A

80%

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6
Q

there is no malignant transformation potential of oral melanotic macule, but it is clinically indistinguishable from what?

A

early melanoma

a biopsy is mandatory

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7
Q

___ is an acquired pigmentation of the oral mucosa that appears to be a reactive process due to trauma

A

oral melanoacanthoma

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8
Q

oral melanoacanthoma is characterized by ___ throughout the epithelium

A

dendritic melanocytes

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9
Q
A

oral melanotic macule

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10
Q
A

labial melanotic macule

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11
Q

is oral melanoacanthoma related to melancanthoma of the skin?

A

no

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12
Q

oral melanoacanthoma is seen almost exclusively in what population, and is it more common in males or females?

A

african americans

F>M

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13
Q

oral melanoacanthoma is most common in what age?

A

20-30s

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14
Q

what is the most common site of oral melanoacanthoma occurrence?

A

buccal mucosa

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15
Q

oral melanoacanthoma is typically asymptomatic, but can cause ___ and ___

A

pain and burning

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16
Q

how does oral melanoacanthoma clinically appear?

A

smooth, dark brown macule

lesions increase rapidly in size

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17
Q

incisional biopsy is indicated in cases of oral melanoacanthoma to rule out ___

A

melanoma

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18
Q

what is the treatment for oral melanoacanthoma? is there a risk of malignant transformation

A
  • biopsy to rule out melanoma
  • no further treatment - lesions regress after incisional biopsy
  • is there a risk of malignant transformation?
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19
Q

bottom photo is after biopsy

A

oral melanoacanthoma

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20
Q

___ is the most commonly recognized nevus

A

acquired melanocytic nevus

aka mole

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21
Q

___ is a benign, localized proliferation of cells from the neural crest, and is the most common of all adult tumors

A

acquired melanocytic nevus

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22
Q

white adults can have how many acquired melanocytic nevus lesions? where are most lesions present?

A
  • 10-40
  • above the waist
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23
Q

what are the 3 clinical stages of acquired melanocytic nevus?

A
  • junctional
  • compound
  • intradermal
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24
Q

which stage of acquired melanocytic nevus is the earliest presentation and appears as a dark macule less than 6mm?

A

junctional

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25
Q

which stage of acquired melanocytic nevus occurs as the nevus cells proliferate and the lesion becomes a slightly elevated, soft papule with a smooth surface; the degree of pigmentation decreases

A

compound

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26
Q

which stage of acquired melanocytic nevus is characterized by the lesion surface becoming somewhat papillomatous; hairs grown from the center; loses most or all of its pigmentation? what is the name give to it if it is in the oral cavity?

A
  • intradermal
  • intramucosal if it is in the oral cavity
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27
Q

are intraoral melanocytic nevi common? what is the fraction that are found in females?

A
  • uncommon
  • 2/3 are found in females
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28
Q

most intraoral melanocytic nevi have an evolution and appearance similar to ___, and have a predilection for the ___

A
  • skin nevi
  • palate
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29
Q

what is the treatment for acquired melanocytic nevi? what is the risk of transformation?

A
  • no treatment necessary unless there is clinical change or found in the oral cavity
  • most will regress
  • risk of transformation of an acquired melanocytic nevus is one in a million
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30
Q
A

acquired melanocytic nevus

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31
Q
A

acquired melanocytic nevus

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32
Q
A

acquired intraoral melanocytic nevus

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33
Q
A

acquired intraoral melanocytic nevus

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34
Q

congenital melanocytic nevi affect ___% of newborns

A

1%

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35
Q

congenital melanocytic nevi are divided into what two categories?

A

small (less than 20cm) and large (greater than 20cm)

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36
Q

small type congenital melanocytic nevi are similar in appearance to ___, except they are usually larger

A

acquired melanocytic nevi

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37
Q

describe large type congenital melanocytic nevi

A
  • plaques with a rough or nodular surface and often change with time
  • common feature is hypertrichosis (excess)
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38
Q

a very large congenital nevus can be called a ___ or ___

A

bathing trunk or garment nevus

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39
Q

up to ___% of large congenital nevi may undergo malignant transformation into melanoma. what should you do with these lesions?

A
  • 15%
  • these lesions should be removed entirely if feasible; otherwise, close follow-up is required
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40
Q

a ___ is a melanocytic nevus with a surrounding pale hypopigmented border

A

halo nevus

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41
Q

halo nevi are thought to result from what?

A

nevus cell destruction by the immune system

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42
Q
A

congenital melanocytic nevus

large type (characteristic hypertrichosis)

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43
Q
A

halo nevus

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44
Q

___ is an uncommon, benign proliferation of dermal (or intramucosal) melanocytes that comes in two forms: common and cellular

A

blue nevus

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45
Q

what is the blue color of blue nevi due to?

A
  • tyndall effect - melanin particles are deep to the surface, so the light reflected back must pass through overlying tissues
  • colors with long wavelenths (red/yellow) are more easily absorbed by the tissues
  • blue has a shorter wavelength and is reflected
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46
Q

how are blue nevi treated? what is the risk of malignant transformation?

A
  • conservative surgical excision with minimal chance of recurrence
  • oral lesions must be biopsied to rule out melanoma
  • malignant transformation has been reported but is very rare
47
Q
A

intraoral blue nevus

48
Q
A

blue nevus

49
Q

___ is an intraoral white plaque that does not rub off and cannot be identified as any well known entity

A

leukoplakia

  • if it can be rubbed off, it is not leukoplakia
  • if it is easily recognizable as a well known entity, it is not leukoplakia
50
Q

why are leukoplakia lesions white?

A

because there is something (keratin, microbial colony, scar tissue, necrosis, etc.) that is blocking the “redness” of the underlying vascular tissue

51
Q

what are some examples of white lesions that can be scraped off?

A
  • materia alba
  • white coated tongue
  • burn (thermal, chemical, cotton roll, etc)
  • pseudomembranous candidiasis
  • sloughing from toothpaste
52
Q

leukoplakia is considered a ___ lesion

A

premalignant

53
Q

leukoplakia comprises ___% of oral precancer

A

85%

54
Q

___ or ___ is seen in 20% of biopsy samples of clinical leukoplakia

A

dysplastic epithelium or squamous cell carcinoma

55
Q

80% of leukoplakia biopsies are ___

A

benign hyperkeratosis

56
Q

what is the malignant transformation potential of leukoplakia?

A

5-50%, depending on the clinical subtype

57
Q

leukoplakia has a strong ___ predilection

A

male

58
Q

what are the 6 etiologies of leukoplakia?

A
  • tobacco
  • smoking
  • sanguinaria
  • UV radiation
  • microorganisms
  • trauma
59
Q

describe leukoplakia with a tobacco etiology

A
  • 80% of patients with leukoplakia smoke
  • smokeless tobacco = tobacco pouch keratosis
60
Q

leukoplakia with an alcohol etiology has a synergistic effect with ___

A

tobacco

61
Q

describe leukoplakia with a sanguinaria etiology

A
  • an herbal extract found in toothpaste or mouth rinses
  • leukoplakia occurs in the maxillary vestibule or alveolar mucosa of the maxilla
  • 80% of patients with leukoplakic lesions here have a history of using sanguinaria products
62
Q

leukoplakia with a UV radiation etiology causes leukoplakia in what location?

A

lower lip vermillion

63
Q

describe leukoplakia with a microorganism etiology

A
  • treponema pallidum (glossitis in 3rd stage syphilis)
  • candida albicans can colonize the superficial oral mucosa to produce a thick plaque (candidal hyperplasia)
    • HPV 16 and 18 has been identified in some leukoplakias
64
Q

describe leukoplakia with a trauma etiology

A
  • not precancerous
  • not true leukoplakia
  • exmamples: nicotine stomatitis and frictional keratosis
65
Q

the prevalence of leukoplakia increases rapidly with ___

A

age

66
Q

70% of leukoplakia lesions are found where?

A

lip vermillion, buccal mucosa, gingiva

67
Q

90% of leukoplakias with dysplasia or carcinoma are found where?

A

lip vermillion, lateral/ventral tongue, floor of mouth

68
Q

lesions that demonstrate scattered red patches are termed ___

A

erythroplakia

69
Q

erythroplakia found in areas of leukoplakia represents site in which ___ cells are so immature they can no longer produce ___

A
  • epithelial
  • keratin
70
Q

red (erythroplakia) and white (leukoplakia) intermixed lesions are termed ___ or ___

A

erythropeukoplakia or speckled leukoplakia

71
Q

erythroplakia and erythroleukoplakia frequently reveal advanced ___ on biopsy

A

dysplasia

72
Q

___ is a special high-risk form of leukoplakia characterized by multiple keratotic plaques with roughened surface projections

A

proliferative verrucous leukoplakia (PVL)

73
Q

proliferative verrucous leukoplakia lesions spread slowly throughout the ___, and as the lesion progresses, ___ can develop

A
  • mouth
  • carcinoma
74
Q

is PVL difficult to treat? do lesions recur?

A

it is difficult to treat, and lesions will recur

75
Q

why is PVL unusual?

A

there is a 4:1 F:M predilection and no association with tobacco use

76
Q

the histoplathology of leukoplakia includes what 4 things?

A
  • hyperkeratosis - thickened keratin layer
  • hyperparakeratosis - no granular cell layer; nuclei are retained
  • hyperorthokeratosis - granular cell layer; nuclei are lost
  • acanthosis - thickened spinous layer
77
Q

when there is concern about malignancy with leukoplakia, ___ techniques such as cytologic testing (including brush biopsy) and lesion staining with supravital dyes should not be considered as substitutes for ___

A
  • noninvasive screening
  • biopsy
78
Q

the first step in treating leukoplakia is arriving at a ___. therefore, ___ is mandatory

A
  • definitive diagnosis
  • biopsy
    • taken from most severe looking areas of involvement
79
Q

describe the alterations found in leukoplakia biopsies that are consistent with mild dysplasia, moderate dysplasia, severe dysplasia, and carcinoma in situ

A
  • mild dysplasia - alterations are limited to the lower 1/3
  • moderate dysplasia - alterations are limited to the lower 1/2
  • severe dysplasia - alterations are present above the lower 1/2
  • carcinoma in situ - alterations are present throughout epithelium
80
Q

management of leukoplakia with mild dysplasia is guided by what?

A

the size of the lesion and the response to more conservative measures (aka smoking cessation)

81
Q

management of leukoplakia with moderate epithelial dysplasia or worse warrants what?

A

complete removal or tissue

82
Q

why is long-term follow up after leukoplakia treatment important?

A
  • recurrences are frequent (85% in verruciform)
  • additional leukoplakias may develop
  • overall, 5% of leukoplakias become squamous cell carcinoma, usually within 2-4 years
83
Q

what are 4 factors that increase the risk for cancer in leukoplakias?

A
  • persistence over several years
  • female patient
  • nonsmoker
  • oral floor or ventral tongue lesions
84
Q

___ is defined as a red patch that cannot be diagnosed as any other condition

A

erythroplakia

85
Q

T or F:

true erythroplakias are benign

A

false

true erythroplakias are never completely benign

86
Q

90% of erythroplakias show ___ on biopsy

A

moderate dysplasia or worse

87
Q

what are the causes of erythroplakia?

A

unknown, but they are assumed to be the same as invasive squamous cell carcinoma

88
Q

erythroplakia predominantly occurs in what age patient, and with what gender predilection?

A
  • middle-aged to older adults (average = 70yo)
  • no gender predilection
89
Q

what are the most common locations of erythroplakia?

A
  • floor of mouth
  • ventral tongue
  • soft palate
90
Q

what does the altered mucosa look like in erythroplakia?

A

well-demarcated macule or plaque with a soft, velvety texture

91
Q

is erythroplakia typically symptomatic or asymptomatic?

A

asymptomatic

92
Q

erythroplakias are red in color due to what?

A
  • lack of keratin and epithelial thinness
    • allows underlying vasculature to show
93
Q

___ is mandatory for erythroplakia, and treatment is guided by ___

A
  • biopsy
  • definitive diagnosis
94
Q

describe recurrence and multifocal oral involvement of erythroplakia

A

both are common, therefore long-term follow up is required

95
Q
A

proliferative verrucous leukoplakia

96
Q
A

proliferative verrucous leukoplakia

97
Q
A

erythroleukoplakia

98
Q

does not rub off

A

leukoplakia

99
Q
A

erythroplakia

100
Q
A

erythroplakia

101
Q

what are the 3 types of smokeless tobacco, and what population most commonly uses each?

A
  • chewing tobacco - men during outdoor activities
  • moist snuff - most popular
  • dry snuff - southern women
102
Q

what is the most common local change seen in patients using smokeless tobacco?

A
  • characteristic, painless loss of gingival tissues in area of tobacco contact
    • gingival recession may be accompanied by destruction of facial surface of alveolar bone; correlates with quantity of daily use and duration of habit
103
Q

a ___ stain on the teeth is common in patients using smokeless tobacco

A

brown-black extrinsic tobacco stain

104
Q

halitosis is a frequent finding of patients using ___

A

smokeless tobacco

105
Q

what is smokeless tobacco keratosis?

A

a characteristic white plaque that is produced on the mucosa in direct contact with smokeless tobacco

106
Q

do smokeless tobacco keratosis lesions develop shortly after tobacco use or after a long history of use?

A

shortly after heavy tobacco use begins; new lesions seldom arise in people with a long history of tobacco use

107
Q

what do smokeless tobacco keratosis lesions look like clinically?

A

thin, gray or white plaque with a border that blends into the surrounding mucosa; appears fissured or rippled

108
Q

do smokeless tobacco keratosis lesions exhibit induration, ulceration, pain, or epithelial dysplasia?

A
  • NO induration, ulceration, or pain
  • epithelial dysplasia is uncommon, but if it is present, it is mild
109
Q

when is a biopsy warranted in smokeless tobacco keratosis lesions?

A

only for more severe lesions or for a lesion remaining 6 weeks after habit is stopped

110
Q

what is the treatment for smokeless tobacco keratosis?

A
  • altnerate the site of tobacco placement
  • habit cessation leads to normal mucosal appearance in 98% of users, usually in 2 weeks
111
Q
A

gingival recession due to smokeless tobacco

112
Q
A

smokeless tobacco keratosis

113
Q
A

smokeless tobacco keratosis

114
Q
A

smokeless tobacco keratosis

Dr. Murrahs class (17 decks)

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