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Oral Pathology - My deck > Chapter 10- Part 1 > Flashcards

Chapter 10- Part 1 Flashcards

1
Q

What term describes a benign proliferation of stratified squamous epithelium?

A

Sqaumous papilloma

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2
Q

What causes squamous papilloma?

A

Human papillomavirus types 6 and 11

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3
Q

What type of virus is human papillomavirus?

A

DNA virus of the papovavirus subgroup

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4
Q

True or False: HPV has high virulence but low infectivity

A

False, HPV has low virulence and low infectivity, only affecting about 1 in 250

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5
Q

What sites are commonly affected by squamous papilloma?

A

Tongue, lips and soft palate

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6
Q

What are some clinical characteristics of squamous papilloma?

A

Painless, pedunculated, enlarges rapidly to 5 mm then stabilizes

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7
Q

What are the 3 differential diagnoses for sqaumous papilloma?

A

Verruca vulgaris, condyloma acuminatum, verruciform xanthoma

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8
Q

How is sqaumous papilloma treated?

A

Surgical excision –> send to pathology to confirm diagnosis

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9
Q

What is the term that describes a focal, benign hyperplasia of stratified squamous epithelium known as a common wart?

A

Verruca vulgaris

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10
Q

What is verruca vulgaris caused by?

A

HPV 2, 4, 6, 40

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11
Q

Is verruca vulgaris contagious?

A

Yes

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12
Q

Describe the clinical presentation of verruca vulgaris in the oral cavity?

A

They almost always appear white as they are usually hyper orthokeratotic

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13
Q

How is verruca vulgaris treated?

A

Surgical excision, but recurrences are possible. Also, many will spontaneously regress in 2 years

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14
Q

What is the chance of malignant transformation of verruca vulgaris?

A

No chance of malignant transformation

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15
Q

What term describes a sexually transmitted wart?

A

Condyloma acuminatum AKA Venereal wart

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16
Q

What causes condyloma acuminatum?

A

HPV 2, 6, 11, 16, 18. 31, 53, 54

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17
Q

What HPV types are the most common cause of condyloma acuminatum?

A

HPV 6 and 11

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18
Q

What HPV types are high risk for malignant transformation pf condyloma acuminatum?

A

HPV 16, 18, 31 (31 not as common)

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19
Q

What is the time of incubation for condyloma acuminatum?

A

1-3 months from time of sexual contact

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20
Q

What are some characteristics of condyloma acuminatum that can be used to distinguis from verruca vulgaris and squamous papilloma?

A

Characteristically clustered with other condyloma, 2x as large as papilloma or verruca culgaris (1-1.5 cm)

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21
Q

How is condyloma acuminatum treated?

A

Conservative surgical excision

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22
Q

What area is at an increased risk for malignant transformation of condyloma acuminatum by HPV 16 and 18?

A

In the anogential area, to squamous cell carcinoma

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23
Q

What term describes multiple lesions that do not spread, appearing during childhood, similar in appearance to condyloma acuminatum?

A

Multifocal epithelial hyperplasia

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24
Q

What is another name for multifocal epithelial hyperplasia?

A

Heck’s disease

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25
Q

What causes multifocal epithelial hyperplasia?

A

HPV 13, 32 but there is a hereditary/genetic component

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26
Q

What is the treatment multifocal epithelial hyperplasia?

A

Conservative surgical excision, but may spontaneously regress

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27
Q

Is there a risk of malignant transformation associated with multifocal epithelial hyperplasia?

A

There is no risk of malignant transformation

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28
Q

What term describes a benign, localized proliferation of respiratory mucosa?

A

Sinonasal papilloma

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29
Q

What term descries a virally induced epithelial hyperplasia typically seen in children?

A

Molluscum contagiosum

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30
Q

What causes molluscum contagiosum?

A

Molluscum contagiosum virus, a member of the DNA poxvirus

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31
Q

Why is it called molluscum contagiosum?

A

Because of molluscum bodies evident in the histology.

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32
Q

What is another name for molluscum bodies?

A

Henderson-Paterson bodies

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33
Q

What is the treatment of molluscum contagiosum?

A

Spontaneous remission after about 9 months, but removed by excision or cryotherapy to decrease risk of transmission

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34
Q

Is there a risk of malignant transformation associated with molluscum contagiosum?

A

No

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35
Q

What term describes an acquired, benign proliferation of epidermal basal cells that appears as small, brown macules?

A

Seborrheic keratosis

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36
Q

In what population is seborrheic keratosis common?

A

Extremely common in elderly patients

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37
Q

Where does seborrheic keratosis develop?

A

On the skin of the face, trunk and extremities. Not in the mouth.

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38
Q

What form of seborrheic keratosis occurs in African americans and is characterized by a scattering of black papules around the periorbital region?

A

Dermatosis papulosa nigra

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39
Q

Is dermatosis papulosa nigra autosomal dominant or recessive?

A

Autosomal dominant

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40
Q

What is the treatment of seborrheic keratosis?

A

Macules can be surgically removed for esthetic reasons

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41
Q

Is there a risk of malignant transformation associated with seborrheic keratosis?

A

No

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42
Q

What term describes numerous seborrheic keratoses with pruritus?

A

Leser-Trèlat sign

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43
Q

What does Leser-Trèlat a sign of?

A

Internal malignancy, usually within the GI tract

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44
Q

What is the professional term for freckle?

A

Ephelis

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45
Q

What is ephelis?

A

Common hyperpignmented macule of the skin, where there is an increased melanin production without an increase in the number of melanocytes

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46
Q

In what population is ephelis common?

A

More prominent in children, and more common in light skinned and light haired persons

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47
Q

Do ephelis become more pronounced with sun exposure?

A

YES, ephelis become more pronounced with sun exposure

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48
Q

What is the treatment for ephelis?

A

No treatment necessary, however, sunscreen can prevent new or darkening of lesions

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49
Q

What term describes a benign, brown macule resulting from chronic UV light damage to the skin?

A

Actinic lentigo

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50
Q

In what population is actinic lentigo common?

A

In caucasians older than 70

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51
Q

What is the clinical appearance of actinic lentigo?

A

Uniformly pigmented tan macules that are well demarcated but have irregular borders

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52
Q

Does actinic lentigo become more prominent with UV exposure?

A

No, actinic lentigo does not become more pronounced with sun exposure

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53
Q

Is there a risk of malignant transformation associated with actinic lentigo?

A

No

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54
Q

What term describes a benign cutaneous melanocytic hyperplasia (increase in the number of melanocytes)?

A

Lentigo simplex

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55
Q

What is the cause of lentigo simplex?

A

The cause of lentigo simplex is unknown

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56
Q

In what population is lentigo simplex common?

A

Lentigo simplex can happen at any age, but is more common in children

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57
Q

What does lentigo simplex clinically present as?

A

Appears as a macule smaller than 5 mm with uniform brown color, on skin that is not exposed to sunlight

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58
Q

Does lentigo simplex change with exposure to sunlight?

A

No, lentigo simplex does not change with UV exposure

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59
Q

Is there a risk of malignant transformation associated with lentigo simplex?

A

No

60
Q

What term describes an acquired, symmetrical, hormonally driven hyperpigmentation of the sun exposed skin of the face?

A

Melasma

61
Q

In what population is melasma common?

A

Pregnant, dark complexioned women

62
Q

How can melasma be hormonally driven?

A

Melanocyte stimulating hormone comes fro the anterior/intermediate pituitary gland, so it can get released with other hormones such as LH and FSH

63
Q

What is the treatment of melasma?

A

Pigmentation can remain faint or darken over time, but avoidance of sun or using sunscreen is necessary for clinical management

64
Q

Is there a risk of malignant transformation associated with melasma?

A

No

65
Q

What term describes a flat, brown hyperpigmented macule found in the oral cavity?

A

Oral melanotic macule (mouth freckle)

66
Q

Where is the most common site of an oral melanotic macule?

A

As a solitary macule on the vermillion zone of the lower, so it is called a labial melanotic macule.

67
Q

Are oral melanotic macules dependent on sun exposure?

A

No

68
Q

What is the treatment for an oral melanotic macule?

A

No treatment necessary, however it can not be clinically distinguished from early melanoma so biopsy is required! (small, symmetrical, and doesn’t grow is a good sign)

69
Q

What does the histology of an oral melanotic macule appear as?

A

Inreased melanin at the basal cell layer of the epithelium

70
Q

What term describes an uncommon, benign acquired pigmentation in the oral mucosa,?

A

Oral melanoacanthoma

71
Q

How can an oral melanoacanthoma be acquired?

A

Appears to be a reactive process due to trauma (lesions increase in size rapidly due to frictional irritation)

72
Q

What is the histology associated with an oral melanoacanthoma characterized by?

A

Characterized by dendritic melanocytes throughout the epithelium

73
Q

In what population are oral melanoacanthomas common?

A

African Americans because they have more melanin, and women in their 20-30s because MSH and the pituitary gland, but are not very common

74
Q

What is the most common site of occurrence of oral melanoacanthomas?

A

Buccal mucosa, and can be associated with pain and burning

75
Q

How are oral melanoacanthomas treated?

A

Biopsy is required to rule out melanoma, but no further treatment is necessary

76
Q

Is there a risk of malignant transformation associated with oral melanoacanthoma?

A

No

77
Q

What term describes a benign, localized proliferation of cells from the neural crest?

A

Acquired melanocytic nevus, the most common of all adult tumors

78
Q

What does nevus mean?

A

The generic term nevus refers to congenital or developmental malformations of the skin, but ascquired melanocytic nevi is the most commonly recognized nevus, so nevus is often used synonymously with it

79
Q

Where are acquired melanocytic nevi found?

A

Most lesions are above the waist, white adults will have 10-40 lesions

80
Q

What term describes “islands of increased melanocytes” associated with an acquired melanocytic nevus?

A

Thèques

81
Q

Are acquired melanocytic nevi common or uncommon in the oral cavity?

A

Uncommon

82
Q

If acquired melanocytic nevi occur in the mouth, what is the most common site of occurrence?

A

The palate

83
Q

What is the treatment for an acquired melanocytic nevus?

A

No treatment is necessary, unless there is a change in appearance

84
Q

Is there a risk of malignant transformation associated with an acquired melanocytic nevus?

A

Yes, the risk of transformation to melanoma is 1 in 1,000,000

85
Q

What term describes a nevus that is present at birth?

A

Congenital melanocytic nevus

86
Q

What are the two types of congenital melanocytic nevi?

A

Small (less than 20 cm) and large (20+ cm)

87
Q

How are congenital melanocytic nevi different from acquired melanocytic nevi?

A

Congenital melanocytic nevi tend to be larger than acquired melanocytic nevi

88
Q

What is a common feature of the large type of congenital melanocytic nevi?

A

Hypertrichosis

89
Q

What term describes when a very large congenital melanocytic nevus?

A

Bathing trunk nevus or garment nevus

90
Q

Is there a risk of malignant transformation associated with congenital melanocytic nevi?

A

Yes, up to 15% of large congenital nevi may undergo malignant transform into melanoma

91
Q

What term describes a melanocytic nevus with a pale hypopigmented border?

A

Halo nevus

92
Q

What is thought to be the cause of halo nevi?

A

Thought to be nevus cell destruction by the immune system

93
Q

What term describes a solitary nodule, that is hard to histologically distinguish from melanoma?

A

Spitz nevus

94
Q

What was the historic name for a spitz nevus?

A

Juvenile melanoma

95
Q

When do spitz nevi appear?

A

Occur during childhood, on the skin of the face or extremities and are usually 6 mm or smaller

96
Q

What term describes an uncommon, benign proliferation of dermal melanocytes that appear blue in color?

A

Blue nevus

97
Q

What are the 2 forms of blue nevi?

A

Common and cellular

98
Q

Where are common blue nevi seen?

A

The dorsa of hands, feet, the scalp and face

99
Q

Are blue nevi common or uncommon in the oral cavity?

A

Blue nevi are the 2nd most frequent melanocytic nevi found in the oral cavity

100
Q

Where do blue nevi occur in the oral cavity?

A

Blue nevi in the oral cavity are almost always found on the palate

101
Q

What are the characteristics of the cellular form of blue nevi?

A

Half are seen on the buttock, and they are slow growing and can reach up to 2 cm

102
Q

What causes the blue color noted in blue nevi?

A

Tyndall effect

103
Q

What is the Tyndall effect?

A

Melanin particles are deep to the surface, so the light reflected back must pass through overlying tissues. Colors with long wavelengths are more easily absorbed, where colors with shorter wavelengths are reflected back

104
Q

How are oral blue nevi treated?

A

Conservative surgical excision, biopsy is required to rule out melanoma

105
Q

Is there a risk of malignant transformation associated with a blue nevus?

A

Yes, it has been reported but it is very rare

106
Q

What term describes an intraoral white plaque that does not rub off and cannot be identified?

A

Leukoplakia

107
Q

Why are leukoplakias white?

A

Because there is something (like keratine, microbial colony, scar tissue, necorsis, etc) that is blocking the redness of the underlying mucosa

108
Q

What are some common diagnoses of white lesions that can be scraped off?

A

Materia alba, white coated tongue, burn (toothpaste), pseudomembranous candidiasis

109
Q

By definition, leukoplakias are _________ and must be ________

A

Leukoplakias are pre-malignant and must be biospied!

110
Q

What percentage of oral premalignancies do leukoplakias comprise?

A

85% of oral precancers are leukoplakias

111
Q

What population is more commonly affected by leukoplakia?

A

Men (etiology… alcohol, tobacco)

112
Q

What are the causes of leukoplakia?

A

Tobacco, alcohol, sanguinaria, UV radiation, microorganisms, trauma

113
Q

What is sanguinaria?

A

A herbal extract found in toothpaste or mouth rinses

114
Q

Where do leukoplakias caused by sanguinaria usually occur?

A

Maxillary vestibule or alveolar mucosa of the maxilla

115
Q

Where do leukoplakias caused by UV radiation usually occur?

A

Lower lip vermillion border

116
Q

What microorganisms are known to be associated with a non-premalignant leukoplakia?

A

Treponema pallidum (glossitis in 3rd stage), and candidia albicans (hyperplastic form)

117
Q

Are trauma caused leukoplakias true leukoplakias?

A

No, they are not precancerous

118
Q

What are some examples of trauma caused leukoplakias?

A

Nicotine stomatitis, and frictional keratosis

119
Q

What factor influences the prevalence of leukoplakia?

A

Age

120
Q

Where are the common sites of occurence of leukoplakias?

A

Lip vermillion, buccal mucosa, gingiva

121
Q

What are the high risk sites for dysplasia or carcinoma?

A

Lip vermillion, lateral/ventral tongue, floor of mouth

122
Q

What term describes lesions that demonstrate scattered red patches and are associated with leukoplakias?

A

Erythroplakia (can;’t be diagnosed as any other condition)

123
Q

Why are erythroplakias red?

A

Those areas represent sites in which epithelial cells are so immature they can no longer produce keratine

124
Q

What term describes lesions that demonstrate white and red patches are are associated with leukoplakias?

A

Erytholeukoplakias (can’t be diagnosed as any other condition)

125
Q

What term describes multiple keratotic plaques with roughened surface projections and is a high-risk form of leukoplakia?

A

Proliferative verrucous leukoplakia

126
Q

How do proliferative verrucous leukoplakis progress?

A

Lesions slowly spread through out the mouth, and as the lesion progress, carcinoma can develop

127
Q

Are men or women more likely to have proliferative verrucous leukoplakia?

A

Women are about 4x more likely, there is no association withe tobacco use

128
Q

What is the treatment of proliferative verrucous leukoplakia?

A

It is difficult to treat. This condition must continually be biospied and will eventually turns into cancer

129
Q

What is the gradient of risk for malignancy of leukoplakias?

A

leukoplakia< erythroleukoplakia< erythroplakia

130
Q

Why should non invasive screening techniques (cytologic testing) not be used as substitutes for biopsies?

A

Because it is easy to miss pathology and so it is not worth the risk.

131
Q

Describe the differences in alteraions between mild dysplasia, moderate dysplasia , severe dysplasia, and carcinoma in situ.

A

Mild = lower 1/3
Moderate = lower 1/2
Severe = in the upper 1/2
Carcinoma in situ = alterations are present throughout the epithelium

132
Q

At what point should leukoplakia be completely removed?

A

When biopsy tissue exhibits moderate epithelial dysplasia

133
Q

Why is long term follow up of leukoplakia important?

A

Recurrences are frequent, additional leukoplakias may develop, and about 5% of leukoplakias become SCCA within 2-4 years

134
Q

What are some factors that increase the risk for cancer in leukoplakia?

A

Persistence over years, female, nonsmoker, oral floor or ventral tongue lesions

135
Q

What are the most common locations of erythroplakia?

A

Floor of mouth, ventral tongue, soft palate

136
Q

True erythroplakias are never _______ _______.

A

True erythroplakias are never completely benign

137
Q

In what population does erythroplakia commonly occur in?

A

Middle aged to older adults

138
Q

What causes the red color in erythroplakia?

A

Lack of keratin and epithelial thinness allows underlying vasculature to show

139
Q

What is the treatment for erythroplakia?

A

Biopsy is mandatory –> surgical excision

140
Q

Why is long term follow up of erythroplakia important?

A

Recurrence and multifocal oral involvement is common

141
Q

What term describes lesions from smokeless tobacco?

A

Smokeless tobacco keratosis

142
Q

What characteristics are common in smokeless tobacco keratosis, besides the tobacco pouch keratosis?

A

Gingival recession, destruction of facial alveolar bone, brown-black extrinsic stain on teeth, halitosis

143
Q

When should tobacco keratosis lesions be biopsied?

A

For more severe lesions, or when a lesion remains after 2 weeks of cessation

144
Q

What is the risk of epithelial dysplasia for tobacco keratosis?

A

Epithelial dysplasia is uncommon

145
Q

How is tobacco keratosis treated?

A

Habit cessation, or alternating the site of tobacco placement

Oral Pathology - My deck (22 decks)

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