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Oral Pathology > Epithelial Pathology > Flashcards

Epithelial Pathology Flashcards

1
Q

ephildes

A

common, small pigmented macules of skin

freckles

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2
Q

transmission of ephelides

A

autosomal dominent predlication

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3
Q

demographics of ephelides

A

blue eyes, fair skin, red or light blond hair

young adutls

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4
Q

clinical features of ephelides

A
  1. face / arms / back
  2. excess melanin in basal cells of epidermis (no increase in melanocytes)
  3. 3-4mm in diameter, sharply demarcated, light brown
  4. from less than 10 to hundreds
  5. lesions darken on sun exposure and lighten in shade
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5
Q

prognosis of ephelides

A

do not progress to melanoma
no treatment necessary

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6
Q

synonyms of actinic lentigo

A

senile lengigo
age spots
liver spots
solar lentigo

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7
Q

etiology of actinic lentigo

A

associated with chronic VU light damage (happens in sun exposed areas - face, dorsum of hands, arms)

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8
Q

demogrpahics of actinic lentigo

A

90% of whites over 70 years of age

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9
Q

clinical features of actinic lentigo

A
  1. benign brown skin macule, even pigmented
  2. well demarcated, border may be regular or irregular
  3. no darkening on sun exposure (unlike ephelides)
  4. 5mm - 1cm
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10
Q

prognosis of actinic lentigo

A

no progression ot melanoma
no treatment required unless for esthetic reasons

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11
Q

actinic chelitis

A

lower lip vermilion counterpart of actinic keratosis

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12
Q

etiology of actinic keratosis

A

cumulative UV radiation induced skin damage

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13
Q

histopathology of actinic keratosis

A

hyperkeratosis with some degree of epithelial dysplasia or even superficially invasive squamous cell carcinoma

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14
Q

demographics of actinic keratosis

A

50% of white adults with history of significant lifetime sun exposure

uncommon under 40 years of age

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15
Q

demographics of actinic cheilitis

A

uncommon under 45 years

almost 10:1 male predilection (due to outdoor / sunlight exposure)

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16
Q

clinical features of actinic keratosis

A

common areas: face neck, hands, bald scalp skin

irregular scale like plaques with sandpaper like texture

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17
Q

clinical features of actinic cheilitis

A

areas of vermillion
obliteraiton of margin between vermilion of lip and skin
chronic scaling
crusting
ulceration
fissuring of lip

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18
Q

treatment of actinic keratosis

A

precancer

cryotherapy, electrocautery, topical agents

long term follow up necessary

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19
Q

treatment of actinic cheilitis

A

lip shave (vermilionectomy)

6-10% cases will progress to lip cancer

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20
Q

different types of eptihelial skin cancers

A

basal cell carcinoma
squamous carcinoma
melanoma

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21
Q

most common type of epithelial skin cancer

A

basal cell carcinoma

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22
Q

etiology of epithelial skin cancer

A

sun exposure

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23
Q

body surfaces affected by BCC

A

80% of skin on face

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24
Q

associations of BCC

A

nevoid basal cell carcinoma syndrome (tumor suppressor gene PTCH1 mutation)

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25
Q

clinical appearance of BCC

A

firm painless papule enlarges with a central depression and rolled borders

umbilication with resultant ulceration - rodent ulcer

fine blood vessels over lesion

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26
Q

MOHs surgery

A

moh’s micrographic surgery for best esthetic results for BCC

excellent aesthetics with this procedure

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27
Q

melanomas

A

-malignancy of melanocytic differentiiation
-most are cutaneous; 3rd most common skin cnacer
-5% of skin cancers; 65% of deaths due to skin cancer
-fair skin patient, 40-70 years

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28
Q

etiology of cutaneous melanoma

A

malignancy of melanocytic differentation

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29
Q

predisposing factors fo cutaneous melanoma

A

-acute sun damage with blistering sunburn early in life
-tendency to burn easily
-indoor occupation; outdoor recreation
-family history
-personal history

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30
Q

statistics of cutaneous melanoma

A

93.3% 5-year survival (because people are aware)

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31
Q

ABCDE of cutaneous melanoma (clinical description)

A

asymmetry
border irregularity
color variation
diameter greater than 6mm
evolving rapidly in shape / size / color / surface

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32
Q

amelanotic melanoma

A

-lack pigment
-challenging to diagnose
-will require immunological stains for accurate diagnosis
-melanoma with ZERO pigment

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33
Q

acral lentiginous melanoma

A

8% of melanomas
-affect palms, soles, oral mucosa (no relation to soalr exposure)
-MOST COMMON CLINICOPATHOLOGIC TYPE OF MELANOMA IN PERSONS OF COLOR
-begins as darkly pigmented macule with irregular borders

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34
Q

cutaneous melanoma treatments

A

-surgical excision with / without lymph nodes
-chemotherapy, radiation therapy with little impact on the disease
-biologica agents ot boose immune system

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35
Q

breslow’s depth of invasion

A

determines prognosis of melanoma

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36
Q

seborrheic keratosis

A

common skin condition (does not occur on mucosa)

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37
Q

transmission of seborrheic keratosis

A

some cases are hereditary (autosomal dominant)

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38
Q

demographics of seborrheic keratosis

A

onset during the 4th decade of life
become more pregalent thereafter

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39
Q

clinical features of seborrheic keratosis

A

-most common on skin of face / trunk / extremities
-begins as small pigmented macules and evolve to enlarge and raise with fine fissured, pitted surface
-stuck on dirty candle wax

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40
Q

dermatosis papulosa nigra

A

-form of seborrheic keratosis in about 30% of blacks
-autosomal dominant trait
-multiple small pigmented papules over skin of zygoma

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41
Q

treatment of seborrheic keratosis

A

no treatment required, except for esthetic purposes

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42
Q

caution with seborrheic keratosis

A

melanomas may look like seborrheic keratosis

sudden eruptions of multiple seborrheic keratosis with pruritus (leser-trelat sign) associated with internal malignancy

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43
Q

squamous papilloma

A

most common benign intraoral epithelial neoplasm

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44
Q

relationship of squamous papilloma with HPV

A

may / may not show human papilloma virus

direct cause / effect is uncertain

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45
Q

clinical features of squamous papilloma

A

solitary lesion, typically found on soft palate / uvula or tongue
-finger like fronds, usually pedunculated, may be sessile
-range of color (reddish to white)

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46
Q

histology of squamous papilloma

A

-orthokeratinized or parakeratinized surface
-papillary proliferation of surface epithelium
-finger like projections of fibrous CT that support the epithelial proliferation

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47
Q

treatment of squamous papilloma

A

conservative excision, including base of lesion

prognosis is excellent

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48
Q

HPV

A

DNA virus
nearly 100 subtypes

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49
Q

HPV types

A

24 types, specifically infect genital and oral mucosa
tropism for epithelial cells

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50
Q

high risk types of HPV

A

16, 18, 31

stornlgy associated with cervical, anogenital and some oropharyngeal cancers

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51
Q

modes of transmission of HPV

A

sexually transmitted

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52
Q

immunization (vaccine) of HPV

A

gardasil
immunization of girls and boys at ages 11 / 12

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53
Q

verruca vulgaris common name

A

common wart

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54
Q

causes of verruca vulgaris

A

common lesion caused by several strains of HPV

HPV 2 / 4 / 6 / 40

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55
Q

clinical features of verruca vulgaris

A

-frequently affects children - hands and facial skin
-usually sessile, exophytic, papillary lesion; often multiple

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56
Q

transmission of verruca volgaris infection

A

contagious
autoinoculation

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57
Q

classic histopathology of verruca vulgaris

A

-hyperkeratotic epithelium raised into finger-like proections
-elongated rete pegs converge towards center of lesion producing a “cupping” effect
-prominent granular cell layer with coarse, clumped keratohyalin granules
-koilocytes

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58
Q

koilocytes

A

virally infected cells with pyknotic nuclei and clear perinuclear cytoplasm

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59
Q

treatment of verruca vulgaris

A

spontaneous regression common in kids

excision, cryotherapy, keratolytic agents
may recur

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60
Q

HPV types associated with multifocal epithelial hyperplasia

A

13 and 32

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61
Q

ethnic predilection of multifocal epithelial hyperplasia

A

isolates of native indians of north and central america and brazil

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62
Q

clinical features of multifocal epithelial hyperplasia

A
  1. multiple sessile, pink and white, papules of the gigniva, buccal and labial mucosa
  2. asymptomatic
  3. mostly found in children, may be foudn in older patients
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63
Q

Transmission of multifocal epithelial hyperplasia

A

HPV virus - contiguous contact of one mucous membrane and another

Between people → between objects (ex. Food, fomites)

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64
Q

mitosoid bodies

A

cells with unusual arrangement of nuclear chromatin resembling abnormal mitotic figures (mitosoid bodies) seen n spinous layer

associated with multifocal epihtelial hyperplasia

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65
Q

Management of multifocal epithelial hyperplasia

A

Tend to regress spontaneously
Topical interferon application

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66
Q

Condyloma

A

gnital warts
venereal warts

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67
Q

Modes of transmission of condyloma acuminatum

A

Spread by direct contact

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68
Q

HPV types involved with condyloma acuminatum

A

Caused by any one of several strains of HPV

High risk strains (HPV 16 and 18) associated with cervical carcinoma

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69
Q

clinical features of condyloma acuminatum

A

-may affect oral mucosa
-usually diagnosed in teenagers and young adults
-clinically presented as multiple sesile papules or plaques with cauliflower-like surface
-affect the labial mucosa, soft palate, and lingual frenum most common

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70
Q

koilocytes

A

Histopathologically, characterized by parakeratotic papillary proliferation of surface epithelium with blunted fronds, acanthosis, broad rete ridges, and increased mitosis

Perinuclear clearing (koilocytosis) is seen in the cells of the spinous layer

associated with condyloma

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71
Q

Molluscum contagiosum

A

common cutaneous infection caused by DNA poxvirus

72
Q

Demographics of molluscum contagiosum

A

Usually seen in children and young adults

73
Q

Clinical appearance of molluscum contagiosum

A

Multiple pink papules affect the skin of the neck, eyelids, trunk, or genitalia

Each papule as a central core or depression

74
Q

Molluscum bodies

A

-Histopathologically distinctive
-Lobular proliferation of surface epithelium
-Epithelial cells exhibit basophilic “molluscum (henderson-paterson) bodies” that are filled with viral particles
-Move to top of skin and exfoliate → release lots of pox virus (creates divot!)

75
Q

Treatment of molluscum contagiosum

A

Consists of curettage or liquid nitrogen, although lesions often resolve spontaneously in the immune competent host in six to nine months

Very difficult to treat

76
Q

melanotic macule

A

common, harmless lesion that may be seen either ont he lip or intraorally

increased amount of melanin pigment in the basal cell layer of epithelium

77
Q

clinical features of melanotic macule

A

-tan to dark brown, uniformly pigmented, demarcated margins
-no change with sun exposure
-could represent post-traumatic melanosis

78
Q

indications for biopsy fo melanic macule

A

-Lesions on vermilion zone of lip are often excised for cosmetic purposes
-Tissues should be submitted for microscopic examination
-Intraoral lesions may need to be excised to rule out early melanoma

79
Q

demogrpahics of melanoacanthoma

A

young, adult african american females

80
Q

Clinical features of melanoacanthoma

A

Occurs on skin and oral mucosa
Dark macule to patch that often arises rapidly
Mimics melanoma

81
Q

Histopathology of melanoacanthoma

A

Long dendrites

82
Q

Treatment of melanoacanthoma

A

Biopsy to establish diagnosis
Spontaneous resolution may be seen following biopsy

83
Q

Prognosis of melanoacanthoma

A

Subsequent additional lesions may arise in same patient

84
Q

acquired melanocytic nevus

A

moles

-One of the most common lesions
-Average 20/person in caucasians
-My develop from first year of life through the fourths decade
-Oftn involute with aging

85
Q

acquired melanocytic nevi types

A

functional
compound
intradermal

86
Q

junctional nevi

A

first stage, appear flat and usually appear dark

-function of epithelium and CT
-nevus cells present among basal epithelial cells

87
Q

compoudn nevus

A

may evolve from jucntioanl nevus as the patient grows older

-proliferaiton of nevus occurs with some of the nevus cells dropping off into the superficial CT
-may begin to dhow elevation clincially

88
Q

intradermal nevus

A

with time, nevus cells may proliferate to the extent that they are completley contained within the dermal CT

-elevated, with variable degree of pigmentation (many are normal skin color)
-no more nevus cells left in epithelium

89
Q

intraoral presentation of acquired melanocytic nevus

A

infrequently, melanocytic nevi can develop in oral cavity

usually located on the hard palate or attached gingiva, but potentially any site an be affected

90
Q

management of acquired melanocytic nevus

A

no treatment absolutely neceesary

91
Q

risk fo malignant transformation of melanocytic nevus

A

1 in a million

changes in nevus or chronic irritation of a nevus would be reason for excision biopsy

92
Q

congenital melanocytic nevi

A

type of melanocytic nevus present at birth

1% of newborns

93
Q

small vs large nevi

A

designated as large or small, with small <15cm being uch more common

large congenital nevus is also known as “garment nevus” or “bathing trunk” nevus due to extensive involvement on patient’s skin

94
Q

risk of malignant transformation for congenital melanocytic nevi

A

high
1% for small
15% for large

95
Q

treatment of congenital melanocytic nevi

A

staged excision for large
excision for small

96
Q

blue nevi

A

-may affect any cutaneous mucosal site
-appear blush / gray due to depth of the melanin pigment
-simpel excision
-excellent prognosis

97
Q

nicotine stomatitis

A

white patch of posteiror hard palate and soft palate

98
Q

Etiology of nicotine stomatitis

A

Acute onset
Secondary to heat of pipe / cigar, cigarette

99
Q

Clinical features of nicotine stomatitis

A

Numerous pinpoint red areas signify inflamed openings of ducts of minor mucous glands of the palate

100
Q

Management of nicotine stomatitis

A

Resolves spontaneously

101
Q

Any malignant potential?

A

no

102
Q

Tobacco pouch keratosis

A

due to placement of quid containing smokeless tobacco

Wrinkled, corrugated hyperkeratosis
Does not show clear margin from surrounding mucosa
Asymptomatic

103
Q

types of smokeless tobacco that have hgher cancer / precancer rates

A

loose leaf tobacco
dry snuff

104
Q

Leukoplakia (definition)

A

white patch of oral mucosa that cannot be scraped off and cannot be diagnosed clinically or microscopically as any other condition

105
Q

White lesions that are not leukoplakia

A

Leukoderma (blend with surroundings, less severe when stretched)

cheek chewing (rigid boundary)

frictional / ridge keratosis, nicotine stomatitis, smokeless tobacco, keratosis

106
Q

Common sites in the oral cavity for oral precancer and cancer

A

Lateral tongue
Ventral tongue
Floor of mouth
Anterior pillar of tonsils
Lateral soft palate

107
Q

Histology of leukoplakia (dysplasia)

A

Typically some degree of hyperkeratosis (wet keratin appears white)

Pre Cancerous changes may be evident microscopically - epithelial dysplasia

Mild (low grade), moderate, severe dysplasia or carcinoma-in-situ (high grade)

108
Q

clinical features of leukoplakia

A
  1. sharply demarcated white plaques with smooth, verrucous or micronodular surface
  2. crisp margins
  3. cracked mud like appearance (because of movement)
109
Q

speckled leukoplakia

A

if red component is present

110
Q

low grad dysplasia

A

not as many changes from normal

111
Q

high grade dysplasia

A

large change from normal (poorer prognosis)

treated just like cancer

112
Q

when to complete excision for leukoplakia

A

when high grade / cancer

113
Q

how to take incisional biopsy from leukoplakia

A

from different areas of the lesion

different portions of lesion will behave differently

114
Q

management of low grade dysplasia

A
  1. discontinue carcinogenic habits and frequent follow up
  2. biopsy if any progressive change (ex increase in size, thickening, ulceration, erosion, pain, mobility of tooth, exophytic growth, atlered sensation)
115
Q

management of high grade dysplasia

A

remove by the most convenient means available

submit tissue for assessment of margins

116
Q

prognosis of leukoplakia

A
  1. prognosis is guarded
  2. 33% of dysplastic lesions will transform to squamous cell carcinoma
  3. 30% of leukoplakia will recur
117
Q

dysplasia

A

altered development

118
Q

dysplasia in context of cancer

A

signifies disorder at cellular and tissue level

microscopically identifiable as changes associated with premalingancy / malignancy

119
Q

cellular changes of precancer / cancer related dysplasia

A
  1. abnormal variation in nuclear size and shape
  2. abnormal variation in cell size and shape
  3. increased nuclear / cytoplasmic ratio
  4. hyperchromatic nuclei
  5. increased mitotic figures
  6. abnormal mitotic fitures
120
Q

arthitectural (tissue) changes of precancer / cancer related dysplasia

A
  1. disordered maturaiton from basal to squamous cells
  2. increased cellular density
  3. basal cell hyperplasia
  4. dyskeratosis
  5. bulbous drop shaped rete pegs
  6. acantholysis
121
Q

hallmark of squamous carcinoma

A

compromise of basement membrane

122
Q

clinical features of proliferative verrucous leukoplakia

A
  1. uncommon, high risk presentation
  2. extensive and often multiple keratotic plques in older adults
  3. hyperkeratosis / hyperplasia with variable dysplasia
123
Q

age impacted by PVL

A

females (mean age 65 years)
males (mean age 49 years)

124
Q

gender impacted by proliferative verrucous leukoplakia (PVL)

A

female predilection (4:1) with only 1/3 having traditional risk factors

125
Q

risk factors for PVL

A

no history of alcohol or tobacco use
common in post-menopausal women

126
Q

treatment of PVL

A
  1. optimal treatment remains to be determined
  2. surgical or ablative therapy, but recurrence common
  3. malignant transformation is frequent complication, even in lesion without previous biopsy evidence of dysplasia
127
Q

prognosis of proliferative veracious leukoplakia - high risk presentation

A

100% will transform to carcinoma

70% of patients developed SCCa within 8 years (40% died as result of carcinoma)

128
Q

erythroplakia

A

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

more serious than leukoplakia

129
Q

etiology of erythroplakia

A

pipe smoking

130
Q

management and prognosis of erythroplakia

A

treatment and prognosis are similar to leukoplakia having a siilar degree of epihtelial

can be excised
patient education is important!

131
Q

causes of sanguinaria leukoplakia

A

associated with use of extract of native indian bloodroot

132
Q

what is sanguinaria found in

A

herbal oral health care products

133
Q

clinical features of sanguinaria leukoplakia

A
  1. homogenous white patch
  2. slight “cracked mud” like appearance
  3. distinct margin
  4. cannot scratch away (not a pseudomembrane)
134
Q

common sites of sanguinaria leukoplakia

A

maxillary gingiva
canine
premolar region

135
Q

sanguinaria vs leukoplakia

A
  1. sites differ
  2. clinically identical to leukoplakia
  3. to be managed like leukoplakia
  4. complete excision with clear margins
  5. close follow up for recurrence or new lesions
136
Q

SCC

A

most common oral malignancy and second most common cutaneous malignancy

137
Q

SCC arises from ____

A

surface epithelial cells

138
Q

etiology of SCC

A

arises from pre-existing actinic keratosis in many instances

due to chronic sun (UV light) exposure

139
Q

common sites of SCC

A

face
helix of ear
dorsum of hands and arms are common sites

140
Q

management of SCC

A
  1. treatment consists of surgical excision
  2. actinically induced SCC generally are well differentiated and grow slowly
  3. prognosis is generally very good if lesion is identified early in course
141
Q

intraoral SCC is known as

A

oral cancer

142
Q

statistics of SCC

A
  1. intraoral squamous cell CAs are usually (75-80%) associated with tobacco cigarettes, with or without alcohol
  2. significant percentage (25-30%) are not associated with any identifiable risk factors - usually lateral tongue of younger people or gingiva of older women
143
Q

etiology of intraoral SCC

A

tobacco
reverse smoking
pipe moking
UV

144
Q

associations of SCC with systemic conditions

A

plummer vinson syndrome
graft vs host disease
syphilitic glossitis
submucous fibrosis
preivous radiation
chronic inflammation, poor oral hygiene

145
Q

demographics of oral SCC

A
  1. oral SCC accounts for 2-4% of all cancers in the US
  2. most occur in older adults
  3. men outnumber women by 2:1 ratio
146
Q

clinical features of carcinoma of oral SCC

A
  1. irregular shape, mixture of red and white clinically
  2. often ulcerated
  3. exophytic (Growing out) or endophytic (growing in) growth pattern
  4. often much firmer than surrounding tissues
  5. early lesions are asymptomatic
147
Q

differential diagnosis of oral SCC

A
  1. nonspecific ulcer
  2. specific indications (TB, histoplasmosis, syphilis)
  3. immune mediated conditions (wegen’ers, crohn’s)
  4. carcinoma should be #1 in differential! (take biopsy!)
148
Q

radiographic features of SCC bone involvement

A
  1. ragged radiolucency is characteristic of bone involvement
  2. due to direct invasion of bone (usually late phenomenon)
149
Q

histopathology of carcinoma

A
  1. microscopically, invades cords and nests of malignant squamous epithelial cells arise from dysplastic surface epithelium
  2. tumor cells show an increase nuclear / cytoplasmic ratio, cellular and nuclear pleomorphism, and mitotic activity
  3. varying degrees of keratin seen
  4. intravascular, lymphatic, and perineural invasion may be seen
150
Q

SCC of lip

A
  1. one of more common sites of involvement
  2. secondary to ultraviolet light exposure
  3. arises in the setting of actinic cheilitis
  4. slow growing, well differentiated lesion
151
Q

SCC of tongue

A
  1. majroity of patients have history of cigarette smoking and alcohol abuse
  2. when oral SCCa is seen in younger (<40) people, almost always develops at tongue
152
Q

SCC of floor of mouth

A
  1. almost equal to lateral tongue as common site fo oral SCCa
  2. most patients have history of cigarette smoking and alcohol abuse
153
Q

SCC of gingiva / alveolar mucosa

A
  1. unusual site epidemiologically for oral SCCa
  2. more common in women at this site
  3. more common in patients with no identifiable risk factors for oral SCCa
154
Q

SCC of buccal mucosa

A

not very common site

155
Q

SCC of palate

A
  1. most SCCa’s affecting the palate arise on the lateral soft palate
  2. rather rare to find this malignancy on the hard palate
  3. may be different to determine whether lesion developed in maxillary sinus and invaded the floor
156
Q

staging helps

A

to dsicern extent of cancer

157
Q

how to stage cancer

A
  1. size of tumor (T)
  2. involvement of regional lymph nodes (N)
  3. whether the cancer has spread to different parts of body (M)
  4. depth of invasion
158
Q

parameters for depth of invasion

A

if less than 5mm, fine! (stay at current staging)

more than 5mm, T value goes up by 1

159
Q

neck level 1a

A

submental

160
Q

neck level 1b

A

submandibular

161
Q

neck level IIa

A

upper jugular (anterior)

162
Q

neck level IIb

A

upper jugular (posterior)

163
Q

neck level III

A

mid jugular

164
Q

neck level IVA

A

lower jugular

165
Q

neck level IVB

A

medial supraclavicular

166
Q

neck level VA

A

upper posterior triangle

167
Q

neck level VB

A

lower posterior triangle

168
Q

neck level VC

A

lateral supraclavicular

169
Q

neck level VI

A

anterior cervical

170
Q

nek level VIIA

A

retro-pharyngeal

171
Q

neck level VIIB

A

retrostyloid

172
Q

nek level VIII

A

parotid

173
Q

neck level IX

A

bucco-facial

174
Q

neck level XA

A

retro-auricular

175
Q

neck level XB

A

occipital

176
Q

treatment of oral carcinoma

A

wide surgical excision / radiation therapy

neck node dissection is based on staging
chemotherapy not much impact

177
Q

prognosis of oral cancer

A

one of the worse cancer prognosis

67% 5-year survival rate

Oral Pathology (14 decks)

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