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Oral Pathology Exam 1 > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

“Textbook” progression of leukoplakias (3 steps)

A
  1. Thin LPs
  2. Thick/homogeneous
  3. Granular/nodular or verrucous/verruciform
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2
Q

Pts with oral submucous fibrosis are ____x more likely to develop SCC

A

19x more likely

This is why it is a high risk lesion

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3
Q

What is the 1 cell in the body that shows reverse polarization

A

Ameloblast

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4
Q

Actinic cheilitis (cheilosis)

A

PREMALIGNANT lesions on lip due to chronic UV exposure

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5
Q

6 histologic features of Granular, Verruciform Leukoplakia

A
  1. Irregular (verruciform) hyperkeratosis
  2. Bulbous rete pegs
  3. Lymphocytes (mod #s)
  4. Mod/severe dysplasia
  5. Congested vessels
  6. Candida hyphae (maybe)
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6
Q

Of the 95% of leukoplakias that are NOT malignant at 1st biopsy, about ___% undergo subsequent malignant transformation

A

5%

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7
Q

In TNM staging, what does TNM stand for?

A 
T = tumor size in cm
N = regional lymph node involvement
M = distant metastasis
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8
Q

What is the main diagnostic feature (microscopically) of focal epithelial hyperplasia (hecks disease)

A

Mitosoid bodies

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9
Q

Erythroleukoplakia (speckled leukoplakia)

A

Leukoplakia with patches of redness

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10
Q

Incidence of proliferative verrucous leukoplakia

A

4x more in females

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11
Q

Cause of verruciform xanthoma

A

Unknown

Most likely reactive or immune response to trauma

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12
Q

The risk for oral SCC in smokeless tobacco users is ____ compared to smoking

A

Less

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13
Q

4 other symptoms associated with smokeless tobacco keratosis

A
  1. Gingival recession
  2. Periodontitis
  3. Caries
  4. Tooth wear
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14
Q

Idiopathic leukoplakia incidence

A

Pts >40 yrs

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15
Q

What role does smoking play in proliferative verrucous leukoplakia

A

No/minor role

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16
Q

Which HPV subtypes may be causative factors for proliferative verrucous leukoplakia?

A

HPV 16 + 18

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17
Q

Acanthosis

A

Diffuse epidermal hyperplasia

Aka thicker epithelium

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18
Q

Betel quid/Guthka

A

*cause of oral submucous fibrosis

Betel leaf, areca nut, slaked lime, catechu, tobacco? Sweeteners?

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19
Q

4 features of Muir Torre syndrome

A
  1. Autosomal dominant
  2. Cutaneous tumors of sebaceous origin
  3. Visceral malignant diseases
  4. Multiple keratoacanthomas
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20
Q

Definition of idiopathic leukoplakia

A

Clinical white lesion that does not rub off + cannot be characterized clinically as any other disease

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21
Q

Leukoplakia is _______

A

PREMALIGNANT

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22
Q

Incidence of oral submucous fibrosis

A

India, South East Asia (where ppl use betel quid)

Young pts

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23
Q

HPV associated oral cancers are different from the others how?

A

Better prognosis

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24
Q

The single most effective measure to lower the risk for oral cancer is…

A

Reduce exposure to tobacco + alcohol

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25
Q

Actinic cheilitis (cheilosis) has the same pathology as ______ but in a different location

A

Actinic keratosis

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26
Q

____% of the dysplasia that present as clinical leukoplakias (thick + granular) will undergo malignant transformation

A

10-15%

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27
Q

Where do you see sanguinaria associated keratosis

A

Mx buccal vestibule

Mx alveolar ridge

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28
Q

Names for a raised lesion

A

Papule

Nodule

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29
Q

3 high risk sites of erythroplakia

A
  1. Floor of mouth
  2. Tongue
  3. RMP
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30
Q

6 danger signals of malignant transformation

A
  1. No cause (risk factors)
  2. Causative agent carcinogen
  3. Location (high risk sites)
  4. Ulceration
  5. Induration
  6. Redness (erythroplakia)
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31
Q

10 signs of epithelial dysplasia

A
  1. Hyperchromatism (dark nuclei)
  2. Pleomorphism (abnormal shape nuc)
  3. Increased nuclear/cytoplasmic ratio
  4. Dyskeratosis (prematrue keratinization)
  5. Increased mitotic activity
  6. Abnormal mitotic figures
  7. Loss of polarity
  8. Bulbous rete pegs
  9. Keratin pearls
  10. Loss of epithelial cell cohesiveness
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32
Q

7 intrinsic risk factors for oral cancer

A
  1. Iron deficiency (plummer vinson syndrome)
  2. Vitamin A defiency
  3. Bacteria (tertiary stage syphilis)
  4. Candida
  5. HPV 16 + 18
  6. Immunosuppression (HIV, drugs)
  7. Oncogenes + tumor suppressor genes
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33
Q

HPV positive tumors have a better prognosis bc…

A

Respond v well to radiation + chemo

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34
Q

Red lesions are red because

A

Epithelium is thin = close to blood vessels

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35
Q

What are the 2 clinical forms of focal epithelial hyperplasia (hecks disease) and how many/where are the lesions

A

Papulonodular
Papillomatous

Multiple lesions on lips, tongue, gingiva, tonsils (typically in anterior)

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36
Q

What cancer can develop from smokeless tobacco keratosis? Risk?

A

Oral squamous cell carcinoma (verrucous)

4x more risk vs. non users (but NOT as high as smoking)

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37
Q

3 microscopic features of focal epithelial hyperplasia (hecks disease)

A
  1. Nodular broad based mass of oral mucosa
  2. Numerous mitosoid bodies
  3. Viral like cytopathic change
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38
Q

4 histologic features of verruciform xanthoma

A
  1. Papillary acanthotic epithelium
  2. Hyperparakeratosis
  3. Clefts + crypts noted
  4. Xanthoma (foam) cells in CT papilla
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39
Q

Metastasis from the posterior mouth occurs through…

A

Superior jugular nodes

Digastric nodes

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40
Q

HPV positive tumors are diagnosed…(6) (compared to HPV negative tumors)

A
  1. Dx @ younger age
  2. Low prevalence of amoking/alch use
  3. Dx @ more advanced TNM stage
  4. Dx @ smaller tumor size
  5. With lumph node positivity
  6. Presence of metastases
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41
Q

Name for a lesion with an irregular surface

A

Papillary

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42
Q

Does every cancer have a precancerous lesion?

A

No

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43
Q

Which 2 conditions increase the risk for development of actinic cheilitis (cheilosis)

A

Xeroderma pigmentation

Albinism

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44
Q

3 histologic features of Thin, Smooth Leukoplakia

A
  1. Hyperkeratosis
  2. Acanthosis (thick epi)
  3. Lymphocytes (sometimes)
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45
Q

Which parts of the tongue are high risk for oral cancer

A

Lateral border

Ventral

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46
Q

What are the 3 theories that explain why HPV positive oropharyngeal cancers respond better to chemo?

A
  1. Low rates of genomic damage
  2. Absence of field cancerization
  3. Presence of immune responses to HPV antigens
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47
Q

8 premalignant + related lesions of the oral mucosa

A
  1. Leukoplakia
  2. Proliferative verrucous leukoplakia
  3. Erythroplakia
  4. Smokeless tobacco keratosis
  5. Oral submucous fibrosis
  6. Nicotine stomatitis
  7. Actinic cheilitis/keratosis
  8. Keratoacanthoma
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48
Q

Nicotine stomatitis clincal presentation

A

Diffuse grey/white mucosa with red punctate papules (= inflamed minor salivary glands + their ductal orifices) on PALATE

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49
Q

Incidence of nicotine stomatitis

A

Men >45 yrs

Pipe + cigar smokers

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50
Q

Hyperchromatism

A

Dark staining nuclei

*sign of epithelial dysplasia

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51
Q

Plummer vinson syndrome

A

Iron deficiency

Risk factor for oral cancer

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52
Q

HPV positive tumors are ____ differentiated

A

Poorly differentaited

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53
Q

What are molluscum bodies

A

Histo feature of molluscum contagiosum

Large intranuclear inclusions inside bloated keratinocytes

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54
Q

How does transmission of molluscum contagiosum vary in different populations

A

Teens/adults = sexual
Kids = nonsexual contact
Immunocompetent pts = warm + humid environments

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55
Q

Are smokeless tobacco keratosis lesions reversible?

A

Yes

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56
Q

Explain the theory that HPV+ tumors respond better to chemo bc of the presence of immune responses to HPV antigens

A

Immune responses to E6 + E7 oncoproteins help in improved tx responses + px

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57
Q

Where do Keratoacanthomas originate from in the skin? Oral mucosa?

A

Skin = pilosebaceous apparatus

Oral mucosa = ectopic sebaceous glands? (FG)

58
Q

Explain the theory that HPV+ tumors are more responsive to chemo because they have an absence of field cancerization

A

HPV believed to arise from limited foci of infection = less 2nd malignancies

59
Q

3 high risk sites for oral cancer

A
  1. Floor of mouth
  2. Tongue (lateral border + ventral)
  3. Soft palate
60
Q

What is the most common malignancy in the mouth

A

Squamous cell carcinoma

61
Q

4 histologic features of Thick, Fissured Leukoplakia

A
  1. Hyperkeratosis
  2. Acanthosis (thick epi)
  3. Lymphocytes (sometimes)
  4. Mild/mod dysplasia
62
Q

Why are white lesions white?

A

Because the epithelium is thickened = further away from blood vessels

63
Q

Types of HPV assoc with Focal Epithelial Hyperplasia (Heck’s disease)

A

HPV 13 + 32

64
Q

90% of leukoplakias show dysplasia or carcinoma in these 3 locations

A
  1. Tongue
  2. Lip vermillion
  3. Floor of mouth
65
Q

2 Tx’s for focal epithelial hyperplasia (hecks disease)

A

Spontaneous regression

Conservative excision

66
Q

Why must all erythroplakias be biopsied?

A

Can’t distinguish clinically

ALMOST ALWAYS squamous cell carcinoma or in situ carcinoma

67
Q

3 reasons why proliferative verrucous leukoplakia is a high risk oral lesion

A
  1. No absolutely predictive histologic pattern
  2. No tests to prove likely progression
  3. Must be re-evel v often + totally removed in recurs
68
Q

How does metastasis of oral squamous cell carcinoma occur?

A

Through the lymphatics to the ipsilateral cervical lymph nodes

69
Q

Cases of molluscum contagiosum are _____ in HIV pts (5-18%)

A

Florid

70
Q

Clinical differential diagnoses of verruciform xanthoma (3)

A

Papilloma
Condyloma
Early carcinoma

71
Q

Multiple keratoacanthomas are a feature of what syndrome?

A

Muir Torre syndrome

72
Q

7 histologic features of Erythroleukoplakia (speckled LP)

A
  1. Irregular hyperkeratosis
  2. Bulbous + crowded rete pegs
  3. Epithelial atrophy
  4. Lymphocytes (mod-numerous)
  5. Severe dysplasia
  6. Carcinoma in situ?
  7. Congested vessels
73
Q

What is different about nicotine stomatitis caused by ‘reverse smoking’

A

Severe keratosis

PREMALIGNANT (otherwise isn’t)

74
Q

Is nicotine stomatitis premalignant?

A

By itself = not premalignant

If caused by ‘reverse smoking’ it IS premalignant

75
Q

Speckled erythroplakia is ALMOST ALWAYS…

A

Carcinoma in situ or squamous cell carcinoma

76
Q

Almost all of oropharyhngeal carcinomas are related to…

A

HPV

77
Q

Traumatic (frictional) hyperkeratosis

A

Hyperplastic response (similar to callus) to chronic mechanical irritation

Reversible after stopping trauma

78
Q

3 histologic features of nicotine stomatitis

A
  1. Hyperkeratosis
  2. Chronic inflammation
  3. Salivary duct metaplasia
79
Q

Pleomorphism

A

Abnormal shaped nuclei

*sign of epithelial dysplasia

80
Q

Cause of nicotine stomatitis

A

Develops in response to HEAT (from pipe/cigars)

81
Q

Symptoms of oral submucous fibrosis

A

Trismus (can’t open) + burning followed by v stiff + blotchy mucosa

Tongue can be stiff + immobile

Leukoplakic lesions can develop

82
Q

What are the 2 things that the MDH says about oral cancer?

A
  1. Most cases are preventable

2. The single most effective measure to lower the risk is to reduce exposure to tobacco and alcohol

83
Q

3 different histologic presentations of erythroplakia (in order from most common to least)

A
  1. 50% Squamous cell carcinoma
  2. 40% severe dysplasia or in situ carcinoma
  3. 10% mild/mod dysplasia
84
Q

Verruciform xanthoma presents in ____ much more than any other site as small lesions <2 cm

A

Gingiva

85
Q

Erythroplakia is usually seen in which pts

A

50-70 yrs

86
Q

Metastasis from the lower lip + floor of mouth happens through…

A

Submental nodes

87
Q

How does molluscum contagiosum present clinically

A

Little papules on skin of face, neck, trunk + genetalia

Less often on mucous membranes

88
Q

__% of leukoplakias are malignant at 1st biopsy

A

5%

89
Q

There are wide ranges of risk of transformation from 1 anatomic site to another. How is the floor of the mouth an example of this?

A

In the floor of the mouth, the transformation rates are HIGH but show only minimal dysplasia

90
Q

Sanguinaria associated keratosis

A

TRUE leukoplakia caused by sanguinaria (herb used in certain toothpaste + mouth rinses)

Persist for years even after stopping use

91
Q

2 features of the histology of molluscum contagiosum

A
  1. Lobular proliferation of epithelium

2. Bloated keratinocytes containing large intranuclear inclusions (molluscum bodies)

92
Q

3 histologic features of actinic cheilitis (cheilosis)

A
  1. Epithelium might show dysplasia
  2. CT shows solar elastosis (sun damage)
  3. Chronic inflammation
93
Q

Describe keratoacanthoma lesions

A

1(+)
Always raised with central depression (cup shaped symmetry)
Verruciform surface

94
Q

Describe Smokeless tobacco keratosis lesion

A

Characteristic white/grey lesion

Velvety feel
Blends w surrounding tissues
Rippled mucosa

95
Q

Molluscum contagiosum can be mistaken for a more localized version of _______

A

Fordyce granules

But FG usually more generalized

96
Q

Clinical presentation of early leukoplakia lesions

A

Thin leukoplakias

Flat/slightly elevated
Greyish white plaque

97
Q

In the US, the majority of oral idiopathic leukoplakias are…

A

Benign + probably will never become malignant

98
Q

Proliferative verrucous leukoplakia is what kind of lesion

A

High risk oral white lesion

99
Q

Does traumatic (frictional) hyperkeratosis, cheek chewing (morsiciatio), or toothbrush trauma of gingiva transform to malignancy?

A

No

100
Q

Verruciform xanthoma is a primarily ____ disease

A

Oral

101
Q

Dyskeratosis

A

Premature keratinization of individual cells (keratin being made before they go up to the cell surface)

*sign of epithelial dysplasia

102
Q

70% of idiopathic leukoplakias happen where? (3)

A
  1. Lower lip vermillion
  2. Buccal mucosa
  3. Gingiva
103
Q

Location of keratoacanthoma

A

Sun exposed skin
Less commonly on mucocutaneous jxn
Rarely intraoral mucosa

104
Q

Keratoacanthoma is a ____ process

A

Squamoproliferative process

105
Q

Erythroleukoplakia (speckled leukoplakia) has a ______ change of dysplasia

A

MUCH higher

106
Q

Clinical term for erythroplakia

A

Idiopathic mucosal red patch

107
Q

What are the 7 high risk sites for malignant transformation (in order)

A
  1. Floor of mouth
  2. Tongue
  3. Lip
  4. Palate
  5. Buccal
  6. Vestibule
  7. Retromolar
108
Q

2% of cases of oral SCC distantly metastasize. What are the 3 common locations?

A
  1. Lung
  2. Liver
  3. Bones
109
Q

Metastasis from the oropharyngeal region occurs through…

A

Jugulodigastric nodes

Retropharyngeal nodes

110
Q

Actinic cheilitis (cheilosis) lesions that show _____ are suspicious for SCC

A

Ulceration

111
Q

Oral cancer is the __ most common cancer in men + ___ most common in women

A

11th most common in men

16th most common in women

112
Q

Progression of proliferative verrucous leukoplakia (5 steps)

*different stages can be present in different sites within the same lesion

A
  1. Clinical leukoplakia
  2. Verrucous hyperplasia
  3. Verrucous carcinoma
  4. Papillary squamous cell carcinoma
  5. Less differentiated squamous carcinoma
113
Q

3 locations for oropharyngeal carcinoma

A
  1. Lateral soft palate
  2. Tonsillar region
  3. Base of tongue
114
Q

6 extrinsic risk factors for oral cancer

A
  1. Smoking
  2. Smokeless tobacco
  3. Betal quid
  4. Alcohol
  5. Occupational exposures (heavy metals)
  6. UV exposure (lip)
115
Q

What 5 diseases must be excluded before you dx leukoplakia

A
  1. Hyperkeratosis (incl frictional)
  2. Candidiasis
  3. Lichen planus
  4. Tobacco pouch keratosis
  5. Hairy leukoplakia
116
Q

Does molluscum contagiosum have malignant transformation?

A

No

117
Q

Thick (homogenous) leukoplakia clinical presentation

A

Progression of thin leukoplakias

Leather like white lesion with distinct borders

⅓ regress

118
Q

Progression of actinic cheilitis (cheilosis) - 4 stages

A
  1. Blotchy, smooth
  2. Dryness + fissures
  3. Blurring of vermillion border
  4. Later stages = scaling, leukoplakic areas, redness, ulceration
119
Q

What organism causes molluscum contagiosum

A

Molluscum contagiosum virus (DNA pox virus)

120
Q

Name for a flat lesion

A

Macule

121
Q

Definition of dysplasia

A

Defect in cell maturation pattern

122
Q

Actinic cheilitis (cheilosis) incidence

A

Men 10x more
UV light exposure
More risk with Xeroderma pigmentation + albinism

123
Q

Sanguinaria associated keratosis is a TRUE leukoplakia, which means it is ____ (although questionable)

A

Premalignant

May show dysplasia

124
Q

Proliferative verrucous leukoplakia is usually multifocal (multiple sites), but the most likely location is…

A

Gingiva

125
Q

Management of oral submucous fibrosis

A 
Mild = steroids
Mod/severe = surgical splitting/excision of fibrous bands

Relapse common

126
Q

Malignant transformation risk of idiopathic LP varies from study to study because…

A

Differences in the underlying pathology

Differences in the use of putative carcinogens (e.g. tobacco)

127
Q

8 anatomic sites for oral cancer (3 HIGH RISK)

A
  1. Lip
  2. Buccal mucosa
  3. Retromolar trigone
  4. FLOOR OF MOUTH
  5. Hard palate
  6. TONGUE (LATERAL BORDER + VENTRAL)
  7. SOFT PALATE
128
Q

Symptoms associated with oropharyngeal carcinoma (3)

A
  1. Dysphagia
  2. Odynophagia (pain during swallowing)
  3. Otalgia (ear pain)
129
Q

Leukoplakia may become _________________ WITHOUT change in clinical appearance

A

Dysplastic or even malignant

130
Q

How can you tell if a lymph node is metastatic?

A

Firm

Feel “fixed”

131
Q

Erythroplakia

A

Red lesions (thinned epithelium, atrophic)

132
Q

Cause of erythroplakia

A

Unknown

Some related to tobacco

133
Q

Induration

A

Localized hardening of soft tissue

Feels thick, firm, like something is underneath in the CT

*danger signal for malignant transformation

134
Q

How does the incidence of oral cancer compare in white men vs. black men >65? Mortality rates? Why?

A

Oral cancer is more common in white men >65 (bc more HPV assoc cases)

Black men >65 have a higher mortality rate (bc of access, socioeconomic)

135
Q

Is verruciform xanthoma malignant?

A

No

136
Q

5 risk factors for idiopathic leukoplakia

A
  1. Tobacco
  2. Alcohol
  3. UV light
  4. HPV
  5. Unknown
137
Q

Incidence of verruciform xanthoma

A

40-70 years
Mostly whites
Slight male predeliction

138
Q

Heck’s disease is also called

A

Focal epithelial hyperplasia

139
Q

Oral cancer is more common in men or women?

A

Men

140
Q

Oral submucous fibrosis

A

High risk premalignant condition caused by betel quid

141
Q

Explanation behind the theory that HPV+ tumors respond better to chemo because of low rates of genomic damage

A

Low frequency of TP53 mutations
Low rates of LOH + microsatellite instability

= intact apoptotic responses (= better response to chemo)

142
Q

Incidence of Focal epithelial hyperplasia (heck’s disease)

A

Children
Immuncompromised
Native americans (high prevalence)
Multiple members of same family (genetic +or infectious)

Oral Pathology Exam 1 (3 decks)

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