Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Oral Pathology > Chapter 10 > Flashcards

Chapter 10 Flashcards

1
Q
A

Squamos Papilloma

Benign proliferation of STRATIFIED SQUAMOUS epithelium

Caused by: HPV 6 & 11 (DNA virus)

Low virulence and infectivity rate

MOST COMMON - intraoral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Sites of predilection of Squamous Papilloma

A

Tongue

Lips

Soft Palate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the clinical manifestations of Squamous Papilloma?

A

Pedunculated

Painless

White, red, or mucosal colored

5mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Squmous Papilloma Differentials

A

Verruca Vulgaris

Condyloma acuminatum

Verruciform xanthoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
A

Verruca Vulgaris

HPV 2, 4, 6, 40

CONTAGIOUS - common on skin (hands)

ORAL LESIONS –> always white

* Hyperkeratized layer

Pedunculated or sessile

5mm

Multiple or clusters are common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
A

Condyloma Acuminatum

(Venereal Wart)

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

Clinically –> Painless, Sessile (short blunted surface projection), Exophytic, Clustered

Large (2x as papilloma or verruca vulgaris)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Condyloma Acuminatum Differential Diagnosis

A

Squamos papilloma

Verruca Vulgaris

Verruciform xanthoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HPV 16 and HPV 18

Condyloma acuminatum

A

increased risk for malignant transformation to squamos cell carcinoma

_** anogenital region – NOT ORAL LESIONS **_

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

HPV 6 and 11

A

Squamous Papilloma

(may be Condyloma acuminatum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

HPV 2, 4, 6, 40

A

Verruca Vulgaris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

Condyloma Acuminatum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Multifocal Epithelial Hyperplasia

A

HECK’S DISEASE

HPV 13 & 32

CHILDHOOD

Multiple lesions

Painless

Flattened or rounded papules –> Cobblestone

Mucosal colored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment for Heck’s Disease?

A

Spontaneously regress

Conservative surgical excision

Risk of recurrence

No risk of malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Heck’s Disease

A

Multifocal Epithelial Hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
A

Sinonasal Papillomas

Benign - localized proliferation of respiratory mucosa

Three histological patterns

Arise from:

* Lateral nasal wall

* Septum

* Sinuses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Sinonasal Papilloma Histological Forms (3)

A

Fungiform

Inverted

Cylindrical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
A

Mulluscum Contagiosum

DNA POXVIRUS

virally-induced epithelial hyperplasia

Sessile, papules

Umbilicated lesions

Skin-colored

Smooth surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Molluscum contagiosum histology

A

Molluscum bodies (Henderson-paterson bodies)

Virally infected epithelial cells (glossy appearance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Treatment of Molluscum Contagiosum

A

Remission occurs in 9 months

Treat to decrease risk of transmission

Remove by curettage or cryotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
A

Verruciform Xanthoma

Hyperplastic condition - likely due to trauma

Lipid-laden histiocytes in the epithelium – XANTHOMA CELLS

Common on gingiva

Painless

Sessile (slightly elevated)

Papillary (roughened surface)

Mucosal, white, yellow, or red

<2cm

Multiple lesions possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Verrucifrom Xanthoma differential diagnosis

A

Squamous papilloma

Verruca vulgaris

Condyloma acuminatum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Treatment of Verruciform Xanthoma

A

Conservative surgical excision

Recurrence is rare

No risk of malignant transformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
A

Seborrheic Keratosis

Benign proliferation of epidermal basal cells (aquired)

DOES NOT OCCUR IN THE MOUTH

SKIN of FACE, TRUNK, and EXTREMITIES

lesions more prevalent with AGE

Tan to brown macules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Dermatosis papulosa nigra

A

Seborrheic Keratosis that occurs in AFRICAN AMERICANS

Genetic inheritance (AD)

Multiple black 2mm papules

Scattered around zygomatic and periorbital region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
A

Dermatosis Papulosa Nigra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q
A

Leser-Trelat Sign

Sudden appearance of NUMEROUS seborrheic keratosis

Associated with INTERNAL MALIGNANCY (not good!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q
A

Sebaceous Hyperplasia

Localized proliferation of SEBACEOUS glands of the skin

** significant because –> Clinically similar to facial tumor – Basal cell carcinoma (BCCA) **

Compression of lesion – sebum is expressed

*Distinguishes from BCCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q
A

Ephelis – FRECKLE

Hyperpigmented macule of skin

** increased of melanin production without the increase of melanocytes **

MORE PRONOUNCED WITH UV LIGHT - sun exposure

Light skinned individuals, bad chilhood sunburns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q
A

Actinic Lentigo

Benign brown macules resulting from chronic UV light damage to skin

Dorsal surface of hands, face, and arms

Uniformly pigmented

NO CHANGE IN COLOR INTENSITY WITH UV LIGHT

Does not undergo malignant transformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Color intensity in UV light:

Increases –> ?

Stays the same –> ?

A

Ephelis

Actinic Lentigo (appearance induced by sun)

Lentigo simplex (found in sunless areas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q
A

Lentigo Simplex

Benign cutaneous melanocytic hyperplasia

(increase in number of MELANOCYTES)

Occurs in skin NOT exposed to UV light (sun)

Color intensity does not change with sunlight

Do not undergo malignant transformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q
A

Melasma

Aquired, symmetrical

Hormonally-driven hyperpigmentation of the sun exposed skin of the face

(Bilateral light brown macules)

Pregnant women (dark skinned more common)

Pigmentation can remain faint or darken over time

No risk of malignant transformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q
A

Oral Melanotic Macule - oral ephelis (freckle)

Brown, asymptomatic macule

Focal increase in malanin deposition

NOT DEPENDENT ON SUN EXPOSURE

most common site –> vermillion border ( labial melanotic macule)

Biopsy is MANDATORY – cannot distinguish clinically from early melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Labial melanotic macule

A

oral melanotic macule

“oral freckle” found on the vermillion border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
A

Oral Melanoacanthoma

Aquired pigmentation of the oral mucosa due to ? –> TRAUMA

Seen almost exclusively in AFRICAN AMERICANS

Most common– 20-30yr females

** BIRTH CONTROL**

Buccal mucosa is the MOST COMMON SITE Incisional biopsy –> rule out MELANOMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q
A

Acquire melanocytic nevus - MOLE

Benign localized proliferation of cells from the NEURAL CREST

Most common ADULT TUMOR

* Junctional, Compound, Intradermal*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Junctional aquired meloncytic nevus

A

earliest presentation

Dark macule - less than 6mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Compound acquired meloncytic nevus

A

nevus cells proliferate

Slightly elevated, smooth surface

Pigmentation decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Intradermal acquired meloncytic nevus

A

Papillomatous surface

hairs grow from center

Losses most or all of it’s pigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Intraoral melonocytic nevi

A

Uncommon

Appearance similar to skin nevi

PALATE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q
A

Congenital Melanocytic Nevus

1% of newborns

Small or Large

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Large congenital melanocytic nevus

A

hypertrichosis

(excess hair)

May undergo malignant transformation into MELANOMA

Should be removed or closely followed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q
A

Halo Nevus

Melanocytic nevus with a surrounding pale HYPOPIGMENTED BORDER

Nevus cell destruction by immune cells - no color

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q
A

Blue Nevus

Proliferation of dermal or intramucosal melanocytes

oral lesions almost always on the PALATE

Tyndall Effect

Oral lesions –> must be biopsied to rule out melanoma

malignant transformation is rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Tyndall Effect

A

Melanin particles are deep to the surface, light reflected back must pass through overlying tissue.

Long wavelenghts are easily absorbed into tissue

Blue has a shorter wavelenght and is reflected

46
Q

Leukoplakia

A

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

*If can be rubbed off – not leukoplakia

considered a PREMALIGNANT LESION

85% of oral precancer

BIOPSY IS MANDATORY

Recurrences are FREQUENT – long term follow ups

47
Q

White lesions

A

Keratin, microbial colony, scar tissue, necrosis are blocking the redness of the underlying vascular tissue

48
Q

White lesions that can be scraped off (5)

A

Materia Alba

White coated tongue

Burn (thermal, chemical, cotton roll)

Pseudomembranous candidiasis

Sloughing from toothpaste

49
Q

Leukoplakia Etiology (6)

A

Tabacco

Alcohol

Sanguinaria

Microorganisms

Trauma

50
Q

Tobacco

(Smokeless)

A

80% – leukoplakia smoke

smokeless tobacco –> tobacco pouch keratosis

51
Q

Sanguinaria

A

Toothpaste and mouthrinses

Maxillary vestibule or alveolar mucosa of the maxilla

80% of pts with leukoplakia have history of using sanguinaria

52
Q

UV radiation

A

Causes luekoplakia on the lower lip vermillion

53
Q

Microorganisms

A

Treponema pallidum –> 3rd stage, glossitis

Candida albicans

HPV 16 and 18

EBV - hairy leukoplakia

54
Q

Trauma

A

Not precancerous

Not true leukoplakia

Nicotene stomatitis and Frictional keratosis

55
Q

Most common LOCATION for leukoplakia

A

Lower lip vermillion border

Buccal mucosa

Gingiva

56
Q

common location for DYSPLASIA or CARCINOMA

A

Lip vermilion - lower lip

Lateral/ventral tongue

Floor of mouth

57
Q

Erythroplakia

A

Scattered red patches

In areas of leukoplakia –> sites where epithelial cells are so immature they CAN NO longer produce KERATIN

Most Advanced Dysplasia

Common locations: FOM, Ventral tongue, Soft palate

Biopsy is MANDATORY

recurrence and multifocal involvement is common

58
Q

Erythroleukoplakia

A

Red and white intermixed lesions

Advanced dysplasia

59
Q
A

Prliferative verrucous leukoplaki (PVL)

Special high-risk form of leukoplaki

Multiple keratotic palques with roughened surface projections

Lesions slowly spread through the mouth

–> carcinoma can devleop

HIGEST RISK FOR MALIGNANT TRANSFORMATION

No association with tobacco use

60
Q

Leukoplakia Histopathology

A

Hyperkeratosis

Hyperparakeratosis (No granular layer, nuclei retained)

Hyperorthokeratosis (Granular layer, nuclei lost)

Acanthosis (thickened spinous layer)

61
Q

Mild dysplasia -

Moderate dysplasia -

Sever dysplasia -

Carcinoma in situ -

A

Alterations in lower 1/3

Alterations in lower 1/2

Alterations above 1/2

Alterations through epithelium

62
Q

Factors that increase the risk of cancer in leukoplakia ( 4)

A

Persistence over several years

Female patient

Nonsmoker

Oral floor or ventral tongue lesions

63
Q
A

Smokeless Tobacco Keratosis

Common local change - painless loss of gingival tissue in area of tobacco contact

Gingival recession may accompany

Correlates with QUANTITY of daily use and duration of habit

White plaque on mucosa in DIRECT contact (faint) - may look similar to luekoplakia

may appear fissured or ripped

longer use – thicker tissue

Biopsy needed if sever lesions

64
Q

Treatment for smokeless tobacco keratosis

A

Alternating the site of tobacco placement

Habit cessation – normal mucosa appears in 2 weeks.

After 6 weeks no normal mucosa appears –> BIOPSY

65
Q
A

Oral Submucosa Fibrosis

Chronic

Progressive scarring (Fibrosis) –> SURFACE IS TYPICALLY WHITE

Mucosal Rigidity

Limits the ability to open wide –> causes trismus

High risk precancerous condition

Caused by: BETEL QUID or POAN Tobacco like found in Indian culture

66
Q

Most commonly affected sites of oral submucosal fibrosis

A

Buccal mucosa

Retrmolar areas

Soft palate

67
Q

Treatment of oral submucosal fibrosis

A

Lesion DOES NOT regress with habit cessation - no new scarring will occur

** Can make incisions in bucall mucosa to release fibrous fibers and allowed a wider opening **

Frequent follow up is MANDATORY –> 1 in 10 biopsies undergo malignant transformation

68
Q
A

Nicotene Stomatitis

White keratotic change on the palate – red dots are salivary gland openings

DUE TO HEAT – long term exposure

Reverse Smoking –> significant potential for malignancy (requires biopsy)

COMPLETELY REVERSIBLE – palate will return to normal within 2 weeks of habit cessation

** if it doesn’t not return to normal in 2 weeks – BIOPSY**

69
Q
A

Actinic Keratosis

cutaneous PREMALIGNANT LESION

developes in adults with significant lifetime sun exposure

Scaly, irregular plaques – keratin formation

Vary in color

Scale peels off but will recur

Sandpaper texture

Some dysplasia may be present in the biopsy

10% will progress to SCCA in 2 years

70
Q

Actinic keratosis treatment and prognosis

A

Treatment –> Destroyed or excised

Prognosis –> 10% will progress to SCCA in 2 years

71
Q
A

Actinic Cheilosis

Common PREMALIGNANT alteration of lower lip vermillion

Loss of vermillion border - blotchy pale areas

Scaly areas develop on the drier protion of the vermillion

Further progression suggests changes to SCCA

Caused by –> LONG TERM UV LIGHT EXPOSURE

72
Q

Treatment for Actinic Cheilisis

A

Chnages are irreversible

Use lip balms with sunscreens to prevent further damage

10% of patients –> SCCA

73
Q

When should an Actinic Cheilisis be biopsied?

A

Induration

Thickening (leukoplakia)

Ulceration

74
Q

Squamous Cell Carcinoma

A

95% of oral cancers are Squamous cell carcinoma –> MOST COMMON CANCER INTRAORALLY

lingual carcinomas - painless, indurated masses or ulcers on the posterior lateral border of tongue

Causes – multifactorial

Exophytic (mass forming - fungatin)

Endophytic

Leukoplakia

Erythroplakic

Erytrholeukoplakic

75
Q

Etiology of SCCA

A

Tobacco

Alcohol

Phenolic agents

Radiation

Ifron deficiency

Vitamin A deficiency

Sphyillis

Oncogenic viruses

Immunosuppression

Oncogenes

Tumor suppresor genes

SCC

76
Q

SCCA - Tobacco

A

80% of patients with oral SCCA have a history of smoking

The risk increases the longer a perso smokes

Greatest risk –> Reverse smoking (no filter)

Pipe smoking, cigar smoking

77
Q

SCAA Alcohol

A

Significant risk factor when combined with tobacco

78
Q

SCC Phenolic agents

A

Phenoxyacetic acids – rood mills

79
Q

SCC radiation

A

UV radiation

X ray radiation increase the risk

80
Q

SCC Iron deficiency

A

Iron is required for –> NORMAL function of epithelial cells

Plummer-Vinson Syndrome – severe, chronic form

Iron deficiency – impaired cell mediated immunity

81
Q

SCC vitamin A defiency

A

Excessive keratinization

Normal levels are protective

82
Q

SCC syphillis

A

tertiary stage

DORSAL tongue

83
Q

SCC oncogenic viruses

A

HPV 16, 18, 31, 33

84
Q

SCC Tumor suppressor genes

A

Allow tumor production when they become inactivated

85
Q

SCC most common location –>

second most common –>

Third –>
Fourth –>

A

Tongue – lateral and vertical

Floor of mouth – associated with leukoplakia or erythroplakia

Soft palate

Gingiva

86
Q

SCC oropharyngeal

A

Soft palate or tonisllar areas

87
Q

Tumor staging

A

Best indicator of patient prognosis

T = size of primary local tumor in cm

N = involvement of local lymph nodes

M = distant metastasis

88
Q

Tumor grading

A

Histologic features (not as good of indicator as clinical staging)

Grade I - tumor resembles parent tissue, well-differentitated

Grade II - tumor somewhat resembles parent tissue, moderately differentiated

Grade III (or IV) - tumor doesn’t resemble parent tissue, poorly differentiated

89
Q

What guides treatment for intraoral lesions?

A

Clinical staging

90
Q

Best therapy for SCC

A

Wide surgical excision and/pr radiation therapy

91
Q

Treatment SCC

A

Intraoral tumors >3 mm depth = radical neck dissection

RADICAL NECK DISSECTION –> removal of neck tissue from collarbone to lower jaw.

Lip carcinoma = wedge resection

92
Q

Field Cancerization

A

Tendency toward development of multiple mucosal cancers

93
Q

Metastasis of SCC

A

Spread largely via lymphatics

Tends to spread ipsilaterally

Nodes = firm/hard, painless, enlarged, fixed

Metastasis most commonly found in:

lungs

liver

bones

94
Q

Verrucous Carcinoma

A

Low grade variant of oral SCC

Can be caused by smokeless tobacco

Common sites:

Mandibular vestibule

Gingiva

Deceptively benign microscopic appearance

95
Q

Malignant transformation potential (most to least)

A

PVL

Nicotine stomatitis

Erythroplakia

Oral submucous fibrosis

Erythroleukoplakia

Granular leukoplakia

Actinic Cheilosis

96
Q

Nasopharyngeal Carcinoma

A

Group of malignancies that arise from lining epithelium in the nasopharynx

Associated with EBV

97
Q

Basal Cell Carcinoma

A

Most common of all cancers

Locally invasive and slow spreading

80% found in head and neck

Results from UV radiation

Metastasis is rare

98
Q

Most common form of BCC

A

Nodular (noduloulcerative)

99
Q

Clinicopathologic varieties of BCC

A

Nodular

Pigmented

Sclerosing

Superficial

Those associated with nevoid BCC

100
Q

Treatment of BCC

A

Less than 1 cm are excised with 3-5 mm margins

101
Q

Melanoma

A

Malignant neoplasm of melanocytic origin

Acute sun exposure is a major causative factor (big time burns)

Third most common skin cancer - MOST DEATHS

102
Q

Risk factors of Melanoma

A

UV radiation - ACUTE

Fair complexion

Light hair

Tendency to sunburn easily

History of painful/blistering sunburns as a child

Personal history of melanoma

Personal history of dysplastic or congenital nevus

FAMILY HISTORY - increases chances by 8%

103
Q

Melanoma growth patterns

A

Radical = malignant cells spread horizontally through basal layer

Vertical = malignant cells invade underlying CT

104
Q

ABCDE of Melanoma

A

Asymmetry

Border irregularity

Color variation

Diameter greater than 6 mm

Evolving lesions

105
Q

Treatment - Melanoma

A

Surgical excision with 3-5 cm margins

Radioresistant

106
Q
A

Squamous Cell Carcinoma

107
Q
A

Basal Cell Carcinoma

** DOES not occur in the MOUTH **

Telangiectactic blood vessels

108
Q

Telangiectactic blood vessels

A

Superficial capillaries

Found on Basal Cell Carcinoma Lesions

109
Q

Prognosis of oral melanoma >.5mm

A

POOR

Survival rate decreases with DEPTH of lesion

110
Q

Melanoma areas with WORST prognosis? (4)

A

BANS

B - interscapular area of back

A - posterior arm

N - Posteriot and lateral NECK

S - Scalp

111
Q

Benign vs Malignant

A

Benign – not a cancerous tumor

Malignant - cancerous tumor, out of controlled growth of tissue?

112
Q

Does seborrheic keratosis occur in the mouth?

A

No

Oral Pathology (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions