1. Benign Epithelial Neoplasms, Melanocytic Lesions Flashcards

1
Q

Etiology of Squamous Papilloma

A

HPV 6, 11

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2
Q

Histo of Squamous Papilloma

A

Epithelial projections, each with fibro-vascular CT cores

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3
Q

Differential Diagnosis of Squamous Papilloma (5)

A
  • Verruca Vulgaris
  • Condyloma Acuminatum
  • Heck Ds - Focal Epithelial Hyperplasia
  • Verrucous Carcinoma
  • Cowden Sx
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4
Q

Children who bite nails or suck fingers with warts

A

Verruca Vulgaris

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5
Q

Etiology of Verruca Vulgaris

A

HPV 2

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6
Q

Histo of Verruca Vulgaris

A

Young lesions have kiolocytes - clusters of clear cells with shrunken raisin-like nuclei in the granular cell layer

  • Kiolocytes = virally infected cells
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7
Q

Etiology of Condyloma acuminatum

A

HPV 6, 11, 16, 18

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8
Q

History of oral sex with a partner having venereal warts

A

Condyloma acuminatum

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9
Q

Histology of Condyloma Acuminatum

A
  • Large papilloma with koilocytes and keratin filled crypts between projections
  • Acanthotic epithelium forming blunted projections with thin CT cores
    • papillary projectes are more blunted and broader than SP and VV
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10
Q

Etiology of Heck Disease (Multifocal Epithelial Hyperplasia)

A
  • HPV 13, 32
  • Producing multiple acanthotic papules
    • Inside of lips, cheeks, and sides of tongue
  • Mostly in Native American Children
    • Also in immunosuppressed HIV pts
  • Tends to resolve
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11
Q
  • A slow growing squamous carcinoma characterized by exophytic papillary growth
  • Much larger than any papilloma
A

Verrucous Carcinoma

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12
Q

Describe Cowden Syndrome - Multiple Hamartoma Sx (7)

A
  • Multiple papules on gingiva, tongue, buccal mucosa
  • Multiple small hair follicle tumors
  • Macrocephaly
  • Intestinal polyps, don’t become malignant
  • Keratosis of palms and soles
  • Early development of malignant tumors of breast and thyroid
  • Autosomal Dominant
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13
Q
  • Benign lesion that imitates SCCA clinically and histologically, but spontaneously resolves
  • Firm fleshy epithelial growth with a central keratin plug
A

Keratoacanthoma

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14
Q

How long does a cycle of a Keratoacanthoma take?

A

4 weeks to 1 year

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15
Q

Histo of Keratoacanthoma

A
  • Arises from hair follicle epithelium
    • Seen on upper and lower lips
  • Pseudoepitheliomatous Hyperplasia - looks similar to SCCA
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16
Q

Appearance of multiple Keratoacanthomas is seen in several inherited syndromes and is associated with what?

A

Internal Malignancies

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17
Q

Describe Seborrheic Keratosis (4)

A
  • Skin only - never oral cavity
  • Soft, sessile, waxy friable growth - can be partially scraped off
  • Common after age 40
  • Never becomes malignant
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18
Q

Etiology of Seborrheic Keratosis

A
  • Autosomal Dominant

or

  • Somatic mutation due to UV light
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19
Q

Sign of Leser-Trelat

A
  • A sudden shower of Seborrheic Keratosis
  • Indicator of undiagnosed internal malignancy (usually stomach cancer)
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20
Q

Micro of Seborrheic Keratosis

A

Exophytic growth of basal cells showing hyperkeratosis, acanthosis, papillomatosis

21
Q
  • Shows increased melanin in basal layer (epidermis) with no increase in melanocytes
  • Darkens with UV light
A

Ephelis (Freckle)

22
Q
  • Flat, brown, macule on lip, gingiva, or palate, no larger than 7mm
  • Histo looks like a freckle but Not UV activated
  • No malignant potential
A

Oral Melanotic Macule

23
Q
  • Benign, brown macule that is considered a hallmark of photodamaged skin
  • No change in color intensity is seen after UV light
  • No malignant transformation
  • Linear increase in melanocytes
A

Actinic Lentigo (Liver Spot)

24
Q
  • Benign localized proliferation of melanocytes
  • Symmetrical brown or flesh colored (differentiate from melanomas)
  • Intraoral lesions are uncommon but the sites the can be seen are - palate, buccal mucosa, gingiva, lips
  • Diameter of < 6mm
  • Most regress slowly with age
A

Nevus (Mole)

25
Q

Junctional Nevus

A
  • Theques of nevus cells are confined to the junction of the epithelium and CT - intraepithelial
  • Always present as a macule
26
Q

Compound Nevus

A
  • Nevus cells are present along the junctional area-epithelium and within the CT
27
Q

Intradermal / Intraoral Nevus

A
  • Nevus cells are found only within the CT
  • Presents as a papule
28
Q
  • Uncommon, benign proliferation of melanin producing spindle cells within the dermis
  • Common on skin of Black and Asain children - Mongolian Spot
  • Located on butt or lower back
  • Mimics bruise of child abuse
  • Oral lesions almost always found on the hard palate
    • small, symmetrical blue macule or papule
A

Blue Nevus

29
Q

Where do you see Racial Pigmentation?

A
  • Attached gingiva
  • Fungiform papillae of tongue
30
Q

What do Cafe-au-lait Spots resemble in Neurofibromatosis?

A

Smooth borders like the coast of California

31
Q

What do Cafe-au-lait Spots resemble in Albright Syndrome?

A

Margins are very irregular like the coastline of Maine

32
Q
  • Freckle like lesions of the hands, perioral skin, and oral mucosa
  • Intestinal polyps and intussusceptions
  • Predispostion for developing cancer of breast, thyroid, and pancreas
  • Autosomal Dominant, but 1/3 are from new mutations
A

Peutz-Jehgers Syndrome

33
Q
  • Adrenal cortical deficiency stimulates pituitary production of ACTH (trying to stimulate the decreased cortisol production)
  • ACTH stimulate melanocytes causing hyperpigmentation
A

Addision Disease

34
Q
  • Mimics Racial Pigmentation
  • Appears mostly in women particularly those on BC
  • Body’s attempt to protect mucosa against chemicals from smoke by producing extra melanin
  • Develops after 1 year of heavy smoking, and resolves 3 years after quiting
A

Smoker’s Melanosis

35
Q

Other causes of Diffuse/Multiple Melanocytic Macules

A
  • Drugs
  • Nutritional and GI Disturbances
  • Respiratory Disturbances/ Nasal Polyps
  • Post-Inflammatory Pigmentation
    • any surface lesion can heal with more, less or the same amount of pigmentation
36
Q

Non-Melanotic causes of Pigmented Lesions (Differental Diagnosis)

A
  • Blood Filled Lesions
  • Exogenous Pigments (Amalgam Tattoo)
  • Heavy Metal Poisoning
    • Symmetrical distribution in the free gingiva (racial pig is in the attached gingiva)
37
Q

Which are Autosomal Dominant?

A
  • Cowden Sx
  • Seborrheic Keratosis
  • Peutz-Jeghers Sx
38
Q

Which mimic Child Abuse?

A
  • Conyloma acuminatum
  • Blue Nevus
39
Q

Which are associated with an increased risk for cancer?

A
  • Condyloma acuminatum
    • Cervical
  • Cowden Sx
    • Breast, Thyroid
  • Keratoacanthoma (~Seb K)
    • Internal malignancies
  • Peutz-Jeghers Sx
    • Breast, Thyroid, Pancreas
40
Q

What is the most common location for Verruca Vulgaris?

A

skin of hands

41
Q

When Verruca Vulgaris is found in the mouth where is it located?

A

Anterior Region (where you put your hands)

42
Q

What is the Tx for Verruca Vulgaris

A
  • Same as SP - surgical excision and biopsy
  • Without tx 2/3 will disappear spontaneously within 2 years
  • Does not transform into malignancy
43
Q

What is the location of oral lesions from Condyloma Acuminatum?

A
  • Labial mucosa and lingual frenum
  • Soft palate
44
Q

What is the clinical appearance of an oral lesion of Condyloma Acuminatum?

A
  • Soft, pink, exophytic mass with short blunted surface projections
45
Q

What is the histology of Blue Nevus?

A
  • Collection of elongated, slender melanocytes with dendritic extensions and numerous melanin granules
  • Cells align parallel to the surface epithelium,
46
Q

What is the histological hallmark of Heck Disease?

A
  • Abrupt acanthosis of surface epithelium (thickened papules)
  • Rete ridges are widened, often confluent and sometimes club shaped
47
Q

What is the tx for Heck Disease?

A
  • Resolve Spontaneously
    • VV, and KA
48
Q

What is the clinical appearance of KA?

A
  • Firm, fleshy epithelial growth with Central Keratin Plug (black or white center)
49
Q

How do you differentiate KA from SCC?

A
  • KA grows faster than SCC, usually gone within 6 months