Benign Cutaneous Lesions, Melanocyte Nevi, and Cutaneous Oncology

Question 1

Tumors may arise from:

Answer 1

activation of oncogenes, inactivation of tumor suppressor gene, down regulation of apoptosis preventing normal cell death.

Question 2

DNA damage may result from various stimuli:

Answer 2

UV light, ionizing radiation, exposure to arsenic, HPV

Question 3

Clinical examples and underlying cause of basal cell nevus syndrome:

Answer 3

inactivation of tumor suppressor genes, pt present w/ large number of basal cell carcinomas from a young age.

Question 4

Clinical examples and underlying cause of xeroderma pigmentosum:

Answer 4

DNA repair defect, dramatic freckling from a young age. Numerous squamous cell carcinomas and melanomas.

Question 5

Progression from DNA damage to pre-cancer to cancer enhanced by decreased immune function:

Answer 5

Locally, UV exposure leads to cutaneous immunosuppresion (Langerhans destruction). Systemically, immunosuppressants, HIV, old age, or health decline.

Question 6

Pathology of benign melanocytic nevi

Answer 6

originate from melanoblasts that migrate from neural crest to epidermis. 3 sub-types: junctional (epidermis), compound (epidermis and dermis), and dermal (fully in dermis). Migrate down as melanocyte matures.

Question 7

Clinical presenation of benign melanocytic nevi

Answer 7

Peak in number of nevi in 3rd decade, decreases with age. Well-circumscribed, oval to round, and show symmetry in shape and pigment distribution. Junctional are uniform macules, compound are variable exophytic, lighter brown, dermal more exophytic, lighter in color.

Question 8

Congenital nevi clinical presentation

Answer 8

present at birth, develop cobbled surface over time, frequently with coarse hair growth. Can be small (20 cm). In 1-2% of newborns. At risk for developing melanoma

Question 9

Pathology of congenital nevi

Answer 9

Pathogenesis unknown. Melanocytes penetrate more deeply than in non-congenital nevi. Frequently surround hair follicles, bv’s, and adnexal structures. Tx: excision, monitoring, or biopsy if changing appearance.

Question 10

Clinical presentation of dysplastic nevi

Answer 10

sporadic or familial, common in fair-skinned individuals. variegated tan, brown, and pink coloration. Macular component always present, larger than common nevi, irregular shape, indistinct borders, trunk most common site.

Question 11

Pathology of dysplatic nevi

Answer 11

Pathogenesis unknown. Histo can be mild, moderate, or severe dysplasia. Risk of conversion to melanoma unknown, but may be marker for increased risk. Mildly dysplastic, observe. Moderate to severe dysplasia, excise.

Question 12

Epidemiology of malignant melanoma

Answer 12

75% of skin cancer deaths.

Question 13

Risk factors for melanoma

Answer 13

numerous, large, or dysplastic nevi, family/ personal hx of melanoma, moderate freckling, UV radiation, sunburns, higher SES, genetic DNA repair defect, immunosuppression.

Question 14

Pathogenesis of melanoma

Answer 14

Evolve from melanocytes at dermoepidermal junction. 1/3 from persisting nevi, 2/3 arise de novo. Begins w/ prolonged, noninvasive, radial growth phase and enlarges asymmetrically. Vertical growth phase means invasion w/ development of papules or nodules. Measured histologically w/ Breslow’s depth.

Question 15

Melanoma subtypes

Answer 15

Superficial spreading melanoma (60-70%): melanoma in situ, confined to epidermis. Long radial growth, rapid vertical growth.
Nodular (15-30%) fastest growing, short radial growth, highest metastasis risk.
Lentigo (5-15%): onset after age 70, most commonly located on the face, flat, asymmetrical color variation, may mimic seborrheic keratosis, longest radial growth phase.
Acral lentiginous (5-10%): most common melanoma in patients with darker skin types. Palmar, plantar, subungal location. Hutchinson's sign: pigment to prox nail fold.

Question 16

Clinical features of melanoma

Answer 16

Asymmetry
Border
Color
Diameter
Evolution

Question 17

Metastatic disease characterized by what? Most common places?

Answer 17

extension to lymphatics, so palpate lymph nodes

common sites of spread: skin, lungs, liver.

Question 18

Tx of melanoma

Answer 18

wide excision w/ appropriate margins (0.5 cm in situ, 1 cm for Breslow depth of 2mm), sentinel lymph node biopsy if 1-4 mm Breslow depth, lymphadenectomy if palpable nodes or if positive sentinel nodes, chemo if metastatic.

Question 19

Clinical presenation of epidermoid cyst

Answer 19

onset after puberty of compressible, mobile subcutaneous mass, attached to epidermis, minimal surface change, punctum may be seen, thick and pasty contents (macerated keratin), rupture may cause inflammation.

Question 20

Pathology of epidermoid cyst

Answer 20

Plugging of the orifice of a hair follicle. Epidermal implantation in scar or deep, penetrating injury. Not sebaceous. Tx: observe, inject steroid or oral antibiotic, excision including cyst wall if recurrent inflammation.

Question 21

Seborrheic cyst pathogenesis

Answer 21

genetic predisposition. Tx: observe, curettage or cryotherapy.

Question 22

Clinical presentation of seborrheic keratoses

Answer 22

flesh, tan, brown, or black colored rough, warty, waxy, or keratotic. Appears “stuck-on.” Common in trunk, may occur at any site. Pseudohorn cyst, small white foic are classical finding.

Question 23

Pathology of actinic keratoses

Answer 23

UV light induces a genetic mutation in affected cells leading to abherrent growth.

Question 24

Risk factors for actinic keratoses

Answer 24

intense, intermittent and/or frequent sunburns, fair skin, male gender, increasing age, prior history of actinic keratoses.

Question 25

Clinical features of actinic keratoses

Answer 25

In sites exposed to UV light. Palpation reveals rough, scaly papule and lesion tender to palpation. Features suspicious for malignant degeneration incl: lesions persist after tx, rapid growth and induration, ulcerated mucosal lesions

Question 26

Pathology of SCC

Answer 26

2nd most common skin cancer, 3x more common than BCC in immunosuppressed. In situ limited to epidermis. Arise from UV damage to squamous cells of epidermis. HPV increases risk, chronic inflammation.

Question 27

Clinical features of SCC

Answer 27

Erythematous, indurate base, thick overlying scale, may become nodular and/or ulcerated. SCC in situ as sharply demarcated, scaly, thin, erythematous plaque, like BCC, psorasis, actinic keratosis, or eczema. Lesions enlarge slowly and rarely grow into invasive squamous cell carcinoma. Lips, genitals, ears, and hands have higher metastasis risk.

Question 28

Pathology of BCC

Answer 28

Most common cancer in the US. Arise from UV damage to cells of basal layer of epidermis.

Question 29

High risk areas for BCC

Answer 29

NOSE MOST COMMON! Central face, behind ear, pinna, ear canal, forehead, scalp.

Question 30

Clinical features of nodular BCC

Answer 30

most common subtype, pearly or translucent, telangiectasis often present, rolled border, friable

Question 31

Clinical features of superficial BCC

Answer 31

favors trunk and extremities, erythematous plaque w/ overlying scale, slow growing, resembles AK or dermatitis

Question 32

Clincal features of morpheaform BCC

Answer 32

depressed, atrophic “scar-like” hypopigmentation papules. Indistinct margins, most aggressive sub-type- recommended tx w/ Mohs surgery.

Question 33

Describe basal cell nevi syndrome

Answer 33

Autosomal dominant inheritance, characterized by numerous BCC, palmar pits, and mandibular cysts. Photoprotection imperative.

Question 34

Describe Mohs surgery

Answer 34

1. apply fixative chemical to skin. 2. skin excision 3. immediate histo analysis. Later refined for fresh tissue for BCC and SCC removal

Question 35

Procedure of Mohs surgery

Answer 35

1. tumor edge plus surgical margins marked
2. tissue removed at 45 degree angle to allow edges and underside of specimen to be visualized
3. tissue inked and correspondence map drawn.
4. microscopic examination. Any residual tumor marked.
5. Steps 2-4 repeated until tumor free-margins.
6. reconstruct defect.