Benign Lesions, Nevi, & Oncology

Question 1

Basal Cell Nevus Syndrome (cause, sxs, tx)

Answer 1

Genetic disease causing loss of tumor suppression → hundreds of BCCs, palmar pits, and mandibular cycts.
Photoprotection is imperative.
Important to check palms to aid diagnosis.

Question 2

Common Melanocytic Nevi - Moles (presentation, population, timing, risk, tx)

Answer 2

Groups of melanocytes. Symmetric.
Lighter skinned individuals tend to have more total nevi than dark-skinned people, who tend to have more on acral sites (palms, soles, nail beds).
Total number associated w/ melanoma risk.
People are typically not born w/ nevi. Accumulate from childhood to 30’s, which then mature and eventually involute.
Tx w/ photoprotection or excision if changing, atypical, repeatedly traumatized, or for cosmetic reasons. Importat to reassure patients that they are not dangerous.

Question 3

Junctional Nevi (presentation and skin layer)

Answer 3

Flat, not raised, and brown. Melanocytes in epidermis.

Question 4

Compound Nevi (presentation and skin layer)

Answer 4

Melanocytes in both epidermis and dermis. Less likely to create visible pigment on surface. Become lighter and more raised as it progresses from junctional to compound.

Question 5

Dermal Nevi (presentation and skin layer)

Answer 5

Melanocytes entirely in dermis. Look pinkish, even more raised.

Question 6

Congenital Nevi (timing, presentation, risk)

Answer 6

Present at birth and darken over time. May be large w/ color irregularity. Often cobbled w/ coarse hair. Giant congenital nevi have risk of melanoma

Question 7

Dysplastic Nevi (presentation, histology, location, population, timing, tx)

Answer 7

Atypical cells on histology.
Variegated (different colors) including tan, brown, and pink. Irregular shape, indistinct borders, and often >5mm.
Most common on trunk and in light-skinned people.
Usually don’t appear until puberty, and unlike common nevi, these continue to develop throughout life.
Tx – observe if mild, excise if moderate / severe

Question 8

Risk factors for melanoma

Answer 8

Intermittent sunburns causes higher risk than chronic sun exposure. Higher risk in high SES.

Question 9

Radial growth phase

Answer 9

Long duration and includes changing shape, size, or color.

Question 10

Vertical growth phase

Answer 10

Fast duration. Papules / nodules become present.

Question 11

ABCDE’s

Answer 11

Asymmetry
Borders - irregular / poorly defined)
Color - more than one is bad)
Diameter (>6mm)
Evolving - most important factor

Question 12

Superficial spreading melanoma / Melanoma in situ (skin layer, level of risk)

Answer 12

Confined to epidermis. Lowest risk.

Question 13

Nodular Melanoma (characteristics and level of risk)

Answer 13

Shortest radial growth phase and fastest overall growth. Highest risk of metastasis

Question 14

Lentigo Maligna Melanoma (sxs, dif dx, population, location)

Answer 14

Longest radial growth phase.  
Flat, asymmetric w/ color variation.  
May mimic seborrheic keratosis.  
Most common in people > 70 yo.  
Commonly located on face.

Question 15

Acral Lentiginous Melanoma (population, location, diagnostic)

Answer 15

Most common type among dark-skinned people.
Palmar, plantar, or subungual location. Hutchinson sign is diagnostic (when spreads beyond nail and appears on cuticle).

Question 16

Amelanotic Melanoma (presentation, dif dx)

Answer 16

Pink / no pigment. Often misdiagnosed as BCC, SCC, or pyogenic granuloma.

Question 17

Melanoma metastasis is most common to which organs?

Answer 17

Skin, lungs, and liver

Question 18

When is sentinel node biopsy done?

Answer 18

Intermediate risk melanoma (1-4 mm depth)

Question 19

Epidermoid Cysts (cause, sxs, tx)

Answer 19

Trapped epidermal cells → pocket of macerated keratin. NOT sebaceous. Caused by injury or blocked hair follicle.
Presents w/ compressible / mobile domed nodule +/- punctum (not pustule as in abscess) and foul-smelling ricotta cheese-like keratin. Rupture may lead to inflammation, but true infection is rare.
Tx w/ intralesional steroids or oral antibiotics if inflamed. If inflammation recurs, excision may be done, but whole wall needs to be cut out or it will recur. Do not excise when actively inflamed.
Do not I/D them b/c they are not filled w/ infection.

Question 20

Seborrheic Keratosis (cause, sxs, location, timing, ddx, key indicator, tx)

Answer 20

Benign overgrowth of epidermis.
“Greasy horn”. Looks like a waxy / warty “stuck on” papule or plaque. Multiple raised bumps. Flesh-colored, tan, brown, or black. Small, dark keratin deposits are visible. May be itchy.
Most common on trunk and in 4th or 5th decade.
May mimic ABCD’s of melanoma.
Pseudohorn cysts are key indicator.
Tx includes curettage (scraping off) or cryotherapy. Reassurance is important.

Question 21

Pseudohorn cysts (associated disease and presentation)

Answer 21

Key indicator of seborrheic keratosis.

Collections of white keratin occur w/in lesion. Don’t see net-like pigment that is common in melanoma.

Question 22

Actinic Keratosis (associated disease, risk factors, location, chromophore, sxs)

Answer 22

“Sun-induced horn”. Pre-cancerous lesions of epidermis. 1-2% convert to SCC.
Risk factors include sun exposure, fair skin, old age, male sex, and prior history.
DNA is chromophore that absorbs UV light → AK
Pink papules / plaques. Feels slightly gritty. More easily felt than seen as textural change may be only presenting sign. Found on sun-exposed areas.
Suspicious w/ rapid growth, indurated (hard), or ulcered.
AK on lips presents with scale.
Tenderness is more common in AK than SCC.
No deep tissue invasion.

Question 23

SCC (risk factors, location, high risk sites, causes, differentiating factors, tx)

Answer 23

3x more likely than BCC in immunocompromised patients.
Affects sites w/ squamous epithelium (skin, mouth, esophagus, penis, anal mucosa).
High risk sites for metastasis include lips, ears, anal / genital regions, and hands.
Caused by DNA disruption from sun, HPV, or chemicals (arsenic). Also caused by chronic inflammation, such as ulcers or burns.
Don’t bleed (unlike BCC).
Tx low risk sites w/ excision. Tx high-risk sites (such as face) w/ Moh’s Surgery.

Question 24

Bowen’s SCC / in situ (sxs and skin layer)

Answer 24

SCC limited to epidermis. Well demarcated thin plaque. Red.

Question 25

Invasive SCC sxs

Answer 25

Erythematous plaque or nodule w/ scale and indurated base. May become ulcerated.

Question 26

What location is highest risk for BCC?

Answer 26

90% on head and neck. Nose most common.

Question 27

Nodular BCC (prevalence, skin layer, sxs)

Answer 27

Most common type.
Nodules of basaloid cells in dermis.
Pearly / translucent papule or nodule. Telangectasias. “Rolled border”. May have central erosion / ulceration. Friable and bleeds easily.

Question 28

Superficial BCC (skin layer, sxs, location, ddx)

Answer 28

Basaloid tumor cells bud directly off epidermis.
Red, thin plaque w/ scale. Translucent, friable / crusting, rolled border.
Favors trunk / extremities. Slowly growing. May resemble dermatitis.

Question 29

Morfeaform BCC (sxs, risk, tx)

Answer 29

Infiltration of surrounding skin.
Depressed, atrophic, “scar-like” hypopigmented papules w/ indistinct margins. Telangectasia may be present.
Most aggressive type b/c it’s hard to find.
Tx w/ Mohs.

Question 30

When is Mohs Surgery used?

Answer 30

Used for high-risk NMSCs (SCC / BCC) in critical sites and recurrent lesions.
Controversial for melanoma

Question 31

When is shave biopsy used?

Answer 31

Good for superficial lesion or diagnosing non-pigmented lesions.

Question 32

When is punch biopsy used?

Answer 32

Removes tissue down to fat. Good for removal of small lesions, but can’t see all different parts / colors if lesion is larger.

Question 33

Characteristics / tx of warts

Answer 33

Often have black dotes (thromboses), which are dried blood vessels. Well circumscribed.
Tx w / cryotherapy.