Benign Lesions, Nevi, & Oncology Flashcards Preview

Dermatology > Benign Lesions, Nevi, & Oncology > Flashcards

Flashcards in Benign Lesions, Nevi, & Oncology Deck (33):

Basal Cell Nevus Syndrome (cause, sxs, tx)

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.


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

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.


Junctional Nevi (presentation and skin layer)

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


Compound Nevi (presentation and skin layer)

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.


Dermal Nevi (presentation and skin layer)

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


Congenital Nevi (timing, presentation, risk)

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


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

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


Risk factors for melanoma

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


Radial growth phase

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


Vertical growth phase

Fast duration. Papules / nodules become present.



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


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

Confined to epidermis. Lowest risk.


Nodular Melanoma (characteristics and level of risk)

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


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

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


Acral Lentiginous Melanoma (population, location, diagnostic)

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


Amelanotic Melanoma (presentation, dif dx)

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


Melanoma metastasis is most common to which organs?

Skin, lungs, and liver


When is sentinel node biopsy done?

Intermediate risk melanoma (1-4 mm depth)


Epidermoid Cysts (cause, sxs, tx)

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.


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

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.


Pseudohorn cysts (associated disease and presentation)

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


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

"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.


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

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.


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

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


Invasive SCC sxs

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


What location is highest risk for BCC?

90% on head and neck. Nose most common.


Nodular BCC (prevalence, skin layer, sxs)

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.


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

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.


Morfeaform BCC (sxs, risk, tx)

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.


When is Mohs Surgery used?

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


When is shave biopsy used?

Good for superficial lesion or diagnosing non-pigmented lesions.


When is punch biopsy used?

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


Characteristics / tx of warts

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