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MSK, Rheum, Derm > Fisher - Moles and Cancers > Flashcards

Fisher - Moles and Cancers Flashcards

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1
Q

This 56 yo light-skinned woman complains of these persistent, firm bumps on the cheeks

They have been present for months without change

They are asymptomatic

She has tried scrubbing them and even squeezing them without benefit

WHAT IS THE BEST DX?

A
  • Milia: small epidermoid cysts
  • Common on cheeks, eyelids, forehead, genitals
  • Occur at any age, including infants
  • Often seen in sun-damaged skin
  • May resolve spontaneously or be easily removed with blade or needle
  • Relatively white, and filled with keratinaceous debris
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2
Q

Your 35 yo physician partner requests removal of this nodule on her calf

It seemed to start as a bug bite, but has persisted for months

It is asymptomatic, but she always cuts it when shaving

It has not grown

HOW WOULD YOU MANAGE THIS LESION?

A

Reassure her that it is benign and tell her to quit shaving it

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3
Q

What is this? Does it require treatment?

A
  • Dermatofibroma: common, benign fibrotic tumors
  • Frequently on extremities; red, brown, but NOT pigmented
  • History of trauma (esp. bites) common, although etiology not well understood
  • Horizontal compression (pinching) of the lesion can lead to dimpling -> DIMPLE SIGN (attached very deep to the dermis)
  • If stable and asymptomatic, require no treatment
  • If lesion is unusual, growing or irregular, consider further evaluation -> do get biopsied if there is ever a question (better to err on the side of biopsy rather than miss something malignant)
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4
Q

What is this?

A
  • Seborrheic keratosis: very superficial lesion
  • Waxy, and somewhat keratotic
  • Different shades of brown, so can get biopsied to rule out a melanocytic lesion
    1. Can also get inflamed and become symptomatic
  • Can feel rough, keratotic to the touch, and don’t extend beyond the epidermis
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5
Q

Seborrheic keratosis is a lesion located on which of layer of the skin?

A

Epidermis

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6
Q

Are seborrheic keratosis benign, malignant, or pre-malignant?

A

Benign

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7
Q

What is up with this dude?

A
  • Numerous seborrheic keratoses
  • Similar to the christmas tree appearance of pityriasis rosea (along the skin lines)
  • Developing all of these in the course of a month, like this guy did, is unusual, and can be a sign of cancer
    1. Acute onset of multiple seborrheic keratosis is a sign of cancer -> paraneoplastic from colon cancer, classically
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8
Q

What is the sign of Leser-Trélat?

A
  • Sudden eruption of multiple SKs can be marker for underlying cancer
  • Associated cancers include adenocarcinoma of colon (classic one), breast, stomach, lung
  • However, many adults have many SKs and this is thought to be rare sign
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9
Q

What is this?

A
  • Seborrheic keratosis: stuck-on appearing, and looks like it could be plucked off
  • Keratotic, rough appearance
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10
Q

What do you see here?

A
  • Seborrheic keratoses: can look like a melanoma
  • Biopsy, if you are concerned (better to be too cautious)
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11
Q

What is this? What should you do next?

A
  • Seborrheic keratosis
  • This could have been easily sampled to rule out a melanoma (based on the color) -> bubbly appearance can be a helpful clue that this is SK
  • Dermatoscopy: magnifier (typically x10), a non-polarised light source, a transparent plate and a liquid medium between the instrument and the skin, and allows inspection of skin lesions unobstructed by skin surface reflections
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12
Q

What is the epi of SK?

A
  • Usually do not appear until after age 30 (lesions of adults)
  • Likely an autosomal dominant (AD) inheritance
  • Males may be affected slightly more often and extensively than females
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13
Q

What will the patient tell you about in their history to clue you in to an SK?

A
  • Patients are often concerned about “moles” that have developed over months to years
  • Lesions are usually asymptomatic unless in an area where friction causes irritation and tenderness
  • Rarely, seborrheic keratoses may be pruritic
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14
Q

What do SKs look like on PE?

A
  • May be small, light tan and macular early on, but usually become larger, darker and raised over time
  • Classic description: round or oval, skin colored to brown or black, slightly raised, “stuck on” papules and plaques on the face, trunk, and upper extremities
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15
Q

What about these?

A
  • Cherry angiomas: raised, bright red, fixed
  • Benign, acquired vascular neoplasms
  • Common on trunk in people > 40
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16
Q

What is this?

A
  • Keloid: suggestive of a shaving distribution
  • Result from exuberant fibrous repair of tissue following a cutaneous injury, extending beyond the original site
  • Usually follows injury to skin, but may also arise spontaneously
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17
Q

What do you see here? Who gets these?

A
  • Keloid: kind of ambiguous whether this is a case of a keloid, or hypertrophic scarring, but it does seem to have broken the boundaries of the injury line
  • Most common in 30s, but can vary widely
  • Equally affects men and women
  • Genetic predisposition: African-American most frequent
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18
Q

What is this? How are these managed?

A
  • Keloid: central chest is a classic location (from thoracotomy scarring: incision into pleural space)
  • No treatment for keloids is perfect
  • Options include: intralesional corticosteroid injections (painful)
    1. Surgical excision—high rates of recurrence; may come back even bigger! Can inject them with steroids after excision, or compress them
    2. Cryotherapy (also painful; liquid nitrogen, but tend to come back)
    3. Combined cryotherapy and intralesional triamcinolone (possibly more painful)
  • PREVENTION IS KEY! Avoid piercings and tattoos, along with other injuries to skin
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19
Q

What is this? What will the pt history look like?

A
  • Keloid: may be pruritic or painful, but often asymptomatic
    1. Can get parasthesias if small nerves are involved
  • Often the cosmetic appearance is the chief complaint
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20
Q

What is an epidermal (epidermoid) cyst?

A
  • Mobile dermal nodule, usually w/central punctum
    1. Filled with keratinaceous debris, oils
  • If traumatized or rupture, can get very inflamed and abscessed
    1. Keratin is something skin makes that is meant to be on the outside -> body considers it foreign material (e.g., ingrown toenail or hair)
    2. If expressed, liberate rancid smelling, cheesy material
  • Commonly referred to as a sebaceous cyst -> not filled with sebum, but rather keratin
  • If it has a central punctum (hole), and is not on the scalp, then it is most likely an epidermoid cyst
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21
Q

How epidermal cysts managed?

A
  • Many probably remain quiescent for years without treatment
  • Surgical removal of entire lesion has best “cure” rate
    1. If you only partially remove them, they may come back
  • If inflamed, may need incision and drainage acutely
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22
Q

What is this?

A
  • 2nd most common cutaneous cyst
  • Smooth, firm, dome-shaped 0.5 to 5 cm, keratin-containing, nodule to tumor, with a predilection for the scalp (90%) -> if you cut into it, it may not drain as much bc solid keratin debris inside
  • Often familial with an autosomal dominant inheritance
  • Much more common on scalp than in other locations
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23
Q

How are nevi and SK different?

A
  • Nevi do not make keratin, and have melanin in them (pigment network that SK do not have)
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24
Q

What are the progenitors of BCC, SCC, and melanoma?

A
  • BCC: germinative keratinocytes associated w/hair follicles (resemble dark blue basal layer)
  • SCC: epidermal keratinocytes (resembles spinous layer)
  • Melanoma: melanocytes
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25
Q

Where do melanocytes come from?

A
  • Neural crest-derived cells, so melanoma and nevi can occur anywhere these cells migrate
  • The dermal-epidermal junction just happens to be the most common site (also eye, medulla, inner ear)
  • Sometimes we don’t see a primary melanoma in the skin (could be a different type of melanoma that metastasized)
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26
Q

What is this?

A

Melanoma

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27
Q

Which factor(s) contribute the most to patient prognosis from this lesion?

A
  • Ulceration and depth of dermal involvement
  • Depth of melanoma is probably the single most important prognostic feature
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28
Q

What is the relationship b/t nevi and melanoma?

A
  • Both are comprised by melanocytes, and can share some mutations (e.g., BRAF)
  • High numbers of nevi (esp. >50) can increase risk of melanoma (more melanocytes in skin)
  • Melanoma can develop from pre-existing nevi:
    1. ~20% develop from nevi
    2. ~80% develop de novo
  • Nevi can sometimes appear clinically (and histo) unusual and mimic melanoma, but are NOT pre-skin cancers (NOT pre-melanomas; BENIGN)
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29
Q

What are the types of nevi?

A
  • Acquired melanocytic nevi:
    1. Junctional (epidermis)
    2. Compound (epi + dermis)
    3. Intradermal (just dermis)
    a. More flat if just in epidermis vs. more raised if in the dermis
  • Halo nevi: common nevi the body regresses (doesn’t necessarily mean it was bad; more likely in patients with vitilligo)
  • Congenital nevi
  • Atypical (“dysplastic”) nevi
  • Most nevi are acquired in the first 30 years of life (unusual after that)
  • Remember: these are benign neoplasms of melanocytes
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30
Q

What are these?

A
  • Junctional nevi: nests of melanocytes are present within the dermis only
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31
Q

What is a melanoma?

A
  • Malignant neoplasm comprised of melanocytes
  • Not all melanocytic nevi are pre-melanomas -> the great majority are NOT
  • However, melanoma can develop in a pre-existing benign nevus (20%), or it can develop de novo
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32
Q

What is this?

A
  • Compound nevus: nests of melanocytes are present within the epidermis and the dermis
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33
Q

What do you see here?

A
  • Intradermal nevus: nests of melanocytes are present within the dermis only
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34
Q

What kind of nevus is this?

A

Acquired compound melanocytic nevus

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35
Q

What are these?

A
  • Common acquired melanocytic nevi
  • Nevus: classic definition is “any congenital lesion of the skin; a birthmark”
  • Melanocytic nevus refers to a benign (either congenital or acquired), localized proliferation of melanocytes within the epidermis and/or dermis
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36
Q

What is the difference between nevi and freckles?

A
  • Nevi tend to swim alone
  • Freckles are very symmetric and come up on sun-exposed surfaces (in groups; fade)
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37
Q

What is a junctional acquired melanocytic nevi?

A
  • 2 to 3 mm in diameter
  • Deeply pigmented and macular
  • Arising at the dermal-epidermal junction above the basement membrane zone
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38
Q

What is a compound acquired melanocytic nevi?

A
  • 3 to 4 mm
  • Slightly raised, and moderately pigmented
  • Melanocytes found both intra-epidermally and dermally
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39
Q

What is a dermal acquired melanocytic nevus?

A
  • Larger and dome-shaped
  • Cells exclusively in the dermis
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40
Q

Where does this lesion most likely originate?

A

Intradermally (bc it is raised)

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41
Q

What are halo nevi?

A
  • Common acquired nevus with a surrounding zone of depigmentation -> halo around them because the body is eliminating them (immune response)
  • Epidemiology - first three decades, equal in males and females, more common in patients with vitilligo, familial tendency
  • Highlights the relationship between melanocytic neoplasia and host immunity
  • More common in children
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42
Q

What are these? What do they mean?

A
  • Halo nevi: immune response
  • When someone develops multiple halos around all of their nevi, they may have melanoma somewhere else -> do full body skin check
    1. Chances very low if a 10-y/o, but if 35-y/o, watch out!
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43
Q

What are congenital nevi?

A
  • Classified according to size: small 20 cm
    1. These are adult measurements (need to be adjusted when looking at a neonate)
  • Clinical features: pigmentation varying from brown to black, grossly irregular surface, hypertrichosis (abnormal amt. of hair growth)
  • Large/giant congenital nevi: 5% risk of melanoma in first 5 years of life if nevus > 5cm in size (large); usually arises in dermis
    1. Otherwise, like any other nevi
  • Can be rough and corrugated on the surface
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44
Q

What is this?

A

Congenital nevus: involved spine; lots of satellite lesions (can cause seizures, in some cases)

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45
Q

What are atypical nevi?

A
  • Controversial, but common acquired nevi that simply appear unusual clinically
  • First described as dysplastic nevus syndrome (BK mole syndrome), a RARE inherited syndrome
    1. Pt, immediate family member may have 100’s of irregular moles with hx/o melanoma
    2. INC risk of melanoma in this very specific setting only
    3. CDNK2 (p16INK4A) tumor suppressor gene (mut only in 10% of non-familial melanoma)
  • Atypical nevi are NOT precursors to melanoma, and do not transform into melanoma at a greater rate than any other acquired nevus
    1. One dysplastic nevus does not increase a patient’s risk of melanoma
    2. Pts with great numbers of atypical nevi probably have INC risk of melanoma, esp. if they have a family history of melanoma
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46
Q

What do you see here?

A
  • Pt with multiple atypical nevi: irregular borders, variegated pigment and asymmetry of the nevi
  • Matters because they look funny clinically, and can break the ABCDE rules
  • Get biopsied and excised a lot
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47
Q

What do you think this is?

A
  • Dysplastic nevus: with a fried egg appearance
  • This is going to get biopsied and called a dysplastic lesion, but their risk of melanoma is no higher than any other patient
  • Fall squarely in the nevi category (not melanoma)
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48
Q

Who gets melanomas?

A
  • Highest risk in Caucasian men >50 y/o
  • Most common type of cancer in ppl 25-29 (and 2nd most common in 15-29)
  • 1 American dies every hour from melanoma: pretty common
  • RISING INCIDENCE
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49
Q

Who catches/finds melanomas most often?

A

Spouses and primary care docs

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50
Q

What is this?

A

Melanoma: asymmetric, streaky borders; jet black, with white streak

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51
Q

How does melanoma progress?

A
  • Not as clearly a step-wise process as SCC, from pre-malignant to malignant lesions (e.g., melanocytic nevi do not all develop into melanoma)
  • But, melanoma in situ when just in the epidermis, and not able to metastasize until it breaks through the BM
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52
Q

How are nevi and melanoma distinct histologically?

A
  • Nevi: small, symmetric, and well-circumscribed
    1. Nests organized and discrete, w/uniform size and shape
    2. Melanocytes ‘mature’ with descent into the dermis (decrease in size), and no melanocytes above basal layer
  • Melanoma: lg, asymmetric, & poorly circumscribed
    1. Nests are confluent, with irregular spacing, irregular sizes and shapes
    2. Melanocytes do NOT ‘mature’ with descent, and are located above the basal layer
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53
Q

What growth phase is this melanoma in?

A
  • Radial growth phase: unorganized melanocytes, INC in # and above basal layer (pagetoid spread)
    1. None have ‘invaded’ into the dermis, so this is an in situ lesion
    2. Until melanoma is in the dermis, it can’t metastasize -> early detection & tx imperative
  • Much more haphazard than the nested nevi that have grouped melanocytes
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54
Q

What growth phase is this melanoma in?

A
  • Vertical growth phase: invaded into the dermis, and can metastasize via lymphatics and blood vessels
  • More risky than radial growth because this can lead to metastasis
  • Deeper it goes, the worse the prognosis
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55
Q

What is the etiology of melanoma?

A
  • MULTIFACTORIAL:
    1. Genetic predisposition (eg. CDNK2; BRAF is in about 15% of melanomas on sun-damaged skin )
    2. Environment (eg. UV)
    3. Underlying immune status
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56
Q

What are the risk factors for melanoma?

A
  • Large # of common nevi (esp. >50)
  • Giant congenital nevi (5% risk first 5 years)
  • Atypical nevi, mostly if multiple and familial
  • History of blistering sunburns
  • Family History of Melanoma
  • Light complexion, tanning bed use
  • Underlying immune dysfunction
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57
Q

What are the ABC’s of melanoma screening?

A

A - Asymmetry

B - Borders: irregular, scalloped

C - Color: mottled, variegated, not uniform

D - Diameter: >6mm

E - Elevation (or evolution, i.e., changing)

  • “Changing mole”
  • “Ugly duckling sign:” when one lesion stands out among all the others
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58
Q

What is this? How can you tell?

A
  • Melanoma
  • Asymmetric
  • Notched, irregular Border
  • Color not uniform
  • Diameter >6mm
  • Elevated
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59
Q

What is this?

A
  • Melanoma: pigmented lesion w/irregular border
  • “Ugly duckling”
  • History of recent color change (in this case)
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60
Q

What is this? Why?

A
  • Melanoma: notched border, asymmetrical, slight elevation
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61
Q

What do you see here?

A
  • Melanoma: asymmetrical, irregular border
  • Diameter >6mm and elevated
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62
Q

What are the 5 subtypes of melanoma?

A
  • Acral lentiginous: hands and feet (higher incidence in skin of color)
  • Lentigo Maligna Melanoma: arises on sun-exposed surface of the face (brown, large patch)
  • Nodular
  • Superficial spreading: largely in radial growth phase (not nodular)
  • Amelonotic: don’t have pigment, and can look very bland -> can be easily missed
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63
Q

What is this? How is this lesion defined?

A
  • Acral lentiginous melanoma: defined by anatomic location on palmar, plantar and subungual skin
  • The most common type of malignant melanoma in pts with darker skin
  • Acral = hands and feet
  • Lentiginous = ‘like lentigo” -> histo pattern that contains melanocytes growing like they do in a lentigo (a proliferation of solitary melanocytes that ‘line up’ along the basal layer)
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64
Q

What is this?

A

Acral lentiginous melanoma

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65
Q

What are these?

A

Acral lentiginous melanomas

66
Q

What is this?

A
  • Lentigo melanoma: older pts on sun-exposed skin; synonym for melanoma in situ
  • Slow growing, still in radial phase (bc melanoma in situ)
  • Irregularly shaped, with different shades of brown
  • NO capability of metastasizing if you catch it in this phase
67
Q

What is going on here?

A
  • Nodule on the background of a lentigo maligna
  • Heralds the progression of the in situ lesion to an invasive one
68
Q

What is this?

A

Nodular melanoma associated with a lentigo maligna

69
Q

What is this?

A

Nodular melanoma

70
Q

What is a nodular melanoma?

A
  • Usually on sun exposed skin
  • 15% of malignant melanoma; 2x M > F
  • Most have focal, short-lived radial growth phase (starts in the epidermis because this is where melanocytes come from)
  • Because the lesion is already in the dermis (it is in ‘vertical’ growth phase), the lesion is capable of metastasizing -> very quickly invade
71
Q

What is this?

A
  • Superficial spreading melanoma: asymmetrical
  • Irregular borders
  • Wide variation in color
  • Diameter >6mm
  • Elevated
  • Red, white, and blue
  • Growing outwards as it’s growing down
72
Q

What do you see here?

A

Superficial spreading melanoma

73
Q

What is this?

A

Seborrheic keratosis: note the indulating, cerebriform shape

74
Q

Are these the same? Different? What are they?

A
  • Left: seborrheic keratosis
  • Right: melanoma
75
Q

What is this? Should you biopsy it?

A
  • Seborrheic keratosis: deep furrows and kind of cerebriform
  • Better biopsy this, just in case
76
Q

What happened here?

A
  • Seborrheic keratosis: much more likely because it just fell off when going to biopsy it
77
Q

What is this?

A

Seborrheic keratosis

78
Q

What are these two lesions?

A
  • Left: melanoma in situ
  • Right: seborrheic keratosis
79
Q

What is this?

A

Melanoma in situ

80
Q

What is this?

A

Melanoma in situ (many of these lesions really could be either melanoma or SK, and need to be biopsied)

81
Q

What is this?

A
  • Melanoma in situ
  • All of these lesions really could be either melanoma or SK, and need to be biopsied
82
Q

What is this?

A

Melanoma

83
Q

What is this?

A

Melanoma

84
Q

What is this?

A

Melanoma

85
Q

Are these the same? Different? What are they?

A
  • Left: pigmented BCC
  • Right: melanoma
  • Dr. Fisher said even he couldn’t really tell which is which -> do a BIOPSY in these cases to ID
86
Q

What is this?

A

Acral lentiginous melanoma

87
Q

What is going on here?

A
  • Melanoma of the iris
  • Nevi can develop in the iris too -> remember, neural crest cells in many parts of the body (see attached)
88
Q

What is this?

A

Mucosal melanoma: vulvar

89
Q

Do melanomas metastasize?

A
  • YES -> often via lymphatics, but not exclusively
  • # 1 organ site for metastasis: SKIN
  • Single most important prognostic factor: lymph node involvement (do sentinel node biopsy)
  • Most important histological prognostic factors:
    1. Breslow thickness and ulceration
90
Q

What is Breslow’s thickness?

A
  • Distance of involvement from the stratum granulosum (top) of the overlying epidermis to the deepest tumor cell (bottom)
    1. Most important histo prognostic factor
  • HUGE differences in survival (see attached)
91
Q

What is this?

A

Metastatic melanoma

92
Q

How is melanoma treated?

A
  • Catch it early and CUT IT OUT
  • Metastatic melanoma treatment: until 2011, no definitive proof that any labwork, imaging study, or intervention increased overall survival
    1. IFNa, combination chemotherapy, XRT, vaccine therapy
    2. Systemic disease once it metastasizes
93
Q

What % of melanomas have BRAF mutations?

A

50%

94
Q

What is Vemurafenib?

A
  • Small molecule inhibitor of BRAF approved for unresectable or metastatic (stage 4) melanoma
  • Provides survival benefit (although modest):
    1. Initial response impressive but melanoma adapts; duration of response only 6 mos
    2. New trials focused on combo tx, esp. with Ipilimumab (inhibits CTLA-4)
  • Pt’s melanoma must be tested prior to therapy, and must harbor an activating mutation in BRAF V600E to be eligible for the drug
  • Around 50% (or greater) patients with melanoma will harbor BRAF V600E mutations
95
Q

What is Ipilimumab?

A
  • Anti-CTLA4 antibody
  • Normally, CTLA4 acts as an inhibitory signal to prevent T cell activation, but w/Ipilimumab, T cells activated, and induce a generalized inflammatory response to fight malignancy
  • Much more sustained duration of response (even years); can be combined with Vemurafenib
96
Q

What is Nivolumab?

A
  • Usually first-line therapy
  • More robust response than with Ipilimumab
  • Being used in mono and combo therapy
97
Q

How do you select a sunscreen?

A
  • Remember: all melanoma is NOT caused by sun exposure
98
Q

What factors contribute to the development of skin cancer?

A
  • Multifactorial:
    1. Genetics
    2. Environment: HIGH EXPOSURE to envo insults
    3. Immune system response
99
Q

Why is there so much potential for early detection of skin cancer?

A
  • It is VISIBLE; non-invasive screening
  • BCC and SCC are the two most common cancers, but neither is reportable
100
Q

What is this? How do you know?

A
  • BCC
  • Telangiectasia is a helpful clue
  • Red in the middle (ulcer)
  • Pearly color
101
Q

What is the most common mutation in sporadic tumors of the type attached here?

A
  • PTCH: tumor suppressor gene -> regulator of basal epidermal cell proliferation
  • Common mutation in sporadic BCCs
  • BCC is the most common invasive neoplasm in the US
102
Q

Which of the following places the patient at greatest risk for metastasis from the lesion shown?

  1. p53 mutation in the tumor
  2. Location on the ear
  3. The patient is immunocompetent
  4. The tumor is HPV mediated
A
  • Location on the ear
    1. Ear and lips are high-risk locations for SCC metastasis -> good vascular supply with a very thin dermis
  • This is a squamous cell carcinoma (most have a p53 mutation, but this is not specific to SCC) -> look like cells from the spinous layer
  • Immunocompromised patient would have a greater risk of metastasis
103
Q

How common are BCC and SCC?

A
  • Two most common skin cancers in the US
  • 1 in 5 lifetime risk
  • Incidence rising among young females
104
Q

What are the risk factors for BCC?

A
  • UV exposure
  • Fair complexion
  • Hx/o sunburns (especially blistering)
  • Family history of BCC
  • Immunosuppression: incidence increased by immunosuppression (10x), but not to same degree as SCC
    1. If immunosuppressed, SCC more common
105
Q

What is this?

A
  • BCC
  • Can be very small, nodular, and pearly (much less disfiguring to catch it early)
106
Q

What is this?

A
  • BCC, nodular type
  • Basophilic (blue) nodules emanating from the surface of the epidermis
  • How to distinguish this from melanoma: note the peripheral palisade of tumor cells and clefting from adjacent stroma in the attached image
107
Q

What do you see here?

A
  • BCC: nodule of basophilic, pleomorphic cells with hyperchromatic nuclei
  • Note the peripheral palisade of tumor cells and clefting from adjacent stroma
    1. Peculiar cleft where the stroma (CT of the dermis) tends to separate from the tumor
108
Q

What are the histo and clinical features of BCC?

A
  • Histo: epidermal-stromal clefting in the middle panel and the peripheral palisade of cells (attached)
  • Clinical features: pearly papules, topped with prominent, dilated subepidermal blood vessels (telangiectasia)
109
Q

What is the histopathology of BCC?

A
  • Basophilic, hyperchromatic cells that form nodules, often extending from surface epidermis
  • Cells at the periphery of the aggregations form a palisade (cells line up like a picket fence)
  • Tumor nodules are set in a mucinous stroma, with retraction (clefting, or ‘retraction artifact’)
    1. Stroma is the CT surrounding the dermis, and is blue-ish (from mucin) and cellular -> it appears different than normal dermis
    2. Retraction from the adjacent stroma is an artifact induced by processing of tissue to create H&E stained sections (slides) -> stroma is not firmly attached, and during processing, it is easy for the tumor to retract from that stroma
110
Q

What are the subtypes of BCC?

A
  • Nodular
  • Superficial: more amenable to superficial tx, like topical immunotherapy (imiquimod), topical chemo (5FU), and superficial destruction (eg cryotherapy)
  • Pigmented
  • Morpheaform (sclerotic): looks like scleroderma (more like a scar)
  • Histo subtypes we’re not expected to recognize: micronodular, cystic, infiltrative
111
Q

Are these the same? Different? What are they?

A
  • Both BCC
  • Superficial type on the left: multifocal growth originating from the epidermis (lives much higher)
  • Nodular type on the right: downward growth into the dermis
112
Q

What is this?

A
  • Classic BCC (nodular): well-circumscribed nodule with pearly rolled border and central erosion
  • Note telangiectasias as well
  • Not all of these are ulcerated
113
Q

What do you see here?

A
  • Superficial BCC with prominent telangiectasias (superficial, dilated vessels)
114
Q

What is this?

A

Nodular BCC

115
Q

What is this?

A

Superficial BCC

  • Can be confused with things like eczema sometimes because they are flatter
  • Clearly an abnormal area with a pearly surface in this example
116
Q

What do you see here?

A

Superficial BCC: note how subtle these can be

117
Q

What is this?

A
  • BCC, pigmented
  • Still has translucent qualities
  • Can sometimes be confused for melanoma
118
Q

What is this?

A

Pigmented BCC

119
Q

What do you see here?

A
  • Morpheaform BCC
  • These can actually be very aggressive (wrapping around nerves, for example)
    1. Once they invade nerves, they have a conduit to go wherever they want (and can cause neuropathies)
  • Tends not to metastasize, but still very much a malignancy -> will grow through cartilage, bone, brain, etc.
120
Q

What is basal cell nevus syndrome?

A
  • Aka, Gorlin Syndrome: auto dom, rare, mutation of PTCH1 tumor suppressor gene
  • BCCs at early age (around 23-y/o); only 20% BCC presents before age 50, and rare prior to age 35
    1. Devo basal cells at an alarming rate, and are disfigured as a result
  • MSK defects and lots of jaw cysts
  • INC risk of other neoplasms: medulloblastoma, fibrosarcoma
121
Q

Does BCC metastasize?

A

Exceedingly rare: 0.0028% to 0.55% of cases

122
Q

How is BCC treated?

A
  • Excision (main option)
  • Electrodessication and curretage
  • Cryosurgery
  • Radiation
  • Topical treatment for superficial BCC: Imiquimod (which was originally approved for warts), 5-FU
  • Vismodegib for advanced BCC: small molecule inhibitor -> competitive antagonist of SMO
    1. Metastatic disease, recurrent disease (post-sx), non-surgical candidates
    2. AEs: can’t taste food (lose weight), terrible muscle cramps, etc.
    3. Numerous o/solid tumors, sarcomas have HH pathway signaling abnormalities, and clinical trials of vismodegib are underway in various stages for noncutaneous malignancies
123
Q

If BCC rarely metastasizes, why is tx so important?

A
  • Lack of metastasis does not mean that treatment is not required: local destruction can be severe (see attached image)
124
Q

What is Mohs surgery?

A
  • Instead of cutting out skin cancer and sending to pathologist to see if margins clear, dermatologist acts as surgeon and pathologist, constantly checking the margins and using different technique (horizontal sections, instead of vertical)
  • Able to target where margin is positive during sx, excising only that part (skin-sparing technique important if near structural things)
125
Q

What is this?

A
  • Squamous cell carcinoma: keratotic surface
  • Doesn’t look like a BCC: not as characteristic -> no classic description like BCC
126
Q

How does SCC develop?

A
  • Cutaneous squamous cell carcinoma from sun-exposed sites often follows stepwise progression:
    1. Non-full thickness atypia -> full-thickness atypia -> invasive carcinoma
    2. Actinic keratosis -> squamous cell carcinoma in situ -> Invasive SCC
  • Can metastasize: very commonly goes to lymph nodes and lung
  • Likes to invade nerves
127
Q

What is SCC? Different expressions?

A
  • 2nd most common skin CA
  • Progression, like cervical CA:
    1. Minimal atypia (actinic keratosis)
    2. Full thickness epidermal atypia confined above the basement membrane (SCC in situ)
    a. Bowen’s Disease: patch that looks like eczema
    b. Erythroplasia of Queyrat: plaque on glans penis à erythroplasia of Queyrat
    3. Invasive (SCC)
    a. Well differentiated: better prognosis
    b. Moderately differentiated
    c. Poorly differentiated
128
Q

What is this?

A

Normal skin histo

129
Q

What do you see here?

A
  • Actinic keratosis morphology
  • Cytologic atypia (dysplasia) in the lower portions of the epidermis (cells are large and abnormal)
  • Stratum corneum is thickened with retention of nuclei (parakeratosis), and loss of underlying granular cell layer -> scale seen in actinic keratosis
  • Lesions may progress to full-thickness atypia, resulting in squamous cell carcinoma in-situ
130
Q

What is this? What are its clinical features?

A
  • Actinic keratosis: b4 overt epidermal malignancy, series of progressively dysplastic changes -> name because dysplasia due to chronic sun exposure and results in hyperkeratosis
  • Clinical features: flat, not firm (if it feels very thick, could be an invasive SCC bc these invade dermis and lift the skin up)
    1. Common in fair-skinned individuals, and predilection for sun-exposed site
    2. <1 cm in diameter, tan-brown, red, or skin colored, & rough, sand paper-like consistency
  • Many regress or remain stable, however, enough become malignant w/evolution to SCC in situ and invasive SCC to warrant treatment
131
Q

What is going on here? How might you treat it?

A
  • Actinic keratoses: thin non-indurated lesions -> lack of induration (hardness) a clue to superficial nature of lesions
  • AK -> SCC risk: 1 in 1000 within 1 yr
  • Can do cryotherapy to some of them
  • Use peel treatments for patients like this; can also use Imiquimod or 5-FU
132
Q

What is this?

A
  • Photodistributed lesions of AK -> pre-skin cancers
133
Q

What is this?

A

AK with crust to it -> warning sign

134
Q

What are these?

A

Actinic keratoses

135
Q

What are these? What next?

A
  • Actinic keratoses: more, thicker lesions -> might need to biopsy some of these
136
Q

What do you see here?

A
  • Actinic keratoses: can become thicker on hands because people rub at them
137
Q

What is this?

A

Actinic keratosis: would be very concerned about this one because it is ulcerated and thick

138
Q

What is this?

A

SCC in situ: note the full-thickness of the atypia (can also look for keratin pearls)

139
Q

What is the morphology of SCC?

A
  • Hyperchromatic, pleomorphic nuclei, disorganized growth, mitoses, invasion through the basal layer
  • Cells are pink and keratinizing, like the stratum spinosum
  • When atypical keratinocytes break through BM zone, squamous cell carcinoma becomes invasive
  • While morphology of SCC may vary, they all share the features of keratinization
140
Q

What are some things that increase the likelihood of metastasis of SCC?

A
  • Risk of metastasis related to size of tumor, depth of invasion into dermis, anatomic site, and host immune status:
    1. Larger than 2cm clinically, greater the risk
    2. Greater than 4mm in depth (subcutaneous extension), greater the risk
    3. Higher risk on lips and ears
  • Tumors that arise in context of actinic keratoses may be less clinically aggressive than those arising in burn scars, ulcers, and in non-sun-exposed sites
  • Remember: SCC is common, arising on sun-exposed skin in older people
141
Q

What is this?

A
  • SCC, invasive: note the islands of squamous epithelial cells extending into the dermis
  • Squamous cells make small nodules of keratin, often called keratin pearls
  • Much more pink that BCC (not blue)
  • The carcinoma is trying to make keratin
142
Q

What is happening here?

A
  • Progression of AK to SCC in situ to SCC across one patient’s temple
  • Raised lesions should make you SUSPICIOUS
  • USMLE books sometimes note that BCC is more common on the upper face, while SCC is more common on the lower face -> this is not particularly helpful in daily practice, but perhaps it is relevant for board preparation
143
Q

What is this?

A

SCC that looks like BCC: sometimes they break the rules

144
Q

What is the etiology of SCC?

A
  • No specific SCC oncogene or tumor suppressor gene has been identified
    1. Increased p53 mutations only (but these are not specific as these mutations are common in many types of cancer)
145
Q

What are the risk factors for SCC?

A
  • MAY BE TESTED ON THESE
  • UV
  • HPV (especially types 16, 18, 31, 35)
  • Chronic inflammation (e.g., osteomyelitis with draining sinus tract, and some chronic inflammatory dermatoses)
    1. Chronic erosive mucosal lichen planus
  • Certain scars (eg. burn): fertile soil for devo of carcinoma because injury to the skin (i.e., ulcers) and chronic inflammation
  • Chemical exposure, especially arsenic
  • Radiation exposure
  • Leukoplakia
  • Immunosuppression
146
Q

How often does SCC metastasize? Where to?

A
  • Overall <5% metastasis rate, but different risk in different settings:
    1. Closer to 0.5-1%: actinic-induced non-mucosal skin
    2. Higher in other clinical scenerios:
    a. Actinic-induced on lip 2-16%
    b. Marjolin’s ulcers 10-30% (aggressive, ulcerating SCC in area of previously traumatized, chronically inflamed, or scarred skin, e.g., burn)
    c. Vulvar, perineal, penile HPV-induced 30%
    d. Leukoplakia
  • Mets to lymph nodes and lung
147
Q

What is this?

A
  • SCC: longstanding, ulcerated plaque on the right forehead
148
Q

What is this? How do you know?

A

SCC: bc it doesn’t look like BCC

149
Q

What is this?

A
  • HPV-associated, peri-ungual SCC: rare, but can happen (transformation of wart to SCC)
150
Q

What do you see here?

A

SCC in situ on lower lip

151
Q

What is this?

A

SCC on lower lip: looks large and deep = high risk bc invasive

152
Q

What is this?

A

SCC on tongue (could be from leukoplakia)

153
Q

What do you see here?

A
  • Bowen’s Disease: SCC in situ that looks like eczema
154
Q

What is this?

A
  • Erythroplasia of Queyrat: SCC in situ on the penis
  • Long-standing, not acute (so less worried about STI)
155
Q

What is this?

A

Radiation-induced SCC: this case was a dentist

156
Q

What do you see here?

A
  • SCC arising in a plaque of leukoplakia, probably secondary to tobacco use
157
Q

What is this?

A
  • Lobular tumor with focal ulceration: SCC
  • Can grow quickly, ulcerate, and involve local lymph node base
158
Q

What do you see here?

A
  • Keratoacanthoma: neoplasm of keratinocytes
  • Related to SCC, possibly a subtype
  • Rapidly grows over 2-6 weeks
  • PAINFUL
  • May involute spontaneously: probably because immune system regresses it
  • Fast-growing, dome-shaped, and keratotic
159
Q

What is this?

A
  • Marjolin’s ulcer: ulcerated invasive SCC arising on a background of chronic inflammation, scarring, radiation, trauma
  • These are risk factors for SCC development, as mentioned before
160
Q

How is SCC treated?

A
  • Depends on degree of progression:
    1. Actinic Keratosis: topical therapy, cryotherapy
    2. SCC in situ: topical therapy, intralesional, excision
    3. Invasive SCC: excision
  • Excision is still the gold standard

MSK, Rheum, Derm (21 decks)

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