Fisher - Moles and Cancers Flashcards

Question 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?

Answer

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

Question 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?

Answer

A

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

Question 3

Q

What is this? Does it require treatment?

Answer

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)

Question 4

Q

What is this?

Answer

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

Question 5

Q

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

Answer

A

Epidermis

Question 6

Q

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

Question 7

Q

What is up with this dude?

Answer

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

Question 8

Q

What is the sign of Leser-Trélat?

Answer

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

Question 9

Q

What is this?

Answer

A

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

Question 10

Q

What do you see here?

Answer

A

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

Question 11

Q

What is this? What should you do next?

Answer

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

Question 12

Q

What is the epi of SK?

Answer

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

Question 13

Q

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

Answer

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

Question 14

Q

What do SKs look like on PE?

Answer

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

Question 15

Q

What about these?

Answer

A

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

Question 16

Q

What is this?

Answer

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

Question 17

Q

What do you see here? Who gets these?

Answer

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

Question 18

Q

What is this? How are these managed?

Answer

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

Question 19

Q

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

Answer

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

Question 20

Q

What is an epidermal (epidermoid) cyst?

Answer

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

Question 21

Q

How epidermal cysts managed?

Answer

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

Question 22

Q

What is this?

Answer

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

Question 23

Q

How are nevi and SK different?

Answer

A

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

Question 24

Q

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

Answer

A

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

Question 25

Q

Where do melanocytes come from?

Answer

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)

Question 26

Q

What is this?

Question 27

Q

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

Answer

A

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

Question 28

Q

What is the relationship b/t nevi and melanoma?

Answer

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)

Question 29

Q

What are the types of nevi?

Answer

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

Question 30

Q

What are these?

Answer

A

Junctional nevi: nests of melanocytes are present within the dermis only

Question 31

Q

What is a melanoma?

Answer

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

Question 32

Q

What is this?

Answer

A

Compound nevus: nests of melanocytes are present within the epidermis and the dermis

Question 33

Q

What do you see here?

Answer

A

Intradermal nevus: nests of melanocytes are present within the dermis only

Question 34

Q

What kind of nevus is this?

Answer

A

Acquired compound melanocytic nevus

Question 35

Q

What are these?

Answer

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

Question 36

Q

What is the difference between nevi and freckles?

Answer

A

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

Question 37

Q

What is a junctional acquired melanocytic nevi?

Answer

A

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

Question 38

Q

What is a compound acquired melanocytic nevi?

Answer

A

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

Question 39

Q

What is a dermal acquired melanocytic nevus?

Answer

A

Larger and dome-shaped
Cells exclusively in the dermis

Question 40

Q

Where does this lesion most likely originate?

Answer

A

Intradermally (bc it is raised)

Question 41

Q

What are halo nevi?

Answer

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

Question 42

Q

What are these? What do they mean?

Answer

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!

Question 43

Q

What are congenital nevi?

Answer

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

Question 44

Q

What is this?

Answer

A

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

Question 45

Q

What are atypical nevi?

Answer

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

Question 46

Q

What do you see here?

Answer

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

Question 47

Q

What do you think this is?

Answer

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)

Question 48

Q

Who gets melanomas?

Answer

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

Question 49

Q

Who catches/finds melanomas most often?

Answer

A

Spouses and primary care docs

Question 50

Q

What is this?

Answer

A

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

Question 51

Q

How does melanoma progress?

Answer

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

Question 52

Q

How are nevi and melanoma distinct histologically?

Answer

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

Question 53

Q

What growth phase is this melanoma in?

Answer

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

Question 54

Q

What growth phase is this melanoma in?

Answer

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

Question 55

Q

What is the etiology of melanoma?

Answer

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

Question 56

Q

What are the risk factors for melanoma?

Answer

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

Question 57

Q

What are the ABC’s of melanoma screening?

Answer

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

Question 58

Q

What is this? How can you tell?

Answer

A

Melanoma
Asymmetric
Notched, irregular Border
Color not uniform
Diameter >6mm
Elevated

Question 59

Q

What is this?

Answer

A

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

Question 60

Q

What is this? Why?

Answer

A

Melanoma: notched border, asymmetrical, slight elevation

Question 61

Q

What do you see here?

Answer

A

Melanoma: asymmetrical, irregular border
Diameter >6mm and elevated

Question 62

Q

What are the 5 subtypes of melanoma?

Answer

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

Question 63

Q

What is this? How is this lesion defined?

Answer

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)

Question 64

Q

What is this?

Answer

A

Acral lentiginous melanoma

Answer 63

A

Acral lentiginous melanomas

Answer 64

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

Answer 65

A

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

Answer 66

A

Nodular melanoma associated with a lentigo maligna

Answer 67

A

Nodular melanoma

Answer 68

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

Answer 69

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

Answer 70

A

Superficial spreading melanoma

Answer 71

A

Seborrheic keratosis: note the indulating, cerebriform shape

Answer 72

A

Left: seborrheic keratosis
Right: melanoma

Answer 73

A

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

Answer 74

A

Seborrheic keratosis: much more likely because it just fell off when going to biopsy it

Answer 75

A

Seborrheic keratosis

Answer 76

A

Left: melanoma in situ
Right: seborrheic keratosis

Answer 77

A

Melanoma in situ

Answer 78

A

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

Answer 79

A

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

Answer 80

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

Answer 81

A

Acral lentiginous melanoma

Answer 82

A

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

Answer 83

A

Mucosal melanoma: vulvar

Answer 84

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

Answer 85

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)

Answer 86

A

Metastatic melanoma

Answer 87

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

Answer 88

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

Answer 89

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

Answer 90

A

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

Answer 91

A

Remember: all melanoma is NOT caused by sun exposure

Answer 92

A

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

Answer 93

A

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

Answer 94

A

BCC
Telangiectasia is a helpful clue
Red in the middle (ulcer)
Pearly color

Answer 95

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

Answer 96

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

Answer 97

A

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

Answer 98

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

Answer 99

A

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

Answer 100

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

Answer 101

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

Answer 102

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)

Answer 103

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

Answer 104

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

Answer 105

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

Answer 106

A

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

Answer 107

A

Superficial BCC with prominent telangiectasias (superficial, dilated vessels)

Answer 108

A

Nodular BCC

Answer 109

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

Answer 110

A

Superficial BCC: note how subtle these can be

Answer 111

A

BCC, pigmented
Still has translucent qualities
Can sometimes be confused for melanoma

Answer 112

A

Pigmented BCC

Answer 113

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.

Answer 114

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

Answer 115

A

Exceedingly rare: 0.0028% to 0.55% of cases

Answer 116

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

Answer 117

A

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

Answer 118

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)

Answer 119

A

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

Answer 120

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

Answer 121

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

Answer 122

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Normal skin histo

Answer 123

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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

Answer 124

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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

Answer 125

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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

Answer 126

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Photodistributed lesions of AK -> pre-skin cancers

Answer 127

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AK with crust to it -> warning sign

Answer 128

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Actinic keratoses

Answer 129

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

Answer 130

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Actinic keratoses: can become thicker on hands because people rub at them

Answer 131

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

Answer 132

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

Answer 133

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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

Answer 134

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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

Answer 135

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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

Answer 136

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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

Answer 137

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SCC that looks like BCC: sometimes they break the rules

Answer 138

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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)

Answer 139

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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

Answer 140

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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

Answer 141

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SCC: longstanding, ulcerated plaque on the right forehead

Answer 142

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SCC: bc it doesn’t look like BCC

Answer 143

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

Answer 144

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SCC in situ on lower lip

Answer 145

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

Answer 146

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SCC on tongue (could be from leukoplakia)

Answer 147

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Bowen’s Disease: SCC in situ that looks like eczema

Answer 148

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

Answer 149

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Radiation-induced SCC: this case was a dentist

Answer 150

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SCC arising in a plaque of leukoplakia, probably secondary to tobacco use

Answer 151

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

Answer 152

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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

Answer 153

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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

Answer 154

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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