Skin Cancer Flashcards

1
Q

Why do basal cell carcinomas appear blue sometimes?

A

Its dervied from germinative keratinocytes from the basal layer

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2
Q

Where do squamous cell CA derive from?

A

These comes from the spinous layer from epidermal keratinocytes and thus are moer foten pink

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3
Q
A

Basal Cell carcinoma- ulcerated nodule with a pearly border and a lot of telangiectasias

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4
Q
A

PTCH- tumor suppressor gene (mutations common in a basal cell carcinoma)

Classic histology: middle- blue, nodules in the dermis that have clefting and a palisyde of nuclei around edge

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5
Q
A

Location on the ear

SCC tend not to metastasize (but it can; risk factors: immunocompromised, being HPV mediated)

the ears and lips are probably the places most common for squamous cell carcinoma because skin is thin and vascular

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6
Q

What are the nonmelanoma skin cancers?

A

Basal cell and squamous cell carcinomas- very common

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7
Q

What are the main risk factors for BCC?

A
  • UV exposure (chronic but intermittent)
  • Fair complexion
  • H/o sunburns (especially blistering)
  • Family history
  • Immunosuppression (but not as common as SCC)
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8
Q

Basal Cell Carcinomas can be very subtle and start as small papules before growing

A
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9
Q
A
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10
Q

How are basal cell carcinomas described?

A

These are basophilic hyperchromatic cells that form nodules, often extending from the surface epidermis with peripheral cells forming a “picket-fence” palisade and showing retraction/clefting from the dermis

Note that there are different patterns (this describes nodular)

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11
Q

Subtypes of Basal Cell CA?

A

Nodular, Superficial, Pigmented, Cystic, Infiltrative, etc.

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12
Q

Look a likely different than nodular BCC because they just sit on the skin but still see telangiectasias

A
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13
Q

Pigmented BCC (pigment made by melanocytes but this is not a tumor of melanocytes)- more common in people with darker skin

A
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14
Q

T or F. BCC are more common in older patients

A

T. Only about 20% of BCC present before the age 50, and it rarely before 25. Note that the presence of one makes it more likely that youll have more

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15
Q

What is Basal Cell Nevus Syndrome (Gorlin Syndrome)?

A

AD disease caused by mutation of PTCH1 (tumor suppressor gene) characterized by BBCs in 20s, jaw cysts, MSK defects, and puts one at an icnreased risk of medulloblastoma or fibrosarcoma

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16
Q

How does PTCH work?

A

part of SHH pathway that prevents SHH binding from SMO (which upregulates basal cell proliferation)

Drug: Vismodegib is aggressive BCC (causes many GI problems so not used lightly)

17
Q

Is metastasis in BCC common?

A

No, 0.5% BUT can be very locally aggressive and destructive (need to be removed)

18
Q

What is Vismodegib approved for?

A
  • Metastatic BCC
  • recurrent disease
  • Gorlin Syndrome patients
19
Q

Step Note

A

BCC are more common on the upper face and

SCC are more common on the lower face and especially the lips (may or may not be true)- due to chronic sun exposure

20
Q

What is this?

A

SSC- more variable in its presentation that BCC but consistently makes more keratin and it derived from the upper layers of the epidermis and the extra-production of keraitn tends to make them more commonly crusted at the top

21
Q

How do SCCs develop?

A

Sunlight is very important in the initation- UV light causes DNA dimerization and sometimes they cannot be contained and give rise to abnormal clones (commonly with a p53 mutation) and as they proliferate can get new mutations (non-specific)

SCC of the epidermis is called in-situ and when it break through the basemnet membrane is called invasive

22
Q

T or F. Sun induced SCC is not likely to metastasize

A

T. More common METs if on the lips or ears

23
Q

Where do SCCs like to go to?

A

through lymph to lungs

24
Q

How do SCCs progress?

A
  • minimal atypica (Actinic keratosis)
  • Full thickness epidermal atypia confined above the basement membrane (SCC in situ) (aka Bowen’s disease or Erythroplasia of Queyrat- if develops on glans penis (HPV induced))
  • Invasive SCC (well, moderately, or poorly differentiated)
25
Q

Normal skin with basket weave orthokeratosis

A

Can parakeratotis

26
Q

Parakeratosis

Clinically: flat, scaly, and usually multiple on sun exposed areas of the body

A
27
Q

Actinic keratosis

A
28
Q
A
29
Q
A
30
Q

Invasive SCC

A

Invasive SCC (dont be fooled by the telangiectasias)

31
Q

What are some genetic causes of SCCs?

A

no specific SCC oncogene or tumor suppressor has been ID’d but p53 mutations common

32
Q

What are the main risks of developing SCC?

A

Chronic UV exposure

HPV (types 16, 18, 31, and 35)

Immunosuppression

Arsenic exposure

Chronic inflammation (e..g osteomyelitis with draining sinus dract)

Burn scars

Leukoplakia

33
Q

What is a common cause of SCC in women?

A

POST-RADIATION (just in general) but particularly in breast cancer

34
Q

The risk of metastasis in CUTANEOUS SCC is related to what?

A

size of tumor, depth of invasion into dermis, anatomic site, and host immune status:

-larger than 2cm in diameter or deeper than 4mm in depth and higher risk on lips and ears

35
Q

What are some situations with increased risk of METS in a SCC?

A
  • actinic-induced on lip
  • Marjolin’s ulcers (10-30%)
  • Vulvar, penile HPV induced (30%)

Leukoplakia

METS to lymph and lungs

36
Q

SCCs can be locally destructive as well

A
37
Q
A
38
Q
A
39
Q

How are SCC treated?

A

Depends ond degree of progression

Actinic keratosis: topical therapy, cryotherapy

SCC in situ: topical some, excision

Invasive SCC: excision needed